Hemorheologic abnormalities associated with HIV infection: altered erythrocyte aggregation and deformability.
OBJECTIVE
To investigate possible alterations of erythrocyte aggregation and deformability, which are factors that can influence blood flow, in human immunodeficiency virus (HIV)-infected individuals and to determine whether these factors are related to the severity of immunodeficiency.


METHODS
Laboratory evaluations were performed on 46 HIV-infected individuals and 44 HIV-negative control subjects. Current and nadir (lowest previous) CD4+ T-lymphocyte counts were identified for each subject. Erythrocyte aggregation was measured using a fully automatic erythrocyte aggregometer. Factors related to erythrocyte aggregation were also determined: erythrocyte sedimentation rate (ESR), zeta sedimentation ratio (ZSR), and plasma fibrinogen levels. Erythrocyte deformability was observed at various fluid shear stress levels, with a laser diffraction ektacytometer. Correlations were sought between each of these measures and current or nadir CD4+ T-lymphocyte counts, and each measure was compared between three subgroups based on current and nadir CD4+ T-lymphocyte counts (severely immunosuppressed, immune reconstituted, never severely immunosuppressed).


RESULTS
The following parameters were significantly different between HIV-infected subjects and controls: increased erythrocyte aggregation, at stasis (P < 0.001) and low shear stress (P < 0.001), increased ESR (P < 0.001), increased ZSR (P < 0.028), increased serum fibrinogen (P = 0.015), and decreased erythrocyte deformability (P < 0.001). Only erythrocyte aggregation at stasis correlated significantly with current CD4+ T-lymphocyte count (r = - 0.344, P = 0.022). None of the parameters was significantly different between HIV-infected subgroups.


CONCLUSIONS
Increased aggregation and decreased deformability of erythrocytes are associated with HIV-infection regardless of the severity of immunodeficiency. HIV-infected individuals may be at risk for progressive retinal microvascular damage from persistent hemorheologic abnormalities, despite immune reconstitution associated with potent antiretroviral drug therapies.
Kim
Alisa
A
Ocular Inflammatory Disease Center, Jules Stein Eye Institute, Los Angeles, CA 90095-7003, USA.
Dadgostar
Hajir
H
Holland
Gary N
GN
Wenby
Rosalinda
R
Yu
Fei
F
Terry
Brian G
BG
Meiselman
Herbert J
HJ
D000328:Adult; D001799:Blood Sedimentation; D018791:CD4 Lymphocyte Count; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology; D004903:Erythrocyte Aggregation; D004906:Erythrocyte Count; D004907:Erythrocyte Deformability; D005340:Fibrinogen / Q000032:analysis; D015658:HIV Infections / Q000097:blood* / Q000150:complications; D006801:Humans; D008875:Middle Aged; D012166:Retinal Hemorrhage / Q000097:blood* / Q000209:etiology; D012171:Retinal Vessels / Q000473:pathology; D012307:Risk Factors
D005340:Fibrinogen