Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.7.7.7 (DNA polymerase)
17,007 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Among 262 inpatients with hematologic diseases who were referred for chemotherapy or immunosuppressive therapy between January, 1985, and December, 1989, nine (3.4%) patients, including two with Hodgkin's disease (HD), three with acute myeloblastic leukemia, one with chronic myelogenous leukemia, two with multiple myeloma and one with aplastic anemia, were found to be hepatitis B virus (HBV) carriers before their chemotherapy began. All six HBV carriers who received chemotherapy containing glucocorticoid showed mild-to-moderate elevations in serum transaminase levels after the chemotherapy. Five showed a rise in titer of the hepatitis B surface antigen, HBsAg. In contrast, three HBV carriers not receiving glucocorticoid showed no change in serum transaminase after chemotherapy. One HBV carrier with HD suffered from severe icteric hepatitis after the withdrawal of multiagent chemotherapy containing glucocorticoid. The HBV-DNA polymerase rose markedly and was accompanied by a marked rise in titer of HBsAg. The results warn us to keep in mind the possibility of glucocorticoid inducing an activation of HBV infection, which may result in severe hepatitis in some HBV carriers. Although further investigation is required, it is recommended that HBsAg-positive patients with hematologic malignancies should, if possible, be treated without glucocorticoid.
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PMID:Activation of hepatitis B virus infection by chemotherapy containing glucocorticoid in hepatitis B virus carriers with hematologic malignancies. 175 16

Both ganciclovir-sensitive and -resistant human cytomegaloviruses (HCMV) were isolated from a patient with aplastic anemia complicated with CMV retinitis and encephalitis. Ganciclovir-resistant clinical isolate, 93-1R, also showed cross-resistance against (s)-1-(3-hydroxy-2-phosphonylmethoxypropyl) cytosine (cidofovir). Molecular analysis of plaque-cloned strains revealed that a single nucleotide substitution at 2160 (C to T) resulted in amino acid substitution at codon 501 from leucine to phenylalanine in the DNA polymerase gene. This mutation at codon 501 was easily identified by means of AluI digestion of the selected PCR product. The same mutation existed in the DNA fragment amplified from the patient's brain, suggesting that cross-resistant mutant 93-1R caused encephalitis. Furthermore, ganciclovir-resistant 93-1R-3 replicated much faster and was released more efficiently into the culture medium than ganciclovir-sensitive 91-7S-1.
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PMID:Genetic analysis of a clinical isolate of human cytomegalovirus exhibiting resistance against both ganciclovir and cidofovir. 912 39

Parvovirus B19 infection is known to cause chronic anemia in immunocompromised hosts, including organ transplant recipients. Most reported cases of parvovirus B19-associated aplastic anemia in renal transplant recipients responded to intravenous immunoglobulin (IVIG) infusion. Tacrolimus is of special interest; it was proposed to be associated with pure red cell aplasia (PRCA) on its own because resolution of anemia on withdrawal of tacrolimus was previously observed. Interaction between parvovirus B19 infection and tacrolimus has not been reported. We report a case of parvovirus B19-associated PRCA in a renal transplant recipient treated with tacrolimus who failed to clear the virus despite repeated courses of IVIG. She showed complete recovery promptly after tacrolimus was switched to cyclosporine A. A well-documented concomitant decrease in serum parvovirus DNA polymerase chain reaction titer was also observed. This shows another mechanism by which tacrolimus can aggravate PRCA because of impaired clearance of parvovirus B19 infection in transplant recipients. For those patients receiving tacrolimus who have parvovirus B19 infection with refractory anemia and who fail to recover with IVIG, replacement of tacrolimus with cyclosporine A can be considered.
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PMID:Parvovirus B19 infection causing red cell aplasia in renal transplantation on tacrolimus. 1058 25