Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An electroneurographic study performed on the peripheral nerves of 25 patients with severe cirrhosis following viral hepatitis showed slight slowing (P greater than 0.05) of motor conduction velocity (CV) and significant diminution (P less than 0.001) of sensory CV and mixed sensorimotor-evoked potentials, associated with a significant decrease in the amplitude of sensory evoked potentials. The slowing was about equal in the distal (digital) and in the proximal segments of the same nerve. A mixed axonal degeneration and segmental demyelination is presumed to explain these findings. The CV measurements proved helpful for an early diagnosis of hepatic polyneuropathy showing subjective symptoms in the subclinical stage.
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PMID:Electroneurographic evidence of polyneuropathy in chronic liver disease. 20 28

296 cases of delirium tremens treated in 1958-69 were analysed retrospectively. Forty-one patients died in delirium or shortly thereafter. In 72 by now dead patients cirrhosis of the liver was the most common cause of death. Of 68 patients re-examinated, 12 were now teetotallers and six had markedly reduced there intake. Fifty patients had continued drinking and most of them had signs of liver failure, one had hypertension and one also had a polyneuropathy. Those who were abstaining, as well as the patients with a favourable course,and most of them were married. Although the acute death-rate of delirium has been markedly reduced since the introduction of clomethiazole treatment, it remains high after discharge. In almost half of those who were still drinking there had been a slide downwards in their social status. Delirium tremens is almost always precipitated by alcohol withdrawal.
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PMID:[Prognosis of alcoholic delirium (author's transl)]. 52 Jan 53

Eight patients with chronic (mean 52 months) type B hepatitis (chronic active hepatitis and active cirrhosis) and markers of active viral replication (presence of HBeAg and HBV-DNA in serum) were treated with Ara-AMP for 7-12 weeks. The mean follow-up time was 18.3 months. All but one patient responded to treatment. In seven patients, HBeAg and HBV-DNA became negative and developed anti-HBe. One patient lost HBsAg as well as HBeAg and HBV-DNA. HBcAg in liver tissue became undetectable or greatly reduced in the seven patients in whom it was strongly positive. Aminotransferase and immunoglobulin levels reverted to normal in the seven responders and remained normal through the entire follow-up period. A second liver biopsy, performed after completion of therapy, showed improvement in six of eight cases, with disappearance of lobular activity. Two patients treated for 12 weeks developed a severe polyneuropathy lasting for 6 months. A 7-week course of Ara-AMP seems to induce long-lasting inhibition of viral replication, along with an improvement in liver function tests and liver histology, without significant side effects. On the other hand, a 12-week course was associated with the development of a severe and prolonged polyneuropathy.
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PMID:Prolonged inhibition of hepatitis B virus replication with vidarabine monophosphate in chronic active type B hepatitis. 242 52

Porphyrin metabolism was investigated in a 63-year-old male patient who developed a subacute onset polyneuropathy with predominance of motor signs in the upper limb. The screening for lead, cadmium, mercury, aluminum and thallium was negative. The study of porphyrin metabolism showed remarkable abnormalities, particularly a very high level of plasmatic 5-aminolaevulinic acid contrasting with a normal level of porphobilinogen and a nearly complete loss of activity of aminolaevulinic acid dehydratase with no regenerative response to dithiothreitol or zinc ions. The other causes of aminolaevulinic acid dehydratase deficiency (tyrosinaemia, alcoholism, smoking, cirrhosis, renal insufficiency, diabetes mellitus) were ruled out. The diagnosis of primary aminolaevulinic acid dehydratase deficiency was proposed and confirmed by the familial study, which revealed the existence of several heterozygous members in this family.
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PMID:Biochemical diagnosis of an hereditary aminolaevulinate dehydratase deficiency in a 63-year-old man. 260 May 50

Two patients developed cirrhosis of the liver following therapy with perhexiline maleate. Liver failure and polyneuropathy caused death in one patient who had received 300 mg daily for three years. Cirrhosis was an unexpected finding in the other patient whose perhexiline dose was 200 mg daily for five years. Perhexiline should be prescribed cautiously and discontinued if liver function tests become abnormal. Monitoring of blood levels may lead to a reduction of toxicity.
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PMID:Cirrhosis of the liver following therapy with perhexiline maleate. 657 24

We carried out a study on 63 patients suffering from alcoholism in order to determine the frequency of 27 HLA antigens. In comparison to healthy blood donors no significant deviation of HLA distributions in alcoholics was found. The data on alcoholic patients with physical consequences such as cerebral seizures, liver cirrhosis and polyneuropathy failed to identify an association with HLA.
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PMID:Genetic markers in alcoholism: no association with HLA. 657 88

A patient with chronic inflammatory demyelinating polyneuropathy (CIDP) associated with type B and type C hepatitis virus infection is reported. A 54-year-old female who had a blood transfusion at the age of 31 years was diagnosed as a carrier of hepatitis B virus at the age of 43. Liver dysfunction was first noted in 1987 and gradually grew worse year by year. Beginning in early June 1992, the patients general fatigue became worse, her serum GOT and GPT levels became elevated, and she complained of a tingling sensation in her arms and legs. Neurological examination revealed moderate sensory disturbance of the glove-and-stocking type in all of her extremities. Deep tendon reflexes were all diminished. Hepatitis C antibody was detected in the serum at this time. On June 12, 1993, progression of her sensory disturbance was found to be associated with generalized muscle weakness. Cerebrospinal fluid studies showed increased protein without pleocytosis. Motor nerve conduction studies revealed marked prolongation of terminal latencies, reduction of conduction velocities, and abnormal temporal dispersion of the motor potentials. No sensory potentials could be evoked at any of the sites stimulated. Sural nerve biopsy showed segmental demyelination and severe loss of large myelinated fibers as well as some onion bulb formation. A diagnosis of CIDP was made. Treatment with corticosteroids was started, but there was little improvement in neurological function. The liver dysfunction progressed further and ultimately the patient died of hepatic failure. An autopsy demonstrated liver cirrhosis, but no malignant tumors were evident.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Chronic inflammatory demyelinating polyneuropathy associated with chronic liver disease due to type B and type C hepatitis virus]. 766 15

We present a case of multiple symmetric lipomatosis Type I (Madelung's disease) with severe organic affection, hepatic cirrhosis, sever sensitive polyneuropathy and neuropathic ulceration at the left lower limb. A nephrotic syndrome developed in a larval form due to proliferative glomerulonephritis as the result of a metainfectious complications of the infection at the lower limb. We discuss the etiopathogenicity of the organic affection and we highlight the pathogenic links between the disease and its complications.
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PMID:[Nephrotic syndrome associated with symmetrical multiple lipomatosis (Madelung's disease)]. 779 19

A 39-year-old man developed sequential acute mononeuropathies involving both median, both ulnar, and the right radial and left peroneal nerves. Electrophysiology demonstrated an asymmetric sensorimotor axonal polyneuropathy; nerve biopsy confirmed a vasculitis. Laboratory evaluation revealed a mixed cryoglobulinemia and active hepatitis C infection. The patient stabilized with prednisone/cyclophosphamide/interferon-alpha. Hepatitis C should be considered in the differential diagnosis of mononeuropathy multiplex. Accurate diagnosis is important, as interferon-alpha may prevent transition to chronic hepatitis/cirrhosis.
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PMID:Nonsystemic vasculitic mononeuropathy multiplex, cryoglobulinemia, and hepatitis C. 894 Dec 74

We performed living donor liver transplantation (LDLT) for 40 patients at Kyushu University Hospital, Fukuoka Japan during the period from October 1996 to April 2000. The patients consisted of 32 adults and 8 children with a mean age of 35.8 years (range: 1 year and 10 months to 65 years old). The underlying liver diseases of the 40 patients included the fulminant hepatic failure (n = 14), biliary atresia (n = 7), liver cirrhosis (HCV) (n = 6), primary biliary cirrhosis (n = 5), primary sclerosing cholangitis (n = 2), familiar amyloidotic polyneuropathy (n = 2), Alagille syndrome (n = 1), glycogen storage disease (n = 1), huge hepatic hemangiomas (n = 1), and Wilson's disease (n = 1). All liver grafts were obtained from each patient's family members except for one domino transplant donor's case, comprised of 13 parents, 13 sons and daughters, 11 brothers and sisters, and 3 wives. The donors are presently all doing well. The patient survival rate is presently 92.5%.
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PMID:[Living donor liver transplantation in Kyushu University]. 1100 65


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