Volume 50, Issue 1 , Pages 149-150, January 2004
Development of Kaposi's sarcoma in an AIDS patient after treatment with topical tacrolimus
Article Outline
To the Editor:
Kaposi's sarcoma (KS) is an AIDS-defining illness which has become increasingly uncommon in HIV-positive individuals in developed countries because of highly active antiretroviral therapy (HAART).1 We describe a case of KS appearing in a HAART-treated AIDS patient, on areas of the skin where topical tacrolimus ointment was applied.
A 28-year-old African American homosexual man with AIDS who had been taking stavudine, lamivudine, and efavirenz for 2 months, was admitted for shortness of breath, hemoptysis, and chest pain. On review of systems, he noted asymptomatic violaceous papules in the axilla, groin, and glabellar region, which had developed three weeks before admission (Fig l). He previously had inverse psoriasis and seborrheic dermatitis in these areas, which resolved with one month of topical tacrolimus 0.1% ointment use twice a day. He had discontinued the ointment ten days before admission. On physical exam, he had a violaceous macule on the right buccal mucosa in addition to the lesions noted above. The hospital course included a workup for infectious etiologies, which showed negative cultures for Pneumocystis carinii, fungus, atypical mycobacteria, and routine bacteria. Pertinent laboratory findings included a CD4 cell count of 143/mm3 and a viral load of 2,261 copies/mL. Mixed interstitial alveolar infiltrates of the lower lobes were noted on chest computed tomographic scan, and bilateral patchy red mucosal lesions were found on bronchoscopy, consistent with Kaposi's sarcoma. Skin biopsy specimens from the right axilla showed a normal epidermis, with a dermal spindle cell proliferation and abundant slit-like vascular spaces, extravasated red blood cells, extracellular eosinophilic globules, and lymphoplasmacytic infiltrate (Fig 2). A Warthin-Starry stain was negative. Because of the history of topical tacrolimus use, systemic tacrolimus levels were obtained on the second day of admission and measured to be less than 3 μg/L, which was below the therapeutic range.
Fig 1.
A, Red-purple oval papules on the glabella. B, Poorly demarcated hyperpigmented patch in the left axilla, with a few red-purple oval papules within the patch.
Fig 2.
A and B, Proliferation of endothelial cells lining slit-like vascular spaces with rare mitotic figures, extravasated red blood cells, and small extracellular eosinophilic globules. (A and B, Hematoxylin-eosin stain; original magnifications: A, ×40; B, ×400.)
To our knowledge, this is the first report of KS developing after the use of topical tacrolimus in an AIDS patient. Our patient developed systemic KS at approximately the same time he developed his cutaneous lesions despite having significantly improved on HAART, with CD4 cell counts increasing from 18 to 143/mm3 and viral loads decreasing from 535,678 to 2261 copies/mL 2 months before the development of his KS lesions. With such low CD4 cell counts, our patient may have been susceptible to KS formation and coincidentally formed cutaneous lesion in the areas of topical tacrolimus application. It seems unlikely that his limited topical use of tacrolimus would have had enough absorption to cause systemic immunosuppression and precipitate his pulmonary KS. The literature reports significant absorption mainly in ichthyotic disorders.2 Local induction of immunosuppression with reactivation of HHV-8 at cutaneous sites, which may have occurred in our patient, raises concerns for the use of topical tacrolimus in AIDS patients with depressed CD4 cell counts and in other immunocompromised individuals who may be infected with HHV-8.
References
PII: S0190-9622(03)02145-5
doi:10.1016/S0190-9622(03)02145-5
© 2003 American Academy of Dermatology, Inc. Published by Elsevier Inc All rights reserved.
Volume 50, Issue 1 , Pages 149-150, January 2004
