CONCEPT OF STRESS

Definition:1
Folkman (1984), defined stress is an internal state and unpleasant feeling which
can be caused by physical demands on the body (disease condition & exercise,
extremes of temperature, and time) by environmental and social situation which are
evaluated as potentially harmful, uncontrollable, or exceeding our resources for coping,
on the other hand psychological responses such as anxiety, hopelessness, depression,
irritability.
Stress is a problem in maximum developed and developing countries. Majority
of body disease are said to be stress related for example, Hypertension, APD,
Conversion reaction, Diabetes etc. Now a days many physicians prescribe tranquillizer
and sedative drugs to many of the patients, which causes addiction of drugs.
Stressors:
The physical, environmental and social causes of the stress state, are termed as
stressors once (stress) induced by stressors, the internal stress state can turn and lead
various response.
Stress cycle
Stress has a number of immediate effects and, if the stressors are maintained for
Long term the behavioral, psychological, emotional & cognitive (thinking) effects
occurs. If these effects hinder adaptation to the environment or create discomfort and
distress, they themselves become stressors.
Neurotransmitter Response to Stress:
Stressors activate noradrenergic system in brain and cause release of
catecholamine from the autonomic nervous system . Stressors also activate serotonorgic
system in the brain as evidenced by increase serotonin turnover. Recent evidence
suggest that although glucocorticoid tends to enhance overall secretion function, there
may be difference in glucocorticoids regulation of serotonin-receptor subtype. Which
may have implication for serotonergic function in depression and related illness for
example; Glucocorticoid may increase serotonin 5-HT2 mediated action, thus
contributing to the intensification and action of these receptors type. Which has been

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implicated in the pathophysiology of major depressive disorder, stress also increases
dopaminergic neurotransmitters in neoprefrontal pathway.
Stress, Anxiety and Gastrointestinal system:
There is a link between stress, anxiety and physiological responsiveness of the
gastrointestinal system. Disturbance in gastrointestinal function occurs through a
central mechanism via humoral effect as the release of catecholamine. Sympathetic
autonomic responses may be generated in the lateral hypothalamus, a region with
neural interaction within the limbic forebrain, Parasympathetic autonomic response also
influence GI function. Parasympathetic impulses originate in periventricular and lateral
hypothalamus and travel to the dorsal motor nucleus of the vagus, the main
parasympathetic output pathway. The vagus is also modulated by the limbic brain,
producing an emotional gut pathway of response.
Enteric nervous system and its relation to stress
The enteric nervous system is a collection of neuron in the GIT that constitute
the brain of the gut and can function independent to CNS. This system controls the
motility, exocrine and endocrine secretion and microcirculation of the GI tract. It also
concerned in regulating immune and inflammatory process. Developmentally the
enteric nervous system is derived from the cells of vagal segment of neural creast
migrate to the cranial portion of the gut and and subsequently more gradually
postulated as nervous system of enteric GIT. Thus ENS is conceived as a displaced part
of CNS that retains communication with CNS through sympthetic and parasympathetic
afferent and efferent neurons. The part of CNS which is connected with the ENS is
termed as central Autonomic Neural Network through which the ENS exercises neural
control of function of GIT.
There is two group of ENS
1- Myentric plexus
2- Submucosal plexus
Both these plexus control the movement and secretion in stomach, intestine,
large intestine by sensitizing the endocrine system.

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 EFFECT OF STERESSORS OF HUMAN HEALTH2

STRESSORS H Immediate effect

Chemical E (1) Behavioral effects
A
Community E.g. over eating
L
Decision T Excessive alcohol consumption
Disease H (2)Physiological effects
Emotional Y E.g. increased blood pressure
Employment I Rapid heart rate
Environmental N Heightened muscle tension
D
Family (3)Emotional effects
I
Financial V
E.g. heightened
Pain I Depression
Phobic D Anger
Physical U (4) Cognitive effects
Social A E.g. Decreased concentration
L Increased distractibility
Work

If stressors continued further

Long term effect (Chronic)

(1) Behavior disorders
E.g. Obesity
Alcoholism
Drug addiction
(2) Medical (psychological) disorders
E.g. Hypertension
Heart disease
Headache
Psychosomatic (3) Emotional disorders
disease E.g. Chronic anxiety
Depression
Phobia
Personality change
Mental illness
(4) Cognitive disorders
E.g. Memory problem
Obsessive thought
Sleep disorder
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GENESIS OF ACID PEPTIC DISORDER DUE TO CHRONIC
STRESS2

Condition of chronic stress e.g. Anxiety, Depression etc.

Stimulation of limbic system of temporoparietal part of cerebral

hemisphere

Increase limbic temporal activity

Increase tone in Vagus nerve

Increased Sensitivity enteric nervous system

Hypersenstivity of M3 receptor in partial cell of stomach

Imbalance of aggrevating and protective factors

Results genesis of Acid Peptic Disorder

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 MODERN VIEW
In Modern medicine, no specific disease is seen that similar to Amlapitta. The
signs and symptoms of Amlapitta disease have given in modern medicine as an under
title of Acid peptic disease. There are number of disease in acid peptic diseases like -
Acute gastritis, chronic gastritis, peptic ulcers, gastro esophageal reflux diseases, non
ulcer dyspepsia, hyperchiorhydria syndrome, menetrier's disease etc. Peptic ulcers
(gastric and duodenal ulcers) have similar symptoms related to Amlapitta. But the
pathophysiology and histopathology said that ulcer's can't be included in Amlapitta. It
may be complication of Amlapitta.
In treatment of Amlapitta, vamana & virechana karmas are mentioned in ancient
classical Indian medicine books. Both are contra indicated in ulcers. Therefore we can't
include peptic ulcers in Amlapitta. So, the acid peptic disease without peptic ulcer can
be included in Amlapitta, So, peptic ulcers are not described anywhere in this chapter.
This chapter is described for the purpose of getting clinical co-relation and similarly
between Amlapitta and non-ulcentive acid peptic disease.
AETIOLOGY OF ACID PEPTIC DISEASES :-
(1) BAD FOOD HABITS:-3 - Irregular pattern of food intake.
- Excessive intake of tea, coffee, cold drinks, caustic soda etc.
- Excessive use of some measles, chilies and other irritant substances in food.
- Faulty meals cause delayed gastric emptying.
- Deficiency of vitamin-A & protein in diet.
Bad food habits may irritate the mucosal membrane of the gastro intestinal tract
and diseases like gastro esophageal reflux disease, gastritis etc. occurs.
(2) PSYCHO-SOMATIC FACTORS:-3
Psychic factors like mental stress, anxiety, depression are lead to the acid peptic
diseases. It leads hyperchlorhydria. Due to this, the secretary & motor functions of the
gastro intestinal tract are disturbed. Psychological stress and significant life event are
important in the cause of functional dyspepsia.

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 In stress induced gastritis, gastric acid secretion is invariably either normal or
decreased. Thus acid hypersecretion is not a significant etiological factor, instead the
breakdown of mucosal defense mechanism is the primary cause.
Stress causes decreased blood flow to the mucosa, leading to ischemia with
subsequent destruction of the mucosal lining. With increasing age atherosclerosis may
play a role in decreased blood supply to gastric mucosa. Hence greater susceptibility to
erosion and ulceration of the gastric mucosa.
(3) DRUGS & ADDICTIONS:-4
Aspirin and other non-steroidal anti-inflammatory drugs likediclofenac,
Ibuprofen etc. inhibits cyclooxygenase, decreases prostaglandin E and decreases
mucosal blood flow resulting in damage of gastric or duodenal mucosa. Steroids also
damage the mucosal memberance & become responsible factor for ulcers.
Theophuline, calcium channel blockers progesterone, tetracycline, potassium
chloride, bisphosphonate etc. drugs are delaying gastric emptying. Addictions like
alcohol, smoking, tobacco chewing etc. are damaging factors of gastro-duodenal
mucosa. High concentrations can cause gastric erosion.
(4) INFECTIONS:-
(a)Bacterial:4,5
Mainly Bacteria like H-pylori is responsible for the acid pepetic diseases. H-
pylori organisms grow in the mucous secreting cells of the stomach lining and create
ulcers or erosions or inflammation in gastric mucosa.
(B)Fungal or viral:5,6
It may develop in people with a prolonged illness or an impaired immune system.
(5) OTHER ASSOCIATED DISEASES:-5
* Ulcerative colitis
* Crohn's disease
* Hiatus hernia
* Hypothyroidism Sarcoidosis
* Diabetes Mellitus
* Zollinger Ellison syndrome (Gastrinoma)
All these diseases lead the aggravation of the acid peptic disorder.

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 Crohn's disease & sarcoidosis lead to duodenitis. Hiatushernia, partial
gastreatomy, ulcerative colitis & crohn's disease are responsible for the chronic
gastritis. Zollinger Ellison syndrome is responsible for peptic ulcers. Diabetes mellitus
may lead diabetis gastropareiss. Hypothyroidism & Hypercalcaemia may lead to
organic dyspepsia.
(6) GENETIC FACTORS:-
Modern medicine has given the 'O' blood group as a predisposing factor for the
acid peptic diseases. Hyperacidity syndrome is seen mainly in person with 'O' blood
group.
(7) ALLERGIC & AUTO IMMUNE DISEASE FACTORS:-8
Some time eosinophillia due to allergic disease causes eosinophilic gastritis.
The atrophic gastritis & gastric atrophy may result when antibodies attack to the gastric
mucosa. It also tends to occur in those who had partial gastrectomy.
These causative factors can be considered as an Ama Dosha in Ayurveda.
(8) IDIOPATHIC:-5,6
Sometime no causative factor was found for acid peptic disease. Menetrier's disease is a
form of gastritis whose cause isn't known.
PATHOPHYSIOLOGICAL AND COMMON SYMPTOMS OF GASTRO
INTESTINAL DISEASE:6
(1) Anorexia:-
Disturbances of appetite such as anorexia and early satiety are common in
digestive disease. Anorexia is the absence of hunger, satiety is the loss of desire to eat
after ingesting food. The control of both appetite and satiety resides in the
hypothalamus.
The level of plasma glucose controls satiety centers.
The causes of anorexia are both physical and psychological. Anorexia nervosa
is the psychological disorder in which appetite virtually does not exist and hunger is
markedly reduced. Anorexia is a nonspecific symptom in that it is associated with
many organic diseases, intestinal and extra intestinal.
(2) Flatulence and Belching:- Flatulence is due to excessive quantities of gas in the
stomach, small intestine or colon. Patients may refer to it as bloating or vaguely as

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heaviness. Most of the gas in this situation is also due to swallowed air. Usually
bacterial action on food, gastric atony or
altered motility of the gut may be the cause in certain cases.

(3) Disturbances of gastric secretary functions:-

(i) The stomach fails to secrete HCl acid and it diagnosed when the PH of gastric
secretion fails to decrease below 6.5 following maximal stimulation. Hypochlorhydria
means diminished acid secretion. Usually acid is not secreted pepsin also is not secreted
and even if it is the lack of acid prevents it from functioning because pepsin requires an
acid medium for activity obviously then, essentially all digestive function in the
stomach is lost when achlorhydira is present.
Though achlorhydira is associated with depressed or even no digestive
capability by the stomach, the overall digestion of food in the entire gastro intestinal
tract is still almost normal.
This is because trypsin and other enzymes secreted by the pancreas are capable
of digesting most of the protein in the diet. Particularly if the food is well chewed, no
portion of the protein is protected by collagen fibers, which need peptic activity for
most effective digestion.
Achlorhydria or hypochlorhydria may be a feature in some cases of atrophic
gastritis. Gastric malignaney and hypothyroidism is associated with a higher incidence
of achlorhydria. Pernicious anemia is characterized by achylia gastrica. Exocrine
pancreatic secreation may be deficient in some of these patients since acid, the
important stimulant of secretin is lacking.
(ii) Hyperchlorhydria :-
In contra distinction to achlorhydria the definition of hyperchorhydria is
difficult since the range of normal values varies widely in healthy persons. The
hyperchlorhydria has important in the genesis of peptic ulcer pain.
DISCRIPTION ON VARIOUS ACID PEPTIC DISEASES
(1) GASTRO-OESOPHAGEAL REFLUX DISEASE:-9
Gastro esophageal reflux disease is caused by excessive exposure of the esophagus to
acid refluxed from the stomach.

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Definition: - It refers to the varied clinical manifestations of reflux of stomach &
duodenal contents in to the esophagus. Although it may associate with sliding hiatus
hernia.

Pathogenesis :-
Lower oesophageal sphincter is a specialised bundle of circular muscle at the
lower end of the oesophagus. A tendency for mean lower oesophageal spincter pressure
is to be significantly lower in patients subjects with gastro oesophageal reflux disease.
The main common problem associated with reflux is an inappropriate relaxation of the
lower oesophageal sphincter.
(2) ACUTE GASTRITIS:-10
Definition:-
The term acute gastritis is usually acute erosive condition that typically results
in necrosis and hemorrhage of the mucosa with relatively inflammation.
It may however, be completely a symptomatic. Its course is self-limiting and
healing usually occurs without any residual damage.
Common factors associated with acute gastritis are: Alcohol, Drugs, Iron,
Salicylates,Stress, Cytotoxic drugs, Uremia, Gastric Irradiation, Acute systemic
infections, Staphylococcal food poisoning.
The major features differentiating acute from chromic gastritis is the tendency
for mucosal changes in acute gastritis to revert to normal.
(3) CHRONIC GASTRITIS:-11
Definition:-
Chronic gastritis is defined as any diffuse chronic inflammation involving the
gastric mucosa. It is by far the most common category of gastritis and incorporates a
heterogeneous group of disorders.
Histopathological classification:-
(i) Superficial gastritis
(ii) Atophic gastritis
(iii) Gastric atrophy
(a) Superficial gastritis:-

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 When inflammatory cells like neutrophils, lymphocytes, plasma cells, few
eosinophils etc. are limited to the gastric pits & upper lamina propria this type of
inflammation is called superficial gastritis.

(b) Atrophic gastritis:-

When inflammatory cells invade deeper in the lamina propria and glandular
epithelium. As the disease progreses, thinning of the mucosa occurs with loss of
glandular elements. In intestinal metaplasia, loss of parietal cells, chief cells, goblet
cells, absorptine cells & loss of intestinal villi.
Based on the anatomical portion of the stomach involved and presence or absent
of parietal cells antibodies. chronic atrophic gastritis has been divided into:
(a) Type A (b) Type B.
TypeA gastritis: - It is the less common form of chronic gastritis. It characteristically
involves the fundus and body of stomach with relative sparing of the antrum and it is
due to autoimmune activity against the parietal cell. Parietal cell antibodies in the
serum are a marker of type A gastritis. In some patients the degree of gastric atrophy is
so severe that the absence of parietal cells leads failure to secret intrinsic factor and
pernicious anemia results. Type A gastritis is asymptomatic. It is important because it
may lead to gastric cancer.
Type B gastritis:
This is the more common form of Chronic Gastritis involves the antrum of stomach but
does spread to the body especially of along the lesser curve.
Studies from various parts of the world have established that H. pylori are the
agent responsible for type B gastritis. It is also occurs after gastric surgery when it may
be caused by a loss of the trophic hormone gastrin and the reflux of bile, pancreatic and
intestinal secretion. The condition is important as a precursor of gastric and duodenal
ulceration and possibly gastric carcinoma.
(C) Gastric atrophy:-
In gastric atrophy Parietal & chief cells are absent, mucosal thickness is
markedly reduced and small number of inflammatory cells are present & end results
leads to persistend & progressive atrophic gastritis.

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 Clinical types of chronic gastritis :-
(i) Eosinophilic gastritis.
(ii) Granulomatous gastritis
(iii) Autoimmune gastritis with pernicious anaemia
(iv) Duodenogastric reflux gastritis
(v) Collagenous gastritis
(vi) Hypertrophic gastritis
(vii) Lymphocytic gastritis
(4) DUODENITIS:-7
Inflammation of the duodenum is called duodenitis. Duodenitis is ususally diagnosed
by the macroscopie appearances at endoscopy.
Common causes :-
i) H-Pylori infection
ii) Crohn's disease
iii) Sarcoidosis
iv) Ectopic Pancreatic tissues.
(5) DYSPEPSIA (NON-ULCERATIVE) 10
Dyspepsia (Indigestion) is a term for non-specific symptoms thought to
originate from the upper gastrointestinal tract. Typical symptoms include upper
abdominal discomfort with/without related to food, anorexia, nausea, vomiting,
bloating & heartburn. It is mainly due to stress or other psychological disturbances,
there are other pathophysilogical abnormalities but it has either not been picked up by
the test or the correct test has not been done.
Multiple factors lead to dyspeptic symptoms in true nonulcer dyspepsia.
Mainly-
(a) Impaired motor and sensory functions:-
- Delayed gastric emptying
- Intestinal dismotlity
(b) Muosal inflammation: - Due to
- Chronic gastritis
- Chemical Irritants
- Autoimmune attack

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 (c) Psychosocial factors:-
- Stress
- Significant life events.
(d) Others:-
- Bad feeding habits.
- Hurriedly consumed food
- Irregular intervals of food consumption.
(6) HYPERACIDITY SYNDROME:-6
Hyperacidity syndrome includes mainly peptic ulcer disease. But in sometimes
it depends upon mucous & concentration of HCL in stomach. In hyperacidity, total
acidity in stomach is higher than the normal. It is mainly due to-
i) Mental stress
ii) Excess amount of circulating amino acids.
iii) Bad food habits
iv) Releasing of histamine substances.
v) Disturbance in feedback inhibition via antral acidification
COMMON SYMPTOMS AND SIGNS OF THE ACID PEPTIC
DISEASE:-4,5,6
(1) Heart burn: - symptoms of the gastro oesophgeal reflux disease. Burning and / or
rising retrosternal discomfort is complained by the patient.
(2) Regurgitation / Water brush: - Water brush, which means the regurgitation of
acid or bile in to the mouth.
(3) Dysphegia: - It is cardinal symptom of the G.E.R.D. painful swallowing is present,
which signifies oesophagitis and a stricture of the lower oesophageal sphincter.
(4) Altered Appetite:-
(5) Sensation of satiety & Anorexia:-
Both above of these symptoms are seen in all the acid peptic diseases in mild or
severe form.
(6) Nausea & Vomiting:-

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 Both of these symptoms are mainly seen in acute & chronic gastritis. Non ulcer
dyspepsia & duodenitis may have nausea or vomitting sometimes. It is mainly due to
irritation of the gastric mucosa.
(8) Epigastric pain:-
It is mainly due to excessive irritation of the mucous membrane of the stomach.

(9) Heaviness in abdomen:-

It is due to anorexia, altered appetite & sensation of satiety which lead ingestion
& delayed gastric emptying. Impaired motor function of the stomach may produce this
symptom.
(10) Hematemesis :-
This symptom occurs in acute type of gastritis when the erosion and
haemorrhage in mucosa of the stomach is there.
(11) Aneamia :-
Pernicious anaemia is found in chronic gastritis & menetrier's disease. It is due
to hypochlorhydria or achlorhydira.
(12) Fatigue:-
It is found in chronic gastritis and in menetrier's diseas. It is due to avitaminosis
of B12 and hypoprotinaemia.
(13) Diarrhoea :-
Diarrhoea is common in hyperacidity & menetrier's disease. It is due to
indigestion of protein materials or hyperactive motor function of the gut or large
intestine.
DIAGNOSIS OF ACID PEPTIC DISEASES :-5,6
(1) BY CLINICAL SIGNS & SYMPTOMS :-
All the acid peptic diseases are diagnosed by clinically with symptoms and
signs. Sometimes it is difficult to differentiate from one another. At that time other
Investigations may help for accurate diagnosis.
(2) HEAMATOLOGICAL INVESTIGATIONS:-
It has no value for diagnosis of these diseases.

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(3) GASTRIC JUICE ANALYSIS:-
It gives the concentration of the acid in gastric jice. It has no value for accurate
diagnosis of acid peptic disease. Hyperchlorhydira, hypochlorhydria & Achlorhydria
conditions are easily diagnosed by this test.
Indications:-
-Patients with pernicires anaemia and achlorhydria.
- Patients with recurrent ulcer especially after vagotomy
- Patients with a gastric ulcer in whom neoplasm is suspected
- Suspected zollinger - Ellison syndrome
Interpretation:-
(i) Hyperchlorhydria :- mainly present in
- In duodenal ulcer
- In gastric ulcer
- Gastric carcinorna
- Gastric neurosis, hyperitability
- Pyloric steriosis, pylorospasm
- Chronic appendicitis etc.
(ii) Hypochlorhydria :-
- In Gasteroenterostomy
(iii) Achlorhydria :- mainly present in:
- Chronic gastritis
- PerniciousAnaemia
- Partial gastrectomy
- Other diseases like hyperthyroidism, Myxoedema etc.
Gastric Jice Analysis test does not give the Complete diagnosis of acid peptic
diseases. This test has not value for accurate diagnosis at present.
(4) RADIOLOGICAL EVALUATION :-
Radiograph with contrast agent like barium meal x-ray can give diagnosis of the
various conditions & they are as follows:
a) Hiatus Hernia
b) Oesophageal varices
c) Peptic Oesophageal stricture

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 d) Reflux oesophagitis
e) Lower oesophageal sphincter structure.
f) Achlasia Cardia
g) Gastric or duodenal ulcear
h) Mass lesion in oesophagus or stomach
i) Erosive gastritis.

(5) ENDOSCOPY :-
This procedure is done entirely with fiberoptic endoscopes. It is suitable & more
reliable test for accurate diagnosis of acid pepetic diseases e.g.
(i) Oesophagitis :-
(ii) Gastritis :-
-Atrophic gastritis
-Antral gastritis
-Erosive gastritis
-Superficial gastritis
(iii) Duodenitis :-
(iv) Mentrier's disease
(6) BIOPSY AND CYTOLOGY
COMPLICATIONS OF ACID-PEPTIC DISEASES:-5,6
There are following complications found in non-ulcerative acid peptic diseases.
(i) Peptic ulcers
(ii) Stricture of the oesophagus & lower oesophageal sphinder.
(iii) Weight loss
(iv) Cachexia
(v) Anemia
(vi) Gastric carcinoma
PROGNOSIS OF ACID PEPTIC DISEASES5,11
(1) Acute gastritis, chronic superficial gastritis & early detectable Gastro oesophageal
reflux diseases are curable easily. But they are difficult to diagnose as early as possible.

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(2) Chronic atrophic gastritis, gastric atrophy, menetrier's disease and complicated
G.E.R.D. are become very difficult to cure. Complicated G.E.R.D. may be curable by
surgical process. Excessive chronoicity of these disease Irreversible condition.
So they become incurable.
(3) Chronic gastritis (Particularly atrophic gastritis) and menetrier's disease are present
with pernicious anemia, loss of weight, diarrhea & peripheral oedema. Both are
incurable disease.

MANAGEMENT:-12,13
(1) Managed by relieving the causative factors.
(2) Drugs:-
- Antacids
- H-2 antagonists / proton pump Inhibitors.
- Prokinetics & Anticholinergics.
- Antibiotics which relieve the infections like H-pylori.
(3) Supportive therapy:-
- Loading dose of Vit - B12
- Protein supplements.
- Intravenous fluid therapy.
(4) Surgical treatment in some cases.

The US Food and Drug Administration has approved some regimens, which are
now accepted internationally, for the treatment of HP infection in patients with
peptic ulcer disease, both gastric and duodenal.
These regimens are also known as triple therapies and have reported cure rates
from 85-90%.
FDA-approved treatment options14
FDA-approved treatment options
Omeprazole 40 mg QD + Clarithromycin 500 mg TID for two weeks, then omeprazole 20
mg QD for 2 weeks
OR

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 Ranitidine bismuth citrate (RBC) 400 mg BID + Clarithromycin 500 mg TID for 2 weeks,
then RBC 400 mg BID for 2 weeks
OR
Bismuth subsalicylate 525 mg QID + Metronidazole 250 mg QID + Tetracycline 500 mg
QID for two weeks + H2 receptor antagonist therapy as directed for 4 weeks
OR
Lansoprazole 30 mg BID + Amoxycillin 1 gm BID + Clarithromycin 500 mg TID for 10
days

OR
Lansoprazole 30 mg TID + Amoxycillin 1 gm TID for 2 Weeks
OR
Ranitidine bismuth citrate (RBC) 400 mg BID + Clarithromycin 500 mg BID for 2 weeks,
then RBC 400 mg BID for 2 weeks
OR
Omeprazole 20 mg BID + Clarithromycin 500 mg BID + Amoxycillin 1 gm BID for 10
days
OR
Lansoprazole 30 mg BID + Amoxycillin 1 gm BID + Clarithromycin 500 mg BID for 10
days

Although not FDA approved, amoxicillin has been substituted for tetracycline for patients
for whom tetracycline is not recommended.

This dual therapy regimen has restrictive labeling. It is indicated for patients who are
either allergic or intolerant to clarithromycin or for infections with known or suspected
resistance to clarithromycin.

This dual therapy regimen has restrictive labeling. It is indicated for patients who
are either allergic or intolerant to clarithromycin or for infections with known or suspected
resistance to clarithromycin.

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