 NCBI

 Skip to main content

 Skip to navigation
 Resources
 How To
 About NCBI Accesskeys

Sign in to NCBI

PMC
US National Library of Medicine
National Institutes of Health
Search database
Search term

 Limits
 Advanced
 Journal list
 Help

 Journal List
 Ther Adv Chronic Dis
 v.4(6); 2013 Nov
 PMC3807765

Ther Adv Chronic Dis. 2013 Nov; 4(6): 287–301.

doi: 10.1177/2040622313503485
PMCID: PMC3807765

Optimal treatment of laryngopharyngeal

reflux disease
Irene Martinucci, Nicola de Bortoli, Edoardo Savarino, Andrea Nacci, Salvatore Osvaldo
Romeo, Massimo Bellini, Vincenzo Savarino, Bruno Fattori, and Santino Marchi
Author information ► Copyright and License information ►
Go to:

Abstract
Laryngopharyngeal reflux is defined as the reflux of gastric content into larynx and pharynx.
A large number of data suggest the growing prevalence of laryngopharyngeal symptoms in
patients with gastroesophageal reflux disease. However, laryngopharyngeal reflux is a
multifactorial syndrome and gastroesophageal reflux disease is not the only cause involved in
its pathogenesis. Current critical issues in diagnosing laryngopharyngeal reflux are many
nonspecific laryngeal symptoms and signs, and poor sensitivity and specificity of all
currently available diagnostic tests. Although it is a pragmatic clinical strategy to start with
empiric trials of proton pump inhibitors, many patients with suspected laryngopharyngeal
reflux have persistent symptoms despite maximal acid suppression therapy. Overall, there are
scant conflicting results to assess the effect of reflux treatments (including dietary and
lifestyle modification, medical treatment, antireflux surgery) on laryngopharyngeal reflux.
The present review is aimed at critically discussing the current treatment options in patients
with laryngopharyngeal reflux, and provides a perspective on the development of new
therapies.

Keywords: gastroesophageal reflux disease, laryngopharyngeal reflux, proton pump

inhibitor, treatment
Go to:

Introduction
Laryngopharyngeal reflux (LPR) is defined as the reflux of gastric content into the larynx and
pharynx [Vakil et al. 2006]. According to the Montreal Consensus Conference, the
manifestations of gastroesophageal reflux disease (GERD) have been classified into either
esophageal or extraesophageal syndromes and, among the latter ones, the existence of an
association between LPR and GERD has been established [Vakil et al. 2006]. LPR may be
manifested as laryngeal symptoms such as cough, sore throat, hoarseness, dysphonia and
globus, as well as signs of laryngeal irritation at laryngoscopy [Vaezi et al. 2003].
Laryngopharyngeal symptoms are increasingly recognized by general physicians, lung
specialists and ear, nose and throat (ENT) surgeons [Richter, 2000]. In particular, there is a
large number of data on the growing prevalence of laryngopharyngeal symptoms in up to
60% of GERD patients [Jaspersen et al. 2003; Koufman et al. 1996; Richter, 2004]. In
addition, some studies support the notion that GERD, as well as smoking and alcohol use, are
risk factors for laryngeal cancer [Freije et al. 1996; Vaezi et al. 2006a]. According to the
Montreal Consensus Conference, some critical issues have been highlighted, as follows:

1. the rarity of extraesophageal syndromes occurring in isolation without a concomitant

manifestation of typical GERD symptoms (i.e. heartburn and regurgitation);
2. extraesophageal syndromes are usually multifactorial with GERD as one of the
several potential aggravating cofactors;
3. data supporting a beneficial effect of reflux treatment on the extraesophageal
syndromes are weak [Vakil et al. 2006].

Subsequently, the American Gastroenterological Association guidelines for GERD

recommended against the use of acid-suppression therapy for acute treatment of patients with
potential extraesophageal GERD syndromes (laryngitis, asthma) in the absence of typical
GERD symptoms [Kahrilas et al. 2008].
The specific reflux-related mechanisms leading to laryngopharyngeal symptoms and signs are
currently unknown. Acidity of gastric juice alone may cause tissue damage at the upper
airway level [Wiener et al. 2009], but several studies have demonstrated that this is not the
only etiologic factor involved in the pathogenesis of laryngopharyngeal reflux disease
(LPRD). Indeed, recently, Pearson and colleagues [Pearson et al. 2011] highlighted that,
although acid can be controlled by proton pump inhibitor (PPI) therapy, all of the other
damaging factors (i.e. pepsin, bile salts, bacteria and pancreatic proteolytic enzymes) remain
potentially damaging on PPI therapy and may have their damaging ability enhanced.
Particularly, pepsin can damage all extragastric tissues at pH up to 6 [Ludemann et al. 1998].
Of note, detectable levels of pepsin have been shown by Johnston and colleagues to remain in
laryngeal epithelia after a reflux event [Johnston et al. 2007a]. The same authors described
that pepsin is taken up by laryngeal epithelial cells by receptor-mediated endocytosis
[Johnston et al. 2007b], thus it may represent a novel mechanism, besides its proteolytic
activity alone, by which pepsin could cause GERD-related cell damage independently of the
pH of the refluxate [Pearson et al. 2011].

To date, the diagnosis of LPR is a very difficult task and several controversies remain
regarding how to confirm LPRD. Laryngoscopic findings, especially edema and erythema,
are often used to diagnose LPR by ENT surgeons [Vaezi et al. 2003]. However, it should be
pointed out that, in a well-performed prospective study, laryngoscopy revealed one or more
signs of laryngeal irritation in over 80% of healthy controls [Milstein et al. 2005]. Moreover,
it has been demonstrated that accurate clinical assessment of LPR is likely to be difficult
because laryngeal physical findings cannot be reliably determined from clinician to clinician,
and such variability makes the precise laryngoscopic diagnosis of LPR highly subjective
[Branski et al. 2002]. The sensitivity and specificity of ambulatory pH monitoring as a means
for diagnosing GERD in patients with extraesophageal reflux symptoms have been
challenged [Vakil et al. 2006]. Furthermore, the sensitivity of 24-h dual-probe (simultaneous
esophageal and pharyngeal) monitoring has ranged from 50% to 80% [Koufman, 1991].
Recently, the availability of multichannel intraluminal impedance and pH monitoring (MII-
pH) seems to show better performances in diagnosing extraesophageal manifestations of
GERD thanks to its ability to evaluate acid and nonacid refluxes other than their proximal
extension [Carroll et al. 2012; Savarino et al. 2009; Sifrim et al. 2005; Tutuian et al. 2006].
However, the poor sensitivity and specificity of all currently available diagnostic tests for
LPR has been highlighted by several review articles [Altman et al. 2011; Katz et al. 2013;
Vaezi et al. 2003]. In a population of patients with laryngoscopic findings of LPR, our group
showed that MII-pH confirmed GERD diagnosis in less than 40% of patients [de Bortoli et
al. 2012], thus highlighting the critical issue of nonspecific symptoms and laryngoscopic
findings of LPR [Zerbib and Stoll, 2010]. New promising diagnostic techniques have been
developed for extraesophageal reflux syndromes, in particular, an immunologic pepsin assay
(PeptestTM), which has been shown to be a rapid, sensitive, and specific tool [Bardhan et al.
2012; Samuels and Johnston, 2010], and a new pH pharyngeal catheter (manufactured by
Restech, San Diego, CA, USA) that recent study documented as highly sensitive and
minimally invasive device for the detection of liquid or vapors of acid reflux in the posterior
oropharynx [Sun et al. 2009]. However, limited data on their diagnostic accuracy and
potential clinical application are available.

In this review, we will discuss the current treatment options in patients with LPRD and their
pro/cons, and we will provide a perspective on the development of new therapies.

Go to:
Lifestyle modifications
Diet and lifestyle modifications are effective interventions for GERD, despite the fact that
few robust data have been published (Table 1) [De Groot et al. 2009; Kaltenbach et al. 2006].
According to treatment used in a UK district general hospital, dietary and behavior
modification has also been supposed to be very effective in the management of LPR [Pearson
et al. 2011].

Table 1.
The positive effects of lifestyle modifications compared with those of uncertain efficacy in
the treatment of laryngopharyngeal reflux disease (LPRD).

Obesity

The incidence of obesity in Western countries has increased dramatically [Nicholls, 2013],
and this has occurred in concordance with an increase in the number of patients suffering
from GERD [El-Serag and Sonnenberg, 1998]. Multiple epidemiological studies clearly
demonstrate an association between obesity and GERD and physiologic investigations
support a biologically plausible relationship between obesity and GERD.

In particular, different studies have shown an association between higher body mass index
(BMI) and GERD [Fass et al. 2005; Nasseri-Moghaddam et al. 2008; Ruigomez et al. 2004;
Savarino et al. 2011] and both obesity (BMI >30 kg/m2) and being overweight (BMI 25–30
kg/m2) are associated with GERD [Dore et al. 2008; Nocon et al. 2007].

The effect of BMI on GERD occurrence seems to be independent of total caloric intake,
dietary intake of fiber, fruits and vegetables, or other macro or micronutrients [El-Serag,
2008]. Obesity is supposed to modify esophagogastric joint (EGJ) morphology and function.
Indeed, obesity generates a mechanical disruption of EGJ by promoting an axial separation
between the lower esophageal sphincter (LES) and the extrinsic crural diaphragm [Pandolfino
et al. 2006]. LES incompetence has also been observed in obese patients [Fisher et al. 1999;
Suter et al. 2004] and among morbidly obese patients a higher esophageal acid exposure was
significantly associated with a lower LES pressure [Sabate et al. 2008].

Observational studies of overweight and obese patients found that weight loss resulted in
improvement in GERD symptoms [Anderson and Jhaveri, 2010; Fraser-Moodie et al. 1999].
Moreover, reflux symptoms have been shown to be exacerbated or improved over time
concomitant with weight gain or loss, respectively [Jacobson et al. 2006]. The HUNT study
showed that, among individuals with GERD-related symptoms, a reduction higher than 3.5
units in BMI is related to a reduction or cessation in weekly antireflux medication use [Ness-
Jensen et al. 2013]. On the other hand, whether weight reduction may improve the subjective
or objective manifestations of reflux is still controversial [Kjellin et al. 1996]. Moreover, few
data are available to determine whether weight loss is able to improve GERD-related
symptoms such as LPR.

Eating habits

Although few data are available on this matter, in clinical practice different foods are
indicated to influence the occurrence of refluxes and, generally, patients are advised against
taking food late in the evening [Pearson et al. 2011].

High-fat foods and chocolate are empirically indicated as foods able to reduce LES pressure
or to prolong gastric emptying; however, there have been no cessation trials evaluating the
impact on GERD outcomes [Murphy and Castell, 1988; Wright and Castell, 1975]. Heartburn
may be exacerbated by spicy foods attributable to direct irritation of already inflamed lower
esophageal mucosa. In particular, Nebel and colleagues [Nebel et al. 1976] described that
88% of patients reported spicy foods as the cause of their heartburn. Orange juice has been
implicated in GERD symptoms even if orange juice infusion did not change LES pressure
[Cranley et al. 1986].

In a cross-sectional study in patients followed at Veterans Administration healthcare

facilities, high dietary fat intake was associated with an increased risk of GERD and erosive
esophagitis [El-Serag et al. 2005]. However, several other studies reported conflicting data
showing that a high-fat diet had no effect on transient LES relaxation or esophageal acid
exposure [Mangano et al. 2002; Pehl et al. 2001; Penagini, 2000; Penagini et al. 1998].
Although it is unclear whether caloric density contributes to esophageal symptoms and acid
exposure, a recent randomized study including a small group of patients found that
esophageal acid exposure was higher with ingestion of a high-calorie diet (1000 kcal versus
500 kcal), and reflux symptoms were affected by the fat content but not density [Fox et al.
2007].

Carbonated beverages have been associated with promoting GERD symptoms by decreasing
LES pressure and were found to predict GERD symptoms in a multivariate analysis [Fass et
al. 2005].

Coffee has been reported to precipitate reflux episodes [Brazer et al. 1995]. A Norwegian
case–control study reported a negative association between GERD and coffee (odds ratio
[OR] 0.5; 95% confidence interval [CI] 0.4–0.6) among subjects who drank 4–7 cups per day
compared with those who did not drink coffee [Nilsson et al. 2004]. In the same study,
consumption of dietary fibers was found to be a protective factor [Nilsson et al. 2004]. In a
large cross-sectional population-based study, consuming bread and fibers at least two meals
per day caused a 50% reduction in reflux symptoms [Terry et al. 2001]. Likewise, in another
cross-sectional study, high fiber intake correlated with a reduced risk of GERD symptoms
[El-Serag et al. 2005]. The mechanism through which fiber is associated with a decreased
risk is unknown, however increased gastric empting could be a reasonable hypothesis.

Voluptuary habits: tobacco and alcohol consumption

Few data are available for voluptuary habits such as cigarettes smoking and alcohol
consumption. Smokers have an increased incidence of reflux symptoms compared with
nonsmokers [Talley et al. 1994; Watanabe et al. 2003]. Nilsson and colleagues [Nilsson et al.
2004] revealed, in a multivariate analysis, that among individuals who had smoked daily for
more than 20 years, the risk of reflux was significantly increased by 70%, compared with
those who had smoked daily for less than a year (OR 1.7; 95% CI 1.5–1.9). A relation has
been considered between smoking cigarettes and a prolonged acid exposure, a decrease in
LES pressure, and diminished salivation, which decreases the rate of esophageal acid
clearance [Kahrilas and Gupta, 1989]. However, pH-metry failed to report an increased
esophageal acid exposure time in smokers compared with nonsmokers despite the former
experiencing increased reflux episodes [Pehl et al. 1997]. Overall, there are inconclusive data
regarding the effect of cessation of cigarette smoking on GERD outcome.

Alcoholic beverages are considered able to precipitate heartburn perception [Pehl et al.
1993]. Even if few data are available, there are no differences in increasing risk between
large amounts of high-alcohol beverages such as whiskey and vodka [Kaufman and Kaye,
1978; Vitale et al. 1987], and even moderate amounts of beer or red and white wine [Pehl et
al. 1993]. However, when compared with red wine, white wine caused more esophageal acid
exposure and a greater decrease in LES pressure [Pehl et al. 1998]. Similar effects were
demonstrated after ingestion of white wine and beer in patients with endoscopic evidence of
reflux esophagitis and abnormal pH study [Pehl et al. 2006].

Sleep position

There are different indications that body position during the sleeping period is related to
reflux of gastric content in the esophagus. The sleep period alters basic physiologic
mechanisms that physiologically protect against GERD. The mechanisms that are depressed
during sleep include the warning signal of heartburn, the frequency of swallowing, and the
suppression of salivary secretion [Freidin et al. 1989]. Several investigations have shown that
esophageal acid clearance is significantly prolonged during sleep compared with the waking
state; this is true even when sleeping subjects are compared with awake subjects in the supine
position [Orr et al. 1981].

Head-of-the-bed elevation can be achieved by putting either 6–8 inch blocks under the bed
legs at the head of the bed or a foam wedge under the mattress. Randomized trials have
shown that this practice can decrease esophageal acid exposure and lead to shorter reflux
periods and a rapid esophageal clearance [Hamilton et al. 1988]. Elevating the head of the
bed is important for people with nocturnal or laryngeal symptoms. Right lateral recumbent
position has also been shown to cause prolonged reflux time and increased LES relaxations,
thus patients with GERD or LPRD should avoid recumbence in this position [Khoury et al.
1999].

Physical exercise

Physical exercise has been found to be a protective factor against reflux. In particular, in a
large population-based study, a correlation has been documented between the number of
exercise sessions lasting at least 30 min and a decreased risk of GERD symptoms (OR 0.5;
95% CI 0.4–0.7) [Nilsson et al. 2004]. Frequently, scheduled programs of body weight
reduction, which are considered helpful to reduce reflux symptoms, are often associated with
aerobic physical activity [Djarv et al. 2012; Ness-Jensen et al. 2013; Yamamichi et al. 2012].
Indeed, a mechanism of an exercise-strengthened antireflux barrier, probably constituted by
striated muscle, was hypothesized [Nocon et al. 2006]. What is more, Nocon and colleagues
have also reported that subjects with GERD symptoms are physically less active than those
without symptoms [Nocon et al. 2006]. However, esophageal acid exposure increases
significantly in healthy volunteers and GERD patients during intense exercise periods
compared with the nonexercise periods [Pandolfino et al. 2004]. Pandolfino and colleagues
have suggested that the anatomical compromise of the esophagogastric junction, as a
consequence of frequent abdominal straining associated with strenuous exercise, may
predispose to exercise-induced reflux [Pandolfino et al. 2004]. Different studies have
suggested that an agonistic physical activity could play a pathogenetic role in inducing
GERD symptoms (i.e. running, cycling, resistance exercise) [Collings et al. 2003; Pandolfino
et al. 2004; Parmelee-Peters and Moeller, 2004]. It has been suggested that GERD may be
increased in athletes because of a decreased gastrointestinal blood flow, alterations of
hormone secretion, changes in the motor function of the esophagus and the ventricle, and
constrained body position during exercise [Jozkow et al. 2006].

Go to:

Medical therapy
Considering the poor sensitivity and specificity of all currently available diagnostic tests, an
empiric trial of therapy represents the first step to confirm LPRD and to treat it accordingly.
However, there is no accepted protocol for the most effective treatment of patients with
LPRD. Since their introduction in the 1980s, PPIs have demonstrated the most potent
suppression of gastric acid secretion, clearly showing a distinct advantage (either for healing
and symptom relief) over H2 receptor antagonists [Chiba et al. 1997]. Thus, H2 receptor
antagonists have restricted their role mainly for patients who suffer from nocturnal acid
breakthrough despite twice-daily PPI therapy [Xue et al. 2001], or for long-term management
of reflux symptoms on an ‘as-needed’ basis [Scarpignato et al. 2006]. Prokinetic agents,
although scarcely evaluated, are usually considered unhelpful in LPRD [Pearson et al. 2011].
A summary of different pharmacological options to treat LPRD are reported in Table 2.

Table 2.
Summary of different medical therapies in laryngopharyngeal reflux disease (LPRD) with
proven or uncertain efficacy.

Proton pump inhibitors

PPI therapy is considered to be the mainstay of care in patients with GERD; however, its
efficacy for the treatment of LPRD remains doubtful. In clinical practice, consistently with
the assumption that the upper aerodigestive tract is more sensitive to acid refluxes than the
esophagus, it is believed that patients with reflux-related laryngitis require higher doses and a
longer trial of PPIs to achieve an improvement of laryngeal symptoms than those with typical
GERD symptoms [Ford, 2005; Koufman et al. 2002; Park et al. 2005]. On the other hand,
placebo-controlled trials have failed to demonstrate any therapeutic benefit of PPIs [Eherer et
al. 2003; El-Serag et al. 2001; Noordzij et al. 2001; Steward et al. 2004; Wo et al. 2006]. In
2006, a prospective multicenter randomized study, with 145 patients having symptoms and
endoscopic signs of LPR, did not show any benefit in patients treated with esomeprazole 40
mg twice daily for 4 months versus placebo [Vaezi et al. 2006b]. In addition, a Cochrane
systematic review of 302 studies did not find any high-quality trials meeting the inclusion
criteria to assess the effectiveness of antireflux therapy for hoarseness [Hopkins et al. 2006].
A systematic review and a meta-analysis of randomized controlled trials failed to demonstrate
superiority of PPIs over placebo for the treatment of suspected LPR [Karkos and Wilson,
2006; Qadeer et al. 2006].

Conversely, more recent studies have demonstrated effectiveness in treating reflux symptoms
and improving laryngeal inflammation. Reichel and colleagues [Reichel et al. 2008] reported
a randomized, double-blind, placebo-controlled trial with esomeprazole 20 mg twice daily for
3 months in patients with symptoms and endoscopic signs of LPR, which found significant
improvement in both symptoms and laryngeal examination. Likewise, Lam and colleagues
[Lam et al. 2010] performed a prospective, randomized, double-blind, placebo-controlled
study with rabeprazole 20 mg twice daily for 3 months in patients with symptoms and
endoscopic signs of LPR, resulting in a significant improvement of symptoms, but not
laryngeal findings. However, on the basis of a closer examination of these two studies, Vaezi
[Vaezi, 2010] argued that the real significant improvement was for heartburn symptoms and
not for chronic throat symptoms.

Some uncontrolled and observational data recommend the use of twice-daily PPIs for LPRD
[Kamel et al. 1994; Klopocka et al. 2004; Shaw and Searl, 1997; Williams et al. 2004].
Furthermore, some studies have shown that the proportion of patients with improvement in
laryngeal symptoms after PPI therapy is higher in GERD patients than in those without
GERD [Lien et al. 2013; Masaany et al. 2011; Qua et al. 2007]. On the other hand, some
studies assessed that the presence of abnormal acid reflux on pH monitoring did not predict
response to therapy [Vaezi et al. 2006b; Williams et al. 2004].

Overall, considering that most of the therapeutic evidence is based on uncontrolled open-
label studies only and the lack of high-quality evidence supporting treatment efficacy,
assessing the optimal treatment for LPRD is still challenging. Furthermore, the dosage and
duration of PPI therapy in LPRD represent further current matters of debate. To date,
whenever typical GERD symptoms are present in addition to the extraesophageal symptoms
and/or there is objective evidence of GERD by endoscopy or reflux monitoring [Katz et al.
2013], it is a pragmatic clinical strategy to start with an empirical 2-month therapy with
twice-daily PPIs [Kahrilas et al. 2008]. If there is symptom improvement, then tapering to
once-daily PPI followed by reducing the dose or the interval of acid suppression is highly
recommended [Vaezi, 2010]. On the other hand, failing such an empirical PPI trial, etiologies
other than GERD should be explored through concomitant evaluation by ENT, pulmonary,
and allergy specialists [Kahrilas et al. 2008; Katz et al. 2013; Vaezi, 2010; Zerbib et al.
2013].

Refractory patients with objective evidence (reflux monitoring) of ongoing reflux as the
cause of symptoms should be considered for additional antireflux therapies that may include
transient LES relaxation (TLESR) inhibitors or surgery [Katz et al. 2013], which are further
discussed in the present review.

Alginate
Traditional antacids are frequently used as add-on therapy in order to neutralize gastric
acidity and to help control heartburn in GERD patients [Giannini et al. 2006; Savarino et al.
2012; Zentilin et al. 2005]. They are polysaccharides found in algae and convert into a gel
form when they combine with cations. In particular, they form a physical barrier for
gastroduodenal contents, and have the advantage of being a nonsystemic medication.

In a prospective, randomized controlled study, liquid alginate preparations (taken four times
daily) have been shown to be effective in treatment of LPR symptoms and signs [McGlashan
et al. 2009]. Of note, considering that pharyngeal and laryngeal cancer might represent LPR
complications, a statistically significant reduction in squamous cell carcinoma volume was
observed in hamsters that received alginate prior to known carcinogen [7,12-
dimethylbenzanthracene (DMBA)] and human pepsin application, compared with hamsters
painted with DMBA and human pepsin alone. Thus, alginate suspension provided protection
from pepsin-enhanced tumor growth [Pearson et al. 2011].

Alginates should be given after each meal and last thing at night, and nothing should be taken
by mouth after the nocturnal dose [Pearson et al. 2011].

Neuromodulators

PPI-refractory patients with persistent reflux (nonacid or weakly acid), assessed with
ambulatory 24-h MII-pH monitoring, could benefit from reflux-reducing agents or visceral
pain modulators [Zerbib et al. 2013]. Reflux-reducing agents, including GABAB agonists and
metatropic glutamate receptor antagonists, are supposed to reduce the frequency of TLESR,
representing the main pathophysiological mechanism underlying GERD. In particular,
GABAB receptor agonists (i.e. baclofen) have been shown to decrease acid reflux occurrence,
esophageal acid exposure, and improved reflux-related symptoms [Ciccaglione and Marzio,
2003; Cossentino et al. 2012]. However, their use in clinical practice is limited by a poor
tolerability profile. Several researchers have tried to develop more-efficient and better-
tolerated compounds (i.e. lesogaberan, ADX10059, arbaclofen) without attempting such
results [Vakil et al. 2011; Zerbib et al. 2011].

Visceral pain modulators [i.e. tricyclic antidepressants (TCAs) or selective serotonin reuptake
inhibitors (SSRIs)] decrease the perception of reflux episodes increasing the esophageal
perception threshold [Broekaert et al. 2006; Clouse et al. 1987; Peghini et al. 1998], thus may
induce beneficial effects in patients with hypersensitive esophagus, as diagnosed through
reflux monitoring in the case of normal acid exposure time and positive correlation between
symptoms and refluxes [Viazis et al. 2011]. These observations, although preliminary in
nature, encourage the performance of studies aimed at assessing the efficacy of visceral pain
modulators in patients with LPRD refractory to an optimal treatment with PPIs.

Go to:

Surgical therapy
Laparoscopic antireflux surgery (LARS) is a well-established and highly efficacious
treatment for GERD and has been shown to provide durable relief from the typical reflux
symptoms [Papasavas et al. 2003]. In particular, the surgical therapy is helpful in allowing
the majority of patients suffering from GERD to discontinue acid suppression therapy, to
achieve resolution of associated esophagitis, and to arrest or perhaps even reverse the
metaplasia/dysplasia induced by frequent exposure of the esophageal mucosa to gastric
contents [Oelschlager et al. 2003; Parise et al. 2011; Rossi et al. 2006].

Few controversial data are available about surgical outcome of LPRD. A clinical prospective
study in patients with LPRD selected for surgical treatment, in which the symptoms and signs
had responded to antireflux medication, the laparoscopic fundoplication was found to be an
effective and safe treatment of LPRD [Sala et al. 2008]. Moreover, in patients with objective
evidence of GERD, LARS was effective in relieving LPR symptoms [Catania et al. 2007;
Lindstrom et al. 2002]. On the other hand, LARS has shown disappointing results in
controlling LPR-related symptoms in patients unresponsive to aggressive PPI therapy
[Swoger et al. 2006]. Likewise, prior studies demonstrated a poor surgical outcome for the
resolution of laryngeal symptoms especially in PPI nonresponders [Chen and Thomas, 2000;
So et al. 1998].

It is necessary for the surgeon to perform a detailed workup including

esophagogastroduodenoscopy, esophageal manometry, gastric emptying test, MII-pH or pH-
metry, and upper gastrointestinal radiography for all patients scheduled for LARS, primarily
to exclude malignancy and motility problems such as achalasia and gastroparesis and then to
detect a cause–effect relation between pathological acid exposure time and laryngeal
symptoms/findings [Zerbib et al. 2013].

The patients who are selected for LARS must be informed that laparoscopic fundoplication
may correct the underlying mechanical defect but they should be warned that the response of
their laryngeal symptoms to surgery would still be uncertain [Chen and Thomas, 2000]. The
LARS approach could be more strongly suggested if patients showed a complete relief of
laryngeal symptoms during PPI therapy or if 24-h pathophysiological studies demonstrated
that nonacid reflux events are predominant. Moreover, the surgeon must carefully select
patients before suggesting LARS and a Regional Referral Center specialized in esophageal
surgery is recommended to reduce postoperative complications. In this matter, patients
should be warned of possible postoperative dysphagia, bloating, flatulence, diarrhea, and
recurrence of the symptoms [Richter, 2013].

To date, the clinical guidelines of the Society of American Gastrointestinal and Endoscopic
Surgeons (SAGES) recommend antireflux surgery for patients who: (1) have failed or are
unable to tolerate medications; (2) have significant extraesophageal manifestation such as
aspiration, asthma, or cough; (3) have the complication of GERD-like peptic stricture.

Go to:

Speech therapy and rehabilitation techniques

Actually, newer treatment options are considered as alternative possibilities in the treatment
of GERD, and in particular LPRD, deserving careful investigations.

The LES, surrounded by diaphragmatic muscle, prevents gastroesophageal reflux and,

indirectly, LPR. It is believed that synergy of the function of the LES and its surrounding
crura of the diaphragm, when superimposed, are of importance for competent closure [Mittal
and Balaban, 1997]. When these structures became incompetent, gastric contents may be
traced back along the esophagus and cause LPR. The importance of the diaphragm muscle is
also demonstrated by experimental studies: even after surgical removal of LES, a pressure
zone is detectable due to contractions of the crura of the diaphragm [Klein et al. 1993]. Like
any other striated muscle of the body, the diaphragm muscle should be amenable to improved
performance by physical exercise. For these reasons, alternative therapies for the treatment of
reflux disease have recently been studied, and in particular speech therapy/relaxation
techniques such as training of the diaphragm muscle with maneuvers and breathing exercises
have been considered.

In the literature, there are few scientific publications regarding the rehabilitation treatment of
reflux and in some centers such therapy is proposed in an empirical way without medical
evidence-based support. In addition, the proposed rehabilitation treatments have been studied
in relation to the symptoms and not in relation to the demonstration of a real reduction of acid
reflux events.

One of the most characteristic symptoms of the LPRD is globus pharyngeus [Chevalier et al.
2003; Park et al. 2006; Tokashiki et al. 2002]. Given the benign nature of the condition and
the recent notion that GERD is a major cause of globus, empirical therapy with high-dose
PPIs has been tried [Lee and Kim, 2012]. In patients nonresponsive to this therapy, when
GERD was demonstrated by tests such as endoscopy, MII-pH monitoring, and manometry,
alternative therapies may be considered, including speech and language techniques. In some
studies, a number of exercises to relieve pharyngolaryngeal tension, voice exercises, and
vocal tract voice hygiene to relieve discomfort and tension have provided significant results
in reducing persistent globus symptoms [Khalil et al. 2003]. However, further research is
needed to determine whether speech and language rehabilitation techniques have a specific
effect or whether patients with globus pharyngeus simply benefit from general attention and
reassurance [Millichap et al. 2005].

More recently laryngeal rehabilitation therapies have been applied in cases of chronic cough
associated with GERD, with significant symptom improvement [Pacheco et al. 2013].
Carvalho de Miranda Chaves and colleagues [Carvalho de Miranda Chaves et al. 2012]
showed, by performing esophageal manometry, that inspiratory muscle training incremented
LES pressure in patients with GERD after an 8-week program. Eherer and colleagues [Eherer
et al. 2012], in a randomized controlled study, showed that actively training the diaphragm
muscle by breathing exercise, can improve reflux disease. Quality-of-life scales, pH-metry,
and on-demand PPI usage were assessed to monitor patients in the short- and long-term
follow up [Eherer et al. 2012].

All of these studies confirm that the rehabilitation therapy that acts on the crural diaphragm is
a potential alternative method to treat GERD and LPRD, reducing long periods of drug
treatment or surgical procedures. These findings need to be confirmed in further studies with
a larger sample, longer follow up and controlled with quality of life scores and instrumental
examinations such as MII-pH.

Go to:

Discussion
The effects of the symptoms of both GERD and LPRD are believed to be secondary to the
irritative effects of gastric refluxate on the sensitive esophageal and pharyngeal mucosa
[Bough et al. 1995]. The optimal treatment of LPRD is neither standardized nor validated
[Hogan and Shaker, 2001]. This is due to the multifactorial nature of the disease, whose
symptoms are nonspecific, and to the difficulty of making an accurate diagnosis of LPRD for
the poor sensitivity and specificity of all currently available diagnostic tests. New techniques
(i.e. Peptest, Restech) may be of great interest to improve the diagnostic accuracy of LPRD,
paving the way towards the development of new targeted therapies. Indeed, pepsin inhibitors
and pepsin receptor antagonists are the new possible frontiers of research [Pearson et al.
2011].

As we discussed in this review, the management of LPRD can be divided into lifestyle
modifications, medical and/or surgical treatment. Behavior changes and lifestyle
modifications are considered the first-line treatment with the lowest possibility of side
effects. Weight loss, smoking cessation, alcohol avoidance, meal habit modifications, and
head elevation during sleep need to be strongly suggested to patients. As to the medical
therapy, currently, the treatment is focused on increasing the pH of the refluxate, thus it is
recommended to start with PPIs twice daily for a period of 8–12 weeks. Refractory patients
with objective evidence (reflux monitoring) of ongoing reflux as the cause of symptoms
should be considered for alternative therapies, such as visceral pain modulators or
laparoscopic antireflux surgery. The surgical approach needs to be tailored for each patient
and very carefully considered. Up and coming results are available with speech therapy but
these results need to be evaluated in future trials. Surgery should be indicated in select
patients, in which high-volume refluxate and incompetence of LES are demonstrated with
esophageal pathophysiological evaluations.

To date, we can conclude that, although many studies are still needed to assess the optimal
therapeutic management in LPRD, a multidisciplinary approach including providers in ENT,
pulmonology, and gastroenterology evaluations is recommended to improve diagnosis and
therapy in patients with LPRD.

Go to:

Footnotes
Funding: This research received no specific grant from any funding agency in the public,
commercial, or not-for-profit sectors.

Conflict of interest statement: The authors declare no conflicts of interest in preparing this
article.

Go to:

Contributor Information
Irene Martinucci, Gastroenterology Unit, University of Pisa, Pisa, Italy.

Nicola de Bortoli, Gastroenterology Unit, University of Pisa, and Cisanello Hospital, Via
Paradisa 2 – 56124 Pisa (PI), Italy.
Edoardo Savarino, Division of Gastroenterology, University of Padua, Padua, Italy.

Andrea Nacci, Ear, Nose and Throat Audiology Phoniatrics Unit, University of Pisa, Pisa,
Italy.

Salvatore Osvaldo Romeo, Ear, Nose and Throat Audiology Phoniatrics Unit, University of
Pisa, Pisa, Italy.

Massimo Bellini, Gastroenterology Unit, University of Pisa, Pisa, Italy.

Vincenzo Savarino, Division of Gastroenterology, Department of Internal Medicine (DIMI),

University of Genoa, Genoa, Italy.

Bruno Fattori, Ear, Nose and Throat Audiology Phoniatrics Unit, University of Pisa, Pisa,
Italy.

Santino Marchi, Gastroenterology Unit, University of Pisa, Pisa, Italy.

Go to:

References
 Altman K., Prufer N., Vaezi M. (2011) A review of clinical practice guidelines for
reflux disease: toward creating a clinical protocol for the otolaryngologist.
Laryngoscope 121: 717–723 [PubMed]
 Anderson J., Jhaveri M. (2010) Reductions in medications with substantial weight
loss with behavioral intervention. Curr Clin Pharmacol 5: 232–238 [PubMed]
 Bardhan K., Strugala V., Dettmar P. (2012) Reflux revisited: advancing the role of
pepsin. Int J Otolaryngol 2012: 646901. [PMC free article] [PubMed]
 Bough I., Jr, Sataloff R., Castell D., Hills J., Gideon R., Spiegel J. (1995)
Gastroesophageal reflux laryngitis resistant to omeprazole therapy. J Voice 9: 205–
211 [PubMed]
 Branski R., Bhattacharyya N., Shapiro J. (2002) The reliability of the assessment of
endoscopic laryngeal findings associated with laryngopharyngeal reflux disease.
Laryngoscope 112: 1019–1024 [PubMed]
 Brazer S., Onken J., Dalton C., Smith J., Schiffman S. (1995) Effect of different
coffees on esophageal acid contact time and symptoms in coffee-sensitive subjects.
Physiol Behav 57: 563–567 [PubMed]
 Broekaert D., Fischler B., Sifrim D., Janssens J., Tack J. (2006) Influence of
citalopram, a selective serotonin reuptake inhibitor, on oesophageal hypersensitivity:
a double-blind, placebo-controlled study. Aliment Pharmacol Ther 23: 365–370
[PubMed]
 Carroll T., Fedore L., Aldahlawi M. (2012) pH Impedance and high-resolution
manometry in laryngopharyngeal reflux disease high-dose proton pump inhibitor
failures. Laryngoscope 122: 2473–2481 [PubMed]
 Carvalho de Miranda Chaves R., Suesada M., Polisel F., de Sa C., Navarro-Rodriguez
T. (2012) Respiratory physiotherapy can increase lower esophageal sphincter pressure
in GERD patients. Respir Med 106: 1794–1799 [PubMed]
 Catania R., Kavic S., Roth J., Lee T., Meyer T., Fantry G., et al. (2007) Laparoscopic
Nissen fundoplication effectively relieves symptoms in patients with
laryngopharyngeal reflux. J Gastrointest Surg 11: 1579–1587; discussion 1587–1578.
[PubMed]
 Chen R., Thomas R. (2000) Results of laparoscopic fundoplication where atypical
symptoms coexist with oesophageal reflux. Aust N Z J Surg 70: 840–842 [PubMed]
 Chevalier J., Brossard E., Monnier P. (2003) Globus sensation and gastroesophageal
reflux. Eur Arch Otorhinolaryngol 260: 273–276 [PubMed]
 Chiba N., De Gara C., Wilkinson J., Hunt R. (1997) Speed of healing and symptom
relief in grade II to IV gastroesophageal reflux disease: a meta-analysis.
Gastroenterology 112: 1798–1810 [PubMed]
 Ciccaglione A., Marzio L. (2003) Effect of acute and chronic administration of the
GABA B agonist baclofen on 24 hour pH metry and symptoms in control subjects and
in patients with gastro-oesophageal reflux disease. Gut 52: 464–470 [PMC free
article] [PubMed]
 Clouse R., Lustman P., Eckert T., Ferney D., Griffith L. (1987) Low-dose trazodone
for symptomatic patients with esophageal contraction abnormalities. A double-blind,
placebo-controlled trial. Gastroenterology 92: 1027–1036 [PubMed]
 Collings K., Pierce Pratt F., Rodriguez-Stanley S., Bemben M., Miner P. (2003)
Esophageal reflux in conditioned runners, cyclists, and weightlifters. Med Sci Sports
Exerc 35: 730–735 [PubMed]
 Cossentino M., Mann K., Armbruster S., Lake J., Maydonovitch C., Wong R. (2012)
Randomised clinical trial: the effect of baclofen in patients with gastro-oesophageal
reflux - a randomised prospective study. Aliment Pharmacol Ther, in press. [PubMed]
 Cranley J., Achkar E., Fleshler B. (1986) Abnormal lower esophageal sphincter
pressure responses in patients with orange juice-induced heartburn. Am J
Gastroenterol 81: 104–106 [PubMed]
 de Bortoli N., Nacci A., Savarino E., Martinucci I., Bellini M., Fattori B., et al. (2012)
How many cases of laryngopharyngeal reflux suspected by laryngoscopy are
gastroesophageal reflux disease-related? World J Gastroenterol 18: 4363–4370 [PMC
free article] [PubMed]
 De Groot N., Burgerhart J., Van De Meeberg P., de Vries D., Smout A., Siersema P.
(2009) Systematic review: the effects of conservative and surgical treatment for
obesity on gastro-oesophageal reflux disease. Aliment Pharmacol Ther 30: 1091–1102
[PubMed]
 Djarv T., Wikman A., Nordenstedt H., Johar A., Lagergren J., Lagergren P. (2012)
Physical activity, obesity and gastroesophageal reflux disease in the general
population. World J Gastroenterol 18: 3710–3714 [PMC free article] [PubMed]
 Dore M., Maragkoudakis E., Fraley K., Pedroni A., Tadeu V., Realdi G., et al. (2008)
Diet, lifestyle and gender in gastro-esophageal reflux disease. Dig Dis Sci 53: 2027–
2032 [PubMed]
 Eherer A., Habermann W., Hammer H., Kiesler K., Friedrich G., Krejs G. (2003)
Effect of pantoprazole on the course of reflux-associated laryngitis: a placebo-
controlled double-blind crossover study. Scand J Gastroenterol 38: 462–467
[PubMed]
 Eherer A., Netolitzky F., Hogenauer C., Puschnig G., Hinterleitner T., Scheidl S., et
al. (2012) Positive effect of abdominal breathing exercise on gastroesophageal reflux
disease: a randomized, controlled study. Am J Gastroenterol 107: 372–378 [PubMed]
 El-Serag H. (2008) Role of obesity in GORD-related disorders. Gut 57: 281–284
[PubMed]
 El-Serag H., Lee P., Buchner A., Inadomi J., Gavin M., McCarthy D. (2001)
Lansoprazole treatment of patients with chronic idiopathic laryngitis: a placebo-
controlled trial. Am J Gastroenterol 96: 979–983 [PubMed]
 El-Serag H., Satia J., Rabeneck L. (2005) Dietary intake and the risk of gastro-
oesophageal reflux disease: a cross sectional study in volunteers. Gut 54: 11–17
[PMC free article] [PubMed]
 El-Serag H., Sonnenberg A. (1998) Opposing time trends of peptic ulcer and reflux
disease. Gut 43: 327–333 [PMC free article] [PubMed]
 Fass R., Quan S., O’Connor G., Ervin A., Iber C. (2005) Predictors of heartburn
during sleep in a large prospective cohort study. Chest 127: 1658–1666 [PubMed]
 Fisher B., Pennathur A., Mutnick J., Little A. (1999) Obesity correlates with
gastroesophageal reflux. Dig Dis Sci 44: 2290–2294 [PubMed]
 Ford C. (2005) Evaluation and management of laryngopharyngeal reflux. JAMA 294:
1534–1540 [PubMed]
 Fox M., Barr C., Nolan S., Lomer M., Anggiansah A., Wong T. (2007) The effects of
dietary fat and calorie density on esophageal acid exposure and reflux symptoms. Clin
Gastroenterol Hepatol 5: 439–444 [PubMed]
 Fraser-Moodie C., Norton B., Gornall C., Magnago S., Weale A., Holmes G. (1999)
Weight loss has an independent beneficial effect on symptoms of gastro-oesophageal
reflux in patients who are overweight. Scand J Gastroenterol 34: 337–340 [PubMed]
 Freidin N., Mittal R., Traube M., McCallum R. (1989) Segmental high amplitude
peristaltic contractions in the distal esophagus. Am J Gastroenterol 84: 619–623
[PubMed]
 Freije J., Beatty T., Campbell B., Woodson B., Schultz C., Toohill R. (1996)
Carcinoma of the larynx in patients with gastroesophageal reflux. Am J Otolaryngol
17: 386–390 [PubMed]
 Giannini E., Zentilin P., Dulbecco P., Iiritano E., Bilardi C., Savarino E., et al. (2006)
A comparison between sodium alginate and magaldrate anhydrous in the treatment of
patients with gastroesophageal reflux symptoms. Dig Dis Sci 51: 1904–1909
[PubMed]
 Hamilton J., Boisen R., Yamamoto D., Wagner J., Reichelderfer M. (1988) Sleeping
on a wedge diminishes exposure of the esophagus to refluxed acid. Dig Dis Sci 33:
518–522 [PubMed]
 Hogan W., Shaker R. (2001) Medical treatment of supraesophageal complications of
gastroesophageal reflux disease. Am J Med 111(Suppl. 8A): 197S–201S [PubMed]
 Hopkins C., Yousaf U., Pedersen M. (2006) Acid reflux treatment for hoarseness.
Cochrane Database Syst Rev 1: CD005054. [PubMed]
 Jacobson B., Somers S., Fuchs C., Kelly C., Camargo C., Jr (2006) Body-mass index
and symptoms of gastroesophageal reflux in women. N Engl J Med 354: 2340–2348
[PMC free article] [PubMed]
 Jaspersen D., Kulig M., Labenz J., Leodolter A., Lind T., Meyer-Sabellek W., et al.
(2003) Prevalence of extra-oesophageal manifestations in gastro-oesophageal reflux
disease: an analysis based on the ProGERD Study. Aliment Pharmacol Ther 17:
1515–1520 [PubMed]
 Johnston N., Dettmar P., Bishwokarma B., Lively M., Koufman J. (2007a)
Activity/stability of human pepsin: implications for reflux attributed laryngeal
disease. Laryngoscope 117: 1036–1039 [PubMed]
 Johnston N., Wells C., Blumin J., Toohill R., Merati A. (2007b) Receptor-mediated
uptake of pepsin by laryngeal epithelial cells. Ann Otol Rhinol Laryngol 116: 934–
938 [PubMed]
 Jozkow P., Wasko-Czopnik D., Medras M., Paradowski L. (2006) Gastroesophageal
reflux disease and physical activity. Sports Med 36: 385–391 [PubMed]
 Kahrilas P., Gupta R. (1989) The effect of cigarette smoking on salivation and
esophageal acid clearance. J Lab Clin Med 114: 431–438 [PubMed]
 Kahrilas P., Shaheen N., Vaezi M., Hiltz S., Black E., Modlin I., et al. (2008)
American Gastroenterological Association Medical Position Statement on the
management of gastroesophageal reflux disease. Gastroenterology 135(4): 1383–
1391, 1391 e1381–e1385 [PubMed]
 Kaltenbach T., Crockett S., Gerson L. (2006) Are lifestyle measures effective in
patients with gastroesophageal reflux disease? An evidence-based approach. Arch
Intern Med 166: 965–971 [PubMed]
 Kamel P., Hanson D., Kahrilas P. (1994) Omeprazole for the treatment of posterior
laryngitis. Am J Med 96: 321–326 [PubMed]
 Karkos P., Wilson J. (2006) Empiric treatment of laryngopharyngeal reflux with
proton pump inhibitors: a systematic review. Laryngoscope 116: 144–148 [PubMed]
 Katz P., Gerson L., Vela M. (2013) Guidelines for the diagnosis and management of
gastroesophageal reflux disease. Am J Gastroenterol 108: 308–328; quiz 329.
[PubMed]
 Kaufman S., Kaye M. (1978) Induction of gastro-oesophageal reflux by alcohol. Gut
19: 336–338 [PMC free article] [PubMed]
 Khalil H., Bridger M., Hilton-Pierce M., Vincent J. (2003) The use of speech therapy
in the treatment of globus pharyngeus patients. A randomised controlled trial. Rev
Laryngol Otol Rhinol (Bord) 124: 187–190 [PubMed]
 Khoury R., Camacho-Lobato L., Katz P., Mohiuddin M., Castell D. (1999) Influence
of spontaneous sleep positions on nighttime recumbent reflux in patients with
gastroesophageal reflux disease. Am J Gastroenterol 94: 2069–2073 [PubMed]
 Kjellin A., Ramel S., Rossner S., Thor K. (1996) Gastroesophageal reflux in obese
patients is not reduced by weight reduction. Scand J Gastroenterol 31: 1047–1051
[PubMed]
 Klein W., Parkman H., Dempsey D., Fisher R. (1993) Sphincterlike thoracoabdominal
high pressure zone after esophagogastrectomy. Gastroenterology 105: 1362–1369
[PubMed]
 Klopocka M., Sinkiewicz A., Budzynski J., Pulkowski G., Swiatkowski M. (2004)
Improvement in clinical course and laryngeal appearance in selected patients with
chronic laryngitis after eight weeks of therapy with rabeprazole. Med Sci Monit 10:
PI115–PI118 [PubMed]
 Koufman J. (1991) The otolaryngologic manifestations of gastroesophageal reflux
disease (GERD): a clinical investigation of 225 patients using ambulatory 24-hour pH
monitoring and an experimental investigation of the role of acid and pepsin in the
development of laryngeal injury. Laryngoscope 101(4 Pt 2 Suppl. 53): 1–78
[PubMed]
 Koufman J., Aviv J., Casiano R., Shaw G. (2002) Laryngopharyngeal reflux: position
statement of the committee on speech, voice, and swallowing disorders of the
American Academy of Otolaryngology-Head and Neck Surgery. Otolaryngol Head
Neck Surg 127: 32–35 [PubMed]
 Koufman J., Sataloff R., Toohill R. (1996) Laryngopharyngeal reflux: consensus
conference report. J Voice 10: 215–216 [PubMed]
 Lam P., Ng M., Cheung T., Wong B., Tan V., Fong D., et al. (2010) Rabeprazole is
effective in treating laryngopharyngeal reflux in a randomized placebo-controlled
trial. Clin Gastroenterol Hepatol 8: 770–776 [PubMed]
 Lee B., Kim G. (2012) Globus pharyngeus: a review of its etiology, diagnosis and
treatment. World J Gastroenterol 18: 2462–2471 [PMC free article] [PubMed]
 Lien H., Wang C., Liang W., Sung F., Hsu J., Yeh H., et al. (2013) Composite pH
predicts esomeprazole response in laryngopharyngeal reflux without typical reflux
syndrome. Laryngoscope, in press. [PubMed]
 Lindstrom D., Wallace J., Loehrl T., Merati A., Toohill R. (2002) Nissen
fundoplication surgery for extraesophageal manifestations of gastroesophageal reflux
(EER). Laryngoscope 112: 1762–1765 [PubMed]
 Ludemann J., Manoukian J., Shaw K., Bernard C., Davis M., al-Jubab A. (1998)
Effects of simulated gastroesophageal reflux on the untraumatized rabbit larynx. J
Otolaryngol 27: 127–131 [PubMed]
 Mangano M., Colombo P., Bianchi P., Penagini R. (2002) Fat and esophageal
sensitivity to acid. Dig Dis Sci 47: 657–660 [PubMed]
 Masaany M., Marina M., Sharifa Ezat W., Sani A. (2011) Empirical treatment with
pantoprazole as a diagnostic tool for symptomatic adult laryngopharyngeal reflux. J
Laryngol Otol 125: 502–508 [PubMed]
 McGlashan J., Johnstone L., Sykes J., Strugala V., Dettmar P. (2009) The value of a
liquid alginate suspension (Gaviscon Advance) in the management of
laryngopharyngeal reflux. Eur Arch Otorhinolaryngol 266: 243–251 [PubMed]
 Millichap F., Lee M., Pring T. (2005) A lump in the throat: Should speech and
language therapists treat globus pharyngeus? Disabil Rehabil 27: 124–130 [PubMed]
 Milstein C., Charbel S., Hicks D., Abelson T., Richter J., Vaezi M. (2005) Prevalence
of laryngeal irritation signs associated with reflux in asymptomatic volunteers: impact
of endoscopic technique (rigid vs. flexible laryngoscope). Laryngoscope 115: 2256–
2261 [PubMed]
 Mittal R., Balaban D. (1997) The esophagogastric junction. N Engl J Med 336: 924–
932 [PubMed]
 Murphy D., Castell D. (1988) Chocolate and heartburn: evidence of increased
esophageal acid exposure after chocolate ingestion. Am J Gastroenterol 83: 633–636
[PubMed]
 Nasseri-Moghaddam S., Mofid A., Ghotbi M., Razjouyan H., Nouraie M., Ramard A.,
et al. (2008) Epidemiological study of gastro-oesophageal reflux disease: reflux in
spouse as a risk factor. Aliment Pharmacol Ther 28: 144–153 [PubMed]
 Nebel O., Fornes M., Castell D. (1976) Symptomatic gastroesophageal reflux:
incidence and precipitating factors. Am J Dig Dis 21: 953–956 [PubMed]
 Ness-Jensen E., Lindam A., Lagergren J., Hveem K. (2013) Weight loss and
reduction in gastroesophageal reflux. A prospective population-based cohort study:
the HUNT study. Am J Gastroenterol 108: 376–382 [PubMed]
 Nicholls S. (2013) Standards and classification: A perspective on the ‘obesity
epidemic’. Soc Sci Med 87: 9–15 [PubMed]
 Nilsson M., Johnsen R., Ye W., Hveem K., Lagergren J. (2004) Lifestyle related risk
factors in the aetiology of gastro-oesophageal reflux. Gut 53: 1730–1735 [PMC free
article] [PubMed]
 Nocon M., Labenz J., Jaspersen D., Meyer-Sabellek W., Stolte M., Lind T., et al.
(2007) Association of body mass index with heartburn, regurgitation and esophagitis:
results of the Progression of Gastroesophageal Reflux Disease study. J Gastroenterol
Hepatol 22: 1728–1731 [PubMed]
 Nocon M., Labenz J., Willich S. (2006) Lifestyle factors and symptoms of gastro-
oesophageal reflux - a population-based study. Aliment Pharmacol Ther 23: 169–174
[PubMed]
 Noordzij J., Khidr A., Evans B., Desper E., Mittal R., Reibel J., et al. (2001)
Evaluation of omeprazole in the treatment of reflux laryngitis: a prospective, placebo-
controlled, randomized, double-blind study. Laryngoscope 111: 2147–2151 [PubMed]
 Oelschlager B., Barreca M., Chang L., Oleynikov D., Pellegrini C. (2003) Clinical
and pathologic response of Barrett’s esophagus to laparoscopic antireflux surgery.
Ann Surg 238: 458–464; discussion 464–456. [PMC free article] [PubMed]
 Orr W., Robinson M., Johnson L. (1981) Acid clearance during sleep in the
pathogenesis of reflux esophagitis. Dig Dis Sci 26: 423–427 [PubMed]
 Pacheco A., Cobeta I., Wagner C. (2013) Refractory chronic cough: new perspectives
in diagnosis and treatment. Arch Bronconeumol 49: 151–157 [PubMed]
 Pandolfino J., Bianchi L., Lee T., Hirano I., Kahrilas P. (2004) Esophagogastric
junction morphology predicts susceptibility to exercise-induced reflux. Am J
Gastroenterol 99: 1430–1436 [PubMed]
 Pandolfino J., El-Serag H., Zhang Q., Shah N., Ghosh S., Kahrilas P. (2006) Obesity:
a challenge to esophagogastric junction integrity. Gastroenterology 130: 639–649
[PubMed]
 Papasavas P., Keenan R., Yeaney W., Caushaj P., Gagne D., Landreneau R. (2003)
Effectiveness of laparoscopic fundoplication in relieving the symptoms of
gastroesophageal reflux disease (GERD) and eliminating antireflux medical therapy.
Surg Endosc 17: 1200–1205 [PubMed]
 Parise P., Rosati R., Savarino E., Locatelli A., Ceolin M., Dua K., et al. (2011)
Barrett’s esophagus: surgical treatments. Ann N Y Acad Sci 1232: 175–195
[PubMed]
 Park K., Choi S., Kwon S., Yoon S., Kim S. (2006) Diagnosis of laryngopharyngeal
reflux among globus patients. Otolaryngol Head Neck Surg 134: 81–85 [PubMed]
 Park W., Hicks D., Khandwala F., Richter J., Abelson T., Milstein C., et al. (2005)
Laryngopharyngeal reflux: prospective cohort study evaluating optimal dose of
proton-pump inhibitor therapy and pretherapy predictors of response. Laryngoscope
115: 1230–1238 [PubMed]
 Parmelee-Peters K., Moeller J. (2004) Gastroesophageal reflux in athletes. Curr
Sports Med Rep 3: 107–111 [PubMed]
 Pearson J., Parikh S., Orlando R., Johnston N., Allen J., Tinling S., et al. (2011)
Review article: reflux and its consequences–the laryngeal, pulmonary and
oesophageal manifestations. Conference held in conjunction with the 9th International
Symposium on Human Pepsin (ISHP) Kingston-upon-Hull, UK, 21–23 April 2010
Aliment Pharmacol Ther 33(Suppl. 1): 1–71 [PubMed]
 Peghini P., Katz P., Castell D. (1998) Imipramine decreases oesophageal pain
perception in human male volunteers. Gut 42: 807–813 [PMC free article] [PubMed]
 Pehl C., Pfeiffer A., Waizenhoefer A., Wendl B., Schepp W. (2001) Effect of caloric
density of a meal on lower oesophageal sphincter motility and gastro-oesophageal
reflux in healthy subjects. Aliment Pharmacol Ther 15: 233–239 [PubMed]
 Pehl C., Pfeiffer A., Wendl B., Kaess H. (1998) Different effects of white and red
wine on lower esophageal sphincter pressure and gastroesophageal reflux. Scand J
Gastroenterol 33: 118–122 [PubMed]
 Pehl C., Pfeiffer A., Wendl B., Nagy I., Kaess H. (1997) Effect of smoking on the
results of esophageal pH measurement in clinical routine. J Clin Gastroenterol 25:
503–506 [PubMed]
 Pehl C., Wendl B., Pfeiffer A. (2006) White wine and beer induce gastro-oesophageal
reflux in patients with reflux disease. Aliment Pharmacol Ther 23: 1581–1586
[PubMed]
 Pehl C., Wendl B., Pfeiffer A., Schmidt T., Kaess H. (1993) Low-proof alcoholic
beverages and gastroesophageal reflux. Dig Dis Sci 38: 93–96 [PubMed]
 Penagini R. (2000) Fat and gastro-oesophageal reflux disease. Eur J Gastroenterol
Hepatol 12: 1343–1345 [PubMed]
 Penagini R., Mangano M., Bianchi P. (1998) Effect of increasing the fat content but
not the energy load of a meal on gastro-oesophageal reflux and lower oesophageal
sphincter motor function. Gut 42: 330–333 [PMC free article] [PubMed]
 Qadeer M., Phillips C., Lopez A., Steward D., Noordzij J., Wo J., et al. (2006) Proton
pump inhibitor therapy for suspected GERD-related chronic laryngitis: a meta-
analysis of randomized controlled trials. Am J Gastroenterol 101: 2646–2654
[PubMed]
 Qua C., Wong C., Gopala K., Goh K. (2007) Gastro-oesophageal reflux disease in
chronic laryngitis: prevalence and response to acid-suppressive therapy. Aliment
Pharmacol Ther 25: 287–295 [PubMed]
 Reichel O., Dressel H., Wiederanders K., Issing W. (2008) Double-blind, placebo-
controlled trial with esomeprazole for symptoms and signs associated with
laryngopharyngeal reflux. Otolaryngol Head Neck Surg 139: 414–420 [PubMed]
 Richter J. (2000) Extraesophageal presentations of gastroesophageal reflux disease: an
overview. Am J Gastroenterol 95(8 Suppl.): S1–S3 [PubMed]
 Richter J. (2004) Ear, nose and throat and respiratory manifestations of gastro-
esophageal reflux disease: an increasing conundrum. Eur J Gastroenterol Hepatol 16:
837–845 [PubMed]
 Richter J. (2013) Gastroesophageal reflux disease treatment: side effects and
complications of fundoplication. Clin Gastroenterol Hepatol 11: 465–471 [PubMed]
 Rossi M., Barreca M., de Bortoli N., Renzi C., Santi S., Gennai A., et al. (2006)
Efficacy of Nissen fundoplication versus medical therapy in the regression of low-
grade dysplasia in patients with Barrett esophagus: a prospective study. Ann Surg
243: 58–63 [PMC free article] [PubMed]
 Ruigomez A., Garcia Rodriguez L., Wallander M., Johansson S., Graffner H., Dent J.
(2004) Natural history of gastro-oesophageal reflux disease diagnosed in general
practice. Aliment Pharmacol Ther 20: 751–760 [PubMed]
 Sabate J., Jouet P., Merrouche M., Pouzoulet J., Maillard D., Harnois F., et al. (2008)
Gastroesophageal reflux in patients with morbid obesity: a role of obstructive sleep
apnea syndrome? Obes Surg 18: 1479–1484 [PubMed]
 Sala E., Salminen P., Simberg S., Koskenvuo J., Ovaska J. (2008) Laryngopharyngeal
reflux disease treated with laparoscopic fundoplication. Dig Dis Sci 53: 2397–2404
[PubMed]
 Samuels T., Johnston N. (2010) Pepsin as a marker of extraesophageal reflux. Ann
Otol Rhinol Laryngol 119: 203–208 [PubMed]
 Savarino E., Bazzica M., Zentilin P., Pohl D., Parodi A., Cittadini G., et al. (2009)
Gastroesophageal reflux and pulmonary fibrosis in scleroderma: a study using pH-
impedance monitoring. Am J Respir Crit Care Med 179: 408–413 [PubMed]
 Savarino E., de Bortoli N., Zentilin P., Martinucci I., Bruzzone L., Furnari M., et al.
(2012) Alginate controls heartburn in patients with erosive and nonerosive reflux
disease. World J Gastroenterol 18: 4371–4378 [PMC free article] [PubMed]
 Savarino E., Zentilin P., Marabotto E., Bonfanti D., Inferrera S., Assandri L., et al.
(2011) Overweight is a risk factor for both erosive and non-erosive reflux disease. Dig
Liver Dis 43: 940–945 [PubMed]
 Scarpignato C., Pelosini I., Di Mario F. (2006) Acid suppression therapy: where do
we go from here? Dig Dis 24: 11–46 [PubMed]
 Shaw G., Searl J. (1997) Laryngeal manifestations of gastroesophageal reflux before
and after treatment with omeprazole. South Med J 90: 1115–1122 [PubMed]
 Sifrim D., Dupont L., Blondeau K., Zhang X., Tack J., Janssens J. (2005) Weakly
acidic reflux in patients with chronic unexplained cough during 24 hour pressure, pH,
and impedance monitoring. Gut 54: 449–454 [PMC free article] [PubMed]
 So J., Zeitels S., Rattner D. (1998) Outcomes of atypical symptoms attributed to
gastroesophageal reflux treated by laparoscopic fundoplication. Surgery 124: 28–32
[PubMed]
 Steward D., Wilson K., Kelly D., Patil M., Schwartzbauer H., Long J., et al. (2004)
Proton pump inhibitor therapy for chronic laryngo-pharyngitis: a randomized placebo-
control trial. Otolaryngol Head Neck Surg 131: 342–350 [PubMed]
 Sun G., Muddana S., Slaughter J., Casey S., Hill E., Farrokhi F., et al. (2009) A new
pH catheter for laryngopharyngeal reflux: Normal values. Laryngoscope 119: 1639–
1643 [PubMed]
 Suter M., Dorta G., Giusti V., Calmes J. (2004) Gastro-esophageal reflux and
esophageal motility disorders in morbidly obese patients. Obes Surg 14: 959–966
[PubMed]
 Swoger J., Ponsky J., Hicks D., Richter J., Abelson T., Milstein C., et al. (2006)
Surgical fundoplication in laryngopharyngeal reflux unresponsive to aggressive acid
suppression: a controlled study. Clin Gastroenterol Hepatol 4: 433–441 [PubMed]
 Talley N., Zinsmeister A., Schleck C., Melton L., III (1994) Smoking, alcohol, and
analgesics in dyspepsia and among dyspepsia subgroups: lack of an association in a
community. Gut 35: 619–624 [PMC free article] [PubMed]
 Terry P., Lagergren J., Ye W., Wolk A., Nyren O. (2001) Inverse association between
intake of cereal fiber and risk of gastric cardia cancer. Gastroenterology 120: 387–391
[PubMed]
 Tokashiki R., Yamaguchi H., Nakamura K., Suzuki M. (2002) Globus sensation
caused by gastroesophageal reflux disease. Auris Nasus Larynx 29: 347–351
[PubMed]
 Tutuian R., Mainie I., Agrawal A., Adams D., Castell D. (2006) Nonacid reflux in
patients with chronic cough on acid-suppressive therapy. Chest 130: 386–391
[PubMed]
 Vaezi M. (2010) Benefit of acid-suppressive therapy in chronic laryngitis: the devil is
in the details. Clin Gastroenterol Hepatol 8: 741–742 [PubMed]
 Vaezi M., Hicks D., Abelson T., Richter J. (2003) Laryngeal signs and symptoms and
gastroesophageal reflux disease (GERD): a critical assessment of cause and effect
association. Clin Gastroenterol Hepatol 1: 333–344 [PubMed]
 Vaezi M., Qadeer M., Lopez R., Colabianchi N. (2006a) Laryngeal cancer and
gastroesophageal reflux disease: a case-control study. Am J Med 119: 768–776
[PubMed]
 Vaezi M., Richter J., Stasney C., Spiegel J., Iannuzzi R., Crawley J., et al. (2006b)
Treatment of chronic posterior laryngitis with esomeprazole. Laryngoscope 116: 254–
260 [PubMed]
 Vakil N., Huff F., Bian A., Jones D., Stamler D. (2011) Arbaclofen placarbil in
GERD: a randomized, double-blind, placebo-controlled study. Am J Gastroenterol
106: 1427–1438 [PubMed]
 Vakil N., van Zanten S., Kahrilas P., Dent J., Jones R. (2006) The Montreal definition
and classification of gastroesophageal reflux disease: a global evidence-based
consensus. Am J Gastroenterol 101: 1900–1920 [PubMed]
  Viazis N., Keyoglou A., Kanellopoulos A., Karamanolis G., Vlachogiannakos J.,
Triantafyllou K., et al. (2011) Selective serotonin reuptake inhibitors for the treatment
of hypersensitive esophagus: a randomized, double-blind, placebo-controlled study.
Am J Gastroenterol, in press. [PubMed]
 Vitale G., Cheadle W., Patel B., Sadek S., Michel M., Cuschieri A. (1987) The effect
of alcohol on nocturnal gastroesophageal reflux. JAMA 258: 2077–2079 [PubMed]
 Watanabe Y., Fujiwara Y., Shiba M., Watanabe T., Tominaga K., Oshitani N., et al.
(2003) Cigarette smoking and alcohol consumption associated with gastro-
oesophageal reflux disease in Japanese men. Scand J Gastroenterol 38: 807–811
[PubMed]
 Wiener G., Tsukashima R., Kelly C., Wolf E., Schmeltzer M., Bankert C., et al.
(2009) Oropharyngeal pH monitoring for the detection of liquid and aerosolized
supraesophageal gastric reflux. J Voice 23: 498–504 [PubMed]
 Williams R., Szczesniak M., Maclean J., Brake H., Cole I., Cook I. (2004) Predictors
of outcome in an open label, therapeutic trial of high-dose omeprazole in laryngitis.
Am J Gastroenterol 99: 777–785 [PubMed]
 Wo J., Koopman J., Harrell S., Parker K., Winstead W., Lentsch E. (2006) Double-
blind, placebo-controlled trial with single-dose pantoprazole for laryngopharyngeal
reflux. Am J Gastroenterol 101: 1972–1978; quiz 2169. [PubMed]
 Wright L., Castell D. (1975) The adverse effect of chocolate on lower esophageal
sphincter pressure. Am J Dig Dis 20: 703–707 [PubMed]
 Xue S., Katz P., Banerjee P., Tutuian R., Castell D. (2001) Bedtime H2 blockers
improve nocturnal gastric acid control in GERD patients on proton pump inhibitors.
Aliment Pharmacol Ther 15: 1351–1356 [PubMed]
 Yamamichi N., Mochizuki S., Asada-Hirayama I., Mikami-Matsuda R., Shimamoto
T., Konno-Shimizu M., et al. (2012) Lifestyle factors affecting gastroesophageal
reflux disease symptoms: a cross-sectional study of healthy 19864 adults using FSSG
scores. BMC Med 10: 45. [PMC free article] [PubMed]
 Zentilin P., Dulbecco P., Savarino E., Parodi A., Iiritano E., Bilardi C., et al. (2005)
An evaluation of the antireflux properties of sodium alginate by means of combined
multichannel intraluminal impedance and pH-metry. Aliment Pharmacol Ther 21: 29–
34 [PubMed]
 Zerbib F., Bruley des Varannes S., Roman S., Tutuian R., Galmiche J., Mion F., et al.
(2011) Randomised clinical trial: effects of monotherapy with ADX10059, a mGluR5
inhibitor, on symptoms and reflux events in patients with gastro-oesophageal reflux
disease. Aliment Pharmacol Ther 33: 911–921 [PubMed]
 Zerbib F., Sifrim D., Tutuian R., Attwood S., Lundell L. (2013) Modern medical and
surgical management of difficult-to-treat GORD. United Eur Gastroenterol J 1: 21–31
 Zerbib F., Stoll D. (2010) Management of laryngopharyngeal reflux: an unmet
medical need. Neurogastroenterol Motil 22: 109–112 [PubMed]

Articles from Therapeutic Advances in Chronic Disease are provided here courtesy of SAGE
Publications

Formats:
  Article

 PubReader

 ePub (beta)

 PDF (1.0M)

 Citation

Share

 Facebook

 Twitter

 Google+

Save items

View more options

Similar articles in PubMed

 Diagnosis of laryngopharyngeal reflux.[Curr Opin Otolaryngol Head Nec...]

 Diagnosis and management of laryngopharyngeal reflux disease.[Curr Opin
Otolaryngol Head Nec...]
 Association of laryngopharyngeal manifestations and gastroesophageal reflux.[Eur
Arch Otorhinolaryngol. 2009]
 Evaluation of patients with suspected laryngopharyngeal reflux: a practical
approach.[Curr Gastroenterol Rep. 2011]
 A systematic review of the role of proton pump inhibitors for symptoms of
laryngopharyngeal reflux.[Clin Otolaryngol. 2006]

See reviews...See all...

Links

 PubMed
Recent Activity

ClearTurn Off

 Optimal treatment of laryngopharyngeal reflux disease

Optimal treatment of laryngopharyngeal reflux disease

Therapeutic Advances in Chronic Disease. 2013 Nov; 4(6)287

 Audiologic disturbances in long-term mobile phone users.

Audiologic disturbances in long-term mobile phone users.

J Otolaryngol Head Neck Surg. 2010 Feb ;39(1):5-11.

PubMed

 [Analysis of Electric Stress in Human Head in High-frequency Low-power

Electroma...

[Analysis of Electric Stress in Human Head in High-frequency Low-power

Electromagnetic Environment].

Sheng Wu Yi Xue Gong Cheng Xue Za Zhi. 2015 Apr ;32(2):295-9.

PubMed

 Effects of radiation phone to hearing (22)

PubMed

 The impact of noise exposure on workers in Mobile Support Units.

The impact of noise exposure on workers in Mobile Support Units.

Codas. 2015 May-Jun;27(3):215-222.

PubMed

See more...

 American Gastroenterological Association Medical Position Statement on the

management of gastroesophageal reflux disease.[Gastroenterology. 2008]

 Oropharyngeal pH monitoring for the detection of liquid and aerosolized

supraesophageal gastric reflux.[J Voice. 2009]
 Review Review article: reflux and its consequences--the laryngeal, pulmonary and
oesophageal manifestations. Conference held in conjunction with the 9th International
 Symposium on Human Pepsin (ISHP) Kingston-upon-Hull, UK, 21-23 April
2010.[Aliment Pharmacol Ther. 2011]
 Effects of simulated gastroesophageal reflux on the untraumatized rabbit larynx.[J
Otolaryngol. 1998]
 Activity/stability of human pepsin: implications for reflux attributed laryngeal
disease.[Laryngoscope. 2007]
 Receptor-mediated uptake of pepsin by laryngeal epithelial cells.[Ann Otol Rhinol
Laryngol. 2007]

 Review Laryngeal signs and symptoms and gastroesophageal reflux disease (GERD):
a critical assessment of cause and effect association.[Clin Gastroenterol Hepatol.
2003]
 Prevalence of laryngeal irritation signs associated with reflux in asymptomatic
volunteers: impact of endoscopic technique (rigid vs. flexible
laryngoscope).[Laryngoscope. 2005]
 The reliability of the assessment of endoscopic laryngeal findings associated with
laryngopharyngeal reflux disease.[Laryngoscope. 2002]
 The Montreal definition and classification of gastroesophageal reflux disease: a global
evidence-based consensus.[Am J Gastroenterol. 2006]
 Review The otolaryngologic manifestations of gastroesophageal reflux disease
(GERD): a clinical investigation of 225 patients using ambulatory 24-hour pH
monitoring and an experimental investigation of the role of acid and pepsin in the
development of laryngeal injury.[Laryngoscope. 1991]
 pH Impedance and high-resolution manometry in laryngopharyngeal reflux disease
high-dose proton pump inhibitor failures.[Laryngoscope. 2012]
 Gastroesophageal reflux and pulmonary fibrosis in scleroderma: a study using pH-
impedance monitoring.[Am J Respir Crit Care Med. 2009]
 Weakly acidic reflux in patients with chronic unexplained cough during 24 hour
pressure, pH, and impedance monitoring.[Gut. 2005]
 Nonacid reflux in patients with chronic cough on acid-suppressive therapy.[Chest.
2006]
 Review A review of clinical practice guidelines for reflux disease: toward creating a
clinical protocol for the otolaryngologist.[Laryngoscope. 2011]
 Guidelines for the diagnosis and management of gastroesophageal reflux disease.[Am
J Gastroenterol. 2013]
 How many cases of laryngopharyngeal reflux suspected by laryngoscopy are
gastroesophageal reflux disease-related?[World J Gastroenterol. 2012]
 Management of laryngopharyngeal reflux: an unmet medical
need.[Neurogastroenterol Motil. 2010]

See more ...

 Review Systematic review: the effects of conservative and surgical treatment for
obesity on gastro-oesophageal reflux disease.[Aliment Pharmacol Ther. 2009]

See more ...

 Standards and classification: a perspective on the 'obesity epidemic'.[Soc Sci Med.

2013]
 Opposing time trends of peptic ulcer and reflux disease.[Gut. 1998]
  Predictors of heartburn during sleep in a large prospective cohort study.[Chest. 2005]

See more ...

 Review Role of obesity in GORD-related disorders.[Gut. 2008]

 Obesity: a challenge to esophagogastric junction integrity.[Gastroenterology. 2006]
 Obesity correlates with gastroesophageal reflux.[Dig Dis Sci. 1999]

See more ...

 Review Reductions in medications with substantial weight loss with behavioral

intervention.[Curr Clin Pharmacol. 2010]
 Weight loss has an independent beneficial effect on symptoms of gastro-oesophageal
reflux in patients who are overweight.[Scand J Gastroenterol. 1999]
 Body-mass index and symptoms of gastroesophageal reflux in women.[N Engl J Med.
2006]
 Weight loss and reduction in gastroesophageal reflux. A prospective population-based
cohort study: the HUNT study.[Am J Gastroenterol. 2013]

See more ...

 Review Review article: reflux and its consequences--the laryngeal, pulmonary and
oesophageal manifestations. Conference held in conjunction with the 9th International
Symposium on Human Pepsin (ISHP) Kingston-upon-Hull, UK, 21-23 April
2010.[Aliment Pharmacol Ther. 2011]

 Chocolate and heartburn: evidence of increased esophageal acid exposure after

chocolate ingestion.[Am J Gastroenterol. 1988]
 The adverse effect of chocolate on lower esophageal sphincter pressure.[Am J Dig
Dis. 1975]
 Symptomatic gastroesophageal reflux: incidence and precipitating factors.[Am J Dig
Dis. 1976]

See more ...

 Dietary intake and the risk of gastro-oesophageal reflux disease: a cross sectional
study in volunteers.[Gut. 2005]
 Fat and esophageal sensitivity to acid.[Dig Dis Sci. 2002]
 Effect of caloric density of a meal on lower oesophageal sphincter motility and
gastro-oesophageal reflux in healthy subjects.[Aliment Pharmacol Ther. 2001]

See more ...

 Predictors of heartburn during sleep in a large prospective cohort study.[Chest. 2005]

 Effect of different coffees on esophageal acid contact time and symptoms in coffee-
sensitive subjects.[Physiol Behav. 1995]
 Lifestyle related risk factors in the aetiology of gastro-oesophageal reflux.[Gut. 2004]
 Inverse association between intake of cereal fiber and risk of gastric cardia
cancer.[Gastroenterology. 2001]
  Dietary intake and the risk of gastro-oesophageal reflux disease: a cross sectional
study in volunteers.[Gut. 2005]

 Smoking, alcohol, and analgesics in dyspepsia and among dyspepsia subgroups: lack
of an association in a community.[Gut. 1994]
 Cigarette smoking and alcohol consumption associated with gastro-oesophageal
reflux disease in Japanese men.[Scand J Gastroenterol. 2003]
 Lifestyle related risk factors in the aetiology of gastro-oesophageal reflux.[Gut. 2004]
 The effect of cigarette smoking on salivation and esophageal acid clearance.[J Lab
Clin Med. 1989]
 Effect of smoking on the results of esophageal pH measurement in clinical routine.[J
Clin Gastroenterol. 1997]

 Low-proof alcoholic beverages and gastroesophageal reflux.[Dig Dis Sci. 1993]

 Induction of gastro-oesophageal reflux by alcohol.[Gut. 1978]
 The effect of alcohol on nocturnal gastroesophageal reflux.[JAMA. 1987]

See more ...

 Segmental high amplitude peristaltic contractions in the distal esophagus.[Am J

Gastroenterol. 1989]
 Acid clearance during sleep in the pathogenesis of reflux esophagitis.[Dig Dis Sci.
1981]

 Sleeping on a wedge diminishes exposure of the esophagus to refluxed acid.[Dig Dis

Sci. 1988]
 Influence of spontaneous sleep positions on nighttime recumbent reflux in patients
with gastroesophageal reflux disease.[Am J Gastroenterol. 1999]

 Lifestyle related risk factors in the aetiology of gastro-oesophageal reflux.[Gut. 2004]

 Physical activity, obesity and gastroesophageal reflux disease in the general
population.[World J Gastroenterol. 2012]
 Weight loss and reduction in gastroesophageal reflux. A prospective population-based
cohort study: the HUNT study.[Am J Gastroenterol. 2013]
 Lifestyle factors affecting gastroesophageal reflux disease symptoms: a cross-
sectional study of healthy 19864 adults using FSSG scores.[BMC Med. 2012]
 Lifestyle factors and symptoms of gastro-oesophageal reflux -- a population-based
study.[Aliment Pharmacol Ther. 2006]
 Esophagogastric junction morphology predicts susceptibility to exercise-induced
reflux.[Am J Gastroenterol. 2004]
 Esophageal reflux in conditioned runners, cyclists, and weightlifters.[Med Sci Sports
Exerc. 2003]
 Review Gastroesophageal reflux in athletes.[Curr Sports Med Rep. 2004]
 Gastroesophageal reflux disease and physical activity.[Sports Med. 2006]

 Speed of healing and symptom relief in grade II to IV gastroesophageal reflux

disease: a meta-analysis.[Gastroenterology. 1997]
 Bedtime H2 blockers improve nocturnal gastric acid control in GERD patients on
proton pump inhibitors.[Aliment Pharmacol Ther. 2001]
 Review Acid suppression therapy: where do we go from here?[Dig Dis. 2006]
  Review Review article: reflux and its consequences--the laryngeal, pulmonary and
oesophageal manifestations. Conference held in conjunction with the 9th International
Symposium on Human Pepsin (ISHP) Kingston-upon-Hull, UK, 21-23 April
2010.[Aliment Pharmacol Ther. 2011]

 Review Evaluation and management of laryngopharyngeal reflux.[JAMA. 2005]

 Review Laryngopharyngeal reflux: position statement of the committee on speech,
voice, and swallowing disorders of the American Academy of Otolaryngology-Head
and Neck Surgery.[Otolaryngol Head Neck Surg. 2002]
 Laryngopharyngeal reflux: prospective cohort study evaluating optimal dose of
proton-pump inhibitor therapy and pretherapy predictors of response.[Laryngoscope.
2005]
 Effect of pantoprazole on the course of reflux-associated laryngitis: a placebo-
controlled double-blind crossover study.[Scand J Gastroenterol. 2003]
 Lansoprazole treatment of patients with chronic idiopathic laryngitis: a placebo-
controlled trial.[Am J Gastroenterol. 2001]
 Evaluation of omeprazole in the treatment of reflux laryngitis: a prospective, placebo-
controlled, randomized, double-blind study.[Laryngoscope. 2001]
 Proton pump inhibitor therapy for chronic laryngo-pharyngitis: a randomized placebo-
control trial.[Otolaryngol Head Neck Surg. 2004]

See more ...

 Double-blind, placebo-controlled trial with esomeprazole for symptoms and signs

associated with laryngopharyngeal reflux.[Otolaryngol Head Neck Surg. 2008]
 Rabeprazole is effective in treating laryngopharyngeal reflux in a randomized
placebo-controlled trial.[Clin Gastroenterol Hepatol. 2010]
 Benefit of acid-suppressive therapy in chronic laryngitis: the devil is in the
details.[Clin Gastroenterol Hepatol. 2010]

 Omeprazole for the treatment of posterior laryngitis.[Am J Med. 1994]

 Improvement in clinical course and laryngeal appearance in selected patients with
chronic laryngitis after eight weeks of therapy with rabeprazole.[Med Sci Monit.
2004]

See more ...

 Guidelines for the diagnosis and management of gastroesophageal reflux disease.[Am

J Gastroenterol. 2013]
 American Gastroenterological Association Medical Position Statement on the
management of gastroesophageal reflux disease.[Gastroenterology. 2008]
 Benefit of acid-suppressive therapy in chronic laryngitis: the devil is in the
details.[Clin Gastroenterol Hepatol. 2010]

 Guidelines for the diagnosis and management of gastroesophageal reflux disease.[Am

J Gastroenterol. 2013]

 A comparison between sodium alginate and magaldrate anhydrous in the treatment of

patients with gastroesophageal reflux symptoms.[Dig Dis Sci. 2006]
  Alginate controls heartburn in patients with erosive and nonerosive reflux
disease.[World J Gastroenterol. 2012]

See more ...

 The value of a liquid alginate suspension (Gaviscon Advance) in the management of

laryngopharyngeal reflux.[Eur Arch Otorhinolaryngol. 2009]
 Review Review article: reflux and its consequences--the laryngeal, pulmonary and
oesophageal manifestations. Conference held in conjunction with the 9th International
Symposium on Human Pepsin (ISHP) Kingston-upon-Hull, UK, 21-23 April
2010.[Aliment Pharmacol Ther. 2011]

 Review Review article: reflux and its consequences--the laryngeal, pulmonary and
oesophageal manifestations. Conference held in conjunction with the 9th International
Symposium on Human Pepsin (ISHP) Kingston-upon-Hull, UK, 21-23 April
2010.[Aliment Pharmacol Ther. 2011]

 Effect of acute and chronic administration of the GABA B agonist baclofen on 24

hour pH metry and symptoms in control subjects and in patients with gastro-
oesophageal reflux disease.[Gut. 2003]
 Randomised clinical trial: the effect of baclofen in patients with gastro-oesophageal
reflux--a randomised prospective study.[Aliment Pharmacol Ther. 2012]
 Arbaclofen placarbil in GERD: a randomized, double-blind, placebo-controlled
study.[Am J Gastroenterol. 2011]
 Randomised clinical trial: effects of monotherapy with ADX10059, a mGluR5
inhibitor, on symptoms and reflux events in patients with gastro-oesophageal reflux
disease.[Aliment Pharmacol Ther. 2011]

 Influence of citalopram, a selective serotonin reuptake inhibitor, on oesophageal

hypersensitivity: a double-blind, placebo-controlled study.[Aliment Pharmacol Ther.
2006]
 Low-dose trazodone for symptomatic patients with esophageal contraction
abnormalities. A double-blind, placebo-controlled trial.[Gastroenterology. 1987]
 Imipramine decreases oesophageal pain perception in human male volunteers.[Gut.
1998]

See more ...

 Review Effectiveness of laparoscopic fundoplication in relieving the symptoms of

gastroesophageal reflux disease (GERD) and eliminating antireflux medical
therapy.[Surg Endosc. 2003]
 Clinical and pathologic response of Barrett's esophagus to laparoscopic antireflux
surgery.[Ann Surg. 2003]

See more ...

 Laryngopharyngeal reflux disease treated with laparoscopic fundoplication.[Dig Dis

Sci. 2008]
 Laparoscopic Nissen fundoplication effectively relieves symptoms in patients with
laryngopharyngeal reflux.[J Gastrointest Surg. 2007]
  Nissen fundoplication surgery for extraesophageal manifestations of gastroesophageal
reflux (EER).[Laryngoscope. 2002]
 Surgical fundoplication in laryngopharyngeal reflux unresponsive to aggressive acid
suppression: a controlled study.[Clin Gastroenterol Hepatol. 2006]

See more ...

 Results of laparoscopic fundoplication where atypical symptoms coexist with

oesophageal reflux.[Aust N Z J Surg. 2000]
 Review Gastroesophageal reflux disease treatment: side effects and complications of
fundoplication.[Clin Gastroenterol Hepatol. 2013]

 Review The esophagogastric junction.[N Engl J Med. 1997]

 Sphincterlike thoracoabdominal high pressure zone after
esophagogastrectomy.[Gastroenterology. 1993]

 Globus sensation and gastroesophageal reflux.[Eur Arch Otorhinolaryngol. 2003]

 Diagnosis of laryngopharyngeal reflux among globus patients.[Otolaryngol Head
Neck Surg. 2006]
 Globus sensation caused by gastroesophageal reflux disease.[Auris Nasus Larynx.
2002]
 Review Globus pharyngeus: a review of its etiology, diagnosis and treatment.[World J
Gastroenterol. 2012]

See more ...

 Review Refractory chronic cough: new perspectives in diagnosis and treatment.[Arch

Bronconeumol. 2013]
 Respiratory physiotherapy can increase lower esophageal sphincter pressure in GERD
patients.[Respir Med. 2012]
 Positive effect of abdominal breathing exercise on gastroesophageal reflux disease: a
randomized, controlled study.[Am J Gastroenterol. 2012]

 Gastroesophageal reflux laryngitis resistant to omeprazole therapy.[J Voice. 1995]

 Review Medical treatment of supraesophageal complications of gastroesophageal
reflux disease.[Am J Med. 2001]
 Review Review article: reflux and its consequences--the laryngeal, pulmonary and
oesophageal manifestations. Conference held in conjunction with the 9th International
Symposium on Human Pepsin (ISHP) Kingston-upon-Hull, UK, 21-23 April
2010.[Aliment Pharmacol Ther. 2011]

You are here: NCBI > Literature > PubMed Central (PMC)
Write to the Help Desk
External link. Please review our privacy policy.
NLM
NIH
DHHS
USA.gov
Copyright | Disclaimer | Privacy | Browsers | Accessibility | Contact
National Center for Biotechnology Information, U.S. National Library of Medicine 8600
Rockville Pike, Bethesda MD, 20894 USA

Translate

Perawatan optimal dari penyakit refluks laryngopharyngeal

Irene Martinucci, Nicola de Bortoli,Edoardo Savarino penulis terkait, Andrea Nacci, Salvatore
Osvaldo Romeo, Massimo Bellini, Savarino Special, Bruno Fattori, dan

penulis Marchi Santino ► Informasi Hak Cipta ► Informasi Lisensi dan

pergi ke:

refluks Laryngopharyngeal abstrak didefinisikan sebagai konten lambung-refluks ke larynx dan

faring,. Sejumlah besar data sarankan prevalensi gejala laryngopharyngeal tumbuh pada pasien
dengan penyakit refluks gastroesophageal. Namun, laryngopharyngeal adalah refluks sindrom sebab
dan gastroesophageal penyakit refluks saluran bukanlah satu-satunya menyebabkan terlibat dalam
patogenesa EH. Masalah-masalah penting saat ini mendiagnosis laryngopharyngeal banyak
nonspecific refluks laring gejala dan tanda, dan kepekaan miskin dan keunikan semua yang saat ini
tersedia tes diagnostik. Walaupun ia adalah sebuah strategi klinis pragmatis untuk memulai dengan
persidangan empirik proton pump inhibitors, banyak pasien dengan laryngopharyngeal dicurigai
telah refluks gejala yang tidak kunjung meskipun terapi penindasan asam maksimal. Secara
keseluruhan, ada sedikit hasil berkonflik untuk menilai pengaruh pengobatan refluks (termasuk
modifikasi gaya hidup dan makanan, perawatan kesehatan, antireflux pembedahan) pada
laryngopharyngeal refluks lambung. Masa kini meninjau adalah bertujuan untuk membahas secara
kritis pengobatan saat ini pada pasien dengan laryngopharyngeal opsi, dan menyediakan sebuah
refluks pada perkembangan perspektif terapi baru.

Kata Kunci: gastroesophageal penyakit refluks, laryngopharyngeal refluks lambung, proton pump
inhibitor, pengobatan, kunjungi

Introduction

Laryngopharyngeal refluks lambung (LPR) didefinisikan sebagai konten lambung-refluks ke dalam

larynx dan faring, [Vakil et al. 2006]. Menurut Konsensus Montreal, Konferensi manifestasi
gastroesophageal penyakit refluks (GERD) telah diklasifikasikan ke dalam salah satu robek/
rupturnya kerongkongan atau sejumlah gejala penyakit menurun dan, di antara extraesophageal
yang datang kemudian, keberadaan sebuah association antara LPR dan GERD telah didirikan [Vakil et
al. 2006]. LPR dapat dimanifestasikan sebagai laring gejala seperti batuk, tenggorokan,, dysphonia
serak dan globus, serta tanda-tanda laring di laryngoscopy iritasi [Vaezi et al. 2003]. Gejala
Laryngopharyngeal semakin dikenali oleh dokter umum, dokter spesialis paru-paru dan telinga,
hidung dan tenggorokan (THT) ahli bedah yang [2000], Richter. Dalam keadaan tertentu, ada
sejumlah besar data pada prevalensi gejala laryngopharyngeal tumbuh dalam hingga 60% pasien
GERD [Jaspersen et al. 2003; Koufman et al. 1996;, 2004] Richter. Selain itu, beberapa studi
mendukung anggapan bahwa GERD, serta menggunakan rokok dan alkohol, faktor-faktor risiko
adalah untuk kanker laring [Freije et al. 1996; Vaezi et al. 2006 sebuah]. Menurut Konsensus
Montreal Konferensi, beberapa isu-isu penting telah disorot, sebagai berikut:

Jarangnya ditemukan dari sejumlah gejala penyakit menurun terjadi dalam isolasi extraesophageal
tanpa politikselalu diiringin manifestasi tipikal GERD gejala (iaitu serangan jantung dan regurgitasi/);

extraesophageal sebab biasanya sejumlah gejala penyakit menurun dengan GERD sebagai salah satu
dari beberapa potensi aggravating cofactors;

data mendukung akibat yang menguntungkan bagi pengobatan refluks pada sejumlah gejala
penyakit menurun extraesophageal yang lemah [Vakil et al. 2006].

Selanjutnya, Asosiasi Gastroenterological Amerika panduan untuk GERD disarankan terhadap

penggunaan asam-penindasan terapi pengobatan akut pasien dengan potensi sejumlah gejala
penyakit menurun (laryngitis extraesophageal GERD, asma) dalam ketiadaan tipikal gejala GERD
[Kahrilas et al. 2008].

Dalam mekanisme yang berhubungan dengan refluks tertentu untuk laryngopharyngeal terkemuka
gejala dan tanda saat ini tidak diketahui. Acidity asam lambung saja dapat menyebabkan kerusakan
jaringan di tingkat saluran napas bagian atas [Wiener et al. 2009], tetapi beberapa studi
menunjukkan bahwa ini bukan satu-satunya menjadi faktor yang terlibat dalam patogenesa EH
laryngopharyngeal penyakit refluks (LPRD). Memang, baru-baru ini, Pearson dan rekan-rekan
[Pearson et al. 2011] yang disorot, walaupun acid dapat dikontrol oleh proton pump inhibitor (PPI),
semua dari terapi kerusakan faktor-faktor lain (misalnya pepsin, garam, bakteri empedu dan enzim
proteolytic pankreas) tetap berpotensi terjadinya kerusakan pada terapi PPI dan mungkin memiliki
kemampuan merusak mereka ditingkatkan. Khususnya, pepsin dapat merusak semua jaringan
extragastric pada pH hingga 6 [Ludemann et al. 1998]. Catatan, tingkat detectable pepsin telah
ditunjukkan oleh Johnston dan rekan tetap dalam laring epithelia setelah sebuah acara refluks
[Johnston et al. Jumlah a]. Para penulis yang sama yang dijelaskan bahwa pepsin adalah diambil oleh
laring sel epitel oleh reseptor-dimediasi mutakhir endositosis prokariotis [Johnston et al. Jumlah b],
jadi mungkin mewakili sebuah mekanisme novel, di samping aktivitas proteolytic saja, oleh yang
pepsin dapat menyebabkan kerusakan sel yang berhubungan dengan GERD secara mandiri dari pH-
refluxate [Pearson et al. 2011].
Untuk saat ini, diagnosis LPR adalah tugas yang sangat sulit dan beberapa kontroversi tetap
mengenai bagaimana untuk konfirmasi LPRD. Temuan Laryngoscopic, khususnya edema dan
eritema, sering digunakan untuk mendiagnosis LPR oleh Ahli Bedah THT [Vaezi et al. 2003]. Namun,
ia harus menunjukkan bahwa, serta melakukan kajian prospektif, laryngoscopy dinyatakan satu atau
beberapa tanda-tanda iritasi laring dalam lebih dari 80% dari kontrol sehat [Milstein et al. 2005].
Lebih jauh lagi, ia telah menunjukkan bahwa akurat penilaian klinis LPR kemungkinan besar akan
sulit karena laring penemuan fisik tidak dapat andal ditentukan dari clinician untuk clinician, dan
variasi seperti membuat laryngoscopic tepat diagnosis LPR sangat subjektif [Branski et al. 2002].
Kepekaan dan keunikan ambulatory pH monitoring sebagai sarana untuk mendiagnosis GERD pada
pasien dengan gejala refluks extraesophageal telah ditantang [Vakil et al. 2006]. Lebih jauh lagi,
kepekaan 24-h dual-memasukkan (robek/ rupturnya kerongkongan dan pharyngeal secara
bersamaan) monitoring telah berkisar dari 50% sampai 80% [Koufman, 1991]. Baru-baru ini,
ketersediaan speaker impedansi intraluminal pH monitoring (MII-pH) nampaknya menunjukkan
penampilan yang lebih baik dalam mendiagnosis extraesophageal manifestasi GERD berkat
kemampuannya untuk mengevaluasi dan nonacid asam refluxes selain ekstensi proksimal mereka
[Carrol et al. 2012; Savarino et al. 2009; Sifrim et al. 2005; Tutuian et al. 2006]. Namun, orang-orang
miskin dan kepekaan keunikan semua yang saat ini tersedia tes diagnostik untuk LPR telah disorot
oleh beberapa artikel peninjauan [Altman et al. 2011; Katz et al. Tahun 2013; Vaezi et al. 2003].
Dalam populasi pasien dengan laryngoscopic temuan-temuan LPR, kelompok kami menunjukkan
bahwa MII-pH mengkonfirmasi GERD diagnosis dalam kurang dari 40% pasien [de Bortoli et al.
2012], maka menyoroti isu kritis dari gejala nonspecific dan temuan-temuan laryngoscopic LPR
[Zerbib dan Stoll, 2010]. Teknik diagnostik menjanjikan baru telah dikembangkan untuk
extraesophageal sejumlah gejala penyakit menurun, khususnya refluks, sebuah imunologis pepsin
(PeptestTM "Kesalkah), yang telah ditunjukkan untuk menjadi, cepat, dan sensitif alat bantu tertentu
[Bardhan et al. 2012; dan Johnston, Samuel 2010], dan pH pharyngeal baru kateter (diproduksi oleh
Restech, San Diego, CA, USA) yang didokumentasikan studi baru-baru ini sebagai sangat sensitif dan
perangkat invasif minimal untuk deteksi cairan pembersih atau kabut awan dari refluks lambung
dalam posterior oropharynx [Matahari et al. 2009]. Namun, data terbatas pada akurasi diagnostik
mereka dan aplikasi klinis potensial yang tersedia.

Dalam kajian ini, kita akan membahas opsi pengobatan saat ini pada pasien dengan LPRD dan
pro/kontra mereka, dan kami akan menyediakan sebuah perspektif pada perkembangan terapi baru.

Kunjungi:

perubahan gaya hidup

dan perubahan gaya hidup Diet adalah Intervensi efektif untuk GERD, terlepas dari kenyataan bahwa
beberapa data tangguh telah diterbitkan (Tabel 1) [De Groot et al. 2009; Kaltenbach et al. 2006].
Sesuai dengan pengobatan yang digunakan di rumah sakit umum kabupaten Inggris, dan makanan
modifikasi perilaku juga telah seharusnya sangat efektif dalam pengelolaan LPR [Pearson et al.
2011].

Tabel 1.

Tabel 1.

Pengaruh positif bagi perubahan gaya hidup dibandingkan dengan orang-orang yang pasti
keberhasilan dalam pengobatan penyakit refluks laryngopharyngeal (LPRD).

Obesitas

insidens obesitas di negara-negara Barat telah meningkat pesat [Nicholls, tahun 2013], dan terjadi ini
dalam peningkatan dengan konkordans jumlah pasien menderita GERD [El-Serag dan Sonnenberg,
1998]. Beberapa studi epidemologi yang jelas menunjukkan sebuah association antara obesitas dan
GERD dan penyelidikan fisiologik mendukung biologis masuk akal hubungan antara obesitas dan
GERD.

Dalam keadaan tertentu, studi yang berbeda telah menunjukkan suatu hubungan antara indeks
massa tubuh yang lebih tinggi (IMT) dan GERD [Fass et al. 2005; Nasseri-Moghaddam et al. 2008;
Ruigomez et al. 2004; Savarino et al. 2011] dan kedua obesitas (IMT >30 kg/m2) dan yang berlebih
(IMT 25-30 kg/m2) telah dikaitkan dengan GERD [Dore et al. 2008; Nocon et al. 2007].

Akibat-akibat imt pada kejadian GERD nampaknya terlepas dari total kebutuhan akan kalori, asupan
makanan serat, buah-buahan, dan sayuran, atau makro lain atau mikronutrien [El-Serag, 2008].
Obesitas merupakan seharusnya untuk memodifikasi esophagogastric (EGJ bersama) morfologi dan
fungsi. Memang, obesitas menghasilkan sebuah gangguan EGJ mekanis oleh mempromosikan
sebuah pemisahan aksial antara robek/ rupturnya kerongkongan sphincter lebih rendah (LES) dan
maupun ekstrinsik diafragma crural [Pandolfino et al. 2006]. LES ketidakmampuan juga telah
teramati pada pasien obesitas [Fisher et al. 1999; Suter et al. 2004] dan di antara morbidly pasien
obesitas paparan asam robek/ rupturnya kerongkongan yang lebih tinggi adalah secara signifikan
dikaitkan dengan tekanan yang lebih rendah LES [Sabate et al. 2008].

Studi kohort berat badan berlebih dan kegemukan ditemukan bahwa kehilangan berat badan pasien
mengakibatkan peningkatan gejala GERD [Anderson dan Jhaveri, 2010; Fraser-Moodie et al. 1999].
Lebih-lebih lagi, gejala refluks telah ditunjukkan sebagai diperburuk atau ditingkatkan sepanjang
waktu politikselalu diiringin dengan penambahan berat badan atau kehilangan, masing-masing
[Jacobson et al. 2006]. Perburuan penelitian menunjukkan bahwa, di antara individu dengan gejala
yang berhubungan dengan GERD, pengurangan lebih tinggi dari 3.5 unit di imt ini terkait dengan
pengurangan atau penghentian dalam antireflux mingguan obat-obatan menggunakan [Ness-Jensen
et al. Tahun 2013]. Pada sisi lain, apakah pengurangan berat badan dapat meningkatkan manifestasi-
manifestasi atau obyektif subjektif masih kontroversial refluks [Kjellin et al. 1996]. Lebih-lebih lagi,
hanya sedikit data yang tersedia untuk menentukan apakah kehilangan berat badan adalah dapat
memperbaiki gejala yang berhubungan dengan GERD seperti LPR.

Tabiat memakan

walaupun hanya sedikit data yang tersedia pada hal ini, dalam clinical practice makanan-makanan
yang berbeda yang ditunjukkan untuk mempengaruhi terjadinya refluxes dan, secara umum, pasien
dianjurkan terhadap mengambil makanan akhir pada waktu petang [Pearson et al. 2011].

Makanan lemak tinggi dan cokelat adalah secara empiris yang ditunjukkan sebagai makanan dapat
mengurangi LES tekanan atau untuk memperpanjang sakit maag; walau demikian, ada
mengosongkan telah ada penghentian persidangan evaluasi dampak pada hasil GERD [Murphy dan
Castell, 1988; Wright dan Castell, 1975]. Serangan jantung mungkin diperburuk oleh makanan pedas
ikutan iritasi langsung yang sudah meradang mukosa robek/ rupturnya kerongkongan lebih rendah.
Dalam keadaan tertentu, Nebel dan rekan-rekan [Nebel et al. Tahun 1976] dijelaskan bahwa 88%
pasien melaporkan makanan pedas sebagai penyebab dari serangan jantung. Jus jeruk telah yang
ditimbulkan dalam gejala GERD bahkan jika jus jeruk larutan infus tidak mengubah LES tekanan
[Cranley et al. 1986].

Dalam sebuah salib studi dapat meningkatkan pada pasien diikuti di fasilitas perawatan kesehatan
Administrasi Veteran, asupan lemak makanan tinggi telah dikaitkan dengan peningkatan risiko GERD
dan erosive esophagitis [El-Serag et al. 2005]. Namun, beberapa studi lain melaporkan data yang
berkonflik menunjukkan bahwa fat diet tinggi yang telah tidak berpengaruh pada LES peduli
sementara atau robek/ rupturnya kerongkongan paparan asam [Mangano et al. 2002; Pehl et al.
2001; Penagini, 2000; Penagini et al. 1998]. Walaupun tidak jelas apakah kebutuhan akan kalori
memberikan kontribusi terhadap robek/ rupturnya kerongkongan gejala kepadatan dan paparan
asam, sebuah studi diacak baru-baru ini termasuk sebuah kelompok kecil pasien ditemukan bahwa
robek/ rupturnya kerongkongan paparan asam lebih tinggi dengan fagositosisnya high-diet kalori
(1000 kkal versus 500 kkal), dan gejala refluks yang terkena dampak oleh konten lemak tetapi
kepadatan tidak [Fox et al. 2007].

Minuman bersoda telah dikaitkan dengan mempromosikan GERD gejala dengan menurunkan LES
tekanan dan yang ditemukan untuk memprediksi GERD gejala dalam analisis multivariate [Fass et al.
2005].

Kopi telah dilaporkan ke mencetuskan episode refluks [Brazer et al. 1995]. Sebuah kasus Norwegia-
control study melaporkan asosiasi negatif antara GERD dan kopi (rasio nisbahnya [atau] 0,5; 95% dari
1.58 0,4-0.6) di antara yang minum 4-7 cangkir per hari dibandingkan dengan orang-orang yang tidak
minum kopi [Nilsson et al. 2004]. Dalam studi yang sama, serat makanan konsumsi ditemui menjadi
sebuah faktor pelindung [Nilsson et al. 2004]. Dalam sebuah salib besar dapat meningkatkan studi
berbasis populasi, mengonsumsi roti dan serat makanan sedikitnya dua per hari menyebabkan 50%
pengurangan dalam gejala refluks [Terry et al. 2001]. Demikian juga, dalam salib lain studi dapat
meningkatkan asupan serat tinggi, korelasikan dengan mengurangi risiko GERD gejala [El-Serag et al.
2005]. Mekanisme melalui serat yang dikaitkan dengan penurunan risiko tidak dikenal, namun
peningkatan empting lambung dapat hipotesis yang wajar.

Kebiasaan Voluptuary: konsumsi alkohol dan tembakau

hanya sedikit data yang tersedia untuk kebiasaan voluptuary seperti rokok merokok dan konsumsi
alkohol. Para perokok mempunyai insidens meningkat gejala refluks dibandingkan dengan orang
bukan perokok [Talley et al. 1994; Watanabe et al. 2003]. Nilsson dan rekan-rekan [Nilsson et al.
2004] dinyatakan, dalam sebuah analisis multivariate, bahwa di antara individu yang telah diasapkan
sehari selama lebih dari 20 tahun, risiko adalah signifikan refluks oleh 70%, dibandingkan dengan
orang-orang yang telah diasapkan sehari selama kurang dari setahun (atau 1,7; 95% CI 1,5-1,9).
Suatu hubungan telah dianggap antara menghisap rokok dan berlanjutnya paparan asam, penurunan
tekanan, dan berkurangnya LES salivation, yang berkurang tingkat robek/ rupturnya kerongkongan
jarak asam [Kahrilas dan Gupta, 1989]. Namun, pH-metry gagal untuk melaporkan peningkatan
robek/ rupturnya kerongkongan waktu paparan asam di perokok dibandingkan dengan orang bukan
perokok terlepas dari mantan mengalami peningkatan episode refluks [Pehl et al. 1997]. Secara
keseluruhan, ada data tidak dapat ditentukan mengenai efek penghentian bebas merokok rokok
pada hasil GERD.

Minuman Beralkohol dianggap dapat mencetuskan serangan jantung persepsi [Pehl et al. 1993].
Bahkan jika beberapa tersedia data, tidak ada perbedaan dalam meningkatkan risiko antara
sejumlah besar minuman alkohol tinggi seperti whiskey dan vodka [Kaufman dan Kaye, 1978; Vitale
et al. Tahun 1987], dan bahkan dalam jumlah moderat beer atau anggur putih dan merah [Pehl et al.
1993]. Walau demikian, bila dibandingkan dengan anggur merah, anggur putih disebabkan lebih
robek/ rupturnya kerongkongan paparan asam dan penurunan yang lebih besar di Les tekanan [Pehl
et al. 1998]. Efek-efek serupa menunjukkan setelah ditularkan anggur putih dan bersyeba pada
pasien dengan bukti endoskopi esophagitis refluks dan studi pH abnormal [Pehl et al. 2006].

Posisi tidur

ada indikasi yang berbeda yang posisi tubuh selama periode tidur adalah berkaitan dengan konten
lambung-refluks di kerongkongan. Waktu tidur yang mengubahkan mekanisme fisiologik dasar yang
secara fisiologis melindungi terhadap GERD. Mekanisme yang tertekan saat tidur termasuk sinyal
peringatan dari serangan jantung, frekuensi menelan, dan penindasan terhadap pembesaran
pelepasan [Freidin et al. 1989]. Beberapa penyidikan telah menunjukkan bahwa robek/ rupturnya
kerongkongan jarak asam secara drastis selama tidur berkepanjangan dibandingkan dengan negara
terbangun; ini benar, bahkan ketika tidur subyek dibandingkan dengan terjaga subyek-subyek dalam
posisi telentang [Orr et al. Tahun 1981].

Kepala dan tempat tidur peninggian dapat dicapai dengan menempatkan baik 6-8 inci block di
bawah tempat tidur kaki di kepala tempat tidur atau wedge matras di bawah busa. Uji acak telah
menunjukkan bahawa amalan ini dapat mengurangi paparan asam robek/ rupturnya kerongkongan
dan memimpin untuk periode refluks lebih pendek dan jarak robek/ rupturnya kerongkongan cepat
[Hamilton et al. 1988]. Meninggikan kepala tempat tidur adalah penting bagi orang-orang dengan
nocturnal atau laring gejala. Posisi recumbent lateral kanan juga telah menjadi penyebab
berkepanjangan waktu refluks dan peningkatan LES relaxations, maka pasien dengan GERD atau
LPRD harus menghindari recumbence dalam posisi ini [Khoury jadi et al. 1999].

Latihan Fisik

Latihan Fisik telah ditemukan untuk menjadi faktor pelindung terhadap refluks lambung. Dalam
keadaan tertentu, dalam sebuah studi berbasis populasi yang besar, korelasi telah didokumentasikan
antara jumlah sesi latihan berlangsung sekurangnya 30 min dan penurunan risiko GERD gejala (atau
0,5; 95% CI 0,4-0.7) [Nilsson et al. 2004]. Program-program yang sering, dijadwalkan pengurangan
berat badan, yang dianggap membantu untuk mengurangi gejala refluks, sering dikaitkan dengan
aktivitas fisik aerobic [Djarv et al. 2012; Ness-Jensen et al. Tahun 2013; Yamamichi et al. 2012].
Memang, suatu mekanisme yang menguatkan latihan antireflux barrier, mungkin didasari oleh
melainkan otot, adalah berhipotesis [Nocon et al. 2006]. Apa yang lebih, Nocon dan rekan-rekan juga
melaporkan bahwa subyek-subyek dengan gejala GERD secara fisik kurang aktif dari orang-orang
tanpa gejala [Nocon et al. 2006]. Namun, robek/ rupturnya kerongkongan paparan asam meningkat
secara signifikan dalam sukarelawan dan GERD selama periode latihan yang intens pasien
dibandingkan dengan periode nonexercise [Pandolfino et al. 2004]. Pandolfino dan rekan-rekan
telah mengusulkan bahwa perbedaan anatomis kompromi terhadap esophagogastric junction,
sebagai akibat dari ketegangan dikaitkan dengan perut sering melakukan latihan, mungkin
predispose refluks yang diinduksi oleh latihan untuk [Pandolfino et al. 2004]. Studi yang berbeda
telah mengusulkan bahwa sebuah agonistic aktivitas fisik dapat memainkan sebuah peran
pathogenetic dalam GERD gejala (misalnya dokumener menjalankan, bersepeda, latihan
perlawanan) [Collings et al. 2003; Pandolfino et al. 2004; Parmelee-Peters dan Moeller, 2004]. Ia
telah menyarankan agar GERD dapat ditingkatkan dalam karena menurunnya atlet saluran cerna
aliran darah, perubahan-perubahan, Sekresi hormon dalam fungsi motor kerongkongan dan
ventricle, dan posisi tubuh terbatas selama latihan [Jozkow et al. 2006].

Kunjungi:

terapi medis

mempertimbangkan kepekaan miskin dan keunikan semua yang saat ini tersedia tes diagnostik,
sebuah sidang terapi empirik mewakili langkah pertama untuk konfirmasi LPRD dan
memperlakukannya sesuai dengan itu. Namun, tidak ada diterima protocol untuk pengobatan yang
paling efektif pasien dengan LPRD. Sejak pengenalan mereka di tahun 1980-an, PPIs telah
menunjukkan penindasan paling potensial dari asam lambung pelepasan, menunjukkan dengan jelas
berbeza advantage (baik untuk menyembuhkan dan bantuan gejala) atas H2 pihak antagonis
reseptor [Chiba et al. 1997]. Justru itu, H2 pihak antagonis reseptor telah membatasi peran mereka
terutama untuk pasien yang menderita dari terobosan asam nocturnal meskipun dua kali sehari-
terapi PPI [Xue et al. 2001], atau untuk manajemen jangka panjang gejala refluks pada sebuah
'sebagai dasar, yang sangat dibutuhkan [Scarpignato et al. 2006]. Agen Prokinetic, walaupun jarang
dievaluasi, biasanya dianggap LPRD masyarakatmasih dalam [Pearson et al. 2011]. Ringkasan
berbagai opsi untuk mengobati LPRD farmakologi yang dilaporkan pada Tabel 2.

Tabel 2.

Tabel 2.

Ringkasan terapi medis yang berbeda dalam laryngopharyngeal penyakit refluks (LPRD) yang terbukti
atau efikasi yang tidak pasti.

Proton pump inhibitors

terapi PPI dianggap sebagai alasan utama bagi care pada pasien dengan GERD; namun, efektifitas
pada pengobatan LPRD tetap ragu. Dalam praktek klinik, secara konsisten dengan asumsi bahwa
saluran aerodigestive atas adalah lebih sensitif terhadap refluxes asam dari kerongkongan, diyakini
bahwa pasien dengan yang berhubungan dengan refluks laryngitis memerlukan dosis yang lebih
besar dan coba lagi PPIs untuk mencapai sebuah perbaikan gejala laring dibandingkan dengan gejala
GERD tipikal [Ford, 2005; Koufman et al. 2002; Park et al. 2005]. Pada sisi lain, yang dikendalikan
plasebo pengadilan tersebut gagal untuk memperlihatkan manfaat terapi PPIs [Eherer et al. 2003; El-
Serag et al. 2001; Noordzij et al. 2001; bekerja sebagai bendahara et al. 2004; tidak akan et al. 2006].
Pada tahun 2006, calon diacak, Studi multicenter dengan 145 pasien gejala dan tanda-tanda
endoskopi LPR, tidak menunjukkan manfaat pada pasien dirawat dengan esomeprazole 40 mg 2 kali
sehari selama 4 bulan versus placebo [Vaezi et al. 2006 b]. Selain itu, sebuah kajian sistematis
Cochrane studi 302 tidak menemukan berkualitas tinggi pertemuan ujian penyertaan kriteria untuk
menilai efektivitas terapi antireflux serak untuk [Hopkins et al. 2006]. Kajian yang sistematis dan
sebuah meta-analisis dari controlled persidangan gagal untuk menunjukkan keutamaan PPIs atas
placebo untuk pengobatan yang dicurigai LPR [Karkos dan Wilson, 2006; Qadeer et al. 2006].

Sebaliknya, studi baru-baru ini telah ditunjukkan lebih efektif dalam mengobati gejala refluks dan
meningkatkan laring inflamasi. Reichel dan rekan-rekan [Reichel et al. 2008] melaporkan diacak,
buta ganda, sidang yang dikendalikan plasebo dengan esomeprazole 20 mg 2 kali sehari selama 3
bulan pada pasien dengan gejala dan tanda-tanda endoskopi LPR, yang ditemukan peningkatan
dalam kedua gejala dan laring diperiksa. Demikian juga, Lam dan rekan-rekan [Lam et al. Tahun
2010] dilakukan calon, diacak, buta ganda, placebo studi yang dikendalikan dengan rabeprazole 20
mg 2 kali sehari selama 3 bulan pada pasien dengan gejala dan tanda-tanda endoskopi LPR, yang
menghasilkan peningkatan gejala-gejala, tetapi tidak laring penemuan-penemuan. Namun,
berdasarkan pada penelitian lebih dekat-dua penelitian, Vaezi [Vaezi, tahun 2010] berpendapat
bahwa peningkatan yang signifikan telah nyata bagi serangan jantung gejala dan tidak untuk gejala
tenggorokan kronik.

Beberapa data ilmiah dan tidak terkontrol merekomendasikan penggunaan dua kali sehari-PPIs
untuk LPRD [Kamel et al. 1994; Klopocka et al. 2004; Shaw dan Searl, 1997; Williams et al. 2004].
Furthermo, Selain itu, beberapa penelitian menunjukkan bahwa proporsi pasien dengan peningkatan
dalam laring gejala terapi PPI lebih tinggi daripada pasien GERD dalam mereka tanpa GERD [Lien et
al. Tahun 2013; Masaany et al. 2011; Qua et al. 2007]. Pada sisi lain, beberapa studi menilai bahwa
kehadiran refluks lambung abnormal pada pH monitoring tidak memprediksi terapi untuk respons
[Vaezi et al. 2006 b; Williams et al. 2004].

Secara keseluruhan, mengingat bahwa kebanyakan bukti terapis adalah berdasarkan studi label
terbuka yang tidak terkawal hanya dan kurangnya bukti berkualitas tinggi yang mendukung
keberhasilan pengobatan, menilai pengobatan yang optimal untuk LPRD masih menantang. Lebih
jauh lagi, dosis dan durasi terapi PPI dalam LPRD mewakili masalah-masalah saat ini perdebatan
lebih lanjut. Untuk saat ini, apabila terdapat gejala GERD tipikal selain gejala extraesophageal
dan/atau ada bukti tujuan GERD oleh pemeriksaan endoskopi atau pemantauan refluks [Katz et al.
Tahun 2013], ia adalah sebuah strategi klinis pragmatis untuk memulai dengan sebuah 2 bulan
dengan dua kali sehari-terapi PPIs [Kahrilas et al. 2008]. Jika ada perbaikan gejala, kemudian tapering
untuk sekali-PPI harian diikuti dengan mengurangi dosis atau interval bagi penindasan asam sangat
disarankan [Vaezi, 2010]. Pada sisi lain, kegagalan seperti PPI empiris, etiologi percobaan selain
GERD harus dieksplorasi melalui politikselalu diiringin penilaian oleh THT, dan paru, spesialis alergi
[Kahrilas et al. 2008; Katz et al. Tahun 2013; Vaezi, 2010; Zerbib et al. Tahun 2013].

Pasien dengan bukti tujuan refrakter (refluks lambung monitoring) dari refluks berkelanjutan sebagai
penyebab gejala harus dipertimbangkan untuk terapi antireflux tambahan yang mungkin berisi LES
peduli sementara (TLESR) inhibitors atau pembedahan [Katz et al. Tahun 2013], yang dibahas lebih
jauh di masa kini meninjau.

Alginate

antacids tradisional sering digunakan sebagai terapi add-on untuk menetralkan asam lambung dan
untuk membantu mengontrol serangan jantung dalam GERD pasien [Giannini et al. 2006; Savarino et
al. 2012; Zentilin et al. 2005]. Mereka polysaccharides ditemukan dalam ganggang dan mengkonversi
ke dalam bentuk gel ketika mereka menggabungkan kation dengan. Dalam keadaan tertentu,
mereka membentuk sebuah rintangan fizikal untuk gastroduodenal isi, dan memiliki manfaat
sebagai nonsystemic obat-obatan.
Dalam calon, controlled cairan, alginate persiapan Studi (diambil empat kali sehari) telah terbukti
efektif dalam pengobatan LPR gejala dan tanda [McGlashan et al. 2009]. Catatan, mengingat
pharyngeal dan laring kanker akan mewakili LPR komplikasi, sebuah memeratakan pengurangan
secara signifikan dalam carcinoma sel subtipe volume dipelihara dalam hamsters yang menerima
alginate sebelum dikenal carcinogen [7,12-dimethylbenzanthracene (DMBA)] dan pepsin manusia,
dibandingkan dengan hamsters aplikasi melukis dengan DMBA dan pepsin saja manusia. Justru itu,
suspensi alginate memberikan perlindungan dari pepsin peningkatan pertumbuhan tumor [Pearson
et al. 2011].

Alginate harus diberikan setelah makan dan hal terakhir di malam hari, dan apa yang harus diambil
melalui mulut setelah dosis nocturnal [Pearson et al. 2011].

PPI Neuromodulators-refrakter pasien dengan terus-menerus (nonacid refluks atau asam lemah),
dinilai dengan ambulatory 24-h MII-pH monitoring, dapat memetik manfaat dari refluks lambung-
mengurangi bahan pembersih atau tindakan naluriah penderitaan modulators [Zerbib et al. Tahun
2013]. Refluks lambung-mengurangi agen, termasuk GABAB agonis dan metatropic antagonis
reseptor glutamat, seharusnya untuk mengurangi frekuensi TLESR, yang mewakili mekanisme
pathophysiological utama underlying GERD. Dalam keadaan tertentu, reseptor GABAB agonis (iaitu
baclofen) telah ditunjukkan untuk menurunkan kejadian refluks lambung, robek/ rupturnya
kerongkongan, dan memperbaiki paparan asam lambung berlebih-gejala terkait [Ciccaglione dan
Marzio, 2003; Cossentino et al. 2012]. Namun, penggunaan mereka di clinical practice terbatas oleh
sebuah profil tolerabilitas miskin. Beberapa peneliti yang telah mencoba untuk mengembangkan
lebih hemat dan lebih baik (iaitu lesogaberan senyawa ditoleransi, ADX10059, arbaclofen) tanpa
mencoba hasil seperti [Vakil et al. 2011; Zerbib et al. 2011].

Tindakan naluriah penderitaan modulators [iaitu antidepresan trisiklik (TCAs) atau selective
serotonin reuptake inhibitors (SSRI)] menurunkan persepsi episode refluks meningkatkan robek/
rupturnya kerongkongan ambang batas persepsi [Broekaert et al. 2006; Clouse et al. Tahun 1987;
Peghini et al. 1998], jadi mungkin mendorong manfaatnya pada pasien dengan hipersensitif
kerongkongan, sebagai didiagnosa melalui pemantauan refluks dalam hal waktu paparan asam
normal dan korelasi positif taruhan Dengan itu mungkin mendorong manfaatnya pada pasien
dengan hipersensitif kerongkongan, sebagai didiagnosa melalui pemantauan refluks dalam hal waktu
paparan asam normal dan korelasi positif antara dan refluxes [Viazis gejala et al. 2011]. Pengamatan,
walaupun di awal alam, mendorong kinerja dari studi bertujuan untuk menilai keberhasilan tindakan
naluriah rasa sakit pada pasien dengan LPRD modulators refrakter untuk pengobatan yang optimal
dengan PPIs.

Kunjungi:

terapi bedah
antireflux dengan pembedahan (LARS) adalah yang dibangun dengan baik dan cukup tinggi
pengobatan untuk GERD dan telah ditunjukkan untuk memberikan bantuan awet dari gejala refluks
tipikal [Papasavas et al. 2003]. Dalam keadaan tertentu, terapi bedah adalah membantu
memungkinkan mayoritas pasien menderita GERD untuk menghentikan penindasan asam, untuk
mencapai resolusi terapi dari dikaitkan esophagitis, dan untuk menangkap atau bahkan mungkin
menterbalikkan metaplasia/istilah kedokteran terjadinya displasia dicetuskan oleh paparan sering-
robek/ rupturnya kerongkongan mukosa lambung untuk isi [Oelschlager et al. 2003; Parise et al.
2011; Rossi et al. 2006].

Beberapa data kontroversial tersedia tentang hasil LPRD bedah. Sebuah kajian prospektif klinis pada
pasien dengan LPRD dipilih untuk pengobatan bedah, di mana gejala-gejala dan tanda-tanda telah
merespon antireflux obat-obatan, dengan fundoplication ditemukan yang efektif dan aman
pengobatan LPRD [Hotel Sala et al. 2008]. Lebih-lebih lagi, pada pasien dengan bukti-bukti tujuan
GERD, LARS efektif dalam meringankan gejala LPR [Catania et al. 2007; Lindstrom et al. 2002]. Pada
sisi lain, LARS telah menunjukkan hasil yang mengecewakan dalam mengontrol gejala yang
berhubungan dengan LPR pada pasien tidak responsif untuk terapi PPI agresif [Swoger et al. 2006].
Demikian juga, sebelum mendemonstrasikan studi hasil bedah miskin resolusi bagi laring gejala
khususnya dalam PPI nonresponders [Chen dan Thomas, 2000; jadi et al. 1998].

Ianya perlu untuk seorang ahli bedah untuk melakukan workup termasuk
esophagogastroduodenoscopy terperinci, robek/ rupturnya kerongkongan manometry, sakit maag
mengosongkan tes, MII-pH atau pH-metry, dan radiography saluran cerna bagian atas untuk semua
pasien dijadwalkan untuk LARS, terutama untuk mengecualikan keganasan dan masalah motilitas
usus seperti achalasia dan kemudian gastroparesis untuk mendeteksi menyebabkan efek-hubungan
antara waktu paparan asam patologi dan laring gejala/penemuan-penemuan [Zerbib et al. Tahun
2013].

Pasien yang dipilih untuk LARS harus diberitahu bahwa dengan fundoplication mungkin benar cacat
mekanis yang mendasari tetapi mereka harus memperingatkan bahwa respon laring gejala mereka
pembedahan masih akan dipastikan [Chen dan Thomas, 2000]. Pendekatan yang LARS lebih sangat
dianjurkan jika pasien menunjukkan menyelesaikan relief laring gejala selama terapi PPI atau jika 24-
h studi pathophysiological menunjukkan bahwa kejadian refluks nonacid mendominasi. Lebih-lebih
lagi, seorang ahli bedah harus dengan hati-hati pilih pasien sebelum menyarankan LARS dan sebuah
pusat rujukan regional di khusus robek/ rupturnya kerongkongan pembedahan ini disarankan untuk
mengurangi komplikasi pasca bedah. Dalam hal ini, pasien harus memperingatkan kemungkinan
disfagia, penggelembungan pasca bedah, kembung, diare, dan pantaulah munculnya kembali gejala-
gejala [, tahun 2013] Richter.
Untuk saat ini, panduan klinis dari masyarakat Amerika dan saluran cerna Ahli Bedah Endoskopi
(Bijaksana) merekomendasikan antireflux pembedahan untuk pasien yang: (1) telah gagal atau tidak
dapat mentoleransi obat-obatan; (2) telah manifestasi extraesophageal signifikan aspirasi seperti,
asma, atau batuk; (3) telah komplikasi GERD-seperti ulkus kecaman.

Kunjungi:

terapi berbicara dan teknik-teknik rehabilitasi

Sebenarnya, opsi-opsi pengobatan yang lebih baru dianggap sebagai kemungkinan alternatif dalam
pengobatan GERD, dan dalam LPRD tertentu, yang setimpal dengan berhati-hati penyidikan.

Dalam LES, dikelilingi oleh atas, mencegah refluks gastroesophageal otot dan, secara tidak langsung,
LPR. Ia adalah percaya bahwa sinergi fungsi les dan sekitarnya crura-diafragma, ketika melapiskan,
adalah penting untuk penutupan kompeten [Mittal dan Balaban, 1997]. Ketika struktur ini menjadi
tidak cakap, isi lambung boleh dilukis kembali ke kerongkongan dan menyebabkan LPR. Pentingnya
diafragma yang juga ditunjukkan oleh otot studi eksperimental: bahkan setelah penyingkiran bedah
LES, sebuah zona tekanan detectable karena pengerutan crura diafragma yang [Klein et al. 1993].
Sama seperti yang lain melainkan otot tubuh, otot diafragma harus terbuka untuk meningkatkan
performa dengan latihan fisik. Untuk alasan ini, pilihan terapi untuk pengobatan penyakit refluks
yang baru-baru ini telah dikaji, dan dalam terapi berbicara/peduli tertentu teknik-teknik pelatihan
seperti diafragma yang manuver dengan otot dan latihan bernafas telah dianggap sebagai.

Dalam literatur, ada beberapa terbitan ilmiah mengenai pengobatan rehabilitasi dan dalam
beberapa refluks pusat diusulkan dalam sebuah terapi cara empirikal tanpa dukungan berbasis bukti
medis. Selain itu, pengobatan rehabilitasi yang diusulkan telah belajar di kaitannya dengan gejala-
gejala dan tidak dalam kaitannya dengan demonstrasi dalam pengurangan nyata dari peristiwa
refluks lambung.

Salah satu ciri yang paling gejala-gejala LPRD adalah globus pharyngeus [Chevalier et al. 2003; Park
et al. 2006; Tokashiki et al. 2002]. Diberikan sifat jinak kondisi dan gagasan baru-baru ini bahwa
GERD adalah penyebab utama globus, terapi empirik dengan dosis tinggi PPIs telah mencoba [Lee
dan Kim, 2012]. Pada pasien nonresponsive untuk terapi ini, ketika GERD yang ditunjukkan oleh
menguji seperti pemeriksaan endoskopi, MII-pH monitoring, dan manometry, pilihan terapi dapat
dipertimbangkan, termasuk bahasa dan teknik-teknik percakapan. Dalam beberapa studi, beberapa
latihan untuk meredakan ketegangan pharyngolaryngeal, latihan suara, dan saluran vokal untuk
menghilangkan kebersihan suara rasa tidak nyaman dan ketegangan telah memberikan hasil yang
signifikan dalam mengurangi terus-menerus globus gejala [Khalil et al. 2003]. Namun, penelitian
selanjutnya diperlukan untuk menentukan apakah berbicara bahasa dan teknik-teknik rehabilitasi
memiliki efek tertentu atau apakah pasien dengan globus pharyngeus hanya memperoleh
keuntungan dari perhatian umum dan kepastian [Millichap et al. 2005].

Baru-baru ini lebih laring terapi rehabilitasi telah diterapkan dalam kasus-kasus batuk kronik
dikaitkan dengan GERD, dengan perbaikan gejala signifikan [Pacheco et al. Tahun 2013]. Carvalho de
Miranda Chaves dan rekan-rekan [Carvalho de Miranda Chaves et al. 2012] menunjukkan, dengan
melakukan robek/ rupturnya kerongkongan manometry, bahwa pelatihan otot inspiratory
bertambah nilainya LES tekanan di pasien dengan GERD setelah 8-program minggu. Eherer dan
rekan-rekan [Eherer et al. 2012], dalam sebuah studi controlled, menunjukkan bahwa pelatihan
secara aktif otot diafragma melalui pernapasan latihan, dapat meningkatkan penyakit refluks.
Kualitas Hidup sisik, pH-metry, dan on-demand menilai-penggunaan PPI untuk memantau pasien
dalam jangka pendek dan jangka panjang menindaklanjuti [Eherer et al. 2012].

Semua penelitian ini konfirmasi bahwa terapi rehabilitasi yang berfungsi pada diafragma crural
adalah metode alternatif untuk mengobati GERD dan LPRD, mengurangi jangka waktu yang terapi
obat atau prosedur bedah. Temuan-temuan ini perlu mengkonfirmasi dalam kajian lebih lanjut
dengan sebuah contoh yang lebih besar, lagi tindak lanjut dan dikontrol dengan kualitas hidup dan
skor pemeriksaan instrumental seperti MII-pH.

Kunjungi:

Diskusi

efek-efek gejala-gejala kedua GERD dan LPRD yang diyakini ke irritative sekunder pengaruh refluxate
lambung pada robek/ rupturnya kerongkongan dan mukosa pharyngeal sensitif [Bough et al. 1995].
Perawatan optimal dari LPRD tidak distandardkan dan tidak divalidasi [Hogan dan pengocok garam,
2001]. Ini adalah karena sebab-sebab multifaktor sifat penyakit, yang nonspecific gejala, dan untuk
kesulitan membuat diagnosa yang akurat atas LPRD untuk kepekaan miskin dan keunikan semua
yang saat ini tersedia tes diagnostik. Teknik-teknik baru (mis. Peptest, Restech) mungkin sangat
menarik untuk meningkatkan akurasi LPRD diagnostik, memuluskan jalan ke arah perkembangan
terapi target baru. Memang, pepsin inhibitors dan pepsin pihak antagonis reseptor adalah mungkin
baru batas negara research [Pearson et al. 2011].

Seperti yang dibahas dalam kajian ini, manajemen LPRD dapat dibagi menjadi perubahan gaya hidup,
dan/atau bedah medis pengobatan. Perubahan perilaku dan perubahan gaya hidup tersebut
dianggap pengobatan garis pertama dengan kemungkinan efek samping terendah. Kehilangan berat
badan, merokok penghentian, alkohol, kebiasaan makan objek hindar modifikasi, dan kepala
peninggian selama tidur perlu sangat dianjurkan untuk pasien. Sebagai Terapi medis ke, saat ini,
dengan perawatan yang berfokus pada peningkatan pH refluxate, maka yang direkomendasikan
untuk memulai dengan PPIs dua kali sehari selama jangka waktu 8-12 minggu. Pasien dengan bukti
tujuan refrakter (refluks lambung monitoring) dari refluks berkelanjutan sebagai penyebab gejala
harus dipertimbangkan untuk terapi alternatif, seperti tindakan naluriah penderitaan modulators
atau antireflux dengan pembedahan. Pendekatan dengan bedah harus dirancang untuk masing-
masing pasien dan dengan sangat hati-hati dianggap. Hasil yang akan tersedia dengan terapi
berbicara tetapi hasil-hasil ini perlu dievaluasi pengadilan di masa depan. Pembedahan harus
ditunjukkan di pilih pasien, di mana volume tinggi refluxate ketidakcekapan dan les ditunjukkan
dengan robek/ rupturnya kerongkongan pathophysiological evaluasi.

Untuk saat ini, kita dapat menyimpulkan bahwa, walaupun banyak penelitian masih diperlukan
untuk menilai manajemen terapi dalam LPRD optimal, sebuah pendekatan multidisiplin termasuk
providers di bagian Pulmonologi bagian Ilmu, dan dikirim, evaluasi gastroenterilogi disarankan untuk
meningkatkan diagnosis dan pada pasien dengan LPRD terapi.