Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019163 (hepatitis B)
 38,309 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We studied the histological and ultrastructural changes in the liver and alterations in the liver test results before, during, and after treatment with human interferon-beta from five patients with hepatitis B e antigen-positive chronic active hepatitis. A daily dose of 3 x 10(6) to 6 x 10(6) units of interferon-beta was given intravenously for four weeks. The total index of periportal and portal inflammation, intralobular degeneration, and focal necrosis before treatment was decreased significantly six months after treatment (P less than 0.05). Ultrastructurally, the structure of endoplasmic reticulum was irregularly shaped or fragmentally decreased during treatment, but these disappeared six or 12 months after treatment. Glycogen particles diminished greatly during treatment. The alanine aminotransferase concentrations in these patients increased during treatment. Serum albumin and cholinesterase levels decreased significantly at the fourth week of treatment (P less than 0.01) and at the third day (P less than 0.01) to the second week (P less than 0.05) of treatment, respectively. These results suggest that interferon-beta injures endoplasmic reticulum and glycogen areas and damages the cholinesterase activity in the early stage of treatment and protein synthesis in patients with hepatitis B e antigen-positive chronic active hepatitis.
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PMID:Changes in ultrastructure of hepatocytes and liver test results before, during, and after treatment with interferon-beta in patients with HB(e)Ag-positive chronic active hepatitis. 149 52

Eight liver biopsy specimens from five patients with PAS-negative intracisternal hyalin were investigated by immunofluorescence for: (1) immunoglobulins (Ig) G, A, M, D, E; (2) light chains (kappa and lambda); (3) complement components C1q, C4, C3c, C5, C9; (4) C1-inactivator; (5) C3-activator; (6) alpha 1-antitrypsin; (7) alpha 1-antichymotrypsin; (8) plasminogen; (9) fibrinogen; (10) fibrinogen breakdown products D and E; (11) fibronectin; (12) prealbumin; (13) albumin; (14) betalipoprotein; (15) apolipoprotein; (16) alpha 1- and alpha 2-glycoprotein; (17) cholinesterase; (18) ceruloplasmin; (19) haemopexin; (20) myoglobin; (21) placenta lactogen; (22) transferrin; (23) actin; (24) myosin; (25) cathepsin D; and (26) hepatitis B surface and core antigens (HBsAg and HBcAg). The globules reacted significantly with antisera against C3c (three patients), C4 (three patients), C3-activator (one patient) and fibrinogen (two patients). The cause of the protein accumulation is not clear. Serial studies indicate the possibility of a disturbance of protein secretion and an as yet unidentified immune complex disorder.
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PMID:Immunohistological investigations of PAS-negative globular intracisternal hyalin in human liver biopsy specimens. 285 88

The concentrations of triiodothyronine (T3), thyroxine (T4), T3/T4 ratio, free thyroxine index, and thyroxine-binding globulin were investigated in 114 viral hepatic disease patients and 36 controls. The T3/T4 ratio in healthy hepatitis B virus carriers was significantly greater than those in the controls and fulminant, acute, or chronic active hepatitis patients. The T3/T4 ratio in the fulminant hepatitis patients was significantly less than those in the controls and other liver disease patients. The correlation coefficient between the T3/T4 ratio and microsomal arylamidase activity in liver tissue from 30 patients was 0.78 (p less than 0.001). The correlation coefficient between the T3/T4 ratio and the content of cholinesterase was 0.64 (p less than 0.001). These results suggest that the T3/T4 ratio represents a marker of microsomal function and is useful for estimation of prognosis of fulminant hepatitis or differentiation of various viral hepatic diseases.
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PMID:Serum thyroid hormone, triiodothyronine, thyroxine, and triiodothyronine/thyroxine ratio in patients with fulminant, acute, and chronic hepatitis. 370 63

Alcohol, hepatitis B, and Non A Non B hepatitis were the main aetiologies of 124 patients with hepatic encephalopathy (HE) due to histologically proven liver cirrhosis. All had severe portal hypertension (PH) and usually increased inflammatory activity of the liver. In stage I (n = 27) 7.4% died, in stage II (n = 28) 14.3%, in stage III (n = 32) 50% and in stage IV (n = 37) 94.6%. Even in cirrhotics without PH, serum albumin, cholinesterase activity and prothrombin time (PT) were significantly decreased. But only in the case of PT did the magnitude of the decrease parallel the stage of HE. Hyperammonaemia and serum creatinine were increased in parallel with the stage of HE. Therefore, in liver cirrhosis a quotient derived from decreased PT and increased serum creatinine has a good prognostic value. Early diagnosis of HE is possible on the basis of writing tests and the determination of free or toxic ammonia.
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PMID:The role of protein metabolism in 204 liver cirrhotics with and without hepatic encephalopathy. I. Clinical and general biochemical findings. 372 88

Patients with severe virus hepatitis and a prothrombin concentration below 25% have a bad prognosis. This is due to direct consequences of hepatic failure and to the rather frequent complications of this disease. The clinical course of such patients is essentially dependent upon the degree of liver regeneration, which again is dependent upon the mass of hepatocytes which are able to regenerate and upon the so called hepatotrophic factors. Patients with severe hepatitis suffer during the first weeks rather frequently from nausea and loss of appetite and for that reason their nutrition is insufficient. In the study recorded here 9 cases were investigated (7 patients with hepatitis B, 2 patients with hepatitis non A non B). The question was asked, if partial parenteral nutrition in addition to a liver diet not containing meat would improve liver function. It could be shown that the prothrombin concentration, which could not be improved by vitamine K1 supplements, was increased during a 7 day parenteral nutrition period from 19,3 +/- 2,9% to 41,5 +/- 8,1% (p less than 0,05), serum albumine and cholinesterase activity improved as well. During the first day of treatment there was a significant fall of ammoniac from 115 +/- 10 mumol to 73 +/- 10 mumol/l (p less than 0,05), at the same time production of urea did not increase. All patients survived. The results show, that parenteral nutrition can improve liver function and decrease the catabolic status of metabolism.
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PMID:[Partial parenteral nutrition in severe virus hepatitis]. 643 23

The immunological and biological properties of a liver-specific antigen (LSA) from rat liver are described. LSA gave interspecies cross-reactions with liver extracts from several mammalian species, but no reaction of complete identify was observed. Moreover, no cross-reaction was found with chicken or frog livers, thus indicating the rather late appearance of LSA in the process of evolution. Experiments with fetal and neonatal liver extracts have indicated that LSA appears late in fetal development and is always present at birth. The biological properties of LSA were explored by several independent approaches. LSAg-Ab immunoprecipitates were stained positively with carbon naphthoxycholine iodide, an indirect evidence of choline esterase activity. LSA was also found to bind bile acids, thus suggesting organic anion properties. Finally, LSA was detected in the circulation of rats with acute carbon tetrachloride- and galactosamine-induced hepatocellular injury. This LSA is immunologically distinct from hepatitis B antigen, alpha-fetoprotein, carcino-embryonic antigen and, from each of several serum and liver proteins tested.
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PMID:LSA--a new liver-specific antigen in the rat. II: Immunological and biological properties. 773 Jul 35

We compared the etiology and prognosis of liver cirrhosis in patients age 60 and older with that of patients under age 60 during the 1980s (1981-89, n = 207). Non-A, non-B hepatitis (NANB) was significantly more prevalent in the elderly (p < 0.05), and the mean age of NANB and alcoholic cirrhosis (Alc) were significantly older than those with hepatitis B virus (HBV) (p < 0.05). Evaluation using hepatitis C virus (HCV) antibody also revealed significantly higher mean age of HCV (p < 0.05). Male patient was predominant in the younger patients than in the elderly patients. (M/F = 2.94 and 1.33, respectively) The estimated 5-year survival rate was 73.1% in the younger patients and 60.2% in the elderly patients (p < 0.05). Multivariate analysis revealed that male sex, a lower serum albumin level, and the presence of the encephalopathy were significantly associated with poor prognosis in the elderly, while a lower serum cholinesterase level and a higher indocyanin green retention rate at 15 minutes (ICGR15) were significantly associated with poor prognosis in younger patients. However, causes of deaths were not significantly different between the younger patients and the elderly patients, the proportion of deaths unrelated to liver disease predominated in the elderly patients. Thus, the etiology and the prognostic factors of liver cirrhosis in elderly patients differ from those in younger patients.
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PMID:Etiology and prognosis of liver cirrhosis in elderly patients. 856 28

The intercellular adhesion molecule 1 (ICAM-1, CD54) and the lymphocyte associated antigen 3 (LFA-3, CD58) have been found in soluble form (sCD54 and sCD58) in human sera. Data concerning their role in chronic liver disease and their usefulness in disease monitoring are contradictory. We addressed the question whether elevated sCD54/sCD58 correlated either with disease activity or with decreased elimination secondary to reduced liver function in chronic hepatitis B. We studied 31 patients with chronic hepatitis B undergoing interferon alpha therapy in a longitudinal fashion. Serum concentrations of sCD54 and sCD58 were measured at four weeks interval by specific Sandwich ELISA during a follow-up period of ten months. The maximal difference in concentration of each biochemical parameter, e.g., delta AST, delta gGt, delta bilirubin, was determined for each patient during the whole follow-up period. These differences were correlated with the variation in sCD54 (delta sCD54) and sCD58 (delta sCD58) at the respective time points. Using this method, we were able to eliminate interindividual differences in serum concentrations for sCD54 and sCD58 and to avoid bias due to preselection of patients. We found that delta sCD54 correlated with delta AST (p = 0.001) and delta ALT (p = 0.002), whereas there was no such correlation for delta sCD58. Interferon therapy did not affect sCD54 or sCD58 levels. Neither hepatitis B viremia nor the immune response to hepatitis B during the time of seroconversion to anti-HBe did significantly increase sCD54 or sCD58 levels. However, delta sCD54 was associated with delta gamma GT (p = 0.005) and delta sCD58 correlated with delta bilirubin (p = 0.037); a negative correlation was found for delta sCD54 with delta cholinesterase (p = 0.007). Our findings imply that sCD54 and sCD58 may be associated with a decrease in liver function that accompanies hepatic disease activity. sCD54 and sCD58 did not prove useful to monitor disease activity or response to interferon therapy in chronic hepatitis B. From our data we conclude, that decreased elimination of soluble adhesion molecules sCD54 and sCD58 in advanced liver disease may be responsible for increased serum concentrations detected.
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PMID:Circulating ICAM-1 (sCD54) and LFA-3 (sCD58) in chronic hepatitis B--a longitudinal study in patients treated with interferon-alpha. 923 90

We report two cases of pressure ulcers in liver cirrhosis patients. In case 1, a 64-year-old Japanese woman had suffered from liver cirrhosis caused by hepatitis C virus and developed a pressure ulcer on her sacral and coccygeal area due to long-term bedrest. After she received a living donor liver transplantation from her child, the ulcer healed synchronizing with improvement of serum cholinesterase and bilirubin. Likewise, her systemic condition also got much better after the transplantation. In case 2, a 53-year-old Japanese man with hepatitis B virus cirrhosis and hepatocellular carcinoma developed a pressure ulcer on his sacral area. Although he received a living donor liver transplantation from his brother, his general status and pressure ulcer were fluctuating in conformity with the variance of serum bilirubin. However, at 5 weeks after the transplantation, the ulcer gradually started improving, entrained to serum bilirubin decrease. From these findings, the condition of the pressure ulcer in liver cirrhosis patients synchronized with serum bilirubin as well as systemic condition, suggesting a possible influence of bilirubin for wound healing.
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PMID:Two cases of pressure ulcer healing after liver transplantation in cirrhosis patients. 1753 9

Biochemical markers are one of the mainstays in the diagnosis of ill health. Plasma cholinesterase is one such marker of the ill health caused by acute organophosphorus pesticide poisoning. Organophosphorus pesticides are powerful inhibitors of plasma cholinesterase; consequently, the reduced level of this biochemical marker has been used in the diagnosis of cases of acute poisoning. But how dependable is this biochemical marker in the diagnosis of suspected organophosphorus pesticide poisoning without adequate clinical signs and symptoms? In the case reported here, the low level of plasma cholinesterase which was suspected to be due to organophosphorus poisoning was found to be caused by pulmonary Koch's and hepatitis B with associated malnutrition.
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PMID:Plasma cholinesterase: double-edged parameter in the diagnosis of acute organophosphorus poisoning. 2113 70


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