2004
DOI: 10.1089/108729104322994810
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Severe Lactic Acidosis in Association with Reverse Transcriptase Inhibitors with Potential Response to L-Carnitine in a Pediatric HIV-Positive Patient

Abstract: We report a case of life-threatening lactic acidosis in a 10-year-old male with HIV stage B2 infection, presumed to be vertically acquired. This occurred after several months of therapy with d4t, ddl, and nevirapine. His most recent CD4 count was 347 cells per microliter and viral load 16,000 copies per milliliter 3 weeks prior to admission. The peak lactic acid level was 12.4 mmol/L. Although multiple therapeutic interventions took place, the patient showed rapid improvement and resolution temporally associat… Show more

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Cited by 10 publications
(11 citation statements)
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“…Only 4.3% of all children on a stavudine-containing regimen changed drugs because of toxicity, lower than in other cohorts [12,14,18,19,24]. Consistent with previous literature, the predominant toxicity was lipodystrophy and toxicity clearly rose with duration of drug exposure.…”
Section: Discussionsupporting
confidence: 78%
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“…Only 4.3% of all children on a stavudine-containing regimen changed drugs because of toxicity, lower than in other cohorts [12,14,18,19,24]. Consistent with previous literature, the predominant toxicity was lipodystrophy and toxicity clearly rose with duration of drug exposure.…”
Section: Discussionsupporting
confidence: 78%
“…Although some of these toxicities are life-threatening, others can cause disability and disfigurement that impact on patient adherence and quality of life, and consequently on virological and clinical outcomes of ART. Although children may develop similar stavudine toxicities to adults, serious conditions appear less frequent [12][13][14]. Clinically significant lactic acidosis is uncommon in children receiving stavudine [12,[15][16][17], although sub-clinical hyperlactataemia may occur in one-third of these children [15].…”
Section: Introductionmentioning
confidence: 99%
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“…In our study, patient 5, who received AZT + 3TC + amprenavir, had a non-renal metabolic acidosis picture with an increased plasma anion gap (Table 3), possibly secondary to viral reverse transcriptase inhibitors [5]. We were unable to measure lactate levels in this patient to confirm a potential mitochondrial dysfunction caused by those drugs [7], which is the postulated mechanism leading to this subtype of metabolic acidosis in HIV-infected subjects [24,34]. We also observed two patients with mild metabolic acidosis who were in the B3 and C3 stages of HIV infection and received AZT + ddI + nelfinavir (Table 3).…”
Section: Discussionmentioning
confidence: 72%