Jpn. J. Infect. Dis., 166-167, 2000

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Laboratory and Epidemiology Communications

Highly Active Antiretroviral Therapy for the Treatment of Kaposi's Sarcoma Associated with Primary Human Immunodeficiency Virus Type-1 Infection

Ikumi Genka, Akira Yasuoka, Kiyoshi Saitoh1 and Shinichi Oka*

AIDS Clinical Center and 1Department of Pathology, International Medical Center of Japan, Toyama 1-21-1, Shinjuku-ku,Tokyo 162-8655

Communicated by Hiroshi Yoshikura

(Accepted August 1, 2000)

Kaposi's sarcoma (KS) is a well-known symptom of acquired immunodeficiency syndrome. KS can be present in patients with wide-ranging CD4+ T cell counts (CD4 count) but becomes increasingly common as immune function declines. Highly active antiretroviral therapy (HAART) consisting of a human immunodeficiency virus type-1 (HIV-1) protease inhibitor in combination with two nucleoside analogues has been shown to decrease the plasma viral load, leading to an increase in the CD4 count. This reconstitution of the immune function has been shown to be an effective treatment for KS and obviates the need for a specific KS therapy (1). In this study, we describe a patient who developed KS shortly after primary HIV-1 infection and who achieved complete remission of the KS lesions by means of HAART.

A 52-year-old homosexual male was admitted to a hospital on May 22, 1998, with a history of headache, fever, muscle weakness of the lower extremities and difficulty in urination. He had sensory disturbances of the face, trunk, both lower extremities, and weakness of both iliopsoas muscles. The cerebrospinal fluid (CSF) showed lymphocyte dominant pleocytosis. He was suspected of having an inflammatory radiculoneuropathy. Starting on June 5, he was treated for 2 weeks with prednisolone at a dose of 60 mg/day, and then doses were decreased by 10 mg every week to reach a dose of 20 mg/day 4 weeks later. The dose was further decreased to 15 mg/day on July 21, and this level was maintained till the medication was stopped. On July 3, his blood and CSF were tested for syphilis using the fluorescent treponemal antibody absorption test; both samples were positive. A diagnosis of neurosyphilis was made; treatment with aqueous crystalline penicillin G was commenced on July 6 and continued for 10 days.

On July 27, he was found to be infected with HIV. HIV-1 RNA in the plasma was 7.5×105 copies/ml. His CD4 count was 620/μl. In Western blot, p24 was detected. He was referred to our hospital on August 11. He had oral candidiasis. Neurological findings were normal. His only medication was prednisolone at a dose of 15 mg/day. On August 11, his CD4 count decreased to 158/μl, and in Western blot, gp160 and gp41 bands, in addition to the p24 band, became positive. HIV-1 RNA in the plasma remained at 7.5×105 copies/ml, however. One month later, hematoma-like tumors appeared in the oral cavity, on the back, on the right side of the chest, and on the lower extremities. These tumors were diagnosed as KS by skin biopsy (Figure). On a visit the following month, the CD4 count was 177/μl. HIV-1 RNA in the plasma was 8.3×105 copies/ml. The p24, gp41, and gp120 bands were positive in Western blot. These results suggested that this patient was experiencing a primary HIV-1 infection.

HAART with zidovudine, lamivudine and indinavir was commenced on October 6, and prednisolone was discontinued on October 20. After 4 months of HAART, the CD4 count increased to 558/μl and HIV-1 RNA in the plasma decreased to 560 copies/ml. During this time, the oral KS lesions disappeared, and the anterior chest and leg lesions turned into scars. No specific treatment for KS had been given.

The neurological signs and symptoms seen in this patient included headache, muscle weakness, and lymphocyte dominant pleocytosis of the CSF. Though the symptoms were first attributed to inflammatory neuropathy and late neurosyphilis, they were probably due to a primary HIV-1 infection (2,3). KS is the most common neoplasm affecting HIV-1 infected individuals, particularly in the gay population. The presence of human herpesvirus 8 (HHV-8) (4) and immune-suppression appeared to be important factors for the development of KS (5). It is interesting to note that, in our patient, the incubation time from the infection to the development of KS lesions was very short, only 4 months. A possible reason for this rapid development of KS lesions was the use of steroids. Progressive KS is usually treated with interferon-α and other cytotoxic drugs (6) However, these therapies often cause myelo- and immune-suppressive side effects. In our case, HAART cured the KS lesions without any serious side effects. Recovery of immune responses produced by antiviral agents probably enabled tumor regression to occur (1,7). HAART should perhaps be the first choice of therapy for early stage KS.

This work was supported by the Ministry of Health and Welfare of Japan. The authors thank Helen Fraser for carefully reading and editing the manuscript.

REFERENCES

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  2. Tindall, B. and Cooper, D.A.(1991): Primary HIV infection: host responses and intervention strategies. AIDS, 5, 1-13.
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  4. Chang, Y., Cesarman, E., Pessin, M.S., Lee, F., Culpepper, J., Knowles, D.M. and Moore, P.S. (1994): Identification of herpesvirus like DNA sequences in AIDS-associated Kaposi's sarcoma. Science, 226, 1865-1869.
  5. Antiman, K. and Chang, Y. (2000): Kaposi's sarcoma. N. Engl. J. Med., 342, 1027-1038.
  6. Yarchoan, R. (1999): Therapy for Kaposi's sarcoma: recent advances and experimental approaches. J. Acquir. Immune Defic. Syndr., 21, Suppl. 1, 66-73.
  7. Parra, R., Leal, M., Delgrado, J., Macias, J., Rubio, A., Gomez, F., Soriano, V., Sanchez-Quijiano, A., Pineda, J.A. and Lissen, E. (1998): Regression of AIDS-related Kaposi's sarcoma following antiretroviral therapy. Clin. Infect. Dis., 26, 218-219.

*Corresponding author: Tel/Fax: +81-3-5273-5193, E-mail: oka@imcj.hosp.go.jp

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