[Anatomopathologic study of five cases of leprosy in HIV seropositive patients]. / Etude anatomopathologique de 5 cas de lèpre chez des sujets séropositifs pour le virus de l'immunodéficience humaine (VIH).

In an effort to establish whether the human immunodeficiency virus (HIV) modifies the histological image of lepromatous skin lesion, a comparative study was conducted in 1994 at the Marchoux Institute in Bamako, Mali, on persons newly suffering from leprosy who had been tested seropositive and seronegative for the HIV virus. These new leprosy patients had never been treated and could be grouped as follows: 5 HIV-positive (1 TT, 1 BT, 1 BL, 2 LL) and 10 controls testing HIV-negative, selected according to the following criteria: each seropositive leprosy subject was matched with two seronegative controls having the same clinical features, same stage under the Ridley classification system, same age and sex. No discordance between the clinical classifications and the histological features in the subjects testing HIV-positive has been observed. They display features similar to those testing negative, with the presence of histiocytes, in particular epithelioid cells and giant cells in normal proportion depending on the form of leprosy. The only remarkable difference was a greater incidence of oedema in the subjects testing seropositive, compared with patients testing seronegative. In conclusion, HIV infection does not appear to cause major modifications in cellular response to Mycobacterium leprae, and no changes should be made in leprosy control programmes.

Clinical classification of African Kaposi's sarcoma: time for reappraisal.

PIP: African Kaposi's sarcoma (KS) remains a medical curiosity which continues to intrigue and elude medical science. While impaired cell-mediated immunity has been associated with some subtypes of African KS before and after the advent of AIDS, its role in the pathogenesis of African KS has never been defined. Determining the role of host immunity in the pathogenesis of African KS could, however, yield important insights into the tumor. The author notes that immune impairment from causes other than AIDS could exert similar influences upon the biological and clinical behavior of African KS. Unfortunately, preoccupation with the relationship between AIDS and atypical KS has overshadowed interest in the relation between immunosuppression in general and African KS. That different morphologic subtypes of African KS have identical histology suggests that they are manifestations of the same disease. Clinical manifestations of African KS in a susceptible host is probably determined by a complex interplay between host immunity and putative cofactors such as infectious agents, KS antigens, hormones, and genetic and environmental factors. African KS has a clinical spectrum ranging from localized to generalized. Hosts with relatively good cellular immunity develop localized lesions, while hosts with markedly impaired immunity develop generalized cutaneous or lymphadenopathic KS. The author draws an analogy with leprosy to help clarify the role of host immunity in the clinical manifestations and behavior of African KS.^ieng