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Primary hypertrophic tuberculosis of the pyloroduodenal area: report of 2 cases. S Agrawal, SV Shetty, G BakshiDepartment of General Surgery, Dr. R.N. Cooper Hospital and Seth G.S. Medical College, Mumbai, India., India
Correspondence Address: Source of Support: None, Conflict of Interest: None PMID: 0010734324
Tuberculosis of the stomach and duodenum is rare in patients with pulmonary tuberculosis. Primary involvement is even rarer. Two cases of primary tuberculosis of the localised to the pyloro-duodenal area are presented. The most common symptoms are non-specific leading to a difficulty in establishing a pre-operative diagnosis. A high degree of suspicion is therefore required for its diagnosis and to differentiate it from more frequent causes of gastric outlet obstruction such as chronic peptic ulcer disease and gastric carcinoma. The treatment of gastric tuberculosis is primarily medical with anti-tuberculous drug therapy. The role of surgery lies in the cases with obstruction following hypertrophic tuberculosis. The surgery done is usually a gastroenterostomy. With the relative rate of extra-pulmonary tuberculosis increasing, tuberculosis of the pyloro-duodenal area should be considered in the differential diagnosis of gastric outlet obstruction. Keywords: Adolescent, Adult, Case Report, Duodenal Diseases, complications,diagnosis,Female, Gastric Outlet Obstruction, diagnosis,etiology,Human, Pyloric Antrum, Tuberculosis, Gastrointestinal, complications,diagnosis,
Tuberculosis of the stomach and duodenum is rare; it usually develops secondary to other tuberculous lesions, most commonly pulmonary. Primary involvement is very rare, only eight cases having been reported in the literature[1]. We report two cases of primary tuberculosis of the stomach and duodenum localised to the pyloro-duodenal area, who presented with gastric outlet obstruction.
Case 1: A 28-year-old woman presented with a two-month history of progressively increasing epigastric pain, immediately after meals and relieved by vomiting. The vomitus consisted of old ingested food. She also complained of anorexia and loss of weight. She denied any history suggestive of peptic ulcer disease. There was no history of cough, fever, haematemesis and malena. On abdominal examination, there was visible peristalsis in upper abdomen, waves moving from left to right and increasing after ingestion of water. A succussion splash was also present. The rest of the physical examination was essentially negative. Investigations: haemoglobin - 12.5g/dl; total leukocyte count - 8300/cmm; erythrocyte sedimentation rate - 28 mm in the first hour. Serum chemistry was normal. Test for HIV antibody was negative. Chest skiagram was normal. There was no sign of active pulmonary disease and no evidence of post-tuberculous disease. Abdominal sonography showed no abnormality and no evidence of abdominal lymphadenopathy. Fibre-optic endoscopy showed an annular lesion involving almost the entire pylorus implanting a strong suspicion of malignancy. Multiple biopsies revealed non-specific gastritis. Case 2: A 16-year-old girl was referred with a five months history of upper abdominal pain and gastric outlet obstruction. She also complained of loss of weight but no history of fever, cough, haematemesis or malena. On abdominal examination, there was epigastric fullness with visible peristalsis after ingestion of food. The rest of the physical examination was normal. Investigations: haemoglobin - 10.1g/dl; total leukocyte count - 6600/cu. mm; erythrocyte sedimentation rate - 7l mm. in the first hour. Serum chemistry was normal. Test for HIV antibody was negative. Chest skiagram was normal. Patient came to us with Barium study already done that revealed grossly distended stomach with coarse mucosal folds and evidence of narrowing in pyloric region suggestive of pyloric stenosis. No ulcer crater or growth was detected. Fibre-optic endoscopy revealed pyloric stenosis. Gastric mucosa was normal. Both the patients were subjected to exploratory laparotomy. In both cases, the pyloroduodenal serosa was studded with multiple tubercles of 2 to 3 mm in size along with thickening of the wall. The stomach was grossly distended. There was no free fluid. The liver appeared normal. Enlarged juxtapyloric nodes were noticed. An anterior gastrojejunostomy was performed in both the cases and biopsies of gastric wall and of juxtapyloric lymph-nodes were taken, which subsequently confirmed the suspicion of tuberculosis. Antitubercular treatment was started on the first post-operative day. Recovery was uneventful. There was complete relief of symptoms with significant weight gain on follow -up.
Tuberculosis of the stomach and duodenum is rare, even in patients with pulmonary tuberculosis. In such cases, the incidence of gastric and duodenal tuberculosis, found at autopsy around 0.4%[2]. Duodenal involvement occurs in 10% of patients with gastric tuberculosis[3]. Primary pyloroduodenal tuberculosis is much rarer[1]. This rarity may be due to gastric acidity, rapid transit of ingested organisms, the scarcity of lymph follicles in the gastric wall, and an intact gastric mucosa[4]. The possible routes of infection that have been considered include: (a) direct infection through the mucosa, most likely route in primary pyloroduodenal tuberculosis, (b) haematogenous spread, (c) lymphatic spread, and (d) spread from the serosa by continuity from adjacent structures, especially the lymph-nodes[5]. The pathologic types of gastric tuberculosis have been classified into ulcerative, hypertrophic, solitary or miliary tubercles, larger nodular foci, and diffuse tuberculous gastritis[3],[4],[5],[6],[7]. Combinations of these lesions do frequently occur[8],[9]. The ulcerative and hypertrophic types are the commonest[3]. Ulcerative lesions are single or multiple with ragged, overhanging margins and are located in the antrum. Perforation is rare because the ulcers seldom penetrate the muscle layer. The duodenal lesions are classified as ulcerative, hyperplastic, infiltrative, and enteroperitoneal[10],[11]. There is usually extensive lymph node involvement in the surrounding areas[3],[5]. Hypochlorhydria and achlorhydria are the most frequent abnormalities in gastric tuberculosis[9]. The most common symptoms are non-specific and include postprandial epigastric pain, vomiting, weakness, weight loss, fever, haematemesis, and gastric outlet obstruction[12], some of which were present in our patients. In the presence of gastric outlet obstruction, the most common differential diagnostic considerations are chronic peptic ulcer disease and gastric carcinoma. In our two cases, there was no past history of peptic ulcer disease and gastric carcinoma could not be ruled out pre-operatively. The radiological appearances are classified as of predominantly ulcerative and predominantly hyper-plastic type[2],[3]. Case 2 showed narrowing in pyloric region, with grossly distended stomach in Barium study. Gastroscopy has been used to establish tissue diagnosis pre-operatively. Diagnosis depends on the demonstration of either acid-fast bacilli or caseating granulomas in the biopsy material. Bacilli can be demonstrated in tissue in only one-third of cases and are rarely cultured from gastric washings[13],[14]. In our cases, a specific pathology could not be identified pre-operatively. The treatment of gastric tuberculosis is primarily medical with anti-tuberculous drug therapy[4],[14]. This usually leads to clinical improvement dramatically. The role of surgery lies in the cases with obstruction following hypertrophic tuberculosis. The surgery done is usually a gastroenterostomy. Antituberculosis chemotherapy has to be given postoperatively. We surmise that, with the relative rate of extrapulmonary tuberculosis increasing in our country, tuberculosis of the pyloro-duodenal area should be considered in the differential diagnosis of gastric outlet obstruction. [Figure - 1], [Figure - 2]
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