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Biomedical subjects

K H Holtermüller

Publications and source records attributed to K H Holtermüller.

At least 37 records · Page 2Linked to original sources

European Cooperative Crohn's Disease Study (ECCDS): clinical features and natural history.

In the European Cooperative Crohn's Disease Study patients from 14 centers were included in whom diagnosis was made within 2 years before study entry on the basis of generally accepted radiological, endoscopical and/or histological criteria or a combination of all. Reasons for exclusion were: diagnosis older than 2 years in patients who did not require active treatment, age less than 18 years, duration of symptoms less than 3 months, presence of complications which potentially required emergency surgery. Data on clinical features were obtained in 633 patients, of whom 452 were eligible to participate in the study. In 110 patients randomized to placebo the natural course of Crohn's disease was studied. Patients with ileocolonic involvement were younger than patients with either colonic or small intestinal involvement only. Classic ileitis terminalis was present in 14% of the patients. 49% of the patients had combined involvement of both the small and large intestine. 30% of patients had only small intestinal involvement, and in 21% colonic disease was present. Small intestinal involvement was associated with a significantly lower Crohn's Disease Activity Index (CDAI) than other anatomical locations of the disease. Perianal disease was more often associated with colonic than with small intestinal involvement. 60% of placebo patients with active disease at entry achieved at least a transient remission within the initial 5 months of study. After 2 years, 23% of patients with active disease at entry and 68% of patients with quiescent disease had reached or maintained a remission, respectively. By stepwise multiple linear regression analysis long duration of disease between diagnosis and randomization, normal serum albumin and combined involvement of small intestine and colon were identified as predictors of a more favorable outcome of patients treated with placebo. In contrast, extensive small bowel disease, treatment with steroids and bowel resection prior to study entry correlated with a less favorable outcome. However, by life table analysis outcome of previously untreated and treated patients in the placebo group was similar.

Adrenal Cortex Hormones↗

[Stress ulcerations: pathogenesis and prevention].

Clinically inapparent gastric stress ulcerations are a frequent complication of extensive trauma, intracranial diseases, burns, sepsis, respiratory insufficiency etc. With improvement of the underlying disease the acute erosions will disappear, however, approximately 20% of the patients will develop major gastro-intestinal bleedings. Besides the known and above mentioned risk factors gastric acid must be present for acute stress lesions to develop. Therefore, attempts at prophylaxis against stress erosions have focused on a decrease of intragastric hydrogen ion concentration. In a number of clinical trials during recent years it was documented that neutralization of gastric content (elevation of intragastric pH to 3.5 or higher) will prevent stress ulcers and their life threatening complication: exsanguinating hemorrhage. Therefore critically ill patients should receive high doses of antacids or cimetidine in combination with antacids to prevent acute stress ulcerations.

Animals↗

[The chemistry of antacids].

Antacids are relative simply assembled salts and salt-like compounds which neutralize acids. This neutralization reactions lead to several products (other salts, water, and possibly carbondioxid), resulting in steps, like hydrolysis and precipitations of insoluble compounds. When antacids containing aluminum are neutralized in the presence of organic acids, peptones, and polypeptides, there is a marked loss in their neutralizing capacity and neutralization rate.

Aluminum Hydroxide↗

[Postvagotomy complications: stomach bezoars - case report and review of the literature].

A 59 year old female with multiple gastric surgical procedures (Billroth I and Billroth II) for recurring ulcer disease developed a gastric phytobezoar following an additional truncular vagotomy within 2 months. Already 1 month after complete endoscopic removal the phytobezoar recurred in spite of dietary restrictions. The phytobezoar was successfully dissolved by oral Cellulase-therapy. The truncular vagotomy and its influence on gastric motility has to be considered as the cause of the repeated bezoar formation.

Bezoars↗

[Treatment of jejunal peptic ulcer with cimetidine or an antacid? Results of a long-term study].

The effectiveness of cimetidine or antacid in healing recurrent jejunal peptic ulcers after Billroth II gastric resection without vagotomy was tested in a randomized study of 18 in-patients. Mean stimulated acid secretion of the cimetidine group was 11.2 +/- 4.3 mmol/h, in the antacid group 12.6 +/- 5.6 mmol/h. Serum gastrin levels were within the normal range in all patients. Within four weeks the ulcers had healed completely in eight of the nine patients on cimetidine (1,000 mg/d), but in only three of the nine patients on antacids (magnesium-aluminiumhydroxide, neutralization capacity 564 mmol/d). The difference is statistically significant (P less than 0.025). All 11 patients with healed ulcers were given prophylactically either 800 mg cimetidine daily or magnesium-aluminiumhydroxide (neutralization capacity 564 mmol/d). During a follow-up period of one year recurrences occurred in two of the five patients on antacids, but in none of the six treated with cimetidine. The results indicate that cimetidine also accelerates the healing of recurrent jejunal peptic ulcers. But further studies are required to elucidate whether long-term treatment with histamine-H2-receptor antagonists is as good as surgery in the long-term prevention of ulcer recurrences.

Adult↗

The influence of oral contraceptives on the composition of bile.

The increased risk of cholelithiasis during intake of oral contraceptives may be due to estrogen-induced saturation of the bile with cholesterol. In a randomized, prospective, crossed-over double-blind study 20 healthy women after roentgenological exclusion of gall-stones received either 1.0 mg of norethindrone acetate and 50 microgram ethinyl estradiol daily - as usual in oral contraception - for 21 days with 7 days of placebo treatment in each cycle or one fifth of this hormone dose in form of a continuous daily medication. After a 4 month's treatment the medication form was crossed-over. At the beginning of the study, before the cross-over and after the study bile was collected by duodenal intubation after a 12-h fast and the lithogenic index as a measure for cholesterol saturation of the bile was determined. No correlation between the dose and the lithogenic index was demonstrated, neither in 15 women, who had used oral contraceptives before the study nor in five women without any previous hormonal contraceptives.

Adult↗

D-penicillamine in Wilson's disease presenting as acute liver failure with hemolysis.

Wilson's disease in a young woman presenting with an acute course is described. The clinical manifestations were fulminant hepatic failure associated with marked intravascular hemolysis. Immediate D-penicillamine and high-dose steroid therapy did not influence the course of the disease. Necropsy revealed an increased hepatic copper content and cirrhosis with extensive necrosis of the liver.

Acute Disease↗

Influence of nonsteroidal anti-inflammatory compounds on healing of chronic gastric ulcers in rats.

Pre-treatment with NOSAC led to an increase of ulcer index in a dose-dependent manner indicating the aggravation of gastric lesions under the influence of NOSAC. The severity of mucosal lesions was diminished by lengthening the time between the last day of pre-treatment with NOSAC and the day on which ulcers were induced. When NOSAC were administered after the induction of gastric ulcers, the healing of the latter was significantly delayed.

Animals↗

Antacid therapy--changes in mineral metabolism.

Antacid ingestion may lead to side-effects related to their chemical composition. Aluminum hydroxide may cause the phosphate depletion syndrome even during short-term administration of high doses in patients at high risk, such as alcoholics. Long-term intake may lead to bone demineralization and to osteomalacia. Fluoride complexing in the gut and prevention of fluoride absorption may be an additional factor. The clinical relevance of aluminum absorption in patients with normal renal function is not clear. In contrast, in patients with renal failure, aluminum hydroxide ingestion may contribute to an increasing hyperaluminemia. Hyperaluminemia and tissue deposition of aluminum in these patients may contribute to the dialysis-associated encephalopathy. Magnesium hydroxide causes an alkalinization of the urine due to magnesium absorption and urinary excretion. Thus, in renal insufficiency, a life-threatening hypermagnesemia may develop if magnesium-aluminum-containing antacids are prescribed. The milk-alkali syndrome, rarely observed nowadays, may be caused by calcium carbonate- and sodium bicarbonate-containing antacids. Hypercalciuria and alkaluria predispose to nephrolithiasis. The possibility that these disturbances in mineral metabolism will develop in patients with normal renal function is unlikely unless there is an abuse of these "over the counter" antacids.

Aluminum Hydroxide↗

Antacids and hormones.

Antacids are neutralizing compounds which have been shown to hasten ulcer healing and to prevent bleeding from stress ulcerations. Owing to gastric alkalinization, gastrin will be released following antacid ingestion, a condition similar to that following the ingestion of a meal. Gastrin release and, more important, acid rebound also occur when the gastric mucosa comes into contact with calcium chloride. These findings indicate that acid rebound is independent of antral neutralization. Acid rebound and gastrin release will also be induced in duodenal ulcer patients by magnesium hydroxide. The magnitude of acid rebound represents one fourth to one third of the peak acid response to pentagastrin and is more marked following calcium than magnesium antacid intake. The mechanism of acid rebound may be in part due to gastrin release, but may also be due to the direct effect of calcium on the parietal cell. In the duodenum, calcium and magnesium evoke pancreatic enzyme secretion and gall bladder emptying. This effect of both cations is attributed to the release of cholecystokinin. Owing to their chemical composition, antacids stimulate the release of gastrointestinal hormones, cause acid secretion and stimulate pancreatic enzyme secretion and gall bladder concentration. So far, it has not been proven that these effects of antacids and of their chemical constituents will limit their therapeutic use.

Antacids↗

[Antacids: A comparison of their in vitro neutralizing capacity in hydrochloric acid and in acidified peptone solution (author's transl)].

Using a simple and reproducible in vitro-test the neutralizing capacity of different liquid commercial antacids was measured at pH 2.0 and at pH 3.5 in diluted hydrochloric acid and in acidified peptone solution. In peptone solutions corresponding to postprandial gastric juice, antacids containing aluminum hydroxide and aluminate forming components demonstrated a marked loss in their neutralizing capacity when compared to peptone free hydrochloric acid as control. This loss in buffering capacity is dependent on the reaction time, the pH of the reaction mixture, the concentration of peptone in the solution and the amount of aluminum in the different antacid compounds. Furthermore the neutralizing capacity of aluminum hydroxide is also diminished by dibasic organic acids which mimicked fasting gastric juice in the experiment. The different availability of neutralizing potency of aluminum hydroxide containing antacids in acid and in acidified peptone solution will need to be considered when antacids are recommended for the treatment of patients with peptic ulcer disease.

Aluminum Hydroxide↗

Fecal blood loss in patients with colonic polyps: a comparison of measurements with 51chromium-labeled erythrocytes and with the Haemoccult test.

The quantitative determinations of fecal daily blood loss after intravenous administration of 51Cr-labeled erythrocytes in 44 patients with colonic polyps and in 11 controls were compared with the results of the daily performed Haemoccult test without dietary restrictions. A total of 642 stool specimens was analyzed for 51Cr loss and the Haemoccult test. The mean fecal daily blood loss in the 34 patients with adenomatous polyps of the descending colon and rectosigmoid was 1.36 +/- 0.14 ml/day (mean +/- SEM), in the 10 patients with polyps of the ascending and transverse colon it was 1.28 +/- 0.31 ml/day, and in the 11 controls 0.62 +/- 0.07 ml/day. There was no positive Haemoccult test in the controls. In fecal specimens from patients with polyps in the descending colon and rectosigmoid containing 2.0-3.99 ml blood/day, the Haemoccult-test was positive in 86%. Fecal specimens from patients with polyps in the ascending colon and transverse colon containing equal blood loss yielded a positive Haemoccult test result in 26%. Thus, the positivity of the Haemoccult test is determined by the fecal daily blood loss and the anatomic location of colonic bleeding sites.

Chromium Radioisotopes↗