A 55-year-old man presented to a dermatology clinic with the chief complaint of sunken cheeks (see accompanying figure), which he first noticed two months earlier. Past medical history included testing positive for human immunodeficiency virus (HIV) and taking highly active antiretroviral therapy (HAART), consisting of one protease inhibitor (indinavir) and two nucleoside transcriptase inhibitors (zidovudine and didanosine) for the previous 10 months. On physical examination, the patient had loss of subcutaneous tissue in the cheeks and upper legs and increased subcutaneous tissue in the region of the abdomen and the back of the neck. The patient felt fine otherwise, but was concerned about his appearance.
Discussion
The answer is B: lipodystrophy, most likely caused by the protease inhibitor. With the advent of protease inhibitors, patients diagnosed with acquired immunodeficiency syndrome (AIDS) have had markedly improved health, despite living with this chronic disease. The combination therapy of one protease inhibitor and two nucleoside transcriptase inhibitors has markedly increased the number of CD4 cells and decreased the viral load of patients.(1) This has led to better health and less occurrence of opportunistic diseases in patients with AIDS.
Shortly after beginning HAART, patients usually feel healthier, but sometimes notice the characteristic changes in body fat redistribution several months after starting the medications. The relatively recent observation of lipodystrophy includes: hypertrophy in the neck fat pad (buffalo hump) similar to a Cushingoid patient,(2) increased fat in the abdominal region (protease paunch),(3) gynecomastia,(4) and loss of fat in the midface(5) and extremities.(6) Also noted in HAART patients are increased triglyceride and cholesterol levels.(7) The etiology of the lipodystrophy may be caused by similar binding sites on the HIV protease and other enzymes involved in lipid metabolism.(8)
It has been observed that different protease inhibitors may have varying rates of lipodystrophy. It has been estimated that approximately 64 percent of patients taking protease inhibitors experience lipodystrophy.(9) Treatment for lipodystrophy secondary to a protease inhibitor may include liposuction in areas with excess fat,(9) with injection of the harvested fat into areas of fat loss.
Niacin (vitamin B3) deficiency, also known as pellagra, has the characteristic three Ds, (dermatitis, diarrhea, and dementia) but does not cause adipose tissue abnormalities.
Bulimia and anorexia nervosa are eating disorders usually associated with teenage girls, and would not lead to increased abdominal and neck fat.
Vitamin B12 deficiency is associated with glossitis, paresthesias, and macrocytic anemia.
REFERENCES
(1.) Deeks SG, Smith M, Holodniy M, Kahn JO. HIV-1 protease inhibitors. A review for clinicians. JAMA 1997;227:145-53.
(2.) Lo JC, Mulligan K, Tai VW, Algren H, Schambelan M. 'Buffalo hump' in men with HIV-1 infection. Lancet 1998;351:867-70.
(3.) Mishriki YY. A baffling case of bulging belly. Protease paunch. Postgrad Med 1998;104:45-6.
(4.) Schurmann D, Bergmann F, Ehrenstein T, Padberg J. Gynaecomastia in a male patient during protease inhibitor treatment for acute HIV disease. AIDS 1998;12:2232-3.
(5.) Viraben R, Aquilina C. Indinavir-associated lipodystrophy. AIDS 1998;12:F37-9.
(6.) Carr A, Samaras K, Burton S, Law M, Freund J, Chisholm DT, et al. A syndrome of peripheral lipodystrophy, hyperlipidemia and insulin resistance in patients receiving HIV protease inhibitors. AIDS 1998;12:F51-8.
(7.) Pujol RM, Domingo P, Xavier-Matias-Guiu, Francia E, Sanbeat MA, Alomar A, et al. HIV-1 protease inhibitor-associated partial lipodystrophy: clinicopathologic review of 14 cases. J Am Acad Dermatol 2000;42:193-8.
(8.) Panse I, Vasseur E, Raffin-Sanson ML, Staroz F, Rouveix E, Saiag P. Lipodystrophy associated with protease inhibitors. Br J Dermatol 2000;142:496-500.
(9.) Wolfort FG, Cetrulo CL Jr., Nevarre DR. Suction-assisted lipectomy for lipodystrophy syndromes attributed to HIV-protease inhibitor use. Plast Reconstr Surg 1999;104:1814-22. n
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