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Biomedical subjects

G Strohmeyer

Publications and source records attributed to G Strohmeyer.

At least 37 records · Page 2Linked to original sources
PubMed1995

Effect of intestinal resection on serum antibodies to the mycobacterial 45/48 kilodalton doublet antigen in Crohn's disease.

Interest in the role of mycobacterial infection in Crohn's disease has been revived by the cultural detection of Mycobacterium paratuberculosis in patients with Crohn's disease. This hypothesis was examined serologically using assays with high specificity for Crohn's disease. The effect of intestinal resection on serum antibodies specific for Crohn's disease was investigated with an immunoblot assay and an enzyme linked immunosorbent assay using the 45/48 kilodalton doublet antigen of Mycobacterium tuberculosis. Antibodies were detected in 64.7% of patients with Crohn's disease (n = 17), 10% of patients with ulcerative colitis (n = 10), 5% of patients with carcinoma of the colon (n = 20), and none of 10 healthy subjects with the immunoblot assay. Statistical comparison of the Crohn's disease patients with each control group resulted in p = 0.0000236. Immunoglobulin G was essentially unchanged 75 days (mean) after surgery. After more than 180 days, however, the antibody response was reduced in all of five patients studied, and was no longer demonstrable in two of them (40%). Simultaneously, the Crohn's disease activity index (CDAI) decreased. Both the high specificity of this assay for Crohn's disease and the diminished antibody response after intestinal resection in parallel with decreased CDAI support a mycobacterial aetiology of Crohn's disease.

Adolescent↗
PubMed1995

[Diagnosis and therapy of autoimmune hepatitis].

Thorough differential diagnosis in patients with autoimmune hepatitis is important since other liver disorders need different treatment regimen. Elevated transaminases and gamma-globulines and autoantibodies should make one think of autoimmune hepatitis. Liver biopsy is helpful but usually not a definitive proof of the diagnosis. Immunosuppressive therapy has to be administered for years and possibly leads to serious side effects. Therapy should only be discontinued if a complete remission is induced. Relapses after cessation of medical treatment occur frequently. If no remission is achieved lifelong immunosuppressive therapy has to be given. In decompensated disease liver transplantation offers a treatment with good prognosis.

Autoantibodies↗
PubMed1995

Glucagon effect on intracellular proteolysis and pericanalicular location of hepatocyte lysosomes in isolated perfused guinea pig livers.

In guinea pigs, glucagon choleresis is accompanied by a significant, but transient, stimulation of biliary protein secretion, which can be accounted for mainly by biliary discharge of lysosomal enzymes. To clarify whether intracellular proteolysis--a process regulated by glucagon and taking place predominantly in the lysosomes--may interact with biliary protein secretion, we determined hepatic proteolytic activity and bile secretory function during substrate deprivation, amino acid supplementation, and glucagon administration in isolated perfused guinea pig livers. To further elucidate the nature of transient lysosomal enzyme release into bile during glucagon infusion, we analyzed pericanalicular distribution of lysosomes by quantitative electron microscopy. The results demonstrate that intracellular proteolysis is accompanied by biliary excretion of lysosomal enzymes. Glucagon-induced secretion of these enzymes as well as labeled proteins into bile occurs independent of protein breakdown and cannot be modulated by addition of amino acids as potent inhibitors of intracellular proteolysis. During glucagon administration, bile canalicular area and pericanalicular distribution of secondary lysosomes show a rapid increase, which persists during the entire infusion period and thus does not explain the transient biliary release of lysosomal enzymes. We therefore postulate that regulation of this process must be located beyond the lysosomal compartment, either involving transport processes or intracellular kinetics of lysosome formation or altered fusion kinetics at the bile canalicular membrane compartment. Metabolic and biliary effects of glucagon seem to occur independent of each other and to underly different regulatory mechanisms.

Amino Acids↗
PubMed1995

[Neuroimmune interactions in the gastrointestinal tract].

The enteric nervous system and immune system are integrated systems that play an important role in the regulation of gastrointestinal functions. Recent studies suggest a bidirectional interaction between both systems. The relationship is based on the synthesis and release of neuropeptides from immune cells and the receptor-mediated alteration of nervous and immune functions by neurotransmitters and inflammatory mediators. The activity of the enteric nervous and immune system can be modulated by the central nervous system. These psycho-neuro-immuno-interactions are involved in gut inflammation, in functional bowel diseases and in the physiological control of gastrointestinal functions.

Animals↗
PubMed1994

[Liver transplantation 1994].

Transplantation of the liver has progressed in recent years and has become universally accepted for numerous indications in end-stage liver diseases, predominantly primary biliary cirrhosis, sclerosing cholangitis, biliary atresia and liver-related metabolic disorders. In fulminant and subfulminant hepatitis, prognosis has been improved considerably by liver transplantation. The debate still persists whether liver transplantation might be indicated in diseases recurring after transplantation, such as HBV cirrhosis. Alcoholic cirrhosis as an indication for transplantation remains still controversial. The risk of tumor recurrence after transplantation for small hepatocellular carcinoma in cirrhosis can be calculated; adjuvant chemotherapy might increase prognosis. Transplantation for other malignant liver tumors seems to be obsolete.

Aged↗
PubMed1994

Pathogenesis of glucose intolerance and diabetes mellitus in cirrhosis.

Glucose intolerance and diabetes mellitus are both prevalent in cirrhosis, yet the pathogenesis of impaired glucose metabolism remains unknown. Therefore insulin secretion (hyperglycemic clamp, +125 mg/dl), insulin sensitivity (euglycemic hyperinsulinemic insulin clamp, +10 microU/ml and +50 microU/ml), whole-body glucose oxidation (indirect calorimetry) and glucose turnover ([6,6-2H2]glucose isotope dilution) were evaluated in a homogenous group of cirrhotic patients with glucose intolerance (n = 7) or frank diabetes mellitus (n = 6). The results were compared with those obtained in control subjects (n = 8). In glucose-intolerant patients, whole-body glucose uptake (mainly reflecting glucose utilization by muscle) was significantly impaired in patients during both insulin infusions as a result of decreased stimulation of the two major intracellular pathways of glucose disposal--nonoxidative glucose disposal (i.e., glycogen synthesis) and glucose oxidation. Hepatic glucose production was normal in the basal state and was normally suppressed during stepwise insulin infusion (by 65% and 85%, respectively, p = NS vs. controls). Hyperglycemia-induced increases of plasma C-peptide concentrations were comparable to those in controls (p = NS). In diabetic patients, insulin-mediated glucose uptake was significantly reduced, mainly because of impaired non-oxidative glucose disposal. Glucose oxidation appeared to be reduced, too. Hepatic glucose production was significantly increased in the basal state (3.03 +/- 0.24 vs. 2.34 +/- 0.10 mg/kg min, p < 0.02) and during insulin infusion (+50 microU/ml: 0.67 +/- 0.17 vs. 0.13 +/- 0.08 mg/kg min, p < 0.05) compared with that in controls. Both the first and second phases of beta-cell secretion were significantly reduced in response to steady-state hyperglycemia (both p < 0.01 vs. control values). In conclusion, glucose intolerance in cirrhosis results from two abnormalities that occur simultaneously: (a) insulin resistance of muscle and (b) an inadequate response (even when comparable to that of controls) of the beta-cells to appropriately secrete insulin to overcome the defect in insulin action. Diabetes mellitus in insulin-resistant cirrhotic patients develops as the result of progressive impairment in insulin secretion together with the development of hepatic insulin resistance leading to fasting hyperglycemia and a diabetic glucose tolerance profile.

Adult↗
PubMed1994

Epidemiology, clinical spectrum and prognosis of hemochromatosis.

EPIDEMIOLOGY: Eleven prospective epidemiological studies from various countries have as yet evaluated the gene prevalence of HLA-linked hemochromatosis. The estimated frequency ranged from 0.027-0.107, the frequency of homozygotes from 0.00074-0.0116, and the frequency of heterozygotes from 0.052-0.191. In a meta-analysis of the eleven surveys the frequency is 0.0016 (106/64758 subjects) for homozygotes which corresponds to a gene frequency of 0.041 and a frequency of heterozygotes of 0.078. Further analyses showed that some of these studies have probably underestimated the prevalence which in reality is probably two- to threefold higher than estimated by the meta-analysis. CLINICAL SPECTRUM: In the total group of 251 patients diagnosed with hemochromatosis in the University of Düsseldorf from 1959-1992, abnormality in liver function tests (75%), weakness and lethargy (74%), skin hyperpigmentation (70%), diabetes mellitus (48%), arthralgia (44%), impotence (45% in males), and ECG abnormalities (31%) were the most frequent findings and symptoms at diagnosis. In recent years about 50% of patients were detected without having liver cirrhosis and 20% of patients did not have any symptoms and pathology except iron overload. PROGNOSIS: Survival analysis in the 251 patients showed that in the absence of cirrhosis and diabetes iron removal by phlebotomy therapy prevents further tissue damage and guarantees a normal life expectancy. Sex and presence of arthropathy did not predict prognosis. However, patients with massive and long-lasting iron overload had a worse prognosis than patients with less severe iron excess. Iron removal in general ameliorated liver disease, weakness and cardiac abnormalities, and also prevented the progression of endocrine alterations. Therapy, however, did not influence arthropathy which even got worse in several patients. Iron removal also failed to reverse insulin-dependent diabetes. During a mean followup of 13.4 years 69 deaths occurred in the 251 patients. In 19 patients death was due to liver cancer, in 14 due to liver cirrhosis, in 5 due to cardiomyopathy, and in 3 due to diabetes mellitus (all causes significantly more frequent than expected for the general population). The other causes of death were as frequent as expected including extrahepatic malignancies. All liver cancers were seen in cirrhotic livers, but often occurred many years or even decades after complete iron removal. Further strategies have to evaluate the design of screening programs in order to diagnose more patients in the precirrhotic and asymptomatic stage.

Bloodletting↗
PubMed1994

Long-term efficacy of biofeedback training for fecal incontinence.

PURPOSE: Biofeedback therapy in fecal incontinence has been reported to improve continence in more than 70 percent of patients, but most studies have followed patients for less than two years. METHODS: Patients treated by biofeedback training between 1985 and 1986 were given a questionnaire in 1991, as were incontinent patients who had not entered this treatment program. All were asked for the occurrence, frequency, and severity of incontinence events in the past two weeks. Anamnestic and anorectal manometry data from the initial visit were also compared. RESULTS: Eighteen of 24 treated patients and 40 of 71 untreated patients responded. Of those treated by biofeedback, 78 percent reported episodes of fecal incontinence as compared with 77.5 percent of those not treated by biofeedback. Severity of incontinence, however, was significantly less (P < 0.02) in the treatment group (mean number of events, 0.2/day) than in those without treatment (1/day). In biofeedback-treated patients, it was identical with the frequency and severity reported immediately after therapy. No differences were found with respect to initial clinical data and anorectal manometry between both groups. CONCLUSION: Biofeedback training improves continence in patients not only during treatment and within the first two years but also for several years after therapy.

Adolescent↗
PubMed1994

Motor analysis predicts progression in HIV-associated brain disease.

One hundred HIV-positive individuals without clinically evident central nervous system (CNS) deficits entered this follow-up study and were examined clinically and with a well-defined motor test battery every 3 months over 2 years or until they decreased. They underwent magnetic resonance tomography once a year. None received any form of therapy at onset of the study. Three groups were analyzed: (A) patients without electrophysiologically detectable motor impairment (n = 23), (B) patients with electrophysiologically detectable motor impairment but no virostatic medication (n = 33), and (C) patients with motor deficits undergoing AZT treatment (n = 44) after study onset. Group A patients, although slightly deteriorating over time, had the best clinical and electrophysiological outcome compared to the other groups, whereas group B patients deteriorated markedly in both clinical and electrophysiological tests, even though the majority did not develop cerebral complications during the observation period. Those group C patients belonging to early CDC stages (II and III) improved electrophysiologically under AZT therapy, while 76% of the patients in more advanced stages (CDC IVA-D) died of cerebral AIDS manifestations. Four patients of this group, being alive at the end of the study, were completely demented. It is suggested that early detectable motor impairment predicts future cerebral involvement in AIDS. Late onset of virostatic treatment did not influence the clinical outcome.

AIDS Dementia Complex↗
PubMed1994

Glucocerebrosidase for treatment of Gaucher's disease: first German long-term results.

Until recently, there was no specific therapy available for patients with Gaucher's disease. Since April 1991 a highly purified human placental preparation of glucocerebrosidase (Ceredase, Genzyme) has been available for clinical studies in Germany. Sequential deglycosylation of the native enzyme yields a mannose-terminated preparation that may preferentially bind to the plasma membrane of macrophages. The present report analyzes the first German (and European) long-term results with glucocerebrosidase therapy in five patients with type I Gaucher's disease (four women and one man, aged 29-40 years). All patients suffered from excessive enlargement of the liver and spleen with subsequent pancytopenia and from skeletal complications. Multiple pathological fractures had already occurred in three of the five patients, requiring several surgical procedures. Fatigue and asthenia were present in all patients. The initial dose of glucocerebrosidase was chosen according to the severity of complications in the individual patient (20-50 U/kg given i.v. every 2nd week) and was performed in the five patients for 12-18 months. After a few weeks all patients reported that fatigue and asthenia were markedly reduced. After 12 months, blood counts of erythrocytes, leukocytes and platelets had completely normalized in all but one of the patients. After 4-6 months a significant reduction in the sizes of liver and spleen could be observed in all patients. No further fractures occurred during treatment. Significant side-effects of glucocerebrosidase treatment did not occur. The new glucocerebrosidase preparation offers the first effective drug therapy for patients with Gaucher's disease. Although the treatment proved effective and harmless, it is, at least initially, very expensive.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Effects of Helicobacter pylori on histamine and carbachol stimulated acid secretion by human parietal cells.

Helicobacter pylori (H pylori) infection is associated with hypo, normal, and hypersecretory disorders of the gastric mucosa. Pathophysiological pathways by which H pylori interacts with acid secretion are still unclear. The effects of H pylori on (14C) aminopyrine uptake by human parietal cells were examined as an indirect assay for acid secretion. Isolated oxyntic glands were stimulated with submaximal concentrations of histamine or carbachol and incubated with sonicates of different H pylori strains. Omeprazole and sonicates of Campylobacter jejuni served as positive and negative controls, respectively. Two of four H pylori strains reduced hydrochloric acid sequestration within the parietal cells significantly and in a dose dependent manner in up to 80%. Interaction with acid secretion may therefore constitute a factor contributing to a distinct pathogenicity of H pylori strains.

Aminopyrine↗
PubMed1994

Effect of Helicobacter pylori on dbc-AMP stimulated acid secretion by human parietal cells.

This study examines the effect of different H.p. strains (A-D) on dbc-AMP stimulated acid secretion by human parietal cells in vitro. H.p. strains A and D reduced acid secretion dose-dependently between 20 and 80%. In contrast, H.p. strains B and C had little or no effect. We conclude that H.p. strains vary in their ability to suppress acid secretion, and that the site of inhibition lies beyond the c-AMP level, possibly involving the K+H(+)-ATPase of the parietal cell. Interference with acid secretion may facilitate H.p. colonization of the stomach and may prove to be an important pathogenetic factor.

Aminopyrine↗
PubMed1994

Prevalence of gastrointestinal symptoms in diabetic patients and non-diabetic subjects.

To determine the frequency of gastrointestinal symptoms in diabetic patients, 190 patients, consecutively referred to the Diabetes Research Institute, reported their gastrointestinal symptoms on a standardized symptom list. One hundred and eighty non-diabetic healthy subjects served as (matched) controls. Finally, 75 patients with Type 1 (insulin-dependent) diabetes mellitus (33 male, 43 female; age 34,1 (18-60) yrs, diabetes duration: 11,1 (0,3-41) yrs) and 68 patients with Type 2 (non-insulin-dependent) diabetes mellitus (31 male, 37 female, age: 61,4 (37-88) yrs, diabetes duration: 10,7 (0,3-40) yrs) were studied and compared with two cohorts of controls of the same size. There were no differences in prevalence of symptoms referrable to the upper and lower GI-tract in type 1 diabetic patients as compared with controls. Among patients with type 2 diabetes the main gastrointestinal complaint was constipation (22,1% vs 10,3%; p < 0.05). Upper gastrointestinal symptoms were also more frequent among Type 2 diabetic subjects (nausea 11,8% vs 2,9%, p < 0.05). There was a tendency for an increased symptom prevalence with higher age in both type 1 and type 2 diabetes. Presence of peripheral neuropathy was associated with a higher symptom prevalence in type 1 diabetes. After stratification, diabetes duration and glycaemic control (HbA1c) did not influence the frequency of symptoms. Thus, gastrointestinal symptoms occur frequently among both diabetic patients and non-diabetic subjects. However, significant differences were found only in type 2 (non-insulin-dependent) diabetes, the commonest symptom being constipation. These findings support the need of a nondiabetic control group in epidemiological studies evaluating symptom prevalence in diabetes mellitus.

Adolescent↗