Biomedical subjects

Jürgen Bauditz

Publications and source records attributed to Jürgen Bauditz.

3 recordsLinked to original sources

PubMed2006

Role of intestinal function in cachexia.

PURPOSE OF REVIEW: Cachexia is a prominent feature in many chronic diseases, but its pathogenesis is still not fully understood. This article reviews recent research into the role of the gut barrier in the pathogenesis of inflammation and cachexia with special emphasis on two potentially catabolic diseases: liver cirrhosis and chronic heart failure. RECENT FINDINGS: There is increasing evidence that catabolic diseases such as liver cirrhosis and chronic heart failure are associated with increased gut permeability, endotoxemia and enhanced expression of proinflammatory cytokines. In liver cirrhosis normalization of portal hypertension by insertion of a transjugular intrahepatic portosystemic stent shunt obviously causes improvement not only of gut barrier function, but also of nutritional status. SUMMARY: Although its pathogenesis is not yet completely understood, proinflammatory cytokines have been implicated in the onset and progression of cachexia. Recent data support the hypothesis that impaired gut barrier function and increased permeability further translocation of endotoxins. Increased endotoxemia might be a potent trigger of systemic inflammatory response which is involved in the pathogenesis of the cachexia syndrome. Thus, it is tempting to speculate that therapeutic strategies for the improvement of gut barrier function will concomitantly improve nutritional status.

Bacterial Translocation↗

PubMed2005

Hepatic steatosis in Dunnigan-type familial partial lipodystrophy.

OBJECTIVES: Characterization of familial clusters of subjects with metabolic derangements predisposing to hepatic steatosis and nonalcoholic steatohepatitis could facilitate genomic studies to identify risk factors for their development. Dunnigan-type familial partial lipodystrophy (FPLD) is an autosomal dominantly inherited disorder caused by mutations in the LMNA gene. Affected subjects have loss of subcutaneous fat from the extremities and symptoms similar to those characterizing the metabolic syndrome, including insulin resistance and dyslipidemia. The goal of this study was to determine the prevalence of steatosis in subjects with FPLD. METHODS: We examined 18 subjects from six families with FPLD for mutations in LMNA and analyzed plasma lipid and serum glucose concentrations. Liver ultrasound and serum aminotransferase activities were used as indicators of steatosis or steatohepatitis. In two subjects, histological examination of hepatic tissue was performed. RESULTS: All subjects had FPLD-causing mutations in LMNA. Plasma lipids were measured in 17 subjects, 16 of whom had hyperlipidemia and 14 presented with either documented insulin resistance or diabetes mellitus. Hepatic steatosis was present in 15 subjects who had ultrasound examinations and 9 of these had elevated serum aminotransferase activities. Liver biopsy confirmed steatosis in 2 subjects. CONCLUSIONS: Hepatic steatosis is part of the clinical phenotype of FPLD. This familial disorder may provide a human metabolic model system to facilitate genomic and environmental studies to determine risk factors for hepatic steatosis and nonalcoholic steatohepatitis.

Adipose Tissue↗

PubMed2003

Manifestation of thyrotoxic periodic paralysis in two patients with adrenal adenomas and hyperandrogenaemia.

Hypokalaemic periodic paralysis is a fairly common complication of hyperthyroidism in Asian populations, but a rare event in Caucasians. In the present work we describe 2 male Caucasian patients with thyrotoxic periodic paralysis (TPP) as initial clinical manifestation of Graves' disease. Further diagnostic procedures demonstrated unilateral adrenal adenoma and hyperandrogenaemia in both patients. To date, only few data are available concerning the hormonal status of Caucasian patients with TPP. The constellation of TPP and adrenal adenomas with increased levels of androgens has not been described previously. Since androgens are capable of inducing sodium-potassium ATPase, which is thought to be centrally involved in the pathogenesis of TPP, hyperandrogenaemia may have triggered the manifestation of paralytic attacks in our patients. It may be of interest to focus not only on thyroid dysbalances in patients with TTP but also to investigate other hormonal disturbances.

Adenoma↗