Forty-one patients underwent nonsurgical removal of postoperatively retained bile duct stones in two nonrandomized groups. The endoscopic-retrograde technique was used in 21 patients, and succeeded in 19. The percutaneous approach through the T-tube tract was used in 22 patients, including the two in whom endoscopic stone removal had failed, and was successful in 21 patients. Individual preferences and prior history introduced a selection bias against the percutaneous technique. Auxiliary extracorporeal shockwave lithotripsy (ESWL) was used in 2 patients whose stones could not be fragmented mechanically by the percutaneous basket technique. ESWL was successful in one patient but failed in the second. Because endoscopy had also failed in this case, the patient subsequently underwent repeat surgery. Procedure-related complications were minor with both techniques and were readily treated by conservative measures. We conclude that both the retrograde and the percutaneous approaches are effective and safe. The endoscopic approach appears convenient because there is no need to await maturation of the percutaneous tract, but sphincterotomy carries a small but distinctive risk. Because the percutaneous approach uses an existing tract, is only minimally invasive and leaves the sphincter of Oddi intact, it is preferable in those patients who have T-tubes of appropriate size and position in place.

Adult↗

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Helicobacter pylori and smoking: two additive risk factors for organic dyspepsia.

The hopes to distinguish between organic and functional dyspepsia on the grounds of the patient's symptomatology have not been fulfilled due to the low specificity of the so-called sinister symptoms. There is increasing evidence accumulating that Helicobacter pylori status and other environmental factors such as smoking have a higher discriminant power. Studies performed in our laboratories testing H. pylori status on gastric biopsy samples have shown that preselection of patients according to smoking habits and H. pylori status has a higher potential in avoiding unnecessary endoscopies in primary care patients as compared to risk factors based on patient complaints. Out of a total population of 282 primary care patients, one out of 24 endoscopies revealed significant pathology such as peptic ulcer or reflux esophagitis in the non-smokers with a negative H. pylori status, but when both risk factors were positive, the percentage rose to one out of every two patients. These observation have largely been confirmed by recent studies where H. pylori status was prospectively assessed prior to endoscopy by highly specific H. pylori serology or 13C breath test analysis.

Age Distribution↗

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Pathophysiology and clinical relevance of Helicobacter pylori.

Considerable knowledge has recently accumulated on the mechanism by which Helicobacter pylori (H. pylori) induces chronic gastritis. Although H. pylori is not an invasive bacterium, soluble surface constituents can provoke pepsinogen release from gastric chief cells or trigger local inflammation in the underlying tissue. Urease appears to be one of the prime chemoattractants for recruitment and activation of inflammatory cells. Release of cytokines, such as tumor necrosis factor alpha, interleukin 1 and 6, and oxygen radicals, leads to a further tissue inflammation accompanied by a potent systemic IgA and IgG type of immune response. Chronic inflammation and antigens on glandular epithelial cells lead to a progressive destruction with loss of the epithelial barrier function. Within the gastric mucosa, patches of intestinal metaplasia develop, which may be a risk factor for subsequent development of gastric carcinoma. Hyperacidity in duodenal ulcer patients induces gastric metaplasia in the duodenal bulb, which represents a target for H. pylori colonization and ulcer formation. H. pylori can be detected in the majority of patients with peptic ulcers and, compared to age-matched healthy people, it is also found more often in patients with dyspepsia and gastric carcinoma. Although H. pylori can be detected in healthy people, the marked reduction of the ulcer recurrence rate by eradication of H. pylori (80 percent versus 20 percent relapse within one year) suggests that H. pylori is a major risk factor for duodenal ulcer formation. The potential role of H. pylori in non-ulcer dyspepsia and carcinogenesis is under investigation. Current regimens aimed at eradicating H. pylori use a combination of several drugs that are potentially toxic. Since the risk of complications may exceed the potential benefit in most patients, eradication treatment should be limited to clinical trials and to patients with aggressive ulcer disease. New drug regimens, e.g., the combination of proton pump inhibitors with one antibiotic, may provide less toxic alternatives. Beyond ulcer treatment, effective and well-tolerated eradication regimens may have a place in prophylaxis of gastric carcinoma.

Gastritis↗

PubMedDate not supplied

[Effect of long-term metiamide treatment on gastric secretion and on mucosal cells in the rat].

Explore the source record for details and available documents.

Animals↗

PubMedDate not supplied

Long-term effects of Helicobacter pylori infection on acid and pepsin secretion.

Chronic Helicobacter pylori infection causes a slight postprandial hypergastinemia, generally referred to as exaggerated or inappropriate gastrin release. This can be ablated by eradication of this infective agent. The expectations that this would further unravel the mysteries of the pathogenesis of peptic ulcer disease have not been fulfilled. It is now well established that of conventional acid secretory patterns such as basal acid secretion, maximum gastrin-stimulated acid secretion, and of sensitivity of the parietal cell to gastrin, only basal acid is modified by chronic H. pylori colonization. This particularly relates to basal secretion in duodenal ulcer patients, as basal secretion of otherwise healthy, chronically H. pylori-infected subjects appears to be affected in only a small proportion of subjects. It is of particular interest, however, that chronic H. pylori infection supplies a solid explanation why acid inhibitory pathways are deficient in duodenal ulcer disease, since this is reversible following H. pylori eradication as demonstrated by elegant studies with gastrin-releasing, peptide-stimulated acid secretion. Furthermore, it has gradually become apparent that exaggerated gastrin response is probably no more than an innocent bystander of chronic H. pylori infection. Paradoxically, in a small subset of patients, hypo-or anacidity accompanying chronic H. pylori infection can be reverted by H. pylori eradication, for currently unknown reasons.

Gastric Acid↗

PubMedDate not supplied

Choledocholithiasis at the hepatic confluence mimicking a hilar cholangiocarcinoma.

Adenocarcinomas of the bifurcation of the hepatic ducts (Klatskin tumors) are a relatively rare cause of obstructive jaundice. Differential diagnosis includes other neoplastic lesions, sclerosing cholangitis, Mirizzi's syndrome and benign strictures. We present a 46 year-old white female with a 2 month history of epigastric pain and progressive jaundice. Endoscopic retrograde cholangiopancreaticography (ERCP) revealed a filiform stenosis of the right hepatic duct and an obstructed left hepatic duct, an image strongly suggestive of a Klatskin tumor. The correct diagnosis was achieved, however, by percutaneous transhepatic cholangiography (PTC), which disclosed a gallstone at the common hepatic duct bifurcation and multiple small concrements in the left hepatic duct. After endoscopic removal of the gallstones in the biliary tree and laparoscopic cholecystectomy, the patient was discharged on the third post-operative day. Protuberant tumors and round biliary stones may be confused at ERCP.

Bile Duct Neoplasms↗