The sedative thalidomide was withdrawn from the market 30 years ago because of 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.