The
sedative thalidomide was withdrawn from the market 30 years ago because of its teratogenic and neurotoxic adverse effects. The compound was later discovered to be extremely effective in the treatment of
erythema nodosum leprosum, a complication of
lepromatous leprosy. This effect is probably due to a direct influence on the immune system, because
thalidomide possesses no antibacterial activity. The compound is presently used as an experimental
drug in the treatment of a variety of diseases with an autoimmune character, including recurrent aphthosis of nonviral and nonfungal origin in human immunodeficiency virus (HIV) patients. This article reviews the most important chemical and pharmacokinetic properties of
thalidomide. The possible mechanisms of the nonsedative effects of
thalidomide with respect to the safety of its use in HIV patients are discussed. Because the mechanism of the immunomodulatory effect of
thalidomide is unknown, the possibility that the administration of this compound will accelerate the deterioration of the immunological status of HIV patients cannot be excluded. Clinical evidence suggests that
thalidomide may aggravate the condition of patients with preexisting
peripheral neuropathy.
Hypersensitivity reactions to
thalidomide may occur more frequently in HIV patients than in other patient groups. Because of the teratogenic activity of
thalidomide, reliable
contraception must be provided to female patients of childbearing age. Before the introduction of
thalidomide therapy to an HIV patient presenting with
oral ulcers, a fungal or viral origin of the lesions should be excluded.
Thalidomide should not be used in patients with preexisting HIV-related peripheral
polyneuropathy,
polyradiculopathy or
encephalopathy. In patients experiencing a complete remission, the discontinuation of
thalidomide treatment and its reintroduction in the case of a relapse are preferable to maintenance
therapy.