Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Of 4651 admissions between February 1995 and February 1996, 1043 had a presumed diagnosis of malaria. Six hundred and twenty-seven cases were confirmed by thick blood film examinations. The highest prevalence was in October (124/480 admissions) and the lowest in March (12/303). Sixty-five children died while 562 survived, 12 with defects. The first treatment in 422 children was chloroquine, in 143 quinine, in 59 halofantrin, and in three pyrimethamine with sulfadoxine (Fansidar). 23/422 patients started on chloroquine were switched to halofantrine, two to quinine. A higher mortality was associated with coma, convulsions, hepatosplenomegaly, pulmonary congestion, jaundice, haemoglobinuria, bladder paralysis, anuria. Anaemia and fever were more severe and hypoglycaemia more frequent in children who died than in children who survived (packed cell volume 18.5 +/- 7.1 per cent vs. 25.6 +/- 7.6 per cent, p < 0.001; temperature 39 +/- 1.1 degrees C vs. 38.7 +/- 0.9 degrees C, p < 0.05; random blood sugar < 40 mg/100 ml; 76 vs. 22 per cent, p < 0.01). There was no difference in the median age, pretreatment duration, and prevalence of diarrhoea and sickle cell disease. The male to female ratio was 1.5:1 in the surviving children vs. 1:1.03 in the dead.
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PMID:Malaria prevalence and outcome in the in-patients of the Paediatric Department of the State Specialists Hospital (SSH), Maiduguri, Nigeria. 960 1

DNA repair status is recognized as an important determinant of the clinical efficacy of cancer chemotherapy. To assess the role that a mammalian DNA glycosylase plays in modulating the toxicity and clastogenicity of the chemotherapeutic DNA cross-linking alkylating agents, we compared the sensitivity of wild-type murine cells to that of isogenic cells bearing homozygous null mutations in the 3-methyladenine DNA glycosylase gene (Aag). We show that Aag protects against the toxic and clastogenic effects of 1,3-bis(2-chloroethyl)-1-nitrosourea and mitomycin C (MMC), as measured by cell killing, sister chromatid exchange, and chromosome aberrations. This protection is accompanied by suppression of apoptosis and a slightly reduced p53 response. Our results identify 3-methyladenine DNA glycosylase-initiated base excision repair as a potentially important determinant of the clinical efficacy and, possibly, the carcinogenicity of these widely used chemotherapeutic agents. However, Aag does not contribute significantly to protection against the toxic and clastogenic effects of several chemotherapeutic nitrogen mustards (namely, mechlorethamine, melphalan, and chlorambucil), at least in the mouse embryonic stem cells used here. We also compare the Aag null phenotype with the Fanconi anemia phenotype, a human disorder characterized by cellular hypersensitivity to DNA cross-linking agents, including MMC. Although Aag null cells are sensitive to MMC-induced growth delay and cell cycle arrest, their sensitivity is modest compared to that of Fanconi anemia cells.
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PMID:Mammalian 3-methyladenine DNA glycosylase protects against the toxicity and clastogenicity of certain chemotherapeutic DNA cross-linking agents. 973 10

The chloroethylnitrosoureas (CENUs) are important antineoplastic drugs for which clinical utility has been restricted by the development of severe delayed myelosuppression in most patients. To investigate the potential of DNA repair proteins to reduce bone marrow sensitivity to the CENUs, we transferred the Escherichia coli ada gene, which encodes a Mr 39,000 O6-alkylguanine-DNA alkyltransferase (ATase), into murine bone marrow cells by the use of a high-titer ecotropic retrovirus. The ada-encoded ATase is resistant to O6-benzylguanine (O6-BG), a potent inhibitor of the mammalian ATases, thus affording the bone marrow an additional level of protection against CENUs. In methylcellulose cultures, ada-infected hematopoietic progenitor cells were twice as resistant as uninfected cells to the toxic effects of 1, 3-bis(2-chloroethyl)-1-nitrosourea (BCNU) following treatment with O6-BG. Although showing no obvious protective effects against leukopenia, overexpression of the bacterial ATase activity reduced the severity of anemia and thrombocytopenia in mice treated with O6-BG and BCNU. These effects, which were maximal at a BCNU dose of 12.5 mg/kg, were associated with improved survival when BCNU was given at this dose. At lower BCNU doses cytotoxicity was limited in both transduced and control mice, and at higher doses the protective effect was saturated due to cytotoxicity. These results suggest that ada gene therapy may be a feasible approach to amelioration of delayed myelosuppression following O6-BG plus CENU combination chemotherapy.
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PMID:Retroviral transfer of a bacterial alkyltransferase gene into murine bone marrow protects against chloroethylnitrosourea cytotoxicity. 981 32

The incidence density of infection and disease caused by Plasmodium falciparum in children aged six to 24 months living in the holoendemic Sahel of northern Ghana was measured during the wet and dry seasons of 1996 and 1997. At the beginning of each season, a cohort composed of 259 and 277 randomly selected children received supervised curative therapy with quinine and Fansidar and primaquine for those with normal glucose-6-phosphate dehydrogenase activity. The 20 weeks of post-therapy follow-up consisted of three home visits weekly and examination of Giemsa-stained blood films once every two weeks. Blood films were also taken from children brought to clinic with illness. The incidence density of parasitemia after radical cure was 4.7 infections/person-year during the dry season and 7.1 during the wet season (relative risk = 1.51, 95% confidence interval [CI] = 1.25-1.81; P = 0.00001). Although the mean parasitemia count at time of reinfection in the dry season (3,310/microl) roughly equaled that in the wet season (3,056/microl; P = 0.737), the risk ratio for parasitemia > 20,000/microl during the wet season was 1.71 (95% CI = 1.2-2.4; P = 0.0025). The risk ratio for parasitemia > 20,000/microl with fever during the wet season was 2.45 (95% CI = 1.5-4.1; P = 0.0002). The risk ratio for anemia (hemoglobin < 8 g/dl) at first post-radical cure parasitemia showed no difference between seasons (1.0; 95% CI = 0.73-1.4; P = 0.9915). We did not see seasonal differences in anemia known to exist in this region, probably because the longitudinal cohort design using first parasitemia as an end point prevented the subjects from developing the repeated or chronic infections required for anemia induction. These findings bear upon the design of malaria drug and vaccine trials in holoendemic areas.
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PMID:Seasonal malaria attack rates in infants and young children in northern Ghana. 1213 21

During a five year period, 233 cases of malaria (2.4%) were diagnosed among 9259 children with fever and hepatosplenomegaly seen in Asir Central Hospital, Abha, Saudi Arabia. The majority of these were below four years of age and came from Tihama, a hot, humid valley area in the Asir region. The infection was seasonal and occurred between December and May. Apart from fever, vomiting and hepatosplenomegaly, anemia was a common clinical finding; this was partly due to iron deficiency anemia, probably nutritional. Most of the cases responded to chloroquine therapy; however, three required intravenous quinine and two received Fansidar to effect eradication of the parasitemia. During the study, two patients died, one from cerebral malaria and the other from severe hemolytic anemia and hemoglobinuria. For prevention of malaria in this endemic area, an integrated program is advocated that includes the use of bednets impregnated with permethin, adequate treatment of proven cases and intensive health education on malaria control and nutrition.
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PMID:Malaria in children - experience from Asir region, Saudi Arabia. 1758 50


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