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DOI 10.1080/08820139.2016.1237525

Медицинская библиотека · Immunological investigations · 2016

Mannose-Binding Lectin Deficiency in Brazilian Patients with Spondyloarthritis.

Skare Thelma L, Nisihara Renato, Cieslinski Juliana Z, Zeni João O, Rasera Henrique N, Messias-Reason Iara, Utiyama Shirley R R

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Аннотация

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.

Для цитирования: Skare Thelma L, Nisihara Renato, Cieslinski Juliana Z, Zeni João O, Rasera Henrique N, Messias-Reason Iara, Utiyama Shirley R R. Mannose-Binding Lectin Deficiency in Brazilian Patients with Spondyloarthritis.. Immunological investigations. 2016. DOI: 10.1080/08820139.2016.1237525.

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