Faculty Bibliography

We report four cases of immunologic thrombocytopenic purpura related to human immunodeficiency virus (HIV) transmitted through heterosexual contact in persons who were not homosexual, addicted to intravenous narcotic drugs, or hemophilic. Each transmission occurred in a different setting. A 23-year-old white woman had immunologic thrombocytopenic purpura in July 1985, with a platelet count of 11 X 10(9)/L. In January 1987, she had prominent submandibular and posterior cervical adenopathy. A careful social-sexual history revealed several sexual contacts with a male narcotic addict before July 1985. A 27-year-old heterosexual white man had a platelet count of 8 X 10(9)/L in December 1986. A social-sexual history revealed that his fiancee had been an intravenous narcotic addict 6 years ago. A 64-year-old white woman had a platelet count of 75 X 10(9)/L in May 1986, approximately 2 years after she had resumed having sexual intercourse with her husband who had had a triple coronary bypass in October 1983. The husband had received HIV-seropositive blood. A 42-year-old white man had a platelet count of 45 X 10(9)/L, which was associated with a cutaneous eruption refractory to antibiotics and antifungal agents. He had had sexual contacts with several women, who, to the best of his knowledge, were neither prostitutes nor intravenous narcotic addicts. He denied homosexuality or drug abuse. All four patients were HIV-seropositive and had circulating immune complexes and platelet-associated IgG, C3C4, and IgM values that were considerably higher than those usually measured in patients with classic autoimmune thrombocytopenia, averaging 2.4-, 2.2-, 6.5- and 5.2-fold higher, respectively. Thus, HIV-related immunologic thrombocytopenic purpura can be heterosexually spread and should become part of the differential diagnosis of unexplained thrombocytopenia. Obtaining a careful social-sexual history is mandatory in such patients

An epidemic of disseminated Kaposi's sarcoma in male homosexuals has recently been described. Forty-one evaluable patients with epidemic Kaposi's sarcoma were treated with etoposide. The majority of these patients had early stage disease, no prior opportunistic infections, and no prior therapy. Twelve patients (30%) achieved complete remission, 19 (46%) partial remission, and ten (24%) no response. With follow-up time to 31 months, the median response duration is nine months. The median survival of patients with complete and partial remissions has not been reached. A combination of doxorubicin (Adriamycin, Adria Laboratories, Columbus, Ohio), bleomycin, and vinblastine (ABV) was used in 31 evaluable patients with epidemic Kaposi's sarcoma. The majority of these patients had late stage disease, prior opportunistic infections, or had failed prior treatment. Seven patients (23%) achieved complete remission, 19 (61%) partial remission, and five (61%) no response. With follow-up time to 24 months, the median response duration is eight months. The projected median survival for all patients treated with ABV is nine months. Both regimens were well tolerated, with an overall response rate of 76% for etoposide and 84% for ABV. However, while successfully treating the Kaposi's sarcoma, the underlying immune deficiency in these patients has persisted. Future treatments of Kaposi's sarcoma will need to focus on reversing the underlying immune incompetence as well as controlling the malignant manifestations of Kaposi's sarcoma arising in relation to the acquired immune deficiency syndrome

The clinical findings in eight young homosexual men in New York with Kaposi's sarcoma showed some unusual features. Unlike the form usually seen in North America and Europe, it affected younger men (4th decade rather than 7th decade); the skin lesions wee generalised rather than being predominantly in the lower limbs, and the disease was more aggressive (survival of less than 20 months rather 8-13 years). All eight had had a variety of sexually transmitted diseases. All those tested for cytomegalovirus antibodies and hepatitis B surface antigen of anti-hepatitis B antibody gave positive results. This unusual occurrence of Kaposi's sarcoma in a population much exposed to sexually transmissible diseases suggests that such exposure may play a role in its pathogenesis

Platelet IgG levels, count, and function and easy bruising or bleeding were studied in 25 patients with Graves' disease and 12 with Hashimoto's thyroiditis (normal value for platelet IgG 10.7 +/- 4.5 ng [SD]/10(6) platelets). Eight of 22 patients with Graves' disease and normal platelet counts had elevated platelet IgG averaging 38 +/- 4.0 ng (SEM) (range, 24 to 60). Four of 10 patients with Hashimoto's thyroiditis and normal platelet counts ahd elevated platelet IgG averaging 45 +/- 7.2 ng (range, 27 to 66). Five patients with thrombocytopenia had platelet counts averaging 53000 +/- 12000/microL (SEM) and elevated platelet IgG averaging 154 +/- 40 ng (range, 27 to 300). Twelve of 15 patients with a history of easy bruising or bleeding had elevated platelet IgG compared to five of 22 without easy bruising (p < 0.001). Four of six with elevated platelet IgG had one or more abnormal in-vitro platelet aggregation measurements (particularly with epinephrine) compared to none of six with normal platelet IgG levels (p = 0.03). We conclude that elevated platelet IgG is associated with easy bruising and thrombocytopenia in about half of patients with Graves' disease or Hashimoto's thyroiditis

The gamma heavy-chain subclass of bound antiplatelet antibody was examined in six patients with autoimmune thrombocytopenic purpura (ATP) by a solid-phase radioimmunoassay. Monospecific antisera for gamma G1, gamma G2, gamma G3, and gamma G4 subclasses were employed in a 'sandwich' technique, utilizing the binding of 126I-staphylococcal protein A. We have previously reported that serum antiplatelet antibody was restricted to be gamma G3 subclass in ATP. In contrast, all 4 IgG subclasses were found bound to platelets of ATP patients in the same distribution as that present in normal serum. It is suggested that the differences noted between serum antiplatelet IgG and platelet-bound IgG may represent different mechanisms of platelet injury