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Updated: May 13, 2025

Induction of Experimental Autoimmune Hypophysitis in SJL Mice
Published on: December 17, 2010
Endocrine dysfunction in patients with juvenile idiopathic arthritis
Sayan Mukherjee1, Abilash Krishnan Vijayakumaran1, Mukesh Kumar Maurya1
1Department of Clinical Immunology and Rheumatology, King George's Medical University, Lucknow, India.
Objectives:
To assess the prevalence of endocrine dysfunction in patients with JIA and identify potential contributory factors for growth and sexual development.
Methods:
A prospective observational study was conducted between July 2021 to January 2023, recruited 107 children of JIA fulfilling the revised ILAR classification criteria with disease duration > 6 months, attending Rheumatology department in KGMU, India. Demographic, clinical (anthropometric), and serological (including hormonal) evaluations were assessed at baseline. Growth velocity was recorded after one year. Mann-Whitney U test, chi-square test, and Fisher's exact t test were applied during statistical analysis.
Results:
107 JIA patients were enrolled with a M: F ratio of 2.06:1 (72 boys & 35 girls) with ERA being the most frequent subtype (51.4%). Mean age was 13 (± 4) years with a disease duration of 33 (± 24) months. Mean glucocorticoid intake was 2.17 (± 5.41) mg/day at baseline. 20.6% children were stunted, 22.4% were underweight and 25.2% had low BMI. Stunted children were more likely to have early onset (p = 0.015) & high GH level (p = 0.013). Underweight children had longer disease (p = 0.047) and more damage (p = 0.006). Children with weight z < -2 have high GH and low IGFBP3. Low BMI group had high disease activity, damage, and poor quality of life & functional state (p = < 0.01). Delayed puberty was noticed only in 2.8% of children. Girls with low Estradiol level had longer exposure to corticosteroids. Slower growth velocity was observed in 22.4% of children without any identifiable cause.
Conclusion:
One third of JIA patients experience growth and pubertal disturbances, primarily due to altered GH-IGF1 axis.
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