Description of patients
In this study, the most frequent clinical manifestations among 80 SLE patients were rash, arthritis, and leucopenia, while the most common laboratory manifestations were anti-nuclear antibodies (100%), anti-ds DNA (97.5%) and low complement (83.75%). The clinical and laboratory characteristics of patients with SLE are shown in Table. 1.
Table. 1
The clinical and laboratory characteristics of patients with SLE.
The clinical and laboratory manifestations
|
Total (n=80)
|
Seizure
|
10 (12.5%)
|
Psychosis
|
4 (5%)
|
Rash
|
66 (82.5%)
|
Organic Brain Syndrome
|
2 (2.5%)
|
Visual disturbance
|
2 (2.5%)
|
Cranial nerve disorder
|
3 (3.75%)
|
Lupus headache
|
4 (5%)
|
CVA
|
0 (0.0%)
|
Vasculitis
|
2 (2.5%)
|
Myositis
|
4 (5%)
|
Urinary casts
|
6 (7.5%)
|
Hematuria
|
6 (7.5%)
|
Proteinuria
|
8 (10 %)
|
Pyuria
|
5 (6.25%)
|
Alopecia
|
2 (2.5%)
|
Pleurisy
|
4 (5%)
|
Precardia
|
7 (8.75%)
|
Low complement
|
59 (73.75%)
|
Increased DNA binding
|
25 (31.25%)
|
Fever
|
11 (13.755)
|
Thrombocytopenia
|
9 (11.25%)
|
Leukopenia
|
27 (26.25%)
|
Associations of genotype and allele frequencies of FcγRIIB and FcγRIIIA with SLE susceptibility
Our data revealed that there were no significant differences in FcγRIIB genotype frequencies between patient and control groups (Table. 2). Allelic analysis indicated that C and T allele frequencies of FcγRIIB in patients did not significantly differ from those of control group (Table. 2).
Table. 2
The genotypes and allele frequencies of FcγRIIB (rs1050501) and FcγRIIIA (rs396991) SNPs in patient and control groups.
Positions
|
Genotype
|
Patients
|
Controls
|
OR (95% CI)
|
P value
|
|
and allele
|
2n= 160
|
2n = 190
|
|
|
|
frequencies
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
Rs1050501
|
CC
|
25
|
(31.25%)
|
28 (29.47%)
|
|
0.64
|
|
|
|
|
|
|
|
|
CT
|
30
|
(37.5%)
|
36 (37.89%)
|
|
|
|
|
|
|
|
|
|
|
TT
|
75
|
(46.8%)
|
31 (32.63%)
|
|
|
|
|
|
|
|
|
|
|
C
|
85
|
(53.2%)
|
92 (48.43%)
|
0.93 (0.61-1.43)
|
0.77
|
|
|
|
|
|
|
|
|
T
|
38
|
(47.5%)
|
98 (51.57%)
|
|
|
|
|
|
|
|
|
|
Rs396991
|
TT
|
25
|
(31.25%)
|
42 (44.21%)
|
|
0.73
|
|
|
|
|
|
|
|
|
TG
|
17
|
(21.25%)
|
35 (36.84%)
|
|
|
|
|
|
|
|
|
|
GG
|
101 (63.1%)
|
18 (18.94%)
|
|
|
|
|
|
|
|
|
|
|
T
|
59
|
(36.9%)
|
119 (62.63%)
|
1.02 (0.66-1.57)
|
0.92
|
|
|
|
|
|
|
|
|
G
|
25
|
(31.25%)
|
71 (37.36%)
|
|
|
Values are indicated as count (percent).
The significance level was considered as P < 0.05.
|
In addition, statistical analyses indicated that FcγRIIIA genotype frequencies were not significantly different from those of healthy individuals (Table. 2). As shown in Table. 2, no significant differences were observed between T and G alleles frequencies in patient and control groups. Other results indicated that T allele was the most frequent allele in two SNPs (Table. 2).
Correlations of FcγRIIB and FcγRIIIA with SLEDAI
To determine the associations of FcγRIIB and FcγRIIIA with SLEDAI, the relationships of genotype and allele frequencies of these SNPs with some clinical parameters, which were the most frequent clinical manifestations of SLE patients, were evaluated. Our data indicated that FcγRIIB genotype and allele frequencies were significantly associated with the frequencies of leucopenia, rash, mucosal ulcer, arthritis, thrombocytopenia in SLE patients (P <0.001-0.05, Table. 3). The results of multiple comparisons revealed that there were significant correlations between distribution frequencies of FcγRIIB CC, CT and TT genotypes versus (vs) other genotypes and these clinical factors used to determine SLEDAI (P <0.001-0.05, Table. 3).
Furthermore, other results of statistical analyses showed that the frequencies of some genotype and allele of FcγRIIIA played significant roles in determining SLEDAI. Similar to FcγRIIB, our results indicated that some genotype and allele frequencies of FcγRIIIA were significantly correlated to SLEDAI (P <0.001-0.05, Table. 5). The frequencies of FcγRIIIA TT, TG and GG genotypes vs other genotypes were significantly associated with SLEDAI (P <0.001-0.05, Table. 3).
Table. 3
The correlations of rs1050501 and rs396991 with some clinical manifestations used to SLEDAI
