Serum Vitamin D Status in Iranian Fibromyalgia Patients: according to the Symptom Severity and Illness Invalidation

BACKGROUND: This study was designed to assess serum vitamin D status (25-OHD) in the fibromyalgia (FM) patients and to compare it with a healthy control group. It also aimed to investigate the correlation of serum vitamin D level with FM symptom severity and invalidation experiences. METHODS: A total of 74 consecutive patients with FM and 68 healthy control participants were enrolled. The eligible FM patients completed the Illness Invalidation Inventory (3*I), the Revised Fibromyalgia Impact Questionnaire (FIQR) and a short-form health survey (SF-12). Venous blood samples were drawn from all participants to evaluate serum 25-OHD levels. Mann-Whitney tests and multiple logistic regression analyses were performed and Spearman's correlations were calculated. RESULTS: 88.4% of FM patients had low levels of serum 25-OHD. FM patients had significantly higher level of serum 25-OHD than the control group (17.24 ± 13.50 and 9.91 ± 6.47 respectively, P = 0.0001). There were no significant correlations between serum 25-OHD levels and the clinical measures of disease impact, invalidation dimensions, and health status. Multiple logistic regression analyses revealed that an increased discounting of the disease by the patient's spouse was associated with a 4-fold increased risk for vitamin D deficiency (OR = 4.36; 95% CI, 0.95-19.87, P = 0.05). CONCLUSIONS: This study showed that although high rates of vitamin D insufficiency or deficiency were seen among FM patients and healthy non-FM participants, but it seems there was no intrinsic association between FM and vitamin D deficiency. Addressing of invalidation experience especially by the patient's spouse is important in management of FM.

[Association of HLA-G INDEL polymorphism with systemic lupus erythematosus [SLE] in Guilan Province, in Iran]

Background and Aim: Systemic lupus erythematosus [SLE] is an autoimmune disease that is characterized by the presence of autoantibodies against nuclear antigens. The exact cause of SLE is unknown, but some of these genes are active in the key pathways, including immune complexes, host immune signal transduction, and interferon pathways which have significant roles in the pathogenesis of SLE. Since the classical HLA class I and II molecules are highly involved in the peptide presentation to the components of immune system, the genes that encode these molecules can be primary candidates associated with susceptibility to autoimmune disorders. HLA-G belongs to the family of non-classical HLA class I antigens. The purpose of this study was to evaluate the association of INDEL polymorphism of the 3'UTR region of HLA-G gene with SLE

Material and Methods: In this study, 80 patients with SLE, and 102 healthy individuals were examined. Genomic DNA was extracted from peripheral blood. The genotypes were determined using ARMS-PCR. Data analysis was performed using MedCalc version 12.1

Results: The frequencies of homozygot genotypes for the presence of [+14bp/+14bp]14bp, hetrozygot genotypes for [-14bp/+14bp], and homozygot genotypes with deletion of [-14bp/-14bp]14bp segments in the healthy individuals were 21.57%, 41.18% and 37.25%, and in the patients were 17.5%, 42.5% and 40% respectively. The most frequent genotype in the healthy individuals and hetrozygot patients was [-14bp/+14bp]. We found no statistically significant differences in the genotype distributions between the cases and controls [and Rho;>0.05]

Conclusion: In this study INDEL polymorphism of the 3UTR region of HLA-G gene showed no association with systemic lupus erythematosus. However, further studies are required to confirm the validity of these results