Hindawi Publishing Corporation AIDS Research and Treatment Volume 2013, Article ID 249171, 7 pages http://dx.doi.org/10.1155/2013/249171 Clinical Study Performance of Clinical Criteria for Screening of Possible Antiretroviral Related Mitochondrial Toxicity in HIV-Infected Children in Accra Allison Langs-Barlow, 1 Lorna Renner, 2 Karol Katz, 3 Veronika Northrup, 3 and Elijah Paintsil 1,4 1 Department of Pediatrics, Yale School of Medicine, New Haven, CT 06520, USA 2 Department of Child Health, Korle Bu Teaching Hospital, University of Ghana Medical School, P.O. Box kb77, Accra, Ghana 3 Yale Center for Analytical Sciences, Yale School of Public Health, New Haven, CT 06520, USA 4 Department of Pharmacology, Yale School of Medicine, New Haven, CT 06520, USA Correspondence should be addressed to Elijah Paintsil; elijah.paintsil@yale.edu Received 12 December 2012; Revised 31 January 2013; Accepted 11 February 2013 Academic Editor: Guido Poli Copyright © 2013 Allison Langs-Barlow et al. is is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Mitochondrial damage is implicated in highly active antiretroviral therapy (HAART) toxicity. HIV infection also causes mitochondrial toxicity (MT). Differentiating between the two is critical for HIV management. Our objective was to test the utility of the Mitochondrial Disease Criteria (MDC) and the Enquˆ ete P´ erinatale Franc¸aise (EPF) to screen for possible HAART related MT in HIV-infected children in Ghana. e EPF and MDC are compilations of clinical symptoms, or criteria, of MT: a (+) score indicates possible MT. We applied these criteria retrospectively to 403 charts of HIV-infected children. Of those studied, 331/403 received HAART. Comparing HAART exposed and HAART na¨ıve children, the difference in EPF score, but not MDC, approached significance ( = 0.1). Young age at HIV diagnosis or at HAART initiation was associated with (+) EPF ( ≤ 0.01). Adherence to HAART trended toward an association with (+) EPF ( = 0.09). Exposure to nevirapine, abacavir, or didanosine increased risk of (+) EPF (OR = 3.55 (CI = 1.99–6.33), 4.76 (2.39–9.43), 4.93 (1.29–18.87)). Neither EPF nor MDC identified a significant difference between HAART exposed or na¨ıve children regarding possible MT. However, as indicators of HAART exposure are associated with (+) EPF, it may be a candidate for prospective study of possible HAART related MT in resource-poor settings. 1. Introduction Since the advent of highly active antiretroviral therapy (HAART), morbidity and mortality have been greatly reduced in children living with HIV [1]. Unfortunately, long- term use of HAART, specifically of nucleoside reverse tran- scriptase inhibitors (NRTIs), causes mitochondrial dysfunc- tion manifesting clinically as lipodystrophy, lactic acidosis, peripheral neuropathy, myopathy, and pancreatitis [2–13]. Moreover, HIV infection also causes mitochondrial damage [14–16]. Differentiating between the two could influence HAART regimens, especially in resource-poor settings where the early generation NRTIs are still considered first line therapy [17]. In addition, there are other sequellae of mito- chondrial dysfunction such as anemia, poor growth, and cognitive delay [18] that may have a greater impact on developing children than adults, and unfortunately reports of mitochondrial toxicity in children are increasing [6, 19]. ese side effects are a particular problem in those chil- dren who have acquired HIV perinatally, as they will likely remain on HAART throughout their lifetime. erefore, a need exists for a sensitive and low-cost screening tool to detect HAART associated mitochondrial toxicity in children living in resource-limited settings in order to help guide the allocation of further diagnostic resources where they are available or distribution of second-line HAART regimens.