HUMAN LEUKOCYTE ANTIGEN-B27 AND
DISEASE SUSCEPTIBILITY IN VOJVODINA, SERBIA
Vojvodić S1,*, Ademović-Sazdanić D1, Busarčević I2
*Corresponding Author: Assistant Professor Svetlana Vojvodić, M.D., Ph.D., Department for Laboratory
Testing, Tissue Typing Compartment, Institute for Blood Transfusion of Vojvodina, Hajduk Veljkova 9a,
21000 Novi Sad, Serbia; Tel.: +381-21-4877-963; Mobile: +381-64-861-58-12; Fax: +381-21-4877-978;
E-mail: ssvu@EUnet.rs
page: 55
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MATERIALS AND METHODS
Ninety-seven patients, of whom 58 were male
and 39 were female, with a mean age of 39.6 ± 14.4
years, suffering from different diseases: AS (16), polyarthralgia
(34), lumboishialgia (14), AAU (11), PA
(3), synovitis coxae (16) and RA (3), composed of different
ethnicities, residents of different parts of Vojvodina,
were included in our study. In addition, a group
of 224 healthy, unrelated potential bone marrow/organ
donors, representing the same ethnic groups as the
patients who resided in the same geographic area,
served as a control population. An informed consent
was obtained from all the individuals participating
in the study and all institutional ethics requirements
were met. Three mililiters of venous blood taken in
vacutainers with EDTA as anticoagulant was collected
from the patients and controls. Peripheral mononuclear
cells were isolated by ficoll hypaque gradient
centrifugation from which the T lymphocytes were
separated by immunomagnetic beads (Dynabeads, HLA class I typing was performed by serological immunomagnetic
two-color fluorescence method using
peripheral blood T lymphocytes and antigenspecific
commercially available sera defining a single HLA
specificity. Briefly, Terasaki microtiter plates (Inno-
Train Diagnostik GmbH, Kronberg, Germany), containing
various anti-HLA class I antisera were seeded
with 1 mL of a 2 × 106 cells/mL suspension of immobilized
T-cells. After incubation at room temperature
and addition of 5 mL rabbit complement, the lysed and
vital lymphocytes were assessed using an ethidium
bromide/acridine orange dye (Merck, Darmstadt, Germany)
under an inverse phase contrast microscope
[10,11]. Phenotype frequencies were obtained by a direct
counting method, according to equation: A = n/N,
where n is number of persons with a given antigen
and N is total number of persons studied. The strength
of association of disease with respect to a particular
HLAs is expressed by odds ratio (OR) interpreted as
relative risk (RR). Relative risk is calculated for those
HLAs that are increased or decreased in patients as
compared to the control group. The RR or the number
of times risk of disease is increased or decreased in
individuals with a certain HLA marker, was calculated
according to following formula
where P+ and C+ are the number of patients or healthy
persons who have a given antigen; C– and P– are the
number of patients or healthy persons who do not
have a given antigen, respectively [12,13,14].
The values between 0 and 1 are of significance.
When RR was higher than 1, we calculated an etiological
fraction (EF) or population attributive risk,
according to formula:
where FAD is the frequency of the HLA-B27 antigen
in the subgroup of patients and FAP is the HLA-B27
frequency in controls. The EF indicates the hypothetical
genetic component of the disease and gives the
proportion of disease cases attributable to a marker
in the population (in this case, an HLA-B27 antigen),
that presents a positive association (RR>1) with disease,
and/or with other risk factors associated with
this marker. Preventive fraction (PF) is calculated for
negative association only where RR was lower than
1, according to following equation:
where RR is relative risk and f is the frequency of
the HLA-B27 antigen in the subgroup of patients.
The PF gives the percentage of cases that can be
prevented if the population is exposed to an intervention
compared to unexposed population. The EF
and PF values greater than 0.15 were considered to
reflect positive and negative association, respectively
[15,16]. The χ2 test was performed to find out if there
was a significant difference of HLA-B27 antigen frequency
between controls and investigated subgroups
of patients, according to following formula:
( )( )( )( )
( )2 ( )
2
a b c d a c b d
X ad bc a b c d
+ + + +
− + + +
=
where a and c are the number of patients or healthy
persons who have a given antigen; b and d are the
number of patients or healthy persons who do not
have a given antigen, respectively [17,18].
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