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Biomedical subjects

J Reikowski

Publications and source records attributed to J Reikowski.

14 recordsLinked to original sources
PubMed1988

Hepatic detoxification and hepatic function in chronic active hepatitis with and without cirrhosis.

The detoxification capacity of the liver in chronic active hepatitis (CAH) without liver cirrhosis (LC) is not sufficiently known. Therefore, we examined, in 156 patients with morphologically proven CAH of different stages, plasma ammonia, free phenols, indican, glucuronic acid and urea synthesis rate as parameters for liver detoxification. We found a significant increase of ammonia, phenols, and indican and a significant decrease of glucuronic acid and urea synthesis rate parallel to the stage of CAH without LC. In 34 CAH patients with complete recovery, a retrospective 10-year follow-up was possible. Parallel to the normalization of liver morphology and general liver tests, detoxification parameters also normalized. However, the detoxification disorders in CAH without LC are mild in nature and do not produce hepatic encephalopathy. Probably, they are caused by a reduced synthesis of the urea-cycle enzymes and of glucuronyltransferase in the liver.

Ammonia↗
PubMed1983

[Hepatic coma. Principles of pathogenesis and treatment. 2: Treatment, prognosis].

According to the multifactorial pathogenesis of hepatic coma, generally caused by the increased formation of toxic protein metabolites in the gut, the most important therapeutical measure is the cleaning and acidifying of the gut. This is possible very simply and cheaply by high enemas of sodium acetate buffers of pH 4,5 and lactulose. If necessary, neomycin or paromomycin must be administered in high doses of 6--8 gm/daily to reduce the pathogenic intestinal bacteria. The detoxification capacity of liver and brain can be improved by intravenous and later oral administration of ammonia reducing amino acids such as arginine, ornithine, and aspartic acid (10--20 gm/daily). They diminish also the elevated serum phenols. Very helpful are also branched chain amino acids which improve apparently the detoxification capacity of the muscle. Very important is the normalization of disturbances of the water and electrolyte balance, especially the normalization of hypokalemia. Very difficult is a successful treatment of cerebral edema and the disturbances of blood coagulation. In special cases of endogenous hepatic coma liver perfusions, hemodialysis, charcoal perfusions a.s.o. can eliminate successfully toxic protein metabolites, whilst this treatment is generally insufficient in the more frequent exogenous hepatic coma. In summary the prognosis of hepatic coma is also nowadays very serious and can only be improved by the early recognition and elimination of exacerbating factors.

Combined Modality Therapy↗
PubMed1983

[Causes and diagnostic criteria of hepatic coma--an analysis of 560 cases].

560 patients with hepatic coma were treated during the years 1958 to 1982 in Homburg and Bad Kissingen . 82 patients had an endogeneous and 478 an exogeneous hepatic coma. Endogeneous hepatic coma was caused most frequently by fulminant virus hepatitis, intoxication, and hepatorenal syndrome accompanying serum hepatitis. Exogeneous hepatic coma in patients with cirrhosis of the liver was caused in most cases by gastrointestinal bleeding, by a diet too high in protein, or by excessive diuresis. Early clinical symptoms are changes in writing tests and ability to concentrate, whereas hepatic foetor occurs in coma stage III and IV. Clinical chemistry findings pointing to imminent hepatic coma are increase of arterial ammonia in exogeneous hepatic coma, and increase of free phenols in endogeneous hepatic coma. The increase of prothrombin time is prognostic for imminent hepatic coma in both types. Prognosis of endogeneous hepatic coma is still rather bad; 87% of the patients suffering from it died; in exogeneous hepatic coma prognosis has improved for stage I and II in the last 23 years, whereas however the total prognosis for all 4 stages is still unchanged, letality being 55%.

Adult↗
PubMed1977

[New aspects of the pathogenesis and therapy of alcoholic delirium (author's transl)].

Clinically, and especially biochemically, alcoholic delirium corresponds closely to an incipient but reversible exogenous hepatic coma. The blood levels of ammonia in particular, free phenols and lactate are greatly increased. These same metabolites increase slightly in the blood of persons with healthy livers after a single alcohol loading. The treatment of alcoholic delirium consists of optimal sedation with Distraneurin, which appears to have no side effects on the liver. There is even a lowering of the raised lactate level in the blood after a single administration of Distraneurin. Ammonia and phenols are reduced by ammonia-lowering aminoacids, lactulose and bifidum milk. Most important, however, is strict abstention from alcohol, which alone brings about a rapid improvement of pathological biochemical and morphological liver findings.

Alcohol Withdrawal Delirium↗