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Suramin Antiviral Therapy in the Acquired Immunodeficiency Syndrome: Clinical, Immunologic, and Virologic Results

ALEXANDRA M. LEVINE, M.D.; PARKASH S. GILL, M.D.; JORDAN COHEN, Ph.D; JEAN G. HAWKINS, M.D.; SILVIA C. FORMENTI, M.D.; SCOTT AGUILAR, R.N.; PAUL R. MEYER, M.D.; MARK KRAILO, Ph.D.; JOHN PARKER, M.D.; and SURAIYA RASHEED, Ph.D.
[+] Article and Author Information

▸Requests for reprints should be addressed to Alexandra M. Levine, M.D.; USC School of Medicine, Norris Cancer Hospital and Research Institute, 1441 Eastlake Avenue; Los Angeles, CA 90033-0804.


Los Angeles, California


© 1986 American College of PhysiciansAmerican College of Physicians


Ann Intern Med. 1986;105(1):32-37. doi:10.7326/0003-4819-105-1-32
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The human T-lymphotropic virus type III/lymphadenopathy-associated virus (HTLV-III/LAV) requires reverse transcriptase for viral replication. We treated 12 patients who had acquired immunodeficiency syndrome and active HTLV-III/LAV viremia with suramin, a potent competitive inhibitor of reverse transcriptase, in six weekly induction doses of 1 g, followed by weekly maintenance doses of 500 mg. Three of eleven evaluable patients had complete inhibition of viral reverse transcriptase levels, lasting at least 18 weeks in each. Two additional patients had marked reduction in reverse transcriptase activity. Nadir serum suramin levels at the end of the induction phase correlated with the level of reverse transcriptase reduction. Toxicity included hepatic transaminase elevation, fever, malaise, rash, proteinuria, paresthesias, reversible neutropenia, and adrenal insufficiency. Objective clinical improvement was documented in 1 patient, but no patient had improvement in immune function and 7 patients had recurrent opportunistic infections. Although suramin may suppress HTLV-III/LAV viremia, its significant toxicity and lack of effect on immune variables indicate that alternative therapy will be required.

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