CLINICAL OUTCOME OF HIV-INFECTED HEMOPHILIAC PATIENTS IN HONG-KONG

Citation
Ck. Lee et al., CLINICAL OUTCOME OF HIV-INFECTED HEMOPHILIAC PATIENTS IN HONG-KONG, Haemophilia, 3(3), 1997, pp. 205-208
Citations number
17
Categorie Soggetti
Hematology
Journal title
ISSN journal
13518216
Volume
3
Issue
3
Year of publication
1997
Pages
205 - 208
Database
ISI
SICI code
1351-8216(1997)3:3<205:COOHHP>2.0.ZU;2-Z
Abstract
About half of the haemophiliacs in Hong Kong have been infected by hum an immunodeficiency virus (HIV). This study aimed to determine their c linical course of progression. Forty-seven adult patients with congeni tal coagulation factor deficiency bring followed up regularly from Jan uary 1992 onward in the Department of Medicine of Queen Mary Hospital, Hong Kong, were included in this study. Twenty were positive for HIV antibody and the remaining 27 were negative. Three other HIV-positive patients who died before 1992 were excluded. From January 1992 to June 1996, the 47 patients included in the study were followed up in the c linic every 3-6 months with regular CD4, CD8 lymphocyte counts and bet a 2 microglobulin levels. At the initiation of the study in January 19 92, the HIV-infected patients had already a lower mean CD4 count (360. 4 mu L-1 versus 658.8 mu L-1, P<0.01), a reversed CD4/CD8 ratio (0.53) and a higher mean serum beta 2 microglobulin level (1.853 mu g mL(-1) versus 1.315 mu g mL(-1), P>0.05). On regular follow-up, HIV-positive patients had a more significant progressive fall in their mean CD4 co unt (301.6 mu L-1 versus 360.4 mu L-1, P<0.01) and rise in their mean serum beta 2 microglobulin level (2.60 mu g mL(-1), versus 1.853 mu g mL(-1), P < 0.05). The CD4 and CD8 counts of HIV-positive patients wer e falling at a rate of 1.44 mu L-1 month(-1) and 4.03 mu L-1 month(-1) respectively. During the follow-up period, two of the 20 HIV-positive patients developed clinical acquired immunodeficiency syndrome (AIDS) at 15 and 36 months from the initiation of the study. Both patients h ad typical features of AIDS with a low CD4 count, reversed CD4/ CD8 ra tio and elevated beta 2 microglobulin level. The former patient eventu ally died of fungal brain abscess. The remaining 18 HIV-positive patie nts so far remained clinically asymptomatic. Eleven patients were put on antiretroviral drug therapy when their CD4 counts fell below 200 mu L-1. Only two of the 20 HIV-infected patients developed AIDS during t he observation period of 4 years; this figure-of 10% is relatively slo w. Two of our patients died of AIDS before the study was initiated in 1992. Even if they were included, still only 17.4% had progressed. The figure is in the lowest rate of progression expected from Western exp erience. Although our study population is small, it remains unclear wh y our HIV-infected Chinese haemophiliacs have a slow rate of progressi on to AIDS.