reduced incidence of ulcers because of relative sparing of gastric mucosal prostaglandin, synthesis, Celecoxib and rofecoxib are the first member of a new class of NSAIDs that selectively inhibit eyclooxygenase-2 (COX-2), the principle enzyme involved in prostaglandin production at sites of inflammation while sparing cyclooxygenase-l (COX-I), the principle enzyme involved with prostaglandin production in the gastric mucosa. H. pylori does not increase the likelihood of development of NSAID-associated ulcers. It is increasingly apparent that NSAIDs may cause small intestinal ulcerations, perforations, colitis, and colonic strictures. Clinical Findings. A, Symptoms and Signs: Epigastric pain and dyspepsia are the basic cause of peptic ulcer, which is present in 80% of patients. However, this complaint is not sensitive ot specific enough to serve as a reliable diagnostic criterion for peptic uleer. The clinical history cannot accurately identify duodenal from gastric ulcers, Less than one-fourth of patients with dyspepsia have ulcer disease at endoscopy. Up to 20% of patients with uleer complications such as bleeding have no antecedent symptoms (silent ulcers). In patients with NSAID-induced ulcers, up to half are asymptomatic, up to 60% of patients with complications do not have prior symptoms. Pain is typically well localized to the epigastrium and not severe. It is reported as gnawing, dull, aching, or hunger like. Classic features of peptic ulcer pain are rhythmicity and periodicity. Rhythmicity reflects that the pain fluctuates intensity throughout the day and night. The half of patients report relief of pain with food or antacids (especially duodenal ulcers) and a recurrence of pain 2 - 4 hours later. Two - Thirds of duodenal ulcers and one-third of gastrie ulcers cause nocturnal pain that awakens the patient. A change from patient's typical rhythmic discomfort to constant or radiating pain may reflect ulcer penetration or perforation. Most patients have symptomatic periods lasting up to several weeks with intervals of months to years in which they are pain-free (periodicity),Nausea and anorexia may occur with gastric ulcers. Significant vomiting and weight loss are un-usual with uncomplicated ulcer disease and suggest gastric outlet obstruction or gastric malignancy. ‘The physical examination is often normal in uncomplicated peptic ulcers. Mild, localized epigastric tenderness to deep palpation may be present. Fecal occult blood testing is almost positive in one-third of patients. . Laboratory Findings: Laboratory tests are normal in peptic ulcer but are recorded to exclude ulcer complications or confounding disease entities. Anemia may occur with acute blood loss from a bleeding ulcer or less commonly from chronic blood loss. Leukocytosis suggests ulcer penetration or perforation. An increased serum amylase in a patient with severe epigastric pain interforeted ulcer penetration into the pancreas, A fasting serum gastrin level to screen for Zollinger-Ellison syndrome is obtained in some patients. Because acid inhibition may raise serum gastrin levels. Hy receptor antagonists should be withheld for 24 hours and proton pump inhibitors for one week before a gastrin level is measured, C. Endoscopy: Upper endoscopy is the procedure of choice for the investigative diagnosis of duodenal and gastric ulcers. Endoscopy provides better diagnostic accuracy than barium radiography and the ability to biopsy for the presence of malignancy and H. pylori infection. In most cases of both gastric and duodenal ulcers, gastric mucosal biopsies are required to assess for the presence of H. pylori. Duodenal ulcers are visually never malignant and are not visualized for biopsy. Three to five percent of benign appearing gastric ulcers ultimately prove to be malignant, Hence cytological brushings and biopsies of the ulcer endoscopist margin are almost always preferred and performed. Provided that the gastric ulcer shows benign to the endoscopies and adequate biopsy specimen’s to reveal no evidence of cancer, dyspepsia, or atypia, the patient may be followed without further endoscopy. If these conditions are not fulfilled, follow-upendoscopy should be performed 12 weeks after that Start of therapy to document complete, healing, non-healing ulcers are suspected for malignant growth. D. Imaging: Barium upper gastro intestinal scanning is an acceptable altemative to screening of un-complicated patients with dyspepsia, However because it has limited accuracy in distinguishing benign growth from malignant gastric ulcers, gastric ulcers diagnosed by x-ray should be evaluated with endoscopy after 8-12 weeks of treatment [8]. E. Testing for H.pylori: Given the importance of H. pylori in ulcer pathogenesis, testing for this organism should be carriedout in all patients with peptic ulcers. The patients diagnosed with ulcer through endoscopy, gastric mucosal biopsies should be done both for a rapid increase test and for histologic examination, The specimens for histology are discarded if the urease test is positive [9]. In patients with a history of peptic ulcer or when an ulcer is diagnosed by upper gastrointestinal series, noninvasive assessment for H.pylori with urea breath testing, fecal antigen assay, or serologic testing should be carried out. Proton pump inhibitors may cause false-negative urea breath tests and fecal antigen tests and should be withheld for at least seven days before testing. Differential Diagnosis Peptic ulcer must be recognized from, other causes of epigastric distress (dyspepsia). Over half of patients with dyspepsia have no clear organic explanation for their symptoms and are categorized as having functional dyspepsia. A typical gastroesophageal reflux may be manifested by epigastric symptoms. Biliary tract disease is characterized by discrete intermittent episodes of pain that should not be confused with other causes of dyspepsia. Severe epigastric pain is atypical for peptic ulcer unless complicated by a perforation or penetration. Other causes include acute pancreatitis: acute Pancreatitits pain also occurs in epigastrium or central abdomen but also has associations of alcohol intake or very heavy fatty meal ingestion. Corroborating finding isincreased levels of serum amylase and lipase. Acute cholecystitis: Pain of cholecystitis also can occur in epigastrium like peptic ulcer but in majority of cases its site is right hypochondrium or right side of epigastric quadrant as well as recurring emesis with usual history of mild carlier such clinical episode and the associated finding of leukocytosis as well as pain radiation to right shoulder. Esophageal rupture: having epi severe and spasmodic attacks of recurrent emesis resulting esophageal rupture. Gastric volvulus: usually having history of Sliding Hiatus Hemia and Ruptured aortic ancurysm: having clinical finding of shock, un equal pulses and pain in back between the shoulder (8) ‘Treatment of gastric ulcer is normally aimed at neutralizing hydrochloric acid by frequent administration of antacids or by decreasing the secretory activity of the stomach with effective herbal treatments for ulcers, which are not few. Beside many herbal plants utilized, for the treatment of peptic ulcers, possibly the only effective plant remedy is Glycyrrhiza. Glyeyrrhiza has been one of the novel herbs utilized for the treatment of peptic ulcer. According to controlled clinical studies, glycyrthizic acid accelerates the healing process of peptic Uleers.ETHNOPHARMACOLOGY OF GLYCYRRHIZA Glycyrrhiza (Urdu: Mulaithi; Arabic: Sus; Persian: Mchak or Mazhu) from Glyeyrrhiza glabra and other species belong to genus Glycyrrhiza has been used as medicine since prehistoric times. Recent by new clinical evidences as a cure of peptic ulcer has attracted attention of the medical and the scientific community. To assess and analyze the many variety of claims suggested and/or proposed in the folkloric medicine over a period of four thousand years should be high lighted. It is also the purpose to compare these ethnopharmacological and biological evaluation. Historical Account The earliest records of the medicinal uses of Glycyrrhiza can be traced in Babylonia- Assyria clay tablet writings. The southem region of Babylonian kingdom, which forms a part as today’s Iraq around 3000 BC. developed a novel system of cuneiform writing. ‘Among these medical writing the oldest pharmaceutical document dates back perhaps around 4000 years ago contained Glycyrrhiza as a drug of vegetable origin. An acknowledged medicinal use of Glycyrrhiza is also found in the "Code Hamurabi " engraved in about 2100 BC. A trek of Babylonian-Assytian herbal remedies have also been found by the Assyrian therapy followers of the desert God “Ashur" whose capital fell to Chaldeans in 606 BC. Although it is fairly difficult to predict when Glycyrrhiza was documented in carly Chinese manuscript as folk medicine. The earliest chinese records from late Chou and early Han dynasties 200-300 BC. provide a mythical chronology starting with three "August" rulers" covering a period between 2852 BC. to 2597 BC. The second emperor Shen Nung was the father of agriculture and herbal therapy. Shen Nung gave China its first pharmacopoeia called the Pen Ts'ao. Among herbal prescription contains Glycyrrhiza, including various mixture preparations. ‘Thereafter a predominant drug period of Egyptian medicine appears which was exposed before the world through the eight medical papyry. Papyrus comprises of fall sedge of Cyperus papyrus which grows along the river- Nile. The name therefore, applies to paper like material on which the ancient Egyptian painted their hieroglyphics. Out of which