Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0000737 (abdominal pain)
31,184 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report three cases of hepatic steatosis associated with lactic acidosis occurring in HIV positive patients and due to a toxicity of antiviral nucleoside analogues. The clinico-pathological presentation was similar associating digestive signs (vomiting and abdominal pain), polypnea, lactic acidosis, a lethal clinical course, and an hepatomegaly with a diffuse macrovacuolar steatosis. The ultrastructural study performed in two cases showed mitochondrial alterations in hepatocytes. The toxicity of antiviral nucleoside analogues is due to a mitochondrial DNA polymerase inhibition. The incidence of this disease is actually low but probably underestimated. The diagnosis should be rapidly performed and the treatment immediatly interrupted.
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PMID:[A rare etiology of hepatic steatosis associated with lactic acidosis: the toxicity of antiviral nucleoside analogues]. 1137 88

A hematopoietic stem cell transplant recipient developed abdominal pain, pneumatosis intestinalis, hepatitis, pancreatitis, and inappropriate antidiuretic hormone secretion. Blood for varicella-zoster virus (VZV) DNA polymerase chain reaction was positive. She was treated with acyclovir and subsequently developed VZV antigen-positive zoster. Detection of VZV DNA in blood may be useful for early diagnosis in immunocompromised hosts who present with zoster without skin lesions.
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PMID:Triad of severe abdominal pain, inappropriate antidiuretic hormone secretion, and disseminated varicella-zoster virus infection preceding cutaneous manifestations after hematopoietic stem cell transplantation: utility of PCR for early recognition and therapy. 1827 22

Antiretroviral therapy has changed human immunodeficiency virus (HIV) infection from a near-certainly fatal illness to one that can be managed chronically. More patients are taking antiretroviral drugs (ARVs) for longer periods of time, which naturally results in more observed toxicity. Overdose with ARVs is not commonly reported. The most serious overdose outcomes have been reported in neonates who were inadvertently administered supratherapeutic doses of HIV prophylaxis medications. Typical ARV regimens include a "backbone" of two nucleoside reverse transcriptase inhibitors (NRTI) and a "base" of either a protease inhibitor (PI) or nonnucleoside reverse transcriptase inhibitor. New classes of drugs called entry inhibitors and integrase inhibitors have also emerged. Older NRTIs were associated with mitochondrial toxicity, but this is less common in the newer drugs, emtricitabine, lamivudine, and tenofovir. Mitochondrial toxicity results from NRTI inhibition of a mitochondrial DNA polymerase. Mitochondrial toxicity manifests as myopathy, neuropathy, hepatic failure, and lactic acidosis. Routine lactate assessment in asymptomatic patients is not indicated. Lactate concentration should be obtained in patients taking NRTIs who have fatigue, nausea, vomiting, or vague abdominal pain. Mitochondrial toxicity can be fatal and is treated by supportive care and discontinuing NRTIs. Metabolic cofactors like thiamine, carnitine, and riboflavin may be helpful in managing mitochondrial toxicity. Lipodystrophy describes changes in fat distribution and lipid metabolism that have been attributed to both PIs and NRTIs. Lipodystrophy consists of loss of fat around the face (lipoatrophy), increase in truncal fat, and hypertriglyceridemia. There is no specific treatment of lipodystrophy. Clinicians should be able to recognize effects of chronic toxicity of ARVs, especially mitochondrial toxicity.
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PMID:A review of the toxicity of HIV medications. 2396 94

Herpes simplex virus (HSV) hepatitis by definition constitutes disseminated herpes simplex infection; it is rare, with only approximately 130 cases reported in the literature. Although HSV hepatitis typically occurs in immunocompromised hosts, pregnancy-especially the third trimester, has been identified as a risk factor for its development. This is likely because of the fact that humoral and cell-mediated immunity decrease throughout pregnancy and nadir in the third trimester with decreased T-cell counts and altered B/T lymphocyte ratios. Here, we report on a patient with HSV 2 hepatitis in a previously healthy 27-year-old woman in her 23rd week of pregnancy. She initially presented with nausea, vomiting, and abdominal pain and was found to have acute hepatocellular liver injury and a systemic inflammatory response syndrome. Broad-spectrum antibiotics and acyclovir were promptly initiated. Liver biopsy, serum DNA polymerase chain reaction (PCR) as well as a labial ulcer culture and PCR were all positive for HSV 2. The patient recovered completely; however, her fetus did not survive. Review of the literature emphasizes that presentation with disseminated HSV infection typically occurs in the third trimester of pregnancy. This report emphasizes that abdominal pain combined with fever and hepatic dysfunction in pregnancy should prompt immediate consideration of the diagnosis of HSV hepatitis. Furthermore, given the high mortality rate and effective treatment, empiric treatment with acyclovir should be considered early in all potential cases.
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PMID:A Spotty Liver of Pregnancy. 2642 23