Garsia R J, Gatenby P A, Basten A, Kenny D F, Gallagher K J, Rickard K A, Gust I D, Maskill W
Clinical Immunology Research Centre, University of Sydney, NSW.
Aust N Z J Med. 1987 Aug;17(4):371-8. doi: 10.1111/j.1445-5994.1987.tb00068.x.
One hundred and sixty-one Australian patients with hereditary bleeding disorders comprising hemophilia A (120), hemophilia B (18), von Willebrand's disease (16), and seven symptomatic female hemophilia A or B carriers were screened for clinical and serological evidence of exposure to HTLV-III/LAV/ARV/HIV infection. During the previous five years (1979-1984) they had been treated almost exclusively with blood products derived from Australian voluntary donors. The prevalence of HTLV-III antibodies in 1985 was 45%, with the highest frequency being in those with severe hemophilia A (78%) and the lowest in patients with hemophilia B (6%). Antibody positivity correlated with a reduced absolute T helper (T4) cell numbers and/or an inverted T4:T8 ratio. Lymphadenopathy was detected in 23 subjects but only 13 had an abnormal T cell ratio. Comparison of seropositivity and T4:T8 ratios in 32 patients studied in 1983 and again in 1985 suggested that T4 cell deficiency reflected HTLV-III exposure rather than being a predisposing factor for infection with the virus. Individual patients showed considerable fluctuation in T cell subsets over a 12 month period of follow-up, but as a population there was a slight trend with time towards diminishing T4:T8 ratio only in the antibody positive hemophilia A patients of mild to moderate severity. Three (2%) of the 161 patients screened to date have developed confirmed AIDS with fatal outcome.(ABSTRACT TRUNCATED AT 250 WORDS)