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)

The bone marrow activity in the liver-spleen (RES) scintigraphy has been difficult to estimate correctly. If the activity of the bone marrow is to be decided as counts/time unit it is of importance that structures with a high activity as the liver and spleen are excluded from the registration. A dorsal registration of the pelvis during 180 s will give a rather correct information of bone marrow activity and besides an image of the pelvic bone marrow is obtained. Using 270 to 280 MBq 99Tcm-Albures all 45 normal cases had values below 150 KCNT (1 KCNT = 1 000 counts). All cases with cirrhosis (n = 15) or metastases in the liver (n = 14) had values over 150 KCNT. Values over 150 KCNT were also found in 29 of 34 patients with an increase in ASAT and ALAT (GOT, GPT) as the only pathologic finding and in 12 of 21 patients with a carcinoma but without metastases in the liver.
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PMID:Recording of bone marrow activity in liver-spleen (RES) scintigraphy. 652 33

Fifteen heavy drinkers with the histological features of chronic hepatitis were studied. Chronic hepatitis observed in heavy drinkers can be divided into two categories. One is caused by alcohol, and the other is not etiologically related to alcohol. Chronic hepatitis caused by alcohol showed a definite improvement of clinical features following abstinence, as well as significantly high serum GOT/GPT ratios and high glutamate dehydrogenase activities on admission. These clinical features are distinctly different from chronic hepatitis without etiological relation to alcohol and resemble the other types of alcoholic liver injury. The leukocyte migration inhibition test by ethanol was more frequently positive in chronic hepatitis induced by alcohol than in the other types of alcoholic liver injury except for alcoholic hepatitis. Histological characteristics of the liver in chronic hepatitis induced by alcohol included the coexistence of features of both chronic hepatitis and alcoholic fibrosis. Three of four cases of chronic hepatitis induced by alcohol developed cirrhosis during the follow-up period. These results suggest that chronic hepatitis induced by alcohol is a type of alcoholic liver disease with an immunopathological etiology. It is a step toward the development of liver cirrhosis.
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PMID:Chronic hepatitis induced by alcohol. 682 42

Variation of incidence of HBe antigen (HBeAg) and HBe antibody (anti-HBe) was examined by use of RIA in 72 patients with HBsAg positive liver diseases. 1) Percentage of positive HBeAg was highest (71.5%) in chronic active hepatitis with lobular distortion, followed by chronic active hapatitis without lobular distortion (70.0%) and acute hepatitis in asymptomatic HBsAg carriers (66.7%). In contrast, it was low in chronic inactive hepatitis (35.7%) and liver cirrhosis (38.5%). None of liver cancers showed HBeAg positive reaction. 2) Percentage of positive HBe antibody (anti-HBe) was highest in liver cancer (100%), followed by liver cirrhosis (61.5%) and chronic inactive hepatitis (50.0%). In acute hepatitis from asymptomatic HBsAg carriers no anti-HBe was found. In chronic active hepatitis the percentage of positive anti-HBe was low, 21.4 and 30.0% with and without lobular distortion, respectively. 3) In 45 patients with persistently positive HBsAg liver diseases, fluctuations of HBeAg and anti-HBe were followed over a period of one year in relation to serum GPT values, an indicator of clinical conditions. Serum GPT tended to fluctuate or to remain high in patients with persistently positive HBeAg or with sporadically positive HBeAg or anti-HBe, whereas it tended to become low or normal with persistently positive anti-HBe or with seroconversion from HBeAg to anti-HBe. However, there were some exceptions to this tendency. From these results we concluded that it is clinically of significant value to determine HBeAg and anti-HBe levels for the effective assessment of the activity and time course of HBsAg positive liver diseases.
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PMID:[Clinical significance of HBeAg and anti-HBe in HBsAg positive liver diseases]. 684 Jun 66

The plasma lipid and apoprotein concentrations were monitored in a group of 12 patients with chronic alcohol abuse entering an abstinence program for 3 weeks. 6 of them had a normal liver function as expressed by the levels of liver enzymes gamma GT, GOT, GPT, while 6 had elevated plasma liver enzyme concentrations. None had evidence of either cirrhosis or alcohol hepatitis. Patients with abnormal liver enzymes had elevated HDL-cholesterol, apo AI and apo AII concentrations in plasma, with normal total cholesterol and apo 8 concentrations. In the group of patients with normal liver enzyme concentrations, the apoproteins and lipids did not significantly differ from the control group. In the course of the abstinence treatment a parallel decrease of apoproteins, HDL-cholesterol and liver enzyme concentrations was observed. The values normalized after 10-15 days. These data indicate that the effect of alcohol on the plasma apoprotein and lipids occurs mostly in the HDL fraction, that it correlates with the state of hepatic function and that it can be reversed by an abstinence treatment.
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PMID:Plasma apoproteins levels in chronic alcohol abuse. 710 48

We determined the serum molybdenum concentration by neutron activation analysis in apparently healthy subjects and in patients with diseases of the liver and biliary system. The level was found to be markedly elevated in the initial phase of acute viral hepatitis (mean +/- S.D. 3.10 +/- 1.46 ng/ml vs. 0.55 +/- 0.21 in controls) and to return to normal during convalescence, in parallel with the liver function tests. The most significant correlations were found between the serum molybdenum concentration and the serum levels of GOT ( r = 0.710, p less than 0.001) and GPT (r = 0.683, p less than 0.001). Besides, the serum molybdenum level (mean +/- S.D.) was observed to be definitely increased in patients with HBsAg-positive chronic active hepatitis (0.97 +/- 0.49 ng/ml), HBsAg-positive liver cirrhosis (1.01 +/- 0.50), alcoholic liver disease (1.32 +/- 0.56), liver metastases (1.40 +/-0.39), gallstones (1.28 +/- 0.38), tumors of the gallbladder or extrahepatic bile ducts (1.64 +/- 0.44), and carcinoma of the head of the pancreas (1.61 +/- 0.91). Finally, the serum molybdenum level was found to be raised in two patients with primary biliary cirrhosis and in two out of four patients with drug-induced liver injury. The etiologic mechanism and the clinical importance of the observed abnormality remain to be established. Our study enlarges the existing information concerning the disorders of trace element metabolism in liver diseases.
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PMID:Serum molybdenum in diseases of the liver and biliary system. 720 61

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

Serum alpha-fetoprotein (AFP) has been determined in 86 cirrhotic patients who simultaneously underwent a complete clinical and analytical evaluation. 25.6% of patients had increased levels (19.1% of Child A, 21.9% of B and 33.3% of C) without any significative differences between Child groups. A correlation between AFP and some analytical findings has been found, being GPT included among the latter (r = 0.24, p = 0.023). No correlation has been found with different laboratory and clinical data. Our data suggest that hepatocyte lesion and/or regeneration play a role in the raise of AFP, although other mechanisms must be implied. Extremely high values, especially with a non active cirrhosis, hardly could be attribute to it, that is why AFP is still a good marker of malignant degeneration in these patients.
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PMID:[Serum alpha-fetoprotein in liver cirrhosis]. 768 38

In 1912, Wilson and Fleischer independently reported autopsied patients with progressive neurological disorder associated with cirrhosis of the liver, and they proposed that the syndrome could be a specific disease of toxic origin. In 1952, Scheinberg demonstrated a deficiency of serum ceruloplasmin in Wilson's disease, and it became possible to diagnose the illness while the patient was still asymptomatic. In 1956, Walshe introduced penicillamine as the most excellent drug for treatment of the disease. These epoch-making discoveries encouraged Japanese physicians to make early diagnosis and to try prevention of the disease. This lecture was to review the changing panorama in the diagnosis, treatment and prognosis of the disease in the period of forty years focusing on the experiences in Japan. Early detection of the patients based on hypoceruloplasminemia made it possible to investigate the onset ages of an elevation of serum GOT or GPT and the appearance of Kayser-Fleischer (KF) rings. So far, the youngest patients who exhibited high GPT level and KF rings were three years and five years old, respectively. It became popular that an unexpected elevation of serum transaminase in apparently healthy children of three years or more prompted to examine the possibility of Wilson's disease, and an increasing number of non-familial patients in late infancy have been detected. Now, the mass-screening for Wilson's disease is in progress. Follow-up studies on the prophylaxis for more than thirty years definitely proved that the appearance of clinical symptoms was prevented with the continued penicillamine therapy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Wilson's disease--evolutive panorama of diagnosis and treatment in the last forty years]. 772 59

Family history of hepatocellular carcinoma (HCC) has been identified as a risk factor of HCC. The pathogenesis is still uncertain. In order to evaluate the risk factors and to detect the small HCC. 721 asymptomatic family members (419 males and 302 females with a mean age of 40.21 years) of the index cases of HCC received a series of examinations including: serum GOT, GPT, alpha-fetoprotein (AFP). HBsAg, Anti-HCV, and abdominal ultrasonography (US). Of the 18 patients with liver tumor detected by US. 6 were proved to be HCC, 8 were hemangioma, and the nature of the rest was undetermined. The US found 22 with cirrhosis, 24 with chronic liver disease, 133 with fatty liver, and 14 with a liver cyst. The incidence of HCC in our study was 0.96% in males (4 of 419 cases), and 0.66% in females (2 of 302 cases) which was much higher than that in the general population of Taiwan (0.025% in males and 0.01% in females). The positive rate of HBsAg in the participants, including all the newly detected HCC patients, was 46.5% (335 cases) which was also higher than the prevalence in Taiwan (15-20%). Male, sibling and liver cirrhosis seemed to have higher risk. These results suggest that family members of patients with HCC have a high risk of developing HCC. The hepatitis B virus may be the most important link. Early diagnosis is possible by screening the family members by means of AFP and abdominal US.
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PMID:Risk factors of hepatocellular carcinoma with familial tendency. 776 61

A 48-year-old woman with type II diabetes developed fatigue, arthralgia and myalgia. A few weeks later she was found to have hepatomegaly. The erythrocyte sedimentation rate was raised (53/93 mm), as were liver enzyme activities (GOT 186 U/l; GPT 240 U/l; gamma-GT 199 U/l), the gamma-globulin levels (40.7%;IgG 4470 mg/dl, IgA 698 mg/dl, IgM 245 mg/dl), antinuclear antibodies and antibodies against double-strand DNA, smooth muscles and actin. Laparoscopy revealed small-nodular liver cirrhosis. The autoimmune hepatitis was treated with prednisolone (initially 60 mg daily, then reduced to 10 mg daily) and azathioprine (initially 100 mg daily, reduced to 50 mg daily). The symptoms markedly improved. But one year later, during follow-up examination, gastric polyps were found, excised and histologically found to be carcinoid. The gastrin level was raised to 765 pg/ml. Another year later the liver cirrhosis had advanced further and the type A gastritis was still present, but there was no sign of carcinoid recurrence.
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PMID:[Autoimmune hepatitis, autoimmune gastritis, hypergastrinemia and stomach carcinoid]. 788 17


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