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Diagnosis, Treatment, and Latest Research

reflux (LPR) is defined
as the retrograde flow
of stomach content to
the larynx and
pharynx whereby this
material comes in
contact with the upper
aerodigestive tract.

Increased by 4% every year since 1976

National Cancer Institute of the United States:
Increase in the prevalence of esophageal cancer of 600% since 1975

ltman et al:
500% increase in visits to the otolaryngologist due to LPR between 1990 and 2001

LPR is present in more than 50% of patients with dysphonia.


Physiological Barriers • The physiological barriers to LPR – LES & UES – Esophageal clearance influenced by esophageal peristalsis – Saliva and gravity – Barriers failstomach content comes in contact with the laryngopharyngeal tissue damage to the epithelium. . ciliary dysfunction. and altered sensitivity. inflammation.

Acid • The pH of the pharynx is neutral (pH 7). • Damage to the pharynx caused by: – Decline in pH & exp. and pancreatic enzymes). pepsin. to reflux components (ex. bile salts. – 3 episodes can already cause damage .

4 – Irreversibly inactivated at pH 8 – Reactivated (decline pH) laryngeal injury (by hydrogen ions) – Cause intracellular damage because cell components such as the Golgi complex and lysosomes have a low pH (5.0 and 4.Pepsin – Stable at pH 7.0) .

Bile Acids • Rats Causing laryngeal inflammation at both acid and nonacid pH. – Conjugated bile acids acid pH – Chenodeoxycholic acid pH 5 to .

3% GERD – Heartburn or a burning: 20% LPR vs. 83% GERD . Symptoms • According to Koufman • 899 patients – Throat clearing: 87% LPR vs.

– Belafsky et al. >13 = Abnormal. .• The most common symptoms – Excessive throat clearing – Coughing – Hoarseness (fluctuating. occurs in the morning-improves during the day) – Globus pharyngeus (“lump in the throat sensation”). Reflux Symptom Index (RSI).


Diagnostic Methods .

• Granulomas. – According to severity. Reflux Finding Score (RFS) based on the findings of fiberoptic laryngoscopy. • Belafsky et al. LPR. Laryngoscopy • Nonspecific signs of laryngeal irritation and inflammation. contact ulcers. • Importance: Cancer vs. and pseudosulcus (infraglottic edema) 90% of cases of LPR. location. and presence or absence – 7 or higher LPR – Evaluate the efficacy of treatment in patients with LPR . particularly in the posterior region. edema and erythema.






pH Monitoring • Multichannel intraluminal impedance pH monitoring • Controversy: LPRpH proximal sensor declines to < 4 during or immediately after distal acid exposure (near LES) • no consensus regarding the definition of abnormal pH. .

Empirical Treatment • Alternative diagnostic modality (diagnostic confirmation). • PPI twice a daily for 2 to 3 months. .

tomato sauce. quitting smoking. and red wine. gasified beverages. avoiding alcohol. chocolate. fat. . TREATMENT • Dietary changes and changes in habits (weight loss. and not eating immediately before bedtime) • Dietary restrictions include caffeine.

30 to 60 minutes before a mealhighest concentration of the drug during the period of stimulation of the proton pump by food consumption.• PPIs suppress acid production by directly acting on the Hþ-KþATPase of parietal cells. of 3 months PPIs administered twice a day (40 mg omeprazole or an equivalent PPI). . • Min.

.antireflux treatment PPI two times per day (before breakfast and dinner) and of an H2 receptor antagonist before bed.time.• Max.

Surgery • Laparoscopic or Nissen .

– Alkaline water pepsin is irreversibly inactivated in alkaline water at pH 8. – Nonacid diet for 2 weeks Symptoms improved in 95% of them. • LPR who were resistant to PPI treatment. Latest Research Nonacid Diet and Alkaline Water • Pepsin (laryngeal tissue) activated by exogenous hydrogen ions derived from any source (ex. diet).8 .

Biomarkers of Reflux .

Inflammatory Cytokines • GERD alters IL-6 (mucosal inflammation) induced by reflux. • IL-6 levels increase according to the degree of reflux and decrease after treatment of GERD. .

• In the presence of LPR and pepsin Carbonic anhydrase III decreases in the vocal folds worsening acid-induced damage. . Carbonic Anhydrase • Defense component of the mucosa • Catalyzes the hydration of CO2 producing bicarbonate neutralizes acid reflux in the extracellular space.

• Tumor suppressor loss of expression1st step to tumor invasion. . • E-cadherin decline in LPR – Reflux components (acid or pepsin)/ to the reflux-associated inflammatory response. E-Cadherin • Maintain the integrity and barrier function of the epithelium.

impairing epithelial protection. adhesion & cell signal transduction. hydration. ion concentration. • LPR reduces the secretion of mucins. lubrication. cell cycle modulation. renewal and differentiation of the epithelium. Mucins Glycoproteins expressed by different types of epithelial cells at sites exposed to oscillations in pH. transport. and oxygenation. . • FunctionsProtection.