INTRODUCTION:

Peptic ulcer disease (PUD) is a serious gastrointestinal disorder that requires a well targeted therapeutic strategy.

The dictionariesare against the semantic misappropriation peptic ulcer; Peptic (Gr. Peptikos) means digestive or related to digestion.^1,2 Ulcers are crater-like sores which form in the lining of the stomach (called gastric ulcers), just below the stomach at the beginning of the small intestine in the duodenum (called duodenal ulcers) or less commonly in the oesophagus (called esophageal ulcers). In general, ulcers in the stomach and duodenum are referred to as peptic ulcers. Duodenal ulcers are a common condition characterized by the presence of a well-demarcated break in the mucosa that may extend into the muscularis propria of the duodenum. More than 95% of duodenal ulcers are found in the first part of the duodenum; most are less than 1 cm in diameter.^2,3A duodenal ulcer is a raw area or open sore (ulcer) that develops when there is a break in the lining of the duodenum, the upper part of the small intestine which is connected to the stomach. When food passes from your mouth, it moves through the oesophagus and into your stomach. From the stomach, it travels into the duodenum. The duodenum produces chemicals and mucus, which protects the tissues and covers the surface from the acid.

If the acid damages this protection by breaking through the lining of the duodenum, an ulcer occurs. Ulcer is a dispensable symbol for this larger dyspeptic reality.⁴ It is essential for understanding gastro duodenal ulcer as a clinical disease, It is the concept that the crater is simply a manifestation and is rather unimportant to the whole illness. Peptic ulcer, as medicine has under stood it, is strictly a human privilege. A number of drugs including proton pump inhibitors and H2 receptor antagonists are available for the treatment of peptic ulcer, but clinical evaluation of these drugs has shown incidence of relapses, side effects, and drug interactions. This has been the rationale for the development of new antiulcer drugs and the search for novel molecules has been extended to herbal drugs that offer better protection and decreased relapse. Drugs of plant origin are gaining popularity and are being investigated for a number of disorders, including peptic ulcer. The present article reviews the anti ulcerogenic and ulcer healing property of both pharmacotherapy by allopathic medicines and natural therapy by plants diet and alternative medicines. Here we have highlighted some of the important plants/plant products reported and pharmacotherapy for their anti-ulcer and ulcer healing properties.

Incidence:

Peptic ulcer disease had a tremendous effect on morbidity and mortality until the last decades of the 20th century. The incidence of chronic duodenal ulcer varies in any one population from year to year ^[5,6]. The prevalence of duodenal ulcers is estimated to be 6-15% in the general population. Most individuals do not have clinically significant ulcer disease, peptic ulcer disease is decreasing,and ulcers have become a rare cause for hospital admission.The prevalence is linked to the presence of H pylori. Approximately only 10% of young persons have H pylori infection, and the proportion of people with the infection increases steadily with age. Approximately 10% of the US population has evidence of a duodenal ulcer at some time. Of those infected with H pylori, the lifetime prevalence is approximately 20%.⁷Overall, the incidence of duodenal ulcers has been decreasing over the past 3-4 decades. It is also known that duodenal ulcer is a relatively common condition in many developing countries. However, unlike many industrialized countries, in some young developing countries like India, the diagnosis of duodenal ulcer in some cases is first made after perforation⁸. Men tend to be affected more frequently by duodenum ulcers than women. It is also more common in people with a family history of duodenal ulcers.

Etiology:

Most duodenal ulcers are caused by a chronic infection with bacteria called H. pylori. Anti-inflammatory medications such as aspirin and ibuprofen which many people use for muscle pain relief and arthritis also affects the lining of the duodenum and causes excessive stomach acid. Other factors that may increase the risk of developing a duodenal ulcer include nicotine, caffeine, excessive alcohol consumption and stress. Smoking has been implicated in the etiology of duodenal ulcers and in delaying of healing by many investigators. An ulcer is the result of an imbalance between aggressive and defensive factors. On one hand, too much acid and pepsin can damage the stomach as well as duodenum lining and cause ulcers.^[9] On the other hand (and more commonly), the damage comes first from some other causes, making the stomach lining susceptible to even an ordinary level of gastric acid. If a person does not receive treatment for ulcers, it could lead to a bleeding ulcer (the ulcer has eaten into blood vessels and the blood has seeped into the digestive tract), a perforated ulcer (the ulcer has eaten a hole in the wall of the stomach or duodenum and bacteria and partially digested food has spilled into the hole, causing inflammation) or a narrowing and obstruction of the intestinal opening preventing food from leaving the stomach and entering the small intestine.

Sign and symptoms:

Complications that may develop as a result of a duodenal ulcer include bleeding and perforation, where the ulcer pierces right through the wall of the duodenum. This causes immense pain and immediate medical attention is required.

· Some common symptoms in patients with duodenal ulcers are:

o Epigastric pain can be sharp, dull, burning, or penetrating.

o Many patients experience a feeling of hunger.

o The pain may radiate into the back.

o About 20-40% of patients describe bloating, belching, or symptoms suggestive of gastrooesophagial reflux.

o Ulcer-related pain generally occurs 2-3 hours after meals and often awakens the patient at night. This pattern is believed to be the result of increased gastric acid secretion, which occurs after meals and during the late night and early morning hours when circadian stimulation of gastric acid secretion is the highest.

o About 50-80% of patients with duodenal ulcers experience nightly pain, as opposed to only 30-40% of patients with gastric ulcers and 20-40% of patients with non ulcer dyspepsia (NUD).

o Pain is often relieved by food, a finding often cited as being specific for a duodenal ulcer. However, this symptom is present in only 20-60% of patients and is probably not specific for duodenal ulcers.

· The pain of duodenal ulcers is generally episodic; however, the pain can evolve into a chronic, daily occurrence in some patients.

· Concern is especially warranted in the setting of new-onset nausea and vomiting, decreased appetite, and weight loss.

· GI bleeding is a common complication of duodenal ulcers and can have serious consequences.

o Patients may present with melena, coffee-ground emesis, or hematemesis.

o The passage of frank blood in the stool or maroon-colored stool in the presence of a bleeding duodenal ulcer suggests precipitous GI bleeding.

· Patients who develop gastric outlet obstructon as a result of a chronic, untreated duodenal ulcer usually report a history of fullness and bloating associated with nausea and emesis that occurs several hours after food intake. A common misconception is that adults with gastric outlet obstruction present with nausea and emesis immediately after a meal.

· A few individuals with duodenal ulcers are completely asymptomatic.

o According to one study, typical epigastric pain was rare in patients older than 65 years with peptic ulcer disease (ie, gastric ulcer and duodenal ulcer).

o Elderly patients are more likely than younger patients to present in an asymptomatic fashion, which is especially common in the setting of NSAID use.

Physical:

No characteristic physical findings are associated with duodenal ulcers. In general, most patients have tenderness over the epigastrium, but this finding has a low sensitivity and specificity. Less often, tenderness is present over the right upper quadrant (RUQ), left upper quadrant (LUQ), or supraumbilical region. Most patients with an uncomplicated duodenal ulcer do not have any other physical findings.

· In the presence of a complication, such as gastric outlet obstruction.

· Perforation usually results in classic findings of diffuse peritonitis with abdominal rigidity, guarding, and rebound tenderness.

· Bowel sounds may initially be hyperactive but, with time, become absent.

· Risk factors for mortality from peptic ulceration include preoperative metabolic acidosis, renal insufficiency at the time of admission, reduced serum albumin concentrations on admissions or poor postoperative nutrition.

Diagnosis:

The diagnosis of a duodenal ulcer is based on the patient’s symptoms, medical history and physical examination. Without the initial diagnosis of duodenal ulcer however, the usefulness of all the new ulcer drugs such as Cimetidine, Ranitidine, Tripotassium dicitrate Bismuthate (De Nol) and Omeprazole (Losec) in preventing perforation is questionable^7,10. In addition, certain tests may be ordered to determine the diagnosis and they include:

· Upper GI X-ray

· Blood tests

· Endoscopy

· Biopsy

· The rapid urease test detects the enzyme urease, which is produced by H. pylori.

· A histology test allows the doctor to find and examine the actual bacteria.

· Breath test

· Stool antigen test

Pathophysiology:

The pathophysiology behind chronic duodenal ulcer is not fully understood, but may be explained as an imbalance between aggressive and defensive factors acting on or in the mucosa. Medical therapy may aim to reduce the aggressive factors acid and pepsin by compounds that neutralize the acid or inhibit the secretion of acid.^[11] Peptic activity is reduced by the high acid pH and also by the inhibition. Another group of compounds increases the mucosal defence by stimulating the secretion of mucus, bicarbonate, and growth of the mucosa, or by forming a protective layer on the ulcer crater. Some compounds affect both the aggressive and defensive factors. All modern compounds heal most ulcers in 4 to 6 weeks, but do not alter the natural history of ulcer disease, as indicated by the high rate of ulcer relapses after cessation of treatment.^[12]There is good evidence that the adherent mucus plays an important role in the protection of gastro duodenal mucosa from the endogenous aggressors acid and pepsin. Adherent mucus provides a stable unstirred layer which supports surface neutralization of acid by mucosal bicarbonate output and acts as a permeability barrier to luminal pepsin^[12-14]. The adherent mucus layer is continuous. True thickness of the mucus layer and its continuity can only be observed on unfixed sections of mucosa, since histological fixatives and preparation for electron microscopy can cause dehydration and shrinkage of the mucus gel. The structure of adherent gastric mucus is deficient in patients with peptic ulcer disease because of decreased polymerization of the component glycoproteins. This impairment of the mucus barrier is associated with raised amounts of pepsin 1, which digests the mucus layer more aggressively than the major pepsin, pepsin 3, under conditions that pertain both in the stomach (pH 2) and duodenum (pH 4-5). Adherent mucus does not appear to offer much protection against exogenous damaging agents, e.g. alcohol and aspirin. These agents permeate the mucus barrier, damaging the underlying epithelium^{[10, 16]}. The subsequent epithelial repair process is protected by a gelatinous coat over ten times thicker and distinct from the normal adherent mucus layer. One recent study showed the gelatinous coat to be primarily a fibrin-based gel with mucus and necrotic cells. Human gastric juice contains 3 major proteolytic components (pepsins1, 3 and 5 or gastricsin). Pepsin 1 is increased in peptic ulcer and it's properties are relatively poorly understood. Studies with pepstatin the highly specific aspartic-protease inhibitor have therefore been carried out on individual active and proenzymes to assess any enzymic similarities. Human pepsin 1 was inhibited with high affinity similar to pepsin 3, whereas pepsin 5 (gastricsin) was at least 40 times less sensitive. Inhibition of human pepsinogens 1, 3 and 5 and pig pepsinogen A showed similar trends to the active enzymes. Studies using Sephadex gel filtration showed that pepstatin does not bind to pepsinogens and inhibition arises from pepstatin binding the pepsins released upon activation. Pepstatin inhibition was shown to be relatively independent of pH between 1.5 and 3.8 although at higher pH inhibition was less effective^{[9, 16]}. The evidence suggests that pepsin 1 is similar to pepsin 3 and pepstatin inhibits by a one to one molecular binding to the active site. The explanation for the reduced affinity of pepstatin to pepsin 5(gastricsin) needs further study by co-crystallisation X-ray analysis.

Management of duodenal ulcer:

Along with reducing stress and modifying lifestyle, doctors treat gastric and duodenal ulcers with several types of medicines, including H2-blockers, proton-pump inhibitors and mucosal protective agents. When treating H. pylori, these medications are used in combination with antibiotics. If medication is ineffective or complications arise, surgery may be required.¹⁶

Medications:-

H2-blockers reduce the amount of acid that the stomach makes. These medicines include cimetidine (Tagamet), ranitidine (Zantac), famotidine (Pepcid) and nizatidine (Axid). A single bedtime dose starts healing a duodenal ulcer in four weeks and a gastric ulcer in six to eight weeks.¹⁷

Proton-pump inhibitors modify the stomach's production of acid by stopping the stomach's acid pump - the final step of acid secretion.some PPIs are Esomeprazole (Nexium), Lansoprazole Prevacid), Omeprazole (Prilosec), Pantoprazole Protonix), Rabeprazole (Aciphex). The recently approved and now available drug, omeprazole (Prilosec), is 10 times more powerful in suppressing stomach acid production than the H2-blockers, able to promote duodenal ulcer healing in two to four weeks.^[18] This potent acid-inhibitor can suppress about 95 percent of stomach acid production. It is especially useful for treating people whose ulcers fail to respond to H₂-receptor blockers or other medications and those with Zollinger-Ellison syndrome.

Mucosal protective agents protect the stomach's mucous lining from acid. The prescription medications are sucralfate (Sulcrate or Carafate) and misoprostol (Cytotec). The non-prescription medications are antacids (such as Tums and Rolaids) and bismuth subsalicylate (Pepto-Bismol).¹⁹

Antibiotics: With the discovery of the link between ulcers and H. pylori peptic ulcers can be treated by a short course of combined high dose antibiotic therapy rather than acid-suppression alone. Without antibacterial therapy, there is a 75 percent chance of the ulcer reoccurring. With antibacterial therapy, there is a 1 percent chance of the ulcer reoccurring. There are two types of combination therapies currently being used: triple therapy and dual therapy.²⁰

Triple therapy involves:

· Metronidazole (Flagyl), an antibiotic taken four times a day

· Tetracycline (Achromycin or Sumycin), an antibiotic taken four times a day

· Pepto-Bismol taken four times a day

This regimen lasts two weeks. This treatment is 90 percent effective in destroying the H. pylori bacteria and in reducing the risk of reoccurrence. (physician may substitute amoxicillin (Amoxil or Trimox); physician may substitute clarithromycin (Biaxin))

Dual therapy involves:

· Amoxicillin two to four times a day or Biaxin three times a day

· Prilosec two times a day

This regimen lasts two weeks. This treatment is 80 percent effective in destroying the H. pylori bacteria and in reducing the risk of reoccurrence.

Surgery:

The most common types of surgery for ulcers are vagotomy, antrectomy and pyloroplasty.

Vagotomy involves cutting the vagus nerve that transmits messages from the brain to the stomach. This interruption reduces acid secretion.

Antrectomy removes the lower part of the stomach (antrum) which produces a hormone that stimulates the stomach to secrete digestive juices. This enlarges the opening into the duodenum and small intestine (pyloris), enabling contents to pass more freely from the stomach. Two important developments are associated with the decrease in rates of peptic ulcer disease: the discovery of effective and potent acid suppressants, and of Helicobacter pylori. With the discovery of H pylori infection, the causes, pathogenesis, and treatment of peptic ulcer disease have been rewritten.^[21] We focus on this revolution of understanding and management of peptic ulcer disease over the past 25 years. Despite substantial advances, this disease remains an important clinical problem, largely because of the increasingly widespread use of non-steroidal anti-inflammatory drugs (NSAIDs) and low-dose aspirin. We discuss the role of these agents in the causes of ulcer disease and therapeutic and preventive strategies for drug-induced ulcers. The rare but increasingly problematic H pylori-negative NSAID-negative ulcer is also examined. More effective eradication of C. pylori may alter the natural history of peptic ulcer.Diets modify gastric function in various ways. Fibre influences acidity, pepsin and bile acid concentrations both in vitro and in vivo. Both animal studies and clinical studies in humans give reason to believe that a diet rich in fibre may protect against the development of peptic ulceration. In about 5-10% of duodenal ulcer patients, ulcer healing is difficult or impossible to achieve with H₂-receptor antagonists. Such patients are considered to have a refractory ulcer. The cause of refractoriness remains unknown. Some patients have high acid secretion or inadequate acid suppression on treatment, but this has not been confirmed by all investigators or in all patients. Abnormalities in mucosal defence presumably exist, but none have as yet been identified.^[22] The principal medical therapeutic approach has been to continue suppressing acid or to use mucosal protective agents. Increasing the duration of H₂-receptor antagonist treatment at the same dose had little effect, but doubling or trebling the dose improved healing rates in open studies. In the recent years, attention has been focused at the traditional (Herbal) way of therapy. It is presumed that Ayurvedic Medicines (drugs), which is popular in our country, have lesser side effects as compared to allopathic drugs.

Natural Remedies:-

While prescription drugs are effective for treating the symptoms of digestive problems, they sometimes have negative side effects. For a more natural, healthier approach, herbal remedies safely improve digestive health and reduces inflammation. ^{[23, 24]}Two well known herbs such as Matricaria recutita (German Chamomile) and Filipendula ulmaria (Meadowsweet) have excellent anti-inflammatory and antispasmodic effects that soothe and calm the digestive tract while also reducing stomach acid. Other herbal ingredients include Ulmus fulva (Slippery Elm) and Sutherlandia frutescens ('Cancer Bush') reduces pain and irritation^25,26, and also acts as a powerful tonic.

Home Remedy for Peptic Ulcer:

· The most effective home remedy for treating peptic ulcer is to eat bananas everyday. It is an excellent way to neutralize the hyperacidity of the gastric juices. Banana milk shake is also beneficial in curing peptic ulcer.

· Having cold milk, without sugar, is effective in reducing the acid, thereby providing relief from burning sensation one encounters in peptic ulcer.

· Prepare a paste of 10 grams drumsticks leaves and water. Mix this paste in half a cup of yoghurt. Have this mixture every day, to cure peptic ulcer.

· In 250 ml of water, soak 15 grams leaves of wood apple and keep it overnight. Strain this concoction in the morning and have it.

· Applying a hot pack over the abdomen region is one of the effective ways of curing peptic ulcer.

· Cabbage and carrot, when mixed as juices, have been found to be beneficial in treating peptic ulcer. In half a liter of water, boil 250 grams cabbage until it is reduced to half. In a similar way, prepare carrot juice. Now, combine 125 ml of each juice. Once cool, drink it two times in a day.

· Tea made from fenugreek seeds is effective in curing peptic ulcer. When coated with water, fenugreek seeds become slightly mucilaginous, which helps in treating the ulcer.

· Combining carrot juice with spinach (or beet) and cucumber is effective in treating peptic ulcer. You can either mix 300ml carrot juice and 200 ml spinach juice or combine 300 ml carrot juice and 100 ml each of beet and cucumber juice, to make 500 ml of juice. Consume this daily.

· Blanch 5 almonds everyday and extract their milk. Drink this milk everyday, as it provides protein and also binds the acid in stomach.

· Drinking raw goat milk is effective in peptic ulcers treatment. For best results, drink this juice three times a day.

· Lime is beneficial in curing peptic ulcer. The citric acid and mineral salts present in it help treat the ulcer. You can either have lime juice or use it in salads.

Nutrition and Dietary Supplements

Following these nutritional tips may help reduce symptoms:

· Foods containing flavonoids, like apples, celery, cranberries (including cranberry juice), onions, garlic, and tea may inhibit the growth of H. pylori.

· Eat antioxidant foods, including fruits (such as blueberries, cherries, and tomatoes), and vegetables (such as squash and bell peppers).

· Eat foods high in B-vitamins and calcium, such as almonds, beans, whole grains (if no allergy), dark leafy greens (such as spinach and kale), and sea vegetables.

· Avoid refined foods, such as white breads, pastas, and sugar.

· Eat fewer red meats and more lean meats, cold-water fish, tofu (soy, if no allergy) or beans for protein.

· Use healthy oils, such as olive oil or vegetable oil.

· Reduce or eliminate trans-fatty acids, found in commercially baked goods such as cookies, crackers, cakes, French fries, onion rings, donuts, processed foods, and margarine.

· Avoid beverages that may irritate the stomach lining or increase acid production including coffee (with or without caffeine), alcohol, and carbonated beverages.

· Drink 6 - 8 glasses of filtered water daily.

· Exercise at least 30 minutes daily, 5 days a week.

These supplements may also help:

· Probiotic supplement (containing Lactobacillus acidophilus), 5 - 10 billion CFUs (colony forming units) a day -- Probiotics or “friendly” bacteria may help maintain a balance in the digestive system between good and harmful bacteria such as H. pylori. Probiotics may help suppress H. pylori infection and may also help reduce side effects from taking antibiotics, the treatment for an H. pylori infection. Some probiotic supplements may need to be refrigerated for best results.

· Vitamin C, 500 - 1,000 mg 1 - 3 times daily -- One study found that taking vitamin C along with triple therapy allowed the dose of one antibiotic to be lower. Vitamin C may also be helpful in treating bleeding stomach ulcers caused by aspirin use.

CONCLUSION:

All modern compounds heal most ulcers in 4 to 6 weeks, but do not alter the natural history of ulcer disease, as indicated by the high rate of ulcer relapses after cessation of treatment. Medical therapy may aim to reduce the aggressive factors acid and pepsin by compounds that neutralize the acid or inhibit the secretion of acid. Peptic activity is reduced by the high acid pH and also by the inhibition. Another group of compounds increases the mucosal defense by stimulating the secretion of mucus, bicarbonate, and growth of the mucosa, or by forming a protective layer on the ulcer crater. A history of previously treated duodenal ulcer or an absence do not preclude the diagnosis of perforated duodenal ulcer in cases of sudden, severe, acute abdomen. Most cases of perforated duodenal ulcer have no previous history of duodenal ulcer. When there are contraindications to surgical treatment, perforated duodenal ulcer can be managed successfully by an aggressive conservative treatment. Diets modify gastric function in various ways. Fiber influences acidity, pepsin and bile acid concentrations. People from many parts of the world who have used pharmacotherapy and natural therapy along with special precaution for diet for stomach/duodenal ulcers and gastric problems have reported feeling much better.

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Received on 24.02.2010 Modified on 21.03.2010

Research J. Pharm. and Tech.3 (3): July-Sept. 2010; Page 721-726