Hyperlactataemia During Antiretroviral Therapy: Incidences, Clinical Data and Treatment

Gérard, Y; Viget, N.; Yazdanpanah, Yazdan; Ajana, F.; Tribonnière, Xavier de la; Bocket, Laurence; Deuffic-Burban, Sylvie; Santos, Anabèle Dos; Ballester, L. Rodríguez; Mouton, Y

doi:10.2515/therapie:2003022

Cited by 10 publications

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“…The incidence of MT in our patients was 12%. This value is higher than in HIV-infected patients receiving HAART, in whom reported values vary between 1.8% [21] and 8.3% [22] per year. Hepatitis C may predispose to lactic acidosis as lactate clearance is impaired in the setting of chronic liver disease [23].…”

Section: Discussionmentioning

confidence: 58%

Incidence and Risk Factors for Mitochondrial Toxicity in Treated HIV/HCV-Coinfected Patients

et al. 2005

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Background Coinfection with hepatitis C virus (HCV) and HIV is not uncommon and therapies for both infections are currently available. A major drawback, however, could be a potentially higher risk for mitochondrial toxicity (MT), defined as the elevation of pancreatic enzymes or lactate levels due to the nucleoside analogue reverse transcriptase inhibitors contained in both therapies. Methods Prospective analyses of clinical and laboratory data, including plasma lactate levels and pancreatic enzymes, of 113 consecutive HIV/HCV-coinfected patients were assigned to receive ribavirin (RBV) plus interferon (IFN)-α. Results Fourteen patients (12%) showed increased levels of amylase/lipase and/or hyperlactataemia. No patient developed clinical pancreatitis. Four patients with hyperlactataemia had clinical symptoms of lactic acidosis and recovered uneventfully by 2 weeks after treatment withdrawal. The variables significantly associated with MT in the univariate analysis were: therapy with didanosine (ddI), ddI plus stavudine (d4T), previous history of diabetes and the baseline lactate level. However, ddI use was the only independent risk factor for MT identified in the multivariate analysis. MT was not associated with gender, age, alcohol consumption, type of IFN, degree of steatosis and fibrosis in liver biopsy, presence of lipodystrophy, CD4+ cell count, HCV or HIV viral load, mitochondrial DNA and COXII-expression in liver tissue, or antiretroviral therapy containing d4T or protease inhibitors. Conclusions 12% of HIV/HCV-coinfected patients receiving IFN plus RBV concomitantly with highly active antiretroviral therapy developed laboratory markers of MT. Although most of cases were asymptomatic, our study suggests that concomitant use of RBV plus ddI should be avoided, and that routine monitoring of lactate and pancreatic enzymes may be recommended.

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Section: Discussionmentioning

confidence: 58%

Incidence and Risk Factors for Mitochondrial Toxicity in Treated HIV/HCV-Coinfected Patients

et al. 2005

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“…Les patients restaient cependant asymptomatiques. D'autres études rapportent des ré-sultats similaires avec une incidence plus faible [7,28]. Cependant, il faut considérer que l'augmentation de la lactatémie puisse être également la conséquence d'une diminution de la clairance hépatique des lactates du fait de l'atteinte hépatique liée au VHC [29].…”

Section: Mécanismes De Toxicité Proposés Pour L'hépatotoxicitéunclassified

Toxicité des antirétroviraux chez les patients co-infectés par les virus VIH et VHC

Roser

Soyer

Duclos‐Vallée

et al. 2006

Immuno-analyse & Biologie Spécialisée

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Exenatide improves weight loss insulin sensitivity and β-cell function following administration to a type 2 diabetic HIV patient on antiretroviral therapy

Oriot

Hermans

Selvais

et al. 2011

Annales d'Endocrinologie

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Hyperlactataemia During Antiretroviral Therapy: Incidences, Clinical Data and Treatment

Cited by 10 publications

References 10 publications

Incidence and Risk Factors for Mitochondrial Toxicity in Treated HIV/HCV-Coinfected Patients

Incidence and Risk Factors for Mitochondrial Toxicity in Treated HIV/HCV-Coinfected Patients

Toxicité des antirétroviraux chez les patients co-infectés par les virus VIH et VHC

Exenatide improves weight loss insulin sensitivity and β-cell function following administration to a type 2 diabetic HIV patient on antiretroviral therapy

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