[Differential diagnosis of chronic diarrhea: indicative findings of factitious diarrhea (Munchausen syndrome) with bisacodyl by the pathologist].
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Biomedical subjects
Publications and source records attributed to J Hotz.
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In a randomized, single-center, double-blind, placebo-controlled pilot study, 20 patients with established Crohn's disease suffering from diarrhea and moderate complaints as measured by the BEST Index, were treated with the yeast preparation Saccharomyces boulardii (S.b.) in a dosage of 250 mg t.i.d., initially for two weeks in addition to the basic treatment. A reduction in the frequency of bowel movements (5.0 +/- 1.4 vs. 4.1 +/- 2.3 evacuations/day, p < 0.01) and in the BEST Index (193 +/- 32 vs. 168 +/- 59, p < 0.05) as compared to baseline was registered. After this initial phase, the patients were allocated in randomized order to the control group (n = 7) receiving placebo, or to the verum group (n = 10) receiving S.b.(250 mg t.i.d.) for 7 weeks, while the basic treatment was maintained. The group treated with S.b. showed a significant reduction in the frequency of bowel movements in the tenth week, to 3.3 +/- 1.2 evacuations per day, and in the BEST Index, to 107 +/- 85. In the control group taking placebo, however, this effect was not observed. By contrast, the frequency of bowel movements and the BEST Index rose again in the tenth week until reaching initial values (4.6 +/- 1.9 evacuations daily and 180 +/- 61, respectively). No adverse drug events were observed. In order to confirm these positive effects of S.b. in patients with Crohn's disease, further controlled multicenter trials in a larger patient population should be performed.
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Lansoprazole (AG 1749/CG 4801) is an inhibitor of gastric acid secretion by blocking H+,K(+)-ATPase. In this 2:1 randomized, double-blind, multicentre trial lansoprazole 30 mg am was compared to 40 mg famotidine nocte in 264 out-patients suffering from uncomplicated duodenal ulcer. After 2 weeks of treatment ulcer healing was confirmed endoscopically in a significantly higher proportion (P = 0.027) of patients treated with lansoprazole (94/174 = 54.0%) compared to patients receiving famotidine (35/90 = 38.9%). Cumulative healing rates after 4 weeks were 91.4% for the lansoprazole group and 83.3% for the famotidine group (P = 0.065). Pain relief and decrease of concomitant antacid consumption during treatment were comparable in both groups. Both compounds were well tolerated. Rates of recurrent duodenal ulcer in the 6 months after trial treatment were 45/158 (28.5%) after lansoprazole, and 18/69 (26.1%) after famotidine.
Although new pathogenetic findings of peptic ulcers have been detected, there still remain some open questions. Accurate anamnestic evaluation will find out risk factors as cigarette-smoking, stress and therapy with nonsteroidal antiinflammatory drugs (NSAIDs), and will be helpful in differential diagnosis. Endoscopy is the diagnostic means of choice, and enables to easy helicobacter pylori detection. Since some gastric ulcers are actually carcinomas, it is absolutely necessary to obtain multiple biopsies. The Zollinger-Ellison syndrome and symptoms of other rare diseases of the upper intestine are discussed.
It is generally accepted that ulcer pathogenesis is mainly mediated by an imbalance between aggressive factors as gastric acid and pepsin, and obviously genetically determined defects in protection mechanisms of the gastric and duodenal mucosa. Since at present it is not possible to substitute these defects properly by pharmacological measures, the modern ulcer therapy aims to a distinct acid reduction as the main and most successful therapeutic principle. Recent studies show a direct correlation between the effectiveness and the acid reducing potency of a given anti-ulcer drug, assessed by pH above 3 over time. By long term treatment using H2-blockers and most recently the ATPase inhibitor Omeprazole it is now possible to reduce drastically the relapse rates of gastrointestinal ulcers and to improve significantly quality of life. An effective prophylaxis in duodenal ulcer can also be achieved by combination therapy with bismuth plus antibiotics or with omeprazole plus antibiotics. Even ulcers induced by nonsteroidal-antirheumatic drugs or acetylsalicylate can be adequately treated and prevented by acid reducing drugs. The present article includes pathophysiological and pharmacological backgrounds of medical ulcer therapy as well as guidelines for indication and mode of application of the different antiulcer drugs concerning short and long term treatment.
In consequence of newly developed ulcer drugs as H2-blocker and especially the ATPase-inhibitor omeprazole there is a rising chance to reduce drastically the relapse rate of gastroduodenal ulcers by long term administration of these drugs. By this, it is possible to improve significantly quality of life and ability for work for periods of years and to repress overt symptomatic chronic ulcer disease into a quiescent stage. Incapability for work and early retiring can be prohibited. Therefore the prognosis of chronic duodenal ulcer disease is significantly improved by long term treatment of ulcer disease using modern ulcer drugs.
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The efficacy of omeprazole therapy (40 mg daily) in H2-blocker refractory severe reflux oesophagitis (Grade II-IV; Savary and Miller classification) was investigated in 61 patients. Mean duration of reflux disease and preceding H2-antagonist treatment were 4.3 years and 15 months, respectively. Healing rates at 4, 8 and 12 weeks were 48%, 80% and 92%, respectively. There was a correlation between severity of oesophagitis and duration of omeprazole therapy necessary for healing. Three patients (5%) required higher dosages than 40 mg for healing. Symptomatic responses paralleled healing. It is concluded that omeprazole is a highly effective drug for severe reflux oesophagitis not responding to H2-blocker treatment and that 40 mg daily is the optimal dose.
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A 10-cm-long longitudinal tear in the middle third of the oesophagus--with intact deeper muscle layers--was found endoscopically in a 52-year-old alcoholic man who had developed acute retrosternal pain after severe vomiting. There was a leukocytosis of 16,700/microliters and fever of 38.8 degrees C. Because of the diagnosis of incomplete spontaneous oesophageal rupture (Boerhaave syndrome) he was fed parenterally, a gastric tube was placed, and he received three times daily 2 g ampicillin, twice daily 80 mg gentamicin and 1.2 g cimetidine. The fever disappeared after 24 hours and the leukocytosis regressed after four days. At repeat endoscopy after 16 days the tear had healed completely.
To investigate the effect of aclatonium napadisilate (Ac), a synthetic cholinergic compound, on human interdigestive gastrointestinal function, six healthy volunteers underwent gastrointestinal intubation for measurement of duodeno-jejunal motor activity and pancreatic enzyme secretion. Each subject was studied twice on two separate days and received either aclatonium (300 mg) or placebo intraduodenally in randomized order. Aclatonium significantly increased the overall length of the cycle of interdigestive motor complex (IMC) by a mean of 34% (p less than 0.05) without stimulating the phases of increased motor activity. Aclatonium slightly, but significantly increased output of lipase during phase II of the IMC (p less than 0.05), whereas outputs during phase I and III were not significantly changed. We conclude that aclatonium in a dose of 300 mg has only weak cholinergic effects on motility and exocrine pancreatic secretion in healthy humans during the interdigestive state.
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The mechanism for acute hypercalcaemia increasing pancreatic enzyme secretion is unknown. To determine if raised extracellular calcium concentrations can directly stimulate pancreatic enzyme output, we measured discharges of pulse labelled protein and chymotrypsin from isolated cat pancreatic lobules in the presence of normal and raised calcium concentrations. Incubation in 5.0 mmol/l calcium increased discharges of pulse labelled protein (four fold), chymotrypsin (2.5 fold) and amylase (2.2 fold), compared with control experiments with 2.5 mmol/l calcium (p less than 0.001). This effect was similar to the maximal effect of carbachol or caerulein. Compared with 5.0 mmol/l calcium, incubation at the higher calcium concentration of 10.0 mmol/l induced similar discharges of chymotrypsin and amylase, whereas the increase in discharge of pulse labelled protein was smaller (p less than 0.01). The effects of raised calcium were not altered by atropine. Incubation in a high calcium medium did not impair pancreatic acinar response to subsequent stimulation with carbachol, but incubation in hypothermia abolished the effects of high calcium concentrations, suggesting that increased enzyme discharge is caused by stimulation of secretion not to cell damage. These data are consistent with a direct stimulatory effect of raised extracellular calcium concentrations on pancreatic acinar cell function.