Analysis of Helicobacter pylori vacA and cagA genotypes and serum antibody profile in benign and malignant gastroduodenal diseases. (1/324)
BACKGROUND: Helicobacter pylori species comprise different strains, cytotoxic and non-cytotoxic, which can be identified on the basis of their genomic pattern. AIMS: (1) To evaluate the polymorphism of the vacA gene and to ascertain whether the cagA gene is present in patients with gastric adenocarcinoma. (2) To study the anti-H pylori antibody profile using western blotting. PATIENTS: Twenty one patients with gastric adenocarcinoma and 71 with H pylori associated benign disease (nine gastric ulcer, 29 duodenal ulcer, 25 antral gastritis, and eight duodenitis). METHODS: The polymerase chain reaction was used to verify the presence or absence of cagA and to study the polymorphism of vacA in gastric mucosal samples obtained during endoscopy for patients with benign diseases and at surgery for patients with gastric adenocarcinoma. Fasting sera were used to assess anti-H pylori antibodies against different H pylori antigens by western blotting. RESULTS: CagA gene and the allele s1 of vacA were significantly less frequent in patients with antral gastritis (60% and 60%) compared with patients with gastric adenocarcinoma (94% and 100%) and with other non-malignant gastroduodenal diseases (93% and 87%) (chi 2 = 16.01, p < 0.001; and chi 2 = 13.97, p < 0.01). In patients with gastric adenocarcinoma, antibodies against a 74 kDa H pylori antigen were less frequently found than in patients with benign diseases. CONCLUSIONS: H pylori infection caused by cagA positive/vacA s1 strains is a frequent finding in patients with gastric adenocarcinoma. Prospective studies are needed to confirm whether the low incidence of positive serological response to the 74 kDa H pylori antigen in patients with gastric adenocarcinoma is important. (+info)Definitive diagnosis of intestinal volvulus in utero. (2/324)
Midgut volvulus with or without intestinal malrotation can occur in fetal life. Several reports have described congenital midgut volvulus showing non-specific sonographic findings of intestinal obstruction and perforation in utero. None of the previously reported cases, however, were definitively diagnosed as midgut volvulus by fetal sonography. We report two cases both exhibiting the sonographic 'whirlpool' sign, in utero. Color Doppler interrogation provided a clue to the viability of the involved intestinal segment. (+info)Endoscopic management of bleeding ectopic varices with histoacryl. (3/324)
Bleeding from antral and duodenal varices is an uncommon feature in patients with portal hypertension. We report a patient with cirrhosis and portal vein thrombosis, who had a massive bleed from antral and duodenal varices. Bleeding was controlled with endoscopic injection of varices using histoacryl. Endoscopic treatment and the relatively uncommon occurrence of antral and duodenal varices are highlighted. (+info)Histological and electron-microscopic observations on the mucosa of pediculated duodenal wall graft transplanted to the stomach in Wistar rats. (4/324)
OBJECTIVE: To study the mechanism of gastric metaplasia in duodenum through the transplantation of a flap of duodenal wall with vascular pedicle to the stomach. METHODS: The pediculated duodenal wall flaps of Wistar rats were transplanted to their stomachs. The rats were killed at the 3rd, 6th, 9th and 12th month after the operation respectively, and histological changes of the duodenal grafts were observed with optical and electron microscopy. RESULTS: Gastric metaplasia was found in the mucosa of duodenal grafts transplanted to the stomach at the 6th, 9th and 12th month. CONCLUSIONS: The formation of gastric metaplasia in the duodenal mucosa may be related to a change of the microenvironment around the tissues, and duodenal mucosa may differentiate into gastric epithelium by the decrease of pH value. (+info)Enteric coating of aspirin significantly decreases gastroduodenal mucosal lesions. (5/324)
BACKGROUND: Low-dose aspirin (acetylsalicylic acid, ASA) increases the risk of developing peptic ulceration. AIM: To investigate the gastroduodenal mucosal tolerability of enteric-coated ASA (EC-ASA) 100 mg/day compared to either placebo (study 1) or plain ASA 100 mg/day (study 2) in healthy volunteers. METHODS: Study 1: In this double-blind study 18 volunteers received randomized dosing with either EC-ASA 100 mg or placebo for 15 days. Study 2: 41 volunteers underwent randomized 7-day dosing of either EC-ASA 100 mg or plain ASA 100 mg in this double-blind, parallel-group, comparison study. In both studies acute gastroduodenal mucosal lesions were assessed endoscopically before treatment, on the morning of day 1 after the first dose (only in study 2), and on the morning after the last dose of the test medication. RESULTS: Study 1 did not reveal any significant differences between the lesion scores of EC-ASA and placebo. In contrast, in study 2 significantly higher total gastroduodenal mucosal lesion scores were observed on day 1 after the first dose and after 7 days of dosing with plain ASA (mean sum of the lesion scores in the gastric fundus, body, antrum and in the duodenal bulb: day 1: plain ASA 3.95+/-3.38 vs. EC-ASA 1.43+/-1.91, P = 0.03; day 7: plain ASA 6.35+/-4.10 vs. EC-ASA 2.00+/-2.02, P = 0.0004). Tolerance of the test drugs was good, and no other adverse events were observed. CONCLUSIONS: Enteric-coated aspirin 100 mg/day causes significantly less gastroduodenal damage over 7 days than the same dose of plain aspirin, when given to healthy subjects. There was little gastric injury and no significant differences between EC-ASA and placebo in this respect. (+info)Aortoduodenal fistula after endovascular stent-graft of an abdominal aortic aneurysm. (6/324)
Despite satisfying short- and middle-term effectiveness and feasibility, endovascular stent-grafting for abdominal aortic aneurysm is still under evaluation. We report a case of an aortoduodenal fistula after the use of this technique. Enlargement of the upper aneurysmal neck was followed by caudal migration of the major portion of the stent-graft, which resulted in kinking of the device in the aneurysmal sac. Ulcerations were found on adjacent portions of both the aneurysmal sac and the adjacent duodenum. Only the textile portion of the prosthetic contralateral limb separated the aortic lumen from the corresponding duodenal lumen. Early detection of complications after stent-grafting is essential to allow successful treatment, either surgical or endoluminal. (+info)The pattern of involvement of the gastric mucosa in lymphocytic gastritis is predictive of the presence of duodenal pathology. (7/324)
AIM: To determine whether the pattern of involvement of the gastric mucosa in lymphocytic gastritis is predictive of the presence or absence of duodenal pathology. METHODS: 50 cases (M:F, 26:24; median age 57 years) diagnosed as lymphocytic gastritis between 1986 and 1998 with concurrent duodenal (D2) biopsies were identified from a computer search of the pathology records and validated by counting gastric intraepithelial lymphocytes. Gastric and duodenal intraepithelial lymphocyte counts were performed on haematoxylin and eosin (H&E) and anti-CD3 stained sections. D2 biopsies were assessed for villous atrophy and chronic inflammatory cell infiltration by subjective grading, and gastritis was classified and graded according to the updated Sydney system. A case was designated corpus predominant when the corpus chronic inflammation grade exceeded that of the antrum. If it was less, then the case was antrum predominant, and if they were equal it was diffuse (pan-) gastritis. The ratio between the corpus and antral intraepithelial lymphocyte count in individual patients was calculated. RESULTS: Of 50 cases of lymphocytic gastritis, 21 were classified as corpus predominant. With one exception (a case of mild villous atrophy), all were accompanied by normal duodenal morphology. Cases with a corpus predominant gastritis had median duodenal intraepithelial lymphocyte counts of 19 (H&E) and 14.1 (CD3), whereas 29 subjects with an antrum predominant or diffuse gastritis had median counts of 39.9 (H&E) and 37.9 (CD3). Fifteen of these 29 cases (52%) showed villous atrophy; all were graded as moderate or severe. Patients with any degree of villous atrophy had a mean corpus/antrum intraepithelial lymphocyte ratio (H&E) of 0.59 (representing antral predominance), while those with normal duodenal morphology had a ratio of 2.39 (p < 0.0001). CONCLUSIONS: The pattern of involvement of gastric mucosa in lymphocytic gastritis is closely related to the associated duodenal pathology. Those with the corpus predominant form are unlikely to have duodenal pathology, while those with an antral predominant or diffuse form should have distal duodenal biopsies taken to exclude villous atrophy. (+info)Primary hypertrophic tuberculosis of the pyloroduodenal area: report of 2 cases. (8/324)
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. (+info)Duodenal diseases refer to a range of medical conditions that affect the duodenum, which is the first part of the small intestine. Here are some examples of duodenal diseases:
1. Duodenitis: This is inflammation of the duodenum, which can cause symptoms such as abdominal pain, nausea, vomiting, and bloating. Duodenitis can be caused by bacterial or viral infections, excessive use of nonsteroidal anti-inflammatory drugs (NSAIDs), or chronic inflammation due to conditions like Crohn's disease.
2. Peptic ulcers: These are sores that develop in the lining of the duodenum, usually as a result of infection with Helicobacter pylori bacteria or long-term use of NSAIDs. Symptoms can include abdominal pain, bloating, and heartburn.
3. Duodenal cancer: This is a rare type of cancer that affects the duodenum. Symptoms can include abdominal pain, weight loss, and blood in the stool.
4. Celiac disease: This is an autoimmune disorder that causes the immune system to attack the lining of the small intestine in response to gluten, a protein found in wheat, barley, and rye. This can lead to inflammation and damage to the duodenum.
5. Duodenal diverticulosis: This is a condition in which small pouches form in the lining of the duodenum. While many people with duodenal diverticulosis do not experience symptoms, some may develop complications such as inflammation or infection.
6. Duodenal atresia: This is a congenital condition in which the duodenum does not form properly, leading to blockage of the intestine. This can cause symptoms such as vomiting and difficulty feeding in newborns.