PREVALENCE OF ANTIPHOSPHOLIPID ANTIBODIES IN HIV-INFECTED CHILDREN IN ILE-IFE, NIGERIA

Abstract

BACKGROUND: This was a prospective case-control study that investigated
the prevalence of antiphospholipid antibodies (aPL) in HIV-infected children. It
also evaluated its association with patients’ clinical stage, features of
autoimmunity and presence of cytopaenia. HIV-infected children studied were
either on Highly-active antiretroviral therapy (HAART) or HAART-naïve; while
apparently healthy age and sex-matched HIV-negative children served as
controls.
INVESTIGATIONS: Six milliliters of venous blood was collected from each
consenting HIV-infected child and the HIV-negative controls. Out of this, 1ml
was added to paediatric size vacuum K2 EDTA specimen bottle, 2.25ml added
to 0.25ml 32g/L sodium citrate and the rest clotted for anticardiolipin antibody
assay. Full blood count was done using the Sysmex KX-21N, CD4+
lymphocytes count was done using Cyflow Counter 1 machine, following both
reagent and machine instructions. Direct Coombs’ tests (DCT) and activated
partial thromboplastin time (aPTT) were carried out according to standard
operating procedures (SOP). Kaolin clotting time (KCT) test and
anticardiolipin antibody (aCL) assay were also performed according to SOP
for subjects and controls with prolonged aPTT. These were done in subjects
and controls.
RESULTS: A total of 116 subjects and 61 controls were investigated. Patients
were aged between 18 months and 14 years with a mean age of 7.2 ± 3.3
years. Controls were also aged 18 months to 14 years with their mean age
being 8.7 ± 3.1 years. Male and female subjects were 63 (54.3%) and 53
(45.7%) respectively while controls were made up of 26 (42.6%) males and 35

(57.4%) females. One hundred and four (89.7%) of the subjects were on
HAART and 12 (10.3%) were HAART-naive.
The mean values of the packed cell volume (PCV), platelet count and
CD4+ lymphocyte count of the subjects were 33.6 ± 3.7%, 268 ± 104 x 109/L
and 878 ± 541 cells/µl respectively while those of the controls were 37.5 ±
3.5%, 219 ± 79 x 109/L and 1,178 ± 327 cells/µl. When these values were
compared, the difference was statistically significant (PCV: p <0.0001; platelet
count: p = 0.002; CD4+: p = 0.0002). However, the WBC count and the aPTT
were not statistically significant (WBC: p = 0.2; aPTT: p =0.3).
Thirteen (11.2%) of the 116 subjects were positive for aPLs. Using only
aCL as a determinant of aPL, only 11(9.48%) of the 116 subjects had
antiphospholipid antibodies. When lupus anticoagulant as determined by KCT
was used as a determinant of aPL, only 7 (6.03%) of 116 subjects had
antiphospholipid antibodies. Of the 13 subjects with aPL, 8 were males (i.e 8
of 63 males were aPL positive) and 5 were females (i.e 5 of 53 females were
aPL positive). The difference using the Pearson’s chi square was not
statistically significant (    = 0.321, p = 0.57).
Six (9.8%) of the 61 controls were positive for aPLs. Similarly, many of the
positive results were by aCL as compared with LA (9.8% vs 6.6%). There
were 3 of the 35 females and also 3 of the 26 males that were positive for
aPLs. This was not statistically significant (    = 0.15, p = 0.7).
The effect of antiphospholipid antibodies on PCV, platelet and white cell
counts were not significant.
Eleven (84.6%) of the subjects positive for antiphospholipid antibodies had
been on HAART for more than 6 months. Nine were in World Health
Organization (WHO) clinical stage 1 and two were in stages 2 and 3. None of
the subjects presented with any feature associated with the presence of aPLs
and DCT was negative in all of them.
Comparing prevalence of aPLs in HAART-naïve patients (2 of 12) and
patients on ARV treatment (11 of 104), there is no association established
(= 0.4, p = 0.52). Furthermore, HIV infection did not influence the
development of antiphospholipid antibodies as we document 13 of 116
infected to have aPL and 6 of 61 HIV-negative patients to have aPL. (=0.49,
p = 0.78).

CONCLUSION: This study found antiphospholipid antibodies in both HIV
infected and HIV-negative children. The presence or absence of these
antibodies did not account for any form of cytopaenia and there was absence
of clinical features related to its presence. There was no association between
positivity for aPLs and HAART naivity or being on treatment. Similarly, HIV
infection did not also influence the presence of antiphospholipid antibodies.

PREVALENCE OF ANTIPHOSPHOLIPID ANTIBODIES IN HIV-INFECTED CHILDREN IN ILE-IFE, NIGERIA