Lipoatrophy of the footpad in HIV-treated patients is associated with increased PAI-1.
OBJECTIVE
To describe lipoatrophy of the plantar pedis fat pads in human immunodeficiency virus (HIV) patients with or without long-term antiretroviral therapy (ART); to compare the characteristics of ART patients with and without plantar pedis lipoatrophy; and to examine the effects of HIV and metabolic/cardiovascular risk parameters and treatment history on plantar pedis lipoatrophy.


METHODS
Participants included 134 patients who started protease inhibitors in antiretroviral therapy (ART) in 1996 and 49 treatment-naive patients, recruited in 2004. Participants were examined and graded for lipoatrophy of five body compartments including the plantar fat pads. Baseline HIV- and ART-related factors were documented together with follow-up metabolic/ cardiovascular risk parameters.


RESULTS
Plantar pedis lipoatrophy occurred more often among ART patients (60%) than among treatment-naive patients (12%; p < .001). ART patients with plantar lipoatrophy were older, had higher plasminogen activator inhibitor 1 (PAI-1) values, a higher prevalence of lipoatrophy in other body compartments, and longer stavudine and didanosine treatment history as compared to patients without plantar lipoatrophy. Multiple logistic regression modeling revealed that among the metabolic/cardiovascular parameters, increased PAI-1 was strongly and positively associated with plantar lipoatrophy. Among the treatment history parameters, didanosine was the strongest independent predictor for plantar lipoatrophy. Increased PAI-1 was not associated to lipoatrophy in any other location.


CONCLUSIONS
Plantar lipoatrophy is common among patients on long-term ART and, though often overlooked, may cause significant discomfort. The association to PAI-1, a well-known marker of increased cardiovascular risk, is intriguing and places further focus on the need for an active approach to evaluating and lowering cardiovascular risk factors in long-term HIV treatment.
Eriksson
Lars E
LE
Venhälsan, Stockholm South General Hospital, Stockholm, Sweden. lars.eriksson@ki.se
Nilsson Schönnesson
Lena
L
Bratt
Göran A
GA
D000273:Adipose Tissue / Q000378:metabolism / Q000473:pathology*; D000328:Adult; D019380:Anti-HIV Agents / Q000009:adverse effects*; D001284:Atrophy; D002318:Cardiovascular Diseases / Q000453:epidemiology; D003430:Cross-Sectional Studies; D016049:Didanosine / Q000009:adverse effects; D005528:Foot / Q000473:pathology; D015658:HIV Infections / Q000188:drug therapy / Q000453:epidemiology / Q000378:metabolism; D006801:Humans; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood*; D015995:Prevalence; D012307:Risk Factors; D018119:Stavudine / Q000009:adverse effects*
D019380:Anti-HIV Agents; D017395:Plasminogen Activator Inhibitor 1; D018119:Stavudine; D016049:Didanosine