4.4 Article

Insulin resistance in children with juvenile systemic lupus erythematosus and investigation of the possibly responsible factors

Journal

CLINICAL RHEUMATOLOGY
Volume 41, Issue 3, Pages 795-801

Publisher

SPRINGER LONDON LTD
DOI: 10.1007/s10067-021-05952-9

Keywords

HOMA IR; Insulin resistance; TyG index; Systemic lupus erythematosus

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Children with juvenile systemic lupus erythematosus (jSLE) were found to have higher insulin resistance even after neutralizing the effects of contributing factors. The elevated insulin resistance in jSLE does not seem to be associated with corticosteroid use, disease duration, disease activity, or autoantibody levels.
Objective Insulin resistance (IR) has been described in adults with systemic lupus erythematosus (SLE), though its mechanism has not been fully clarified. In this study, it was aimed to investigate insulin sensitivity for the first time in children with juvenile SLE (jSLE) by considering the effect of the already known contributing factors of IR. Method This is a cross-sectional study including 43 patients with jSLE and the same number of healthy controls matched for age, gender, pubertal stage, body mass index, and physical activity level. IR, as calculated by both homeostatic model assessment for insulin resistance (HOMA-IR) and a relatively new method, triglyceride glucose (TyG) index, was compared between the patients and their matched controls, also among the patients stratified by disease duration, corticosteroid use, and disease activity. Results Insulin resistance in the patient group was higher than the controls according to both HOMA-IR and TyG index (p < 0.001 for both). In the patient group, no significant effect of disease duration, corticosteroid use, disease activity, and levels of anti-dsDNA, anti-cardiolipin IgM, anti-cardiolipin IgG, C3, and C4 on IR was demonstrated. Conclusion Children with jSLE were found to have higher IR even after neutralizing the effects of the contributing factors which are expected to aggravate IR. This elevation in IR in jSLE seems not to be associated with corticosteroid use, disease duration, disease activity, or autoantibody levels. Thus, the presence of IR in jSLE cannot be explained solely with neither the already known contributing factors nor the increased inflammation of the disease.

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