# Metabolic and Anthropometric Alterations in Juvenile Idiopathic Arthritis: A Focus on Cardiometabolic Risk and Non-Invasive Evaluation Methods

**Authors:** Agnieszka Januś, Justyna Roszkiewicz, Elżbieta Smolewska

PMC · DOI: 10.3390/metabo16020090 · Metabolites · 2026-01-24

## TL;DR

This review explores how juvenile idiopathic arthritis affects metabolism and body composition, increasing cardiovascular risk in children.

## Contribution

The paper synthesizes evidence on metabolic alterations and non-invasive diagnostic methods for cardiovascular risk in JIA.

## Key findings

- Children with JIA show dyslipidemia, insulin resistance, and abnormal fat distribution.
- Non-invasive methods like DXA and cIMT detect subclinical metabolic and vascular changes.
- Early detection of these changes may improve long-term outcomes in JIA patients.

## Abstract

Juvenile idiopathic arthritis (JIA) is the most prevalent chronic rheumatologic condition in childhood, with an incidence that continues to rise worldwide. Despite substantial progress in therapeutic strategies over the past two decades, JIA remains a major health concern. Beyond joint inflammation and musculoskeletal impairment, accumulating evidence indicates that JIA is associated with metabolic disturbances and altered body composition, which may predispose affected children to an elevated cardiovascular risk in the long term. The objective of this review is to synthesize current knowledge on these metabolic and anthropometric alterations and to evaluate the role of non-invasive diagnostic methods in detecting early cardiovascular changes. A narrative review of the literature was conducted using PubMed and Scopus databases, focusing on studies assessing lipid metabolism, insulin resistance, adiposity, and cardiovascular markers in pediatric patients with JIA. Special attention was given to non-invasive diagnostic approaches, including bioelectrical impedance analysis (BIA), dual-energy X-ray absorptiometry (DXA), skinfold thickness, transient elastography, carotid intima–media thickness (cIMT), as well as selected biochemical markers. Evidence suggests that children with JIA frequently present with dyslipidemia, increased insulin resistance, and abnormal body fat distribution compared with their healthy peers. Non-invasive assessment methods, particularly DXA and cIMT, have demonstrated sensitivity in detecting subclinical metabolic and vascular changes. These alterations resemble early features of metabolic syndrome and are thought to contribute to premature cardiovascular morbidity in this population. Incorporating non-invasive cardiovascular risk assessment into routine rheumatology practice may improve early detection of metabolic and vascular complications in JIA, support timely preventive interventions, and ultimately enhance long-term outcomes for affected children. Most available evidence is derived from cross-sectional studies, highlighting the need for longitudinal investigations to better define long-term cardiometabolic risk in JIA.

## Linked entities

- **Diseases:** Juvenile idiopathic arthritis (MONDO:0011429), metabolic syndrome (MONDO:0000816)

## Full-text entities

- **Genes:** APOB (apolipoprotein B) [NCBI Gene 338] {aka FCHL2, FLDB, LDLCQ4, apoB-100, apoB-48}, LEP (leptin) [NCBI Gene 3952] {aka LEPD, OB, OBS}, SELE (selectin E) [NCBI Gene 6401] {aka CD62E, ELAM, ELAM1, ESEL, LECAM2, selectin-e}, VCAM1 (vascular cell adhesion molecule 1) [NCBI Gene 7412] {aka CD106, INCAM-100}, MPO (myeloperoxidase) [NCBI Gene 4353], APOA1 (apolipoprotein A1) [NCBI Gene 335] {aka AMYLD3, HPALP2, apo(a)}, CRP (C-reactive protein) [NCBI Gene 1401] {aka PTX1}, IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}, ADIPOQ (adiponectin, C1Q and collagen domain containing) [NCBI Gene 9370] {aka ACDC, ACRP30, ADIPQTL1, ADPN, APM-1, APM1}, PRKAB1 (protein kinase AMP-activated non-catalytic subunit beta 1) [NCBI Gene 5564] {aka AMPK, HAMPKb}, ICAM1 (intercellular adhesion molecule 1) [NCBI Gene 3383] {aka BB2, CD54, P3.58}, LPL (lipoprotein lipase) [NCBI Gene 4023] {aka HDLCQ11, LIPD}, INS (insulin) [NCBI Gene 3630] {aka IDDM, IDDM1, IDDM2, ILPR, IRDN, MODY10}, TNC (tenascin C) [NCBI Gene 3371] {aka 150-225, DFNA56, GMEM, GP, HXB, JI}, IL1B (interleukin 1 beta) [NCBI Gene 3553] {aka IL-1, IL1-BETA, IL1F2, IL1beta}, RETN (resistin) [NCBI Gene 56729] {aka ADSF, FIZZ3, RENT, RETN1, RSTN, XCP1}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}
- **Diseases:** immune dysregulation (OMIM:614878), glucose (MESH:D018149), Lipid disturbances (MESH:D011017), abnormal body fat distribution (MESH:D020243), chronic (MESH:D002908), hypertriglyceridemia (MESH:D015228), type 2 diabetes (MESH:D003924), Proinflammatory Cytokines (MESH:D000080424), underweight (MESH:D013851), deformities (MESH:D009140), adiposity (MESH:D018205), reduced muscle mass (MESH:D009135), brachial (MESH:D020968), Systemic (MESH:D015619), T1D (MESH:D003922), cardiovascular diseases (MESH:D002318), endocrine disturbances (MESH:D004700), JIA (MESH:D001171), joint stiffness (MESH:C535724), autoimmune rheumatic diseases (MESH:D012216), osteoporosis (MESH:D010024), Insulin Resistance (MESH:D007333), Idiopathic Arthritis (MESH:D001168), RA (MESH:D001172), thrombosis (MESH:D013927), abnormalities (MESH:D000014), hypertension (MESH:D006973), venous thromboembolism (MESH:D054556), metabolic and vascular complications (MESH:D020739), atherogenesis (MESH:D050197), metabolic dysregulation (MESH:D021081), metabolic (MESH:D008659), psoriatic arthritis (MESH:D015535), CS (MESH:D003480), psoriasis (MESH:D011565), HD (MESH:D050031), visceral adiposity (MESH:D007418), hypothalamic-pituitary-adrenal (HPA) axis disorders (MESH:D007029), Hepatic Steatosis (MESH:D005234), weight gain (MESH:D015430), autoimmune diseases (MESH:D001327), obese (MESH:D009765), HDL dysfunction (MESH:D052456), fatigue (MESH:D005221), anti (MESH:D006679), Overweight (MESH:D050177), NAFLD (MESH:D065626), endothelial dysfunction (MESH:D014652), DM (MESH:D003920), oligoarticular disease (MESH:D004194), injury to (MESH:D014947), Chronic inflammation (MESH:D007249), muscle atrophy (MESH:D009133), sarcopenia (MESH:D055948), rheumatologic condition (MESH:D020763), fibrosis (MESH:D005355), cardiometabolic abnormalities (MESH:D024821), hyperglycemia (MESH:D006943), Pain (MESH:D010146), dyslipidemia (MESH:D050171)
- **Chemicals:** baricitinib (MESH:C000596027), Glucose (MESH:D005947), Lipid (MESH:D008055), fatty acid (MESH:D005227), carbohydrate (MESH:D002241), Janus (-), cholesterol (MESH:D002784), MTX (MESH:D008727), triglyceride (MESH:D014280), tocilizumab (MESH:C502936)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## References

87 references — full list in the complete paper: https://tomesphere.com/paper/PMC12942494/full.md

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Source: https://tomesphere.com/paper/PMC12942494