Níveis séricos da IL-13 na esclerose sistêmica: uma revisão sistemática com meta-análise / Serum levels of IL-13 in systemic sclerosis: a systematic review with meta-analysis

A interleucina-13 (IL-13) sérica foi investigada na esclerose sistêmica (ES) por meio de uma meta-análise para avaliar a possível diferença nos níveis em pacientes com a doença e pessoas saudáveis. As buscas foram realizadas nas bases de dados Pubmed, ScienceDirect, Cochrane Library, LILACS e Scopus para estudos do tipo caso-controle pertinentes utilizando os descritores. Os níveis séricos dos pacientes com ES em relação aos controles saudáveis foram plotados usando o software Review Manager 5.3. A avaliação da qualidade de cada estudo elegível foi conduzida na Escala de Newcastle-Ottawa (NOS). Quatro estudos de caso-controle foram selecionados para esta meta-análise e continham um total de 120 pacientes com ES e 84 controles saudáveis. Nossos resultados demonstram níveis séricos elevados da IL-13 em pacientes com ES, com um agrupamento médio de 0,70 ng/ml (p=0,00001) (IC 95%: -0,42 a -0,99, p=0,6). A IL-13 está aumentada no soro de pacientes com ES em comparação com os controles saudáveis e pode ser útil como possível biomarcador da doença. 

Genetic variants in LGALS3 are related to lower galectin-3 serum levels and clinical outcomes in systemic sclerosis patients: A case-control study

Introduction Systemic sclerosis (SSc) is a rare complex disease characterized by vascular damage, autoimmunity, and extensive skin and internal organs fibrosis. Galectin-3 (Gal-3) is encoded by gene LGALS3 (Lectin, Galactoside-Binding, Soluble, 3; 14q22.3) and it has been reported to play a central role in self-tolerance, inflammation, and fibrosis. Objective To investigate associations among LGALS3 single nucleotide polymorphisms (SNPs) and serum levels Gal-3 and SSc susceptibility and their clinical features. Methods A case-control study with 88 patients and 151 matched controls was performed. LGALS3 variants were analyzed by the TaqMan real-time polymerase chain reaction (PCR) system whereas Gal-3 serum levels were measured by sandwich enzyme linked immunosorbent assay (ELISA). Associations among genotypes, clinical features, and Gal-3 levels were performed by univariable and multivariable analysis through statistical packages. Results The LGALS3 rs4652 A/C genotype was more frequent in SSc patients than controls according to overdominant model [OR 1.89 (CI 95% 1.01 − 3.52); p = .046]. Also, LGALS3 rs4652 C/C polymorphic genotype was associated with lower patient Gal-3 levels (p = .03) and control group (p = 0.005), as noted by generalized linear model (GLM). The LGALS3 rs1009977 G/T controls showed higher Gal-3 levels than wild-type and polymorphic genotypes (p = .03); however, in SSc patients, no difference was found. None of the LGALS3 SNPs or Gal-3 levels was associated with clinical manifestations in SSc patients. Considering only the SSc group, GLM analysis pointed LGALS3 rs4652 and rs2075601, pulmonary arterial hypertension (PAH), myopathy, and health assessment questionnaire (HAQ) and scleroderma health assessment questionnaire (SHAQ) as important predictors for Gal-3 levels. Conclusion The LGALS3 rs4652 A/C was more frequent in SSc patients and related to lower Gal-3 levels. These findings were corroborated through a GLM to estimate Gal-3 values. Also, by model equations, Gal-3 levels may be predicted by HAQ, SHAQ, PAH, myopathy, and LGALS3 rs4652 and rs2075601 factors. In these ways, we suggest that galectins may be promising biomarkers to identify susceptibility to SSc as well as to identify HAQ, SHAQ, PAH, and myopathy outcomes