1/24. zidovudine-associated type B lactic acidosis and hepatic steatosis in an HIV-infected patient.A 34-year-old obese woman with human immunodeficiency virus (HIV) infection diagnosed a year earlier was seen because of nausea, vomiting, and intermittent diarrhea for 3 weeks. Her current medications included zidovudine. physical examination revealed tachypnea and tender hepatomegaly. Computed tomography of the abdomen showed hepatomegaly with fatty infiltration. liver enzymes were within normal range except for elevated lactate dehydrogenase (LDH). The serum bicarbonate value was low, with a lactate level three times normal. The tachypnea and dyspnea worsened as lactate concentrations rapidly increased to 15 times normal. Although her Po2 and cardiac index were initially adequate, the patient had acute respiratory failure. She died with multiorgan dysfunction, including hepatic failure, severe lactic acidemia, disseminated intravascular coagulation, and renal failure. autopsy revealed hepatomegaly and massive steatosis. physicians should consider lactic acidosis in patients taking zidovudine and having unexplained tachypnea, dyspnea, and low serum bicarbonate concentrations.- - - - - - - - - - ranking = 1keywords = tea (Clic here for more details about this article) |
2/24. Lactic acidosis associated with stavudine administration: a report of five cases.Type "B" lactic acidosis has been described in patients receiving the nucleoside analogs zidovudine, didanosine, and fialuridine. Lactic acidosis has also been described in 4 patients receiving combination therapy with stavudine and lamivudine. We describe the development of chronic type "B" lactic acidosis in 3 patients receiving stavudine as a single agent and in 2 patients receiving combination therapy with stavudine and either lamivudine or delavirdine, a nonnucleoside analog. All patients presented with abdominal pain, vomiting, and hepatic steatosis. Other signs of mitochondrial toxicity included pancreatitis and myopathy (2 cases). The mean duration of stavudine therapy was 9.4 months, and the mean observed peak lactate level /-SD was 10.3 /-5 mmol/L. After discontinuation of stavudine treatment, lactic acidosis improved in 4 patients after 4-60 weeks, and 1 patient died. Evaluations for other causes of lactic acidosis, including hypoxemia, malignancy, sepsis, and cardiogenic shock, were negative.- - - - - - - - - - ranking = 0.2keywords = tea (Clic here for more details about this article) |
3/24. Lactic acidosis and hepatic steatosis associated with use of stavudine: report of four cases.BACKGROUND: An association between use of zidovudine and didanosine and a rare but life-threatening syndrome of hepatic steatosis, lactic acidosis, and myopathy has been reported. OBJECTIVE: To describe the syndrome of hepatic steatosis, lactic acidosis, and myopathy in four patients taking stavudine. DESIGN: Case series. SETTING: A community hospital in washington, D.C., and National Institutes of health Clinical Center, Bethesda, maryland. patients: Two men and two women with hiv-1 infection who were taking stavudine presented with lactic acidosis and elevated levels of aminotransferases. All patients required intensive care. MEASUREMENTS: Levels of lactic acid, alanine aminotransferase, aspartate aminotransferase, amylase, and lipase; computed tomography of the abdomen; liver biopsy (two patients); and muscle biopsy (two patients). RESULTS: Histologic findings consistent with mitochondrial injury confirmed the diagnosis of hepatic or muscle abnormality. CONCLUSION: Because hepatic steatosis may be life-threatening, physicians should consider it as a possible cause of elevated hepatic aminotransferase levels among patients taking stavudine.- - - - - - - - - - ranking = 1.4keywords = tea (Clic here for more details about this article) |
4/24. Hyperlactatemia and hepatic abnormalities in 10 human immunodeficiency virus-infected patients receiving nucleoside analogue combination regimens.During a 6-and-a-half month period, we identified 10 human immunodeficiency virus (HIV)-infected men who were receiving antiretroviral regimens, including nucleoside analogues, and who developed unexplained reproducible hyperlactatemia in association with either abdominal symptoms or an unaccounted-for elevated alanine aminotransferase level, or both. After careful consideration of the possible etiologies, antiretrovirals were discontinued; lactate levels normalized in all patients. The estimated incidence of this phenomenon in our clinic was 20.9 cases per 1000 person-years of nucleoside analogue treatment. These observations extend the spectrum of the nucleoside analogue-induced lactic acidosis/hepatic steatosis syndrome by the identification of a subtle and perhaps earlier form, which has characteristic symptoms and laboratory abnormalities, and a favorable prognosis on discontinuation of antiretroviral therapy.- - - - - - - - - - ranking = 0.2keywords = tea (Clic here for more details about this article) |
5/24. Hepatic steatosis and lactic acidosis caused by stavudine in an HIV-infected patient.Lactic acidosis and hepatic steatosis caused by mitochondrial toxicity of nucleoside reverse transcriptase inhibitors (NRTI) is a rare cause of liver disease with a high mortality rate. This report describes a male, HIV-positive patient with a 4-week history of nausea, vomiting and abdominal pain. His medication consisted of prednisone 5 mg od (because of auto-immune thrombocytopenia), didanosine (for 2 years) and stavudine (for 3 months). Laboratory studies showed cholestasis and elevation of aminotransferases. Lactic level was not measured. liver biopsy revealed steatosis and cholestatic hepatitis. In the absence of other causes of liver disease a probable diagnosis of stavudine-induced hepatic toxicity was made. After discontinuation of NRTI, he recovered completely. Because lactic acidosis had not been confirmed, stavudine was restarted and within 1 week the lactate level increased significantly. Therefore stavudine was discontinued again. One year later the patient is doing well on a double protease inhibitor regimen. In conclusion, clinicians treating patients with NRTI should be aware of the risk of lactic acidosis and hepatic steatosis. When this is suspected, all NRTI must be stopped. The diagnosis can be made when elevated lactate levels and hepatic steatosis are present in the absence of other causes of liver disease.- - - - - - - - - - ranking = 1.8keywords = tea (Clic here for more details about this article) |
6/24. Lactic acidosis secondary to nucleoside analogue antiretroviral therapy.A 53-year-old woman with newly diagnosed HIV infection was treated with the nucleoside analogue antiretroviral agents lamivudine and stavudine and the protease inhibitor indinavir. An illness characterized by severe lethargy, persistent nausea and vomiting, lactic acidosis, hyperglycemia, and microvesicular hepatic steatosis developed. Her symptoms improved gradually after withdrawal of the antiretroviral agents. The illness can be explained by mitochondrial dysfunction caused by inhibition of mitochondrial dna (mtDNA) polymerase by the nucleoside analogues. The patient was successfully treated with nonnucleoside reverse transcriptase inhibitors, which lack affinity for mtDNA polymerase.- - - - - - - - - - ranking = 0.4keywords = tea (Clic here for more details about this article) |
7/24. Acute hepatic steatosis complicating massive insulin overdose and excessive glucose administration.OBJECTIVE: To describe a case of acute hepatic steatosis due to excessive administration of glucose in the setting of massive insulin overdose, a complication which is rapidly and completely reversible if glucose infusion is rapidly tapered. DESIGN: Case report, clinical. SETTING: intensive care unit, university hospital. PATIENT: A single patient admitted to the ICU. INTERVENTION: Intravenous glucose after insulin overdose. MEASUREMENTS AND MAIN RESULTS: On the 3rd day, increases in transaminase (ASAT 420 IU/l, ALAT 610 IU/l), bilirubin (147 mmol/l) and lactate (6.8 mmol/l), a decrease in arterial pH (7.32) and slightly increased liver size on ultrasound examination suggested acute hepatic steatosis. Clinical and laboratory abnormalities resolved rapidly after discontinuation of excessive glucose infusions (1,400 g/day for 3 days). CONCLUSIONS: Very large amounts of glucose after massive insulin overdose are potentially dangerous. Even though the fear of hypoglycemia-induced neurologic damage should be a constant preoccupation in this situation, glucose administration should be titrated on closely monitored blood glucose levels.- - - - - - - - - - ranking = 1.2keywords = tea (Clic here for more details about this article) |
8/24. Antiretroviral-induced hepatic steatosis and lactic acidosis: case report and review of the literature.As the prevalence of human immunodeficiency virus (HIV) infection continues to rise the clinician is encountered with a diagnostic challenge. Nonsurgical diseases such as acute colitis or enteritis can appear similar to such true surgical emergencies as abscess, perforation, or mesenteric ischemia. We report a case of fulminant hepatic failure associated with didanosine and masquerading as a surgical abdomen and compare the clinical, biologic, histologic, and ultrastructural findings with reports described previously. This entity should be kept in mind when evaluating the acute abdomen in the HIV-positive patient.- - - - - - - - - - ranking = 0.8keywords = tea (Clic here for more details about this article) |
9/24. riboflavin treatment of antiretroviral induced lactic acidosis and hepatic steatosis.BACKGROUND: Antiretroviral induced lactic acidosis and hepatic steatosis is a rare syndrome caused by inhibition of deoxyribonucleic acid (dna) polymerase gamma by the Nucleoside Reverse Transcriptase Inhibitor (NRTI) class of antiretrovirals. There have been recent reports of NRTI-induced lactic acidosis treated with high-dose riboflavin. INTERVENTION AND RESULTS: We report a case of NRTI lactic acidosis reversed with high-dose riboflavin. Treatment with 50 mg of riboflavin per day was initiated on hospital day 10 after the patient developed respiratory failure. Arterial lactate decreased from 11.9 mmol/dL to 2.1 mmol/dL. Despite lactic acidosis reversal the patient developed acute respiratory distress syndrome (ARDS) and expired. autopsy confirmed extensive hepatic steatosis with no infectious agents identified. CONCLUSION: Nucleoside Reverse Transcriptase Inhibitor lactic acidosis will likely become more prevalent with the trend toward aggressive antiretroviral treatment. This report provides additional support for the efficacy of riboflavin treatment to reverse this serious complication of antiretroviral therapy. Clinicians should have a high index of suspicion for lactic acidosis in a patient on NRTIs and the medications should be stopped at the earliest sign of toxicity.- - - - - - - - - - ranking = 1.2keywords = tea (Clic here for more details about this article) |
10/24. Symptomatic lactic acidosis in hospitalized antiretroviral-treated patients with human immunodeficiency virus infection: a report of 12 cases.We retrospectively investigated the clinical and histopathologic features of hospitalized patients infected with human immunodeficiency virus who had symptomatic lactic acidosis syndrome at a university teaching hospital during 1995-2000. Twelve patients were identified, 11 during 1998-2000; of these, 5 died with rapid progression to otherwise unexplained multiple-organ failure. All had extensive prior exposure to nucleoside analog reverse-transcriptase inhibitors (NRTIs). At presentation, the most commonly identified NRTI component of antiretroviral regimens was stavudine plus didanosine. Eleven patients presented with abdominal pain, nausea, and/or emesis. Eight patients had prior acute weight loss (mean [ /-SD], 12 /-5.3 kg). Median venous plasma lactate levels were > or =2-fold greater than the upper limit of normal (2.1 mmol/L). serum transaminase levels were near normal limits at presentation. Histopathologic studies confirmed hepatic macrovesicular and microvesicular steatosis in 6 patients. Concurrent chemical pancreatitis was identified in 6 patients. The increasing number of cases identified during the study period suggests that physicians better recognize symptomatic lactic acidosis and/or that cumulative NRTI exposure may increase the risk for this syndrome.- - - - - - - - - - ranking = 0.4keywords = tea (Clic here for more details about this article) |
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