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)

We report a case of recurrent hepatic encephalopathy accompanied by transient cortical blindness. The patient with cryptogenic liver cirrhosis had six attacks of hepatic encephalopathy of grades II to III during 1 yr after admission. In the beginning of each episode of encephalopathy, when the patient was conscious, a complete loss of vision occurred, but with a normal pupillary reflex to light. At the same time, the visual evoked potential recorded the second negative wave with a prolonged latency and a diminished amplitude. His sight completely returned, and the electroencephalogram tracing and the visual evoked potential response normalized after treatment for the encephalopathy. The loss of vision was thought to be cortical blindness accompanied by hepatic encephalopathy. Thus, in rare cases of hepatic encephalopathy, the visual cortex may be affected, and cortical blindness may occur before the loss of consciousness.
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PMID:Hepatic encephalopathy and reversible cortical blindness. 338 12

A newly-born male affected by extrahepatic biliary atresia with an alpha-1 antitrypsin pi ZZ deficiency is presented. Parents, Pi MZ, showing no signs of affection either in liver or lungs. His two brothers and one sister died at nine months, 7 years and 22 months respectively. Two brothers showed cirrhosis of the liver, the sister showed extrahepatic biliary atresia, and in all three patients there was an alpha-1 antitrypsin deficiency. Authors want to emphasize the presence of extra-hepatic biliary atresia in both brother and sister who had also an alpha-1 antitrypsin deficiency because this is an infrequent association which requires different treatment.
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PMID:[Alpha 1-antitrypsin deficiency and atresia of the bile ducts]. 349 22

Supplementation may benefit patients with liver cirrhosis. Zinc uptake from zinc-histidine complex 1:2 was assessed in eight patients with liver cirrhosis. Influence of the time of application was also studied. Compared with healthy controls, patients showed a 40% lower uptake of zinc after 20 mg zinc from zinc histidine. Bioavailability was identical when zinc was taken 6 h or 1 h before a meal but an order of magnitude greater than with or 1 h after a meal. No significant increase of serum zinc was found when zinc was given with a meal or 1 h after. Lower doses of zinc-histidine complexes than of zinc sulfate may be used to supplement patients with liver cirrhosis. Time of application is of great importance if this substitution is to be successful.
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PMID:Bioavailability of zinc from zinc-histidine complexes. II. Studies on patients with liver cirrhosis and the influence of the time of application. 359 29

Evidence from several sources suggest that blood-brain transport of the large neutral amino acids (NAA) is abnormal in animals with a portacaval anastomosis (PCA) and in patients with liver cirrhosis and portal-systemic shunting and encephalopathy, but the underlying mechanisms are unknown. After PCA, the concentration of glutamine (Gln) in brain is markedly increased as a by-product of cerebral ammonia detoxification, and the rate of efflux of Gln from brain is also increased. The following studies were undertaken to clarify the relationships among plasma and brain concentrations of NAA after PCA in rats and to examine the relationship of brain Gln concentration to plasma and brain NAA concentrations. After PCA plasma phenylalanine, tyrosine and histidine were elevated and leucine, isoleucine and valine were lowered. In brain, phenylalanine, tyrosine, histidine and methionine were markedly elevated after PCA and their concentrations in brain far exceeded the concentrations in plasma. Analyses of single, partial and multiple correlations of plasma NAA ratios expressed as plasma competitor function (PCF), brain NAA and brain Gln showed significant correlations between PCF nd brain NAA in shunted rats. A better correlation was found between brain NAA and brain Gln. Correlation coefficients obtained from multiple correlation analysis equalled or exceeded those obtained in the partial correlation or in the single correlation, suggesting that the effects of PCF and brain Gln on brain NAA were separate and additive. Gln was shown to compete with other NAA for blood brain transport by inhibiting brain 14C phenylalanine uptake.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Relationship of brain glutamine and brain neutral amino acid concentrations after portacaval anastomosis in rats. 393 Feb 56

An autopsy case of hypertrophic obstructive cardiomyopathy with extensive myocardial fibrosis is reported in a 43-year-old male. His mother died suddenly at 55. At the age of 39 the patient felt fatigue and feverish sensation followed by dyspnea and palpitation on exertion. He responded to beta-blocker and was discharged on the 51st hospital day. He died suddenly during his work three years and one month after discharge. The heart weighs 700 g. The thickness of the ventricular septum measures up to 3.2 cm, and that of the left ventricular posterior wall 2.2 cm. Subaortic endocardium is moderately thickened. Many patchy fibroses of various sizes and broad linear fibroses are mainly observed in the ventricular septum and in the left ventricular free wall. Microscopic examination shows severe fascicular disarray of hypertrophied myocardial fibers in the ventricular septum and in a part of the left ventricular anterior wall. Pericardial fibrosis, granulation tissue with many capillaries, and slight lymphocytic infiltrate are also noted. These findings suggest that the patient have both congenital hypertrophic cardiomyopathy and myocarditis. There are following possibilities as regards the relation between the two: first, haphazard association of cardiomyopathy with myocarditis; secondly, myocarditis triggered the onset or progression, or both, of cardiomyopathy. He also had liver cirrhosis, probably alcoholic, which appears to accelerate the progression of myocardial disarray and fibrosis.
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PMID:[Hypertrophic obstructive cardiomyopathy with extensive myocardial fibrosis: case report with autopsy]. 403

Reversibility of hepatic fibrosis was demonstrated histologically in a case with subacute hepatitis. His first liver biopsy showed the transformation to liver cirrhosis. Gamma-globulin, TTT and ZTT gradually recovered to normal range, and serial second to fourth liver biopsy revealed the gradual decrease in newly formed fibrous tissues of the liver.
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PMID:A case of subacute hepatitis with reversible liver fibrosis. 617 86

Hepatocellular carcinoma associated with hepatitis B virus (HBV) infection occurring in a boy who was 6 years 2 months old is reported. The patient is thought to have been infected with HBV by exchange blood transfusion (horizontal infection) in the neonatal period. Jaundice appeared eight months after birth. He was subsequently treated and follow-up with a diagnosis of hepatitis B surface (HBs) antigen (Ag)-positive chronic persistent hepatitis. His mother and other family members were HBsAg-negative. Postmortem examination revealed a multinodular growth of hepatocellular carcinoma of trabecular and solid pattern, mainly of the right lobe, complicated with mild fibrosis of the liver. Numerous HBsAg-positive hepatocytes demonstrated by orcein staining and the indirect immunoperoxidase method were present in the noncancerous area. This hepatocellular carcinoma is considered to have occurred within six years two months after HBV infection and not to have been associated with liver cirrhosis. The present case may be valuable for assessing the oncogenic properties of HBV and the incubation period of HBV infection before it develops into hepatocellular carcinoma.
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PMID:A 6-year-old boy having hepatocellular carcinoma associated with hepatitis B surface antigenemia. 625 92

A 9-year-old boy with non-resectable hepatocellular carcinoma was treated with irradiation and intra-hepatic arterial infusion of antitumor agents. His blood was positive for hepatitis B surface antigen (HBs Ag), but negative for hepatitis B e antigen (HBe Ag). Maternal transmission was suspected, because his mother's blood was positive for HBs Ag and his grand mother died from hepatic cirrhosis. The patient received a total dose of 4000 rad in 30 fractions. A chemotherapy cycle consisted of 5-FU (6 mg/M2/day, given continuously), EX (300 mg/M2, given on 1st, 3rd, 5th, 7th, and 9th week), VCR (1.5 mg/M2, on 2nd, 4th, 6th, 8th, and 10th week), and ADM (30 mg/M2, on 13th and 16th week). Since 6 months after the initiation of the chemotherapy, alpha-fetoprotein has become negative (less than or equal to 100n g/ml), and now, 2 years and 11 months after the diagnosis was settled, the patient remains a disease free state. His blood continues to be positive for HBs Ag.
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PMID:[HBs antigen-positive adult type liver cancer in a child with sustained remission induced by infusion of antineoplastic agents into the hepatic artery]. 630 70

The patient was a 59-year-old man who had been in hospital suffering from aplastic anemia with transfusion hemosiderosis. Sudden onset of weakness, shaking chills and headache was observed after his staying out overnight on July 25, 1981. His temperature was 39.3 degrees C and he complained of abdominal pain and abdominal distension. His blood pressure dropped to a dangerous level and tonic convulsions that had begun in the upper body gradually extended to the whole body and he died 23 hours after his return. V. vulnificus was isolated by the blood culture performed before death. During his stay away from the hospital, he had eaten raw cuttlefish, which was considered to be the source of infection. V. vulnificus is one of the halophilic marine vibrios and is isolated frequently in summertime from the sea foods and sea water near Japan. It has been disclosed that the presence of underlying diseases such as liver cirrhosis, hemochromatosis can predispose a person to fatal sepsis by V. vulnificus. In this case, besides leukocytopenia, the presence of hemosiderosis induced by many transfusions was considered to be a major cause leading to the fulminating course of the disease.
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PMID:[Fatal Vibrio vulnificus infection in a patient with aplastic anemia]. 667 24

A renal transplant recipient presented with bleeding esophageal varices. Needle biopsy, later confirmed by operative wedge biopsy, showed slight periportal fibrosis but no cirrhosis or hepatitis. No etiology for his liver disease could be determined and he could not be differentiated from other reported patients with idiopathic noncirrhotic portal hypertension (IPH). His liver biopsy did show massive hepatic iron deposition. He had received about 115 units of blood while on hemodialysis and had taken oral iron supplementation for 8 years. IPH has been associated with toxin exposure, especially arsenic and vinyl chloride. This case suggests that excessive iron deposition may also lead to IPH and the indiscriminate use of iron supplementation in hemodialysis or renal transplant patients should be avoided.
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PMID:Hemosiderosis without cirrhosis: an unusual case of portal hypertension. 700 99


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