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1.
Autoimmunity ; 50(7): 409-413, 2017 Nov.
Article in English | MEDLINE | ID: mdl-28898115

ABSTRACT

OBJECTIVE: To investigate the association between mannose-binding lectin (MBL) serum level and MBL2 polymorphisms, and the frequency of spontaneous miscarriages in rheumatoid arthritis (RA) patients. METHODS: One hundred seventy seven women (mean age 50 years) with RA from Southern Brazil were studied and 4.5% had a history of abortion (8/177). The MBL levels were determined by ELISA. MBL2 polymorphisms in the promoter (-550H/L, -221X/Y), 5' untranslated region (4 P/Q) and exon 1 (p.Gly54Asp: B allele, p.Arg52Cys: D allele and p.Gly57Glu: C allele; collectively labelled O) were genotyped by sequencing. RESULTS: Mannose-binding lectin levels of RA patients ranged from ≤100 ng/mL to 6640 ng/mL (median 541.5 ng/mL). There was a significant difference in MBL median levels (100 ng/mL vs. 625 ng/mL, respectively, p = .001) and frequency of MBL deficiency (75.0% vs. 24.1%, p = .007, OR = 10.3, 95%CI = 1.9-55.4), in patients with a history of miscarriage vs those without it. Patients with RA and miscarriage had more frequently haplotypes related with low MBL levels (p = .007, OR = 10.5, 95%CI = 1.3-84) than high producers. Moreover, LYPB haplotype and O allele were significantly associated with the occurrence of miscarriage (p = .001, OR = 9.7, 95%CI = 2.4-39.1 and p = .009, OR = 5.9, 95%CI = 1.4-23.4, respectively). CONCLUSIONS: The results suggest that MBL deficiency and the presence of MBL2 gene polymorphisms that lead to MBL deficiency are risk factors for the occurrence of miscarriage in patients with RA.


Subject(s)
Abortion, Spontaneous/blood , Abortion, Spontaneous/etiology , Arthritis, Rheumatoid/complications , Mannose-Binding Lectin/blood , Mannose-Binding Lectin/deficiency , Metabolism, Inborn Errors/complications , Adult , Alleles , Amino Acid Substitution , Biomarkers , Female , Genotype , Haplotypes , Humans , Male , Mannose-Binding Lectin/genetics , Metabolism, Inborn Errors/genetics , Middle Aged , Odds Ratio
2.
Immunol Invest ; 46(2): 183-189, 2017 Feb.
Article in English | MEDLINE | ID: mdl-27911110

ABSTRACT

BACKGROUND: Infections are usually involved in the pathogenesis of spondyloarthritis (SpA). Mannose-binding lectin (MBL) is a component of the innate immune system with an important role in microbial defense. OBJECTIVE: To study the prevalence of MBL deficiency in SpA patients as well as its influence in the clinical profile of these diseases. METHODS: We studied 89 SpA patients and 89 healthy individuals, paired for age and gender. MBL serum levels were measured by ELISA test. Individuals with levels ≤100 ng/mL were considered deficient. SpA patients had determination of Bath Ankylosing Spondylitis Disease Activity Index (BASDAI), Ankylosing Spondylitis Disease Activity Score (ASDAS)-CRP, Bath Ankylosing Spondylitis Functional Index (BASFI), C reactive protein (CRP), erythrocyte sedimentation rate (ESR), and review of their clinical profile. RESULTS: SpA patients had MBL levels ranging from 100 to 4100 ng/mL (median = 375 ng/mL); controls levels ranged from 100 to 4703 ng/mL (median = 1204 ng/mL; p < 0.0001). The prevalence of MBL deficiency was 27/89 (30.3%) in SpA patients and 12/89 (13.5%) in controls, with p = 0.01; OR = 2.5 (95% IC = 1.2-5.3). No association/correlation was found between MBL levels with BASDAI, BASFI, age at disease onset, ASDAS-CRP, ESR, CRP, presence of uveitis, HLAB27, peripheral arthritis, or SpA subtype (all p = NS). CONCLUSION: MBL levels may be linked with the occurrence of SpA but do not influence its phenotype.


Subject(s)
Mannose-Binding Lectin/deficiency , Mannose-Binding Lectin/genetics , Metabolism, Inborn Errors/epidemiology , Spondylitis, Ankylosing/epidemiology , Adult , Blood Sedimentation , Brazil/epidemiology , C-Reactive Protein/metabolism , Cross-Sectional Studies , Disease Progression , Female , HLA-B27 Antigen/metabolism , Humans , Immunity, Innate/genetics , Male , Mannose-Binding Lectin/blood , Middle Aged , Phenotype , Prevalence , Severity of Illness Index
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