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Biomedical subjects

N Schaub

Publications and source records attributed to N Schaub.

14 recordsLinked to original sources
PubMed1991

[Gastritis associated with Gastrospirillum hominis--a zoonosis?].

We found spiral bacteria (non-Helicobacter pylori, SB) in gastric biopsies of 5 patients corresponding to an incidence of 0.3%. The bacteria were found on the surface of the gastric mucosa and in part tightly packed within the crypts. Contrary to Helicobacter pylori, most of them had no direct contact to the surface and crypt epithelium. They are distinctly coiled, 3.6-5.5 microns in length and on average 0.5 microns thick. Ultrastructural studies revealed sheathed flagella at each pole. In one case the bacteria displayed periplasmic fibrils in pairs as also described in cultures of SB from cats' stomachs. In all 5 cases there was histological evidence of inflammation of the gastric mucosa, i.e. one acute diffuse gastritis, one case of granulomatous and three of slight to medium grade chronic gastritis. Biopsies of 2 patients showed a positive urease reaction in the CLO test. Morphologically very similar SB occur as commensals in the stomachs of various animals, in particular dogs and cats. We investigated the stomachs of four dogs and four cats and found all to be infested with SB. The bacteria were found not only on the surface of the mucosa and in crypts, but within the glands of the corpus and antrum and often also within parietal (oxyntic) cells. Yet despite bacterial colonization there was no evidence of gastritis in dogs. However, all of the cats' stomachs showed slight to medium grade chronic gastritis. Cultivation of SB has not been successful so far, with the exception of cats' stomachs. Since the germs have been defined only morphologically, the question as to how close the relationship is among SB of various origins must for the time being remain unanswered. Furthermore, species-specific pathogenicity and the possibility of contagion from animal to man has not yet been clarified.

Adult↗
PubMed1990

[Chronic gastritis. Pathogenesis, clinical aspects and therapy].

Based on clinical and histopathological features, three different types of chronic gastritis can be distinguished: gastritis A is confined to the proximal stomach and is the result of an autoimmunological process with antibodies against parietal cells and intrinsic factor. It is a rare disorder and may lead to pernicious anaemia. Distal, antral gastritis B is caused by an infection of the gastric mucosa with Helicobacter pylori (HP). Its incidence increases with age (greater than 50% above age 50). Gastritis C may be caused by drugs and alcohol but is mainly found in gastric remnants after partial resection as a consequence of biliary reflux. Gastritis A rarely causes symptoms. A relationship between gastritis B and C and non-ulcer dyspepsia (NUD) is highly controversial. Gastritis B is very closely associated with peptic ulcer disease. HP-positive antral gastritis seems to be the prerequisite for ulcer formation. All 3 types of gastritis carry an increased risk of malignancy, which seems to be positively correlated with hypoacidity, the chronicity of the inflammation and the histopathological feature of intestinal metaplasia. Noninvasive diagnostic tests (serology, breath tests, scintigraphy) are available, but the diagnosis of gastritis is still mainly based on endoscopy and biopsy. Treatment of gastritis A is not possible. Gastritis B can be healed by eradication of HP using bismuth salts and antibiotics but only combinations of 2-3 compounds seem to afford long-term positive results. Further clinical trials are needed to determine whether such treatment is justified in patients with gastritis and NUD. In patients with chronic recurrent peptic ulcers eradication of HP prevents relapses and heals ulcer disease. Gastritis C complicated by severe symptoms or ulcer can only be successfully treated by a biliary diversion, i.e. Roux-Y-gastrojejunostomy. The discovery that gastritis B is caused by HP improves our understanding of peptic ulcer disease and will change therapeutic concepts.

Algorithms↗
PubMed1988

[Campylobacter pylori, gastritis and ulcer disease. Microbiological, histological and serological studies].

In a prospective study of 70 patients with epigastric pain, gastroduodenoscopy revealed gastric and/or duodenal ulcers in a total of 41 and no ulceration in the remainder. Biopsies were taken to assess the severity of gastritis and the presence of Campylobacter pylori (CP) by histology and culture. Gastritis was found in 54 patients. CP was detected in 78% of the ulcer patients and 52% of the patients without ulcer (p less than 0.05). CP was demonstrated in 83% of the histologically diagnosed cases of gastritis (all grades) but no CP was detectable in patients with normal gastric mucosa. Among the ulcer patients, CP was more frequent in those with no history of medication with nonsteroidal antiinflammatory drugs (p less than 0.01). Sera from CP-positive ulcer and gastritis patients have significantly higher levels of IgG antibodies to CP than sera from those found to be free of ulcer or gastritis. In 200 blood donors an increasing percentage of elevated CP-antibody titres were found with advancing age (50% over 60 years of age). Quantification of circulating CP antibodies, would thus seem a valuable adjunct in the diagnosis of gastritis and probably also of peptic ulcer. The data presented furnish further evidence of the high rate of association of CP and the gastritis-peptic ulcer complex.

Adult↗
PubMed1988

Reduction in early recurrence of variceal bleeding by propranolol.

Survival after variceal bleeding depends greatly on the outcome of the immediate posthaemorrhagic period. This may in turn depend on the recurrence of bleeding. We therefore prospectively evaluated the influence of propranolol on the recurrence of variceal haemorrhage during the early period after the acute bleeding episode. Twenty consecutive patients with acute variceal haemorrhage and liver disease were randomly assigned to treatment either with propranolol or placebo orally for 14 days. Propranolol significantly decreased the rate of recurrence of variceal haemorrhage during this early period (p = 0.0028; 95% confidence interval in the placebo group, 90 +/- 20%; in the beta blocker group, 20 +/- 26%). Whereas a recurrence of variceal bleeding occurred in 9 of 10 patients in the placebo group, only 2 of 10 rebled during treatment with propranolol. These results suggest that propranolol may prevent rebleeding in the crucial early period after acute haemorrhage from oesophageal varices.

Acute Disease↗
PubMed1986

Investigation of ranitidine 150 mg bd or 300 mg bd in the treatment of reflux disease.

Twenty patients with symptoms and endoscopic changes of gastro-oesophageal reflux were randomly allocated to treatment with either ranitidine 150 mg bd, or 300 mg bd for 8 weeks. Symptoms, endoscopic appearances, histopathology of oesophageal biopsies and 22-h intra-oesophageal pH profile in ambulant patients on standard diets were recorded before and at the end of the treatment period. Symptoms improved rapidly and markedly on either dose of ranitidine. Both doses produced significant improvement of the endoscopic appearances, but there were no differences in symptomatic and endoscopic improvement related to the dose. Biopsy appearances and the 22-h oesophageal pH profile remained unchanged on either dose of ranitidine.

Adult↗
PubMed1985

[Ischemic colitis as a cause of intestinal bleeding after marathon running].

A 33-year-old long-distance runner had three episodes of bloody diarrhoea, all occurring after competitive marathon runs. Colonoscopy revealed a small lesion in the caecum histologically compatible with ischaemia of the mucosa. The discussion centres on the pathophysiology of impaired intestinal blood supply during excessive effort and the frequency of gastrointestinal symptoms and occult blood loss due to jogging.

Adult↗
PubMed1985

[Pathogenesis of gastroesophageal reflux].

Gastro-oesophageal reflux (GOR) is common. Nearly all healthy individuals experience occasional or frequent reflux episodes, with or without symptoms, which occur during spontaneous relaxations of the lower oesophageal sphincter, predominantly after meals. It is not known how neural, hormonal and muscular factors contribute to this. A proportion of the patients with reflux disease have normal lower oesophageal sphincter pressures, and their reflux episodes occur during spontaneous sphincter relaxations following the pattern of normals. Nevertheless, most patients with reflux disease have decreased lower oesophageal sphincter pressure, and manoeuvres which increase the intraabdominal pressure provoke "stress" reflux. If the sphincter pressure is very low, "free" reflux occurs; the cause of decreased sphincter pressure is not known. Pharmacological and gastric factors also facilitate GOR. The noxious potency of reflux material on the oesophageal epithelium depends on its components [( H+], pepsin, bile salts, trypsin) and the contact time, which is prolonged during supine and nocturnal reflux episodes, i.e. when clearance function is impaired. In complicated reflux disease it is necessary to consider this multifactorial model of the pathogenesis of reflux disease, and to go on to more sophisticated diagnostic procedures (manometry, scintiscanning, prolonged pH-monitoring) in order to identify an individual patients' predominant pathogenetic factor.

Cholecystokinin↗
PubMed1975

[Incidence of postoperative deep vein thrombosis in general surgical and urological patients an investigation by means of the 125I-Fibrinogen test in 95 patients withoug prophylaxis (author's transl)].

We present the results of a control group of 95 patients who were thoroughly investigated in a prospective, randomized study, where the efficacy of small doses of s.c. heparin and dextran 40 is checked. The 125I-fibrogen test was used in all patients. 1. 35.8% of the patients develop deep vein thrombosis (DVT) during the first post-operative week. More than half of them show bilateral thrombosis. 2. There is no statistically significant difference in the thrombosis incidence between males and females. 3. 47% of the patients over 60 years develop postoperative DVT. Among those younger than 60 years, only 23% have DVT (P less than 0.025). 4. The DVT incidence in surgery of the colon is 58.3%. 5. Surgery for a malignant disease means probably increased risk for DVT (P less than 0.025). 6. More than half of the patients having a previous history of varicose veins develop postoperative DVT (P less than 0.025). 7. Obese patients are statistically seen not more prone to develop DVT than those of normal body build. 8. Immediately after operation 32.4% of DVT are diagnosed, 24 hrs. later 61.8%. 94% of all DVT are diagnosed up to the third postoperative day. 9. With the exeption of one patient, all DVT develop in the calf veins, 3/4 of all abnormal values were measured in the midcalf region.

Adult↗