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Biomedical subjects

J C Bode

Publications and source records attributed to J C Bode.

At least 73 records · Page 4Linked to original sources
PubMed1991

Effect of alcohol-feeding on IgA-producing immunocytes in the small intestine of rats with and without jejunoileal bypass.

Alcohol-feeding to rats subjected to jejunoileal bypass operation has been shown to lead to marked liver injury (fatty liver, necrosis and inflammation). This study investigated the influence of alcohol-feeding over a period of 3 months on the number of IgA-producing immunocytes and the villus surface area in various sections of the small intestine of rats subjected to a jejunoileal bypass or a sham operation. A jejunoileal bypass in animals receiving the control diet led to a decrease in the number of IgA-producing immunocytes in the duodenum and ileum, but not in the bypassed (blind) loop of the jejunum. In animals subjected to a jejunoileal bypass, alcohol-feeding led to an increase in the number of IgA-producing immunocytes in the duodenum and the bypassed jejunal loop as compared with animals with a jejunoileal bypass receiving the control diet. Among the animals with a jejunoileal bypass fed the control diet, the villus surface area within the duodenum and ileum increased as compared with the groups of sham-operated rats. The feeding of alcohol prevented this increase in the villus surface area in animals with a jejunoileal bypass. The increase in the number of IgA-producing immunocytes induced by alcohol in the animals with a jejunoileal bypass, in the duodenum and bypassed jejunum, supports the assumption of a change in antigen uptake in these parts of the small intestine, brought about by alcohol.

Animals↗
PubMed1990

[Computed tomographic detection of liver hemangiomas].

A 67-year old woman had noticed increasing growth of hair on the face and extremities for eight months. The testosterone level was raised at 2.6 micrograms/l and 24-hour urinary cortisol excretion was 160 micrograms. Ultrasound scanning showed a tumour measuring 14 x 10 x 10 cm in the left suprarenal, as well as several irregular space-occupying lesions in the liver, some of which were echo-rich. By computed tomography these structures were hypodense and did not concentrate any contrast medium. A provisional diagnosis of suprarenal carcinoma with hepatic metastases was accordingly made. After surgical removal of the suprarenal carcinoma the hormonal parameters unexpectedly returned to normal. Repetition of the computed tomography failed to elucidate the nature of the liver lesions. However, superselective hepatic angiography revealed the typical picture of haemangiomas of the liver. The existing computed tomograms were therefore reviewed. The diagnostic error was found to be due to incorrect timing of the interval between injection of contrast medium and performance of computed tomography.

Adrenal Gland Neoplasms↗
PubMed1990

[Cardiac findings in alcoholic liver disease].

In a prospective study 53 patients with alcohol-induced liver disease (fatty liver in 27, cirrhosis in 26) were studied clinically and with non-invasive techniques (electrocardiogram, systolic time intervals, M-mode echocardiography, upright bicycle stress test) to detect a possible cardiac involvement. Mean daily alcohol consumption was comparable in both groups (136 g/day over 16 years vs 124 g/day over 14 years). 15 to 41% of patients (more patients with fatty liver) complaint of angina pectoris and dyspnea at exercise or had palpitations. Echocardiography and systolic time intervals demonstrated in both groups (in patients with cirrhosis despite of a more intensive therapy with digitalis and diuretics) a marked enlargement of left ventricular dimensions with a significant (p less than 0.05) degree of dysfunction (PEP/LVET). Electrocardiography showed abnormalities in 26 to 44% of patients: signs of right ventricular enlargement in 26% of patients with fatty liver, and a prolongation of myocardial repolarisation (QTc) in 44% of patients with cirrhosis. Patients with alcohol-induced liver disease deserve more attention of their cardiac complaints, clinical and functional findings.

Adult↗
PubMed1990

Gastric emptying in non-responders to H2-receptor antagonists.

H2-receptor antagonists are known to fail to increase the intragastric pH in some patients (so-called non-responders), and we have recently found a higher frequency of non-responders among cirrhotics. Since intragastric pH is also affected by gastric emptying, in the present study we determined the gastric emptying of 300 ml orange juice labelled with [99mTc]-Solco Nanocoll using a gamma camera. Measurements were made over a period of 60 min in cirrhotic patients and controls without liver disease who either responded to 300 mg ranitidine or showed no response. The mean (+/- SD) liquid half-emptying time (T1/2) was 26.3 +/- 17.5 min (range, 9-75 min) in responders (n = 10), 20.9 +/- 8.6 min (range, 7-34 min) in non-responders (n = 10), 19.4 +/- 19.2 min (range, 7-75 min) in cirrhotics (n = 11), and 27 +/- 4.6 min (range, 17-33 min) in controls (n = 9). In 19 of the 20 subjects gastric emptying was normal (T1/2, less than 40 min). Since gastric emptying was not delayed in any of the non-responders, it would appear very unlikely that gastric motility plays a major role in the non-response to H2-receptor antagonists.

Adult↗
PubMed1990

Sucralfate in the treatment and prevention of gastric ulcer: multicentre double blind placebo controlled study.

A randomised controlled multicentre trial was performed in 160 patients with gastric ulcer, proved by endoscopy and biopsy, to compare ulcer healing with sucralfate and ranitidine (double blind double dummy design) and to assess the effect of maintenance treatment with sucralfate on ulcer recurrence (double blind placebo controlled design). The healing rates were similar with 4 g sucralfate suspension per day and 300 mg ranitidine per day (82% and 88% after 12 weeks, respectively). Of the 109 patients with healed ulcers, 92 were entered into the maintenance trial and treated with sucralfate tablets (2 g per day) or placebo tablets. Maintenance treatment with sucralfate delayed symptoms of gastric ulcer recurrence. Lifetable analysis showed significant differences between sucralfate and placebo, both after six months (p = 0.018) and after 12 months (p = 0.044). The rates of symptom recurrences were 13% and 34% after six months and 34% and 55% after 12 months for sucralfate and placebo, respectively. The rate of asymptomatic recurrences after 12 months was similar in the two groups (9% and 10%, respectively). The recurrence rate was higher in patients who had never taken non-steroidal anti-inflammatory drugs than in those who had but had stopped on admission to the study. It was also higher in patients with recurrent ulcer and in those with scarring deformation and narrowing of the pylorus. Maintenance treatment with sucralfate slowed the appearance of symptom recurrences of gastric ulcer.

Adult↗
PubMed1990

Combined effect of pirenzepine and ranitidine on the nocturnal intragastric pH in non-responders to ranitidine.

Both H2-receptor antagonists and pirenzepine are used in the treatment of peptic ulcer disease. Since we have recently found a higher frequency of non-responders to H2-receptor antagonists among cirrhotics, we tested the effect of the combination of 50 mg pirenzepine and 300 mg ranitidine in 25 patients (12 cirrhotics and 13 controls) in whom a normal 300 mg dose of ranitidine had failed to suppress intragastric acidity. Nocturnal intragastric pH was continuously monitored for 12 hours. A rise in the intragastric pH above 4.0 for more than 6 hours following the oral dose at 18.00 h was considered as response. In all subjects, plasma concentrations of ranitidine and pirenzepine were in the therapeutic range. Coadministration of pirenzepine and ranitidine resulted in sufficient increase of the intragastric pH in only 4 of the 12 patients with cirrhosis, and in 4 of the 13 control patients. This treatment failure in most of our patients does not support the view that excessive vagal drive might play an important role in the non-response to H2-blockers. With regard to the benefit resulting from coadministration of pirenzepine and ranitidine, there seems to be no difference between cirrhotic and control patients.

Adult↗
PubMed1990

Macrolipasemia: a rare cause of persistently elevated serum lipase.

This report describes a variant form of lipase found in a patient with cryptogenic liver cirrhosis. Serum lipase in this patient showed persistently increased activity with simultaneously normal activity of amylase. Results of exclusion chromatography demonstrate that the lipase activity in the serum of this patient eluted as a macromolecule. Since macromolecular complexes were not fixed by protein A, it seems unlikely that lipase is attached to IgG. Tests of the sera from 20 patients with raised serum lipase activity in acute pancreatitis or an acute episode of chronic pancreatitis revealed, in two patients, that a small but reproducible proportion of the total lipase activity eluted in the region of the macrolipase. In addition, 10% and 18% of the total lipase activity was found in the elution region of the macrolipase in two commercial pooled sera used for quality control. The results show that, in rare cases, macrolipasemia must be considered a possible cause of raised serum lipase activity.

Aged↗
PubMed1989

Frequent non-response to histamine H2-receptor antagonists in cirrhotics.

The effect of ranitidine 300 mg po given at 1800 h (famotidine 40 mg/cimetidine 800 mg) on the night time gastric pH was tested using longterm intragastric pH monitoring in 27 patients with and 32 patients without liver cirrhosis. A rise in the gastric pH above 4.0 for more than six hours between 1800 h and 0600 h was considered as sufficient effect (response) of the H2-receptor antagonists on gastric acidity. Among the patients with cirrhosis, there were significantly (p less than 0.005) more non-responders to ranitidine (16 of 27 patients) than in the control group (six of 32). When 13 of the 22 non-responders to ranitidine were subsequently treated with famotidine, only two showed a sufficient rise in their gastric pH. Of the 11 patients not responding to both H2-receptor antagonists, 10 were finally treated with cimetidine and eight did not respond. Plasma levels of all three drugs measured two and four hours after oral administration were not significantly different between cirrhotic and noncirrhotic patients as well as between responders and non-responders. In addition, in all patients plasma levels were far above the corresponding IC50 values. Therefore, differences in the absorption and plasma levels of these drugs cannot account for the frequent non-response in cirrhotics.

Anti-Ulcer Agents↗
PubMed1989

Chromogenic endotoxin assay in plasma. Selection of plasma pretreatment and production of standard curves.

The aim of this study was to define the optimal conditions for the plasma pretreatment and to improve the production of standard curves for plasma endotoxin determination by a chromogenic substrate assay. Endotoxin standard from E. coli O 111:B 4 (0-50 ng/l) was added to pyrogen-free water or to plasma samples from 12 healthy subjects and 24 alcoholics, before pretreatment by heating (75 degrees C, 5 minutes) or with perchloric acid (0.32 mol/l). When endotoxin standard curves were determined using a microprocessor-controlled reader, the slopes of the curves obtained with plasma differed from those with pyrogen-free water. The slope of the standard curve prepared with plasma samples from different patients exhibited marked interindividual variations. Compared with the heating method, the perchloric acid method gave more variable results and a lower recovery of added endotoxin, especially in plasma from alcoholics. The results permit the following conclusion: 1. For plasma endotoxin determination, a standard curve should be prepared for each individual plasma sample. 2. The endotoxin standard should be added before pretreatment of the plasma. 3. Pretreatment of the plasma by heating at 75 degrees C for 5 minutes provides more reliable results than pretreatment with perchloric acid.

Adult↗
PubMed1989

Effect of acute ethanol ingestion on human gastric luminal prostaglandin E2, prostaglandin F2 alpha and 6-keto-prostaglandin F1 alpha.

In healthy human volunteers we evaluated the effect of a single oral dose of 1 g/kg of alcohol (12.5%, v/v) on the output of prostaglandin E2, prostaglandin F2 alpha and 6-keto-prostaglandin F1 alpha in the gastric juice. In control experiments performed at intervals of 5-8 days, the subjects received the identical volume of water. Ninety minutes after the ingestion of alcohol, or water, first the basal secretion and subsequently the secretion after injection of pentagastrin (6 micrograms/kg, i.m.) were collected over periods of 60 min. The concentrations of the three prostaglandins were determined by radio-immunoassay. After ingestion of alcohol, the volume of gastric juice in response to pentagastrin stimulation was reduced by 24.6%, as compared with the control period. Ingestion of alcohol led to a significant reduction in the concentration of prostaglandin E2 (-42.7%) after stimulation with pentagastrin. The prostaglandin E2 output per hour was markedly inhibited by the ingestion of alcohol, both in the basal period (-47%) and after stimulation with pentagastrin (-55%). While stimulation with pentagastrin did not influence the secretion of PGE2 or PGF2 alpha, the output of 6-keto-PGF1 alpha increased appreciably (+88%) after the administration of pentagastrin. Alcohol also significantly (-28%) inhibited the secretion of 6-keto-PGF1 alpha in the period following the administration of pentagastrin. It is supposed that the inhibition of the secretion of prostaglandin E2 and 6-keto-prostaglandin F1 alpha by acute alcohol ingestion, might be of significance for the development of alcohol-induced mucosal damage in the stomach.

6-Ketoprostaglandin F1 alpha↗
PubMed1988

Effect of acute and chronic alcohol feeding on prostaglandin E2 biosynthesis in rat stomach.

The effect of acute and chronic alcohol ingestion on gastric prostaglandin E2 synthesis and the PGE2 content in the stomach was studied in rats. Up to 8 hr following a single oral load of 20% alcohol (v/v; 4 g/kg body weight), the PGE2 synthesis in isolated microsomes from rat stomach remained unchanged as compared with control values. Feeding a liquid alcohol-containing diet (37% of total Joules) for 1, 6, or 12 weeks significantly decreased the rate of PGE2 synthesis (percentage inhibition as compared with control values 39, 27, and 57, respectively). In addition, chronic alcohol feeding led to a drop in the tissue content of PGE2, the decrease being more pronounced after 6 (-49%) and 12 (-58%) weeks than after 1 week (-24%). The results suggest that the inhibition of endogenous PGE2 synthesis in the stomach following ingestion of appreciable quantities of alcohol might play a role in the pathogenesis of alcohol-induced injury of the gastric mucosa.

Animals↗
PubMed1987

[Mesenteric lipomatosis. A rare disease often misdiagnosed as ascites].

A 53-year-old man, a known alcoholic, was admitted to hospital, because of abdominal swelling, with the admission diagnosis of ascites. Treated with diuretics a severe hypokalaemia developed with subileus and moderate clouding of consciousness. Computed tomography revealed the correct diagnosis of intraabdominal extraperitoneal (mesenteric, pelvic, retroperitoneal) soft-tissue lipomatosis.

Alcoholism↗