Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.6.1.2 (alanine aminotransferase)
 26,722 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thus, it can be concluded that: (1) Hepatitis B, even before the introduction of donor screening for HBsAg, probably never accounted for more than one-quarter of all cases of transfusion-associated hepatitis. (2) As of 1988, the frequency of this viral infection in blood recipients, now that sensitive donor screening for HBsAg is routine, is less than 10%. The exception are multiply transfused populations, such as hemophiliacs, the majority of whom have evidence of current or past exposure to hepatitis B. However, new inactivation procedures are likely to reduce the attack rate in virgin populations of hemophiliacs. (3) Interdiction of paid blood has proved far more effective than donor screening for HBsAg in reducing the overall frequency of transfusion-associated hepatitis. (4) The current requirement that all donors be screened for anti-HBc and ALT as surrogate markers of non-A, non-B hepatitis infection, and for anti-HIV, is likely to reduce the hepatitis B attack rate even more, perhaps to near zero. (5) The long-term outcome of transfusion-associated hepatitis B has not been determined, a task that will remain difficult to accomplish because of the paucity of current cases. Information in this regard will need to be derived from the recall and reevaluation of pedigreed patients who participated in prospective studies that were conducted in the distant past.
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PMID:Transfusion-associated hepatitis B: past and present. 298 89

Markers of hepatitis B viral infection and the evolution of immune response to these were compared with serum alanine aminotransferase (ALT) levels in adult male and non-pregnant and pregnant female patients with acute hepatitis B from the time of onset of disease to the seventh week. In the adult male and non-pregnant female patients, the peak ALT levels of about 360 IU/litre, seen at the time of onset, gradually declined during the course of the disease. Significantly, even in the seventh week, the median ALT level was abnormal (80 IU/litre). In contrast, the disease was mild in pregnant patients and the ALT levels declined rapidly, returning to normal by the third week. Markers associated with HBV replication, i.e., serum HBV-DNA and HBeAg, declined early in the course of the disease in both groups. The anti-HBc-IgM and anti-HBe responses were well evolved early in the course of the disease in both groups. HBsAg was present in the serum in large amounts (1-1.5 X 10(4) AU/100 microliter) early in the course of the disease and remained so up to the seventh week. Even the pregnant patients who had recovered clinically by the fourth week continued to have HBsAg in their sera in large amounts in spite of normal ALT levels. LMI and LTT responses to HBsAg, which were practically absent in the first week, gradually increased to a peak during the fourth week and remained elevated up to the seventh week in adult male and non-pregnant female patients. In contrast, LMI response to HBsAg was absent in pregnant patients with acute hepatitis B even up to the fourth week Thus, continued liver cell necrosis after the fourth week, as indicated by raised ALT levels, may be associated with T cell responses to HBsAg.
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PMID:Mechanisms of liver cell damage in acute hepatitis B. 349 6

Eleven patients of Chinese origin experienced spontaneous reactivation of chronic active hepatitis B. Eight HBsAg-positive patients were followed for an average of 15 months prior to, while three others presented during reactivation. Fatigue, hepatomegaly and jaundice were frequent findings. Elevation of both serum ALT (average = 1,212 units per liter) and hepatitis B virus DNA levels were noted in all patients, and reactivation lasted an average of 4.4 months. During resolution, clinical symptoms abated, serum ALT levels reverted toward normal, and in nine patients, the hepatitis B virus DNA values became undetectable. All patients lacked evidence for acute hepatitis A, Epstein-Barr Virus, cytomegalovirus or hepatitis delta virus infection. Histologic findings of liver tissue from eight patients showed piecemeal necrosis and fibrosis. Within the parenchyma, varying degrees of hepatocytolysis with cuffing, perivenular necrosis and acidophilic bodies were noted. Ground-glass cells and regenerative changes also were observed. Cirrhosis was not present in any of the liver biopsies. These findings suggest that spontaneous reactivation of hepatitis B occurs in heterosexual patients with chronic active hepatitis B and contributes to chronic inflammation and to the progression of their liver disease.
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PMID:Spontaneous reactivation of hepatitis B in Chinese patients with HBsAg-positive chronic active hepatitis. 361 49

The plasma clearance of intravenously injected rabbit muscle LDH was studied. In normal mice the clearance followed a biphasic exponential curve comprising an initial fast and subsequent slow phase. Riley virus-infected mice showed only the slow phase of enzyme clearance. The change from fast to slow clearance rate in normal mice appeared to depend upon the level of plasma enzyme activity rather than on the amount of enzyme cleared. Treatment of mice with RES-blocking agents (cholesterol oleate and carbon) inhibited the fast clearance phase, whereas an RES-stimulating agent (stilbestrol) caused an accelerated rate of enzyme clearance. Riley virus infection was found to inhibit the clearance of phosphoglucose isomerase, but had no effect on the clearance of alanine transaminase. The activity of the former enzyme is raised in the plasma of infected mice, whereas the activity of the latter enzyme is unaltered.
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PMID:Studies on the mechanism of action of Riley virus. IV. The reticuloendothelial system and impaired plasma enzyme clearance in infected mice. 495 74

Plasma LDH levels were determined in normal and Riley virus-infected mice following treatment with various drugs known to alter the activity of the RES. The rise in plasma LDH level after Riley virus infection was considerably enhanced by previous treatment with thorotrast (to produce blockade of the RES), and decreased by previous treatment with stilboestrol (to stimulate the RES). A dose of 2000 r whole-body x-irradiation, lethal within 3 to 4 days, did not alter the phagocytic activity of the RES, and was without effect on plasma LDH activity in normal mice, or on the rise in plasma LDH level following infection with Riley virus. Blockade of the RES with cholesterol oleate, thorotrast, or zymosan, resulted in a 2- to 3-fold rise in plasma LDH level within a few hours. The level returned to normal by 1 to 3 days. Stimulation of the RES with stilboestrol resulted in a decrease in plasma LDH level by 1 to 2 days in both normal and infected mice, with a return to normal by about a week. Blockade of the RES in uninfected mice with thorotrast or cholesterol oleate, besides increasing the plasma LDH level caused a rise in plasma phosphoglucose isomerase level, but no significant alterations in plasma aldolase or alanine transaminase levels, studied up to 10 days. Riley virus causes a similar pattern of enzyme elevation. It is suggested that the increased levels of certain plasma enzymes in Riley virus-infected mice may be due to competitive inhibition by virus particles of plasma enzyme clearance by the RES.
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PMID:Studies on the mechanism of action of Riley virus. I. Action of substances affecting the reticuloendothelial system on plasma enzyme levels in mice. 585 75

Sixty-nine consecutive patients with acute type A hepatitis were followed-up to establish the natural history of the disease. Illicit drug abusers were not included in this study. 19% (13/69) of the patients at 6th month, and 6% (4/69) at 12th month showed aminotransferase (ALT) values at least two folds the upper levels. The histological examinations performed in 5 of these cases suggest that persistence of abnormal ALT levels may be related to a misdiagnosed chronic liver disease preexisting the acute type A hepatitis. Three of the 69 patients had a relapsing hepatitis with two peaks of serum ALT 6-8 weeks apart. The illness resolved uneventfully in all these patients. The exclusion of exposure to liver toxins such as alcohol or drugs, as well as other known hepatitis virus infection in these cases, suggests that the two distinct episodes of hepatitis could be the result of the sequential infection of hepatitis A and non-A, non-B viruses.
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PMID:Prolonged course and relapses of acute type A hepatitis. 608 49

There are reports in the literature that infection with hepatitis A virus in hepatitis B carriers can result in resolution of the carrier state. In an attempt to induce clearance of the carrier state of hepatitis B virus in two persistently infected chimpanzees, the chimpanzees were infused with documented non-A, non-B infectious material. Biochemical and histopathological evidence of hepatitis was accompanied by the unique abnormalities of endoplasmic reticulum associated with non-A, non-B hepatitis in the chimpanzees. Elevation of alanine aminotransferase was accompanied by fourfold reduction in one chimpanzee and sixfold reduction in the other in the plasma levels of HBV-associated DNA polymerase activity and simultaneously by twofold reduction in the concentration of hepatitis B surface antigen in both chimpanzees. A mediator may account for these changes in markers of hepatitis B virus infection, and this mechanism may also explain the occurrence of spontaneous regression in some persistently infected carriers. The significance of transient red cell anaemia in non-A, non-B hepatitis, which was observed in one of the chimpanzees, is yet to be established.
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PMID:Non-A, non-B hepatitis in persistent carriers of hepatitis B virus. 640 22

Abrupt increases of alanine transaminase were observed in 6 of 23 non-treated, male homosexuals with chronic hepatitis associated with hepatitis B virus. Before this occurrence, all subjects had hepatitis B e antigen (HBeAg) and elevated DNA polymerase activity. Within 3 months, HBeAg was nondetectable in 3 subjects and elevated DNA polymerase disappeared in 4. These serologic events were not always sustained, however. In 3 subjects, reactivation of hepatitis B virus infection occurred within the subsequent 6-month period. Serologic testing for cytomegalovirus, Epstein-Barr virus, delta agent, and hepatitis B surface antigen (HBsAg) subtype showed that episodes of clearance and reactivation were not explainable by secondary infection with these agents or infection with a different HBsAg subtype. Spontaneous clearance and reactivation of hepatitis B virus infection may commonly occur among male homosexuals with chronic type B hepatitis. These phenomena should be considered when evaluating the need for treatment or interpreting the results of investigations that use anti-viral therapy.
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PMID:Spontaneous clearance and reactivation of hepatitis B virus infection among male homosexuals with chronic type B hepatitis. 669 58

Non-A, non-B hepatitis is a newly recognized disease entity. Although initially described as a transfusion related viral infection, the disease can occur in sporadic, endemic, and epidemic settings. There are no confirmed, reproducible serologic tests for associated antigens or antibodies, but electron microscopy has revealed virus-like particles of different sizes. Nonspecific laboratory tests of hepatic dysfunction, especially alanine aminotransferase, are currently utilized to diagnose non-A, non-B hepatitis in patients and may be used to implicate blood donor carriers of this virus. The existence of an infectious non-A, non-B hepatitis agent and proof of a chronic carrier state in humans have been documented by transmission studies in chimpanzees. Cross challenge studies in chimpanzees, as well as some epidemiologic data, suggest that more than one agent causes non-A, non-B hepatitis.
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PMID:Non-A, non-B viral hepatitis. 680 Sep 28

To investigate the prevalence of hepatitis C virus in the family members of patients with hepatitis C, we examined antibody to hepatitis C virus with a second-generation enzyme-linked immunosorbent assay and viral RNA with a combined assay of reverse transcription and polymerase chain reaction in sera. Among 219 (75 spouses, 110 children, and 34 others), 26 (12%) were antibody positive. The positive rate of antibody to hepatitis C virus was significantly higher than that of the control group (2.0%) and of volunteer blood donors in our district (1.5%), and it increased with age. In particular, the positive rate of antibody to hepatitis C virus among spouses was high (24%). Among family members with elevated ALT, 59% were antibody positive, which was significantly higher than that of the control group (11%). Of the 26 who were antibody positive, 21 (81%) had viral RNA, whereas of the 70 who were antibody negative, only one (1.4%) had viral RNA. These data suggest that hepatitis C virus was transmitted by the infrafamilial route during long duration of contact with patients or sexual transmission. In family members, hepatitis C viral infection is the main cause of liver disorder, and many who were antibody-positive with a second-generation enzyme-linked immunosorbent assay had viremia in the sera.
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PMID:Prevalence of hepatitis C virus in family members of patients with hepatitis C. 750 9


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