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Mary M. Stimmler, MD; Francisco P. Quismorio, Jr, MD; William G. McGehee, MD; Thomas Boylen, MD; Om P. Sharma, MD

Arch Intern Med. 1989;149(8):1833-1835.

Abstract
• We undertook a prospective study of IgG and IgM anticardiolipin antibodies (ACAs) to determine their clinical significance in patients with acquired immunodeficiency syndrome (AIDS). IgG ACAs were found in 24 (92.3%) of 26 patients with AIDS who were hospitalized for pulmonary complaints (group 1) and in 13 (93%) of 14 patients with AIDS-related complex (group 2). In addition, 17 (94%) of 18 patients with AIDS (group 3) who had coagulation tests and were studied retrospectively had IgG ACAs. The prevalence of IgG ACAs in these three groups was significantly higher than in healthy controls, but was comparable to that in 31 consecutive patients with systemic lupus erythematosus (67.7%). The mean titer of IgG ACAs in group 1 was higher than in groups 2 and 3 but was not different from that in the patients with systemic lupus erythematosus. The frequency and titer of IgM ACAs in group 1 (7.6%) or group 2 (14.3%) were not significantly different from those in normal controls (4.7%). In contrast, half of the patients in group 3 had low-titer IgM ACAs. The serum titer of IgG ACAs in patients with AIDS with thrombocytopenia was significantly higher than it was in those with normal platelet counts. There was no association between ACAs and Pneumocystis carinii pneumonia or other infections, cancer, thrombosis, positive VDRL test, or presence of the lupus anticoagulant. The prevalence and titer of IgG or IgM ACAs were not associated with abnormal results of any coagulation test. Although we found IgG ACAs to be associated with thrombocytopenia in AIDS, their presence does not carry exactly the same clinical significance as it does in systemic lupus erythematosus. The high prevalence of ACAs in AIDS, in AIDS-related complex, and in otherwise healthy contacts with antibodies to human immunodeficiency virus suggests that their occurrence may be related to the underlying human immunodeficiency virus infection.

(Arch Intern Med. 1989;149:1833-1835)

Author Affiliations
From the Divisions of Immunology and Rheumatology (Drs Stimmler and Quismorio), Hematology (Dr McGehee), and Pulmonary Medicine (Drs Boylen and Sharma), Department of Medicine, University of Southern California School of Medicine, Los Angeles.

Footnotes
Accepted for publication February 10, 1989.

Reprint requests to Division of Immunology and Rheumatology, University of Southern California School of Medicine, HMR-715, 2015 Zonal Ave, Los Angeles, CA 90033 (Dr Quismorio).

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