Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0016382 (flushing)
 6,387 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To assess the relationship between the polymorphism of aldehyde dehydrogenase (ALDH) isozyme and alcoholic liver injury, ALDH isozyme was analyzed by isoelectric focusing electrophoresis in hair roots from normal volunteers and alcoholics with chronic liver disease. Liver biopsy specimens from alcoholics and non-alcoholics with chronic liver disease were also analyzed. It was found that (1) the frequency of low Km ALDH isozyme in hair roots from chronic alcoholics with liver injury was 90%, which was significantly higher than those from normal volunteers (44%) and from non-alcoholics with chronic liver disease (56%); (2) the isozyme pattern of liver specimens analyzed coincided with that of hair roots; (3) the low Km ALDH isozyme-positive subjects including alcoholics showed no facial flushing, and negative subjects showed facial flushing after drinking alcohol. It is concluded that a much higher frequency of low Km ALDH isozyme was found in chronic alcoholics with liver injury. There was no apparent difference in hepatic biochemical and histological findings between chronic alcoholics with and without low Km ALDH isozyme, suggesting that acetaldehyde does not play a primary role in the pathogenesis of alcoholic liver injury.
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PMID:Low Km ALDH isozyme and alcoholic liver injury. 663 52

Paraneoplastic syndromes are frequently associated with various types of malignant tumors but are fairly rare in the course of hepatocellular carcinoma (HCC). We describe the clinical case of a 76 year old man with chronic hepatitis C infection related to liver disease who had suffered for several months from chronic runny but blood and mucus-free diarrhea, together with progressive weight loss and flushing of the face. Serological tests made on admission confirmed the chronic liver disease and showed an increase of serum levels of some neuroendocrine hormones, i.e. 5-hydroxytryptamine and vasoattive intestinal peptide. Ultrasound and CT scans led to the diagnosis of HCC. The diarrhea and the increase in some neuroendocrine hormones were therefore interpreted as expression of a paraneoplastic-like neuroendocrine syndrome that had preceded the onset of HCC by some months. The patient died a few months after the diagnosis of HCC, from total portal vein thrombosis and consequent liver and renal failure. This clinical report draws the attention to the possibility of paraneoplastic syndrome expression before the clinical onset of HCC and to the role that neuroendocrine hormones may have on the growth and spread of HCC.
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PMID:[Diarrhea as first clinical manifestation of hepatocellular carcinoma]. 1235 85