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

We studied 145 children with acute lymphocytic leukemia (ALL) in remission who had been off chemotherapy for at least 2 years, to assess the prevalence of hepatitis delta virus (HDV) infection, and to determine whether HDV infection was associated with more severe chronic liver disease. The prevalence of chronic HBV infection was 41.5% (60/145). The prevalence of HDV infection among these patients with chronic HBV infection was 50% (30/60). Eighty-five patients were HBsAg-negative. There was evidence that HDV-infected children had more severe chronic liver disease than did HBsAg-positive, anti-HDV-negative patients: (1) their serum ALT levels were significantly more likely to be elevated at long-term follow-up (27/30 vs. 10/26, p = 0.0001); (2) their mean ALT levels were significantly higher 3 years after the cessation of chemotherapy (128 vs. 84 IU/L, p = 0.001); and (3) they were more likely to have either chronic acute hepatitis or cirrhosis when liver biopsy was done (18/23 vs. 6/18, p = 0.0038). Children who were HBsAg-negative had the lowest alanine aminotransferase (ALT) levels and were least likely to have chronic active hepatitis or cirrhosis (3/31). We conclude that infection with HDV in children with ALL is associated with serious chronic liver disease. In long-term survivors, HDV infection is a major cause of morbidity and an adverse prognostic factor in terms of leukemia-free survival.
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PMID:Delta virus and childhood leukemia. 202 65

The results of a prospective controlled randomized clinical study on using of autologous LAK cell reinfusion in the treatment of chronic hepatitis B (including CAH and CPH) were reported. The study was based on the criteria formulated by the National Conference of Viral Hepatitis in 1984 and patients were randomly assigned in two groups (39 cases in treated group and 25 in control group). Patients in the treated group received autologous LAK cell reinfusion treatment alone for 6 weeks and the control group 10% glucose solution intravenous drip also for 6 weeks. HBeAg seronegative rate anti-HBe seropositive rate and normalization rate of ALT after completion of the therapy were 53.8%, 28.2% and 33.3% respectively in the treated group and 20.0%, 8.0% and 4.0% respectively in the control group. The difference of parameters between the treated group and control group as described above was of statistical significance, but definite evaluation of the efficacy of this therapy can only be made after a more extended controlled randomized clinical study.
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PMID:[Prospective study on using of autologous LAK cell reinfusion in the treatment of chronic hepatitis B]. 203 92

Forty-one hepatitis B e antigen (HBeAg) and hepatitis B virus (HBV) DNA positive Chinese patients with chronic active hepatitis B were randomized to receive either prednisolone or placebo oral for 8 weeks. The prednisolone group received 60 mg daily for 2 weeks, 40 mg for 2 weeks, 20 mg for 2 weeks, 10 mg for 1 week and 5 mg for 1 week. In 18 patients receiving prednisolone, serum HBV DNA levels rose during the course of therapy, but dropped abruptly within 1 month of cessation of treatment. Conversely, their serum alanine aminotransferase (ALT) levels decreased during high doses of prednisolone therapy, and then became transiently elevated during the period of withdrawal of prednisolone. At 1 year from initial treatment, the serum HBV DNA and ALT levels were similar between the groups of patients treated with prednisolone or placebo. In the prednisolone treated group, 66.7% of patients became HBV DNA negative, 50% became HBeAg negative, and 33.3% seroconverted to antibody to HBeAg (anti-HBe). In the placebo treated group, 60.9% of patients became HBV DNA negative, 60.9% became HBeAg negative, and 56.5% seroconverted to anti-HBe. Hepatic decompensation was not noted in any of the prednisolone-treated patients. Thus, the effects of the withdrawal prednisolone therapy on serum ALT and HBV DNA levels was temporary, and no differences in serum viral markers or biochemical parameters of liver inflammation between these two groups were noted at the 1 year follow-up period.
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PMID:A randomised double-blind placebo-controlled trial of prednisolone therapy in HBeAg and HBV DNA positive Chinese patients with chronic active hepatitis B. 205 Oct 4

A retrospective study on the evaluation of antituberculous drugs for patients with hepatic dysfunction was undertaken to clarify treatment regimens. The values of GOT, GPT and T. Bil were used as indicators of liver function, and the "deterioration" in the liver function was defined as a level greater than 1.5 times the initial value. Of total 538 cases of active pulmonary tuberculosis, 103 cases (19.1%) had abnormalities in liver functions before chemotherapy, and 21 of 103 cases showed the deterioration in their liver functions during chemotherapy. There was little relationship between the initial status of liver functions and the incidence of their deteriorations after chemotherapy. Nine of 21 cases did not exceed the 3 times of normal ranges of liver functions. These nine cases could tolerate the same regimens of chemotherapy, and showed satisfactory clinical responses to chemotherapy with two exceptions: one died of tuberculosis and the other cerebrovascular disease. On the other hand, of 12 cases with elevated values of hepatic function greater than 3 times the normal limits, 6 cases discontinued chemotherapy. One case, however, died of hepatic failure related to chronic active hepatitis. Eight of 12 cases showed the rapid improvement of liver dysfunctions. These results suggest that antituberculous drugs are acceptable to patients with hepatic dysfunction as long as the elevations of GOT, GPT and T. Bil stay within 3 times of normal limits. Further chemotherapy could be continued under careful monitoring of liver functions even if the cases exhibit elevated levels of liver functions greater than 3 times the normal ranges.
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PMID:[Chemotherapeutic evaluation of pulmonary tuberculosis patients with a complication of hepatic dysfunction]. 205 6

A randomized controlled trial of recombinant interferon alfa-2b has been initiated in patients with chronic active hepatitis who were negative for serum hepatitis B e antigen but positive for serum hepatitis B virus DNA and hepatitis B core antigen expression in the liver. Twenty-five patients received interferon alfa-2b 3 million units thrice weekly for 14-16 weeks and 25 served as untreated controls. Seventeen patients in the treatment and 18 in the control group have already completed a 12-month period of observation. Interferon alfa-2b was well tolerated by all patients. At the end of therapy, complete responses, defined as disappearance of hepatitis B virus DNA from serum and return of alanine aminotransferase to normal, were observed in 10 (59%) of the 17 treated patients compared to none in the control group (p less than 0.01). Twelve months after the onset of interferon alfa-2b therapy, 11 (65%) of the 17 treated patients were complete responders compared to 2 (11%) of 18 in the control group (p less than 0.01). Fifty per cent (4/8) of complete responders to interferon alfa-2b therapy, followed for 16-24 months, experienced reactivations of hepatitis B virus replication with reappearance of serum hepatitis B virus DNA and a return of serum alanine aminotransferase activity. The response to interferon alfa-2b therapy appeared to be independent of pre-treatment serum alanine aminotransferase and hepatitis B virus DNA levels.
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PMID:Interferon alfa-2b treatment of HBeAg negative/serum HBV DNA positive chronic active hepatitis type B. 207 71

Liver biopsies from 52 patients with chronic hepatitis B were investigated for the presence and distribution of HBcAg and the results were compared with the status of hepatitis B virus deoxyribonucleic acid (HBV-DNA). The patients consisted of 37 men and 15 women, aged 16-55 years (mean = 34 years). Serum alanine aminotransferase (ALT) was elevated in 50 patients (range: 18-969 U/L; mean = 290 U/L). Serological testing showed HBsAg in all, HBeAg in 45 (87%), and HBV-DNA in 28 (54%). Liver biopsies demonstrated HBcAg in 35 (67%) patients. HBcAg was not only present in 31 of 45 (69%) patients who were seropositive for HBeAg, but also in four of seven (57%) with antibody to HBeAg (anti-HBe). In 28 of 35 (80%) patients with HBcAg in the liver, serum HBV-DNA was detected. However, no serum HBV-DNA was detected in 17 patients who had no detectable HBcAg in the liver. The distribution of HBcAg in the liver was rather cytoplasmic and nuclear than nuclear alone. Among 33 patients with cytoplasmic HBcAg in the liver, 15 (45%) had an evidence of acute exacerbation of hepatitis with marked ALT elevation (range: 168-894 U/L; mean = 385 U/L) and nine patients showed severe chronic active hepatitis and confluent necrosis, histologically. These results indicate that the presence of HBcAg in the liver correlates with the amount of circulating hepatitis B virus as quantified by serum level of HBV-DNA. The predominant cytoplasmic HBcAg in the liver may suggest the possibility of multiple episodes of acute exacerbation and more severe ongoing hepatitis during the clinical course.
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PMID:Significance of hepatitis B core antigen in the liver in patients with chronic hepatitis B and its relation to hepatitis B virus DNA. 210 4

Pharmacokinetics, tolerance and biological effects of human recombinant gamma-interferon were studied in 12 patients with chronic active hepatitis B. Serum concentrations of gamma-interferon were measured by radioimmunoassay in four patients after a subcutaneous injection of 10 million U (0.5 mg); the peak serum concentration of gamma-interferon (29 +/- 7 U/ml) was reached after 5 to 8 hr and gamma-interferon remained detectable for 24 to 36 hr. Twelve patients received recombinant gamma-interferon, 2.5 to 10 million U daily, for 4 mo. All suffered from a dose-dependent, flulike syndrome similar to that induced by alpha-interferon. Recombinant gamma-interferon induced a marked increase of serum ALT and a significant decrease of serum hepatitis B virus-DNA. Serum hepatitis B virus-DNA disappeared in one patient during administration of recombinant gamma-interferon. Serum hepatitis B virus-DNA disappeared in four additional patients, and HBeAg disappeared in two patients during the 12 mo after administration of recombinant gamma-interferon. These results indicate that subcutaneous injection is suitable for administration of recombinant gamma-interferon and that recombinant gamma-interferon has an antiviral effect in patients with chronic active hepatitis B.
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PMID:Recombinant human gamma-interferon in patients with chronic active hepatitis B: pharmacokinetics, tolerance and biological effects. 211 94

Thirty-three Swedish patients with chronic post-transfusion non-A, non-B hepatitis entered a randomized trial of interferon alfa-2b treatment (INTRON A, Schering-Plough Corporation) (3 million units, three times weekly, subcutaneously for 36 weeks). Twenty-two patients (67%) were reactive for antibodies against hepatitis C virus. Nineteen patients completed the course of therapy; 11 (58%) had a complete response with normalization of serum alanine aminotransferase levels, compared to none of the 12 controls (p less than 0.001). Four treated patients with chronic active hepatitis were non-responders. Non-responders had a significantly higher mean body weight than responders (p less than 0.05) and tended to have a longer duration of prior disease. During the 10-month follow-up period post treatment, 4/11 (36%) complete responders had a sustained response and three (75%) of these four were reactive for antibodies against hepatitis C virus, whereas 7/11 (64%) relapsed, of whom four (57%) were reactive for antibodies against hepatitis C virus. All patients who were treated again responded but relapsed once more after retreatment was stopped. We conclude that the majority of patients with chronic post-transfusion non-A, non-B hepatitis will respond to 9 months' interferon alfa-2b treatment, but that only one of three responders will have a sustained response 10 months post treatment. Reactivity for antibodies against hepatitis C virus is not predictive of the outcome of therapy.
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PMID:Therapy of chronic post-transfusion non-A, non-B hepatitis with interferon alfa-2b: Swedish experience. 212 89

A 41 year old woman developed chronic active hepatitis with prominent cholestasis. She was treated with prednisolone over 3 years with symptomatic benefit and improvement in serum biochemistry. However, various steroid-related side effects were encountered and steatorrhoea eventually occurred with very troublesome nocturnal diarrhoea. Therapy with ursodeoxycholic acid 750 mg daily was started. Serum alanine aminotransferase and gamma-glutamyl transferase normalized for the first time since her illness began. Steatorrhoea was abolished. There was good control of symptoms as prednisolone therapy was gradually reduced. However, when prednisolone was completely withdrawn there was a prompt biochemical deterioration. Addition of low-dose azathioprine has maintained normal blood tests over 24 months without return of the original symptoms. There are no side effects of ursodeoxycholic acid in subjects without gallstones and this agent may be effective treatment for cholestatic liver disease.
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PMID:Ursodeoxycholic acid therapy in chronic active hepatitis. 223 18

Using the paired method and the same observation standard, 35 pairs of patients (70 patients) suffering from chronic active hepatitis B were treated with FHST or glucose in 5 hospitals. After three months of treatment a significant decrease in ALT, TTT and a significant increase in PTA were observed in FHST group as compared with the control group (p less than 0.05-0.01). There was no significant change in HBVM in both groups. No side effect was observed during the period of treatment.
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PMID:[Fetal hepatocellular suspension transfusion in the treatment of chronic active hepatitis B]. 228 73


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