Abstract
Objectives
Studies which report cystatin C’s (Cys-C) role in immunological disorders are increasing. However, data in the pediatric age group is limited. In this study, we aimed to evaluate the association between serum Cys-C levels and thyroid autoantibodies in children and adolescents diagnosed with euthyroid Hashimoto’s thyroiditis.
Methods
The patient group was included 50 participants aged between 3 and 18 years, and the control group included 50 healthy children matched for age, gender, and body mass index. Patients with hypothyroidism or taking any medication were not included in the study. Fasting glucose, liver enzymes, urea, creatinine, lipid profile, Cys-C, free thyroxine (fT4), free triiodothyronine (fT3), thyroid-stimulating hormone (TSH), thyroid peroxidase antibody (TPOAb), and thyroglobulin antibodies (TGAb) levels were recorded in all subjects.
Results
The mean age of control group was 13.5 ± 2.5 years, and the mean age of Hashimoto thyroiditis (HT) group was 14.2 ± 2.7 years, no statistically significant differences existed (p=0.205). Cys-C values were significantly higher in the HT group than in the control group (p=0.041). When all cases were evaluated, Cys-C levels were statistically positively correlated with fT3, TPOAb, and TGAb values (p<0.001, p=0.029, p=0.013 respectively).
Conclusions
Based on the results of our study, Cys-C levels in children and adolescents with euthyroid Hashimoto thyroiditis were statistically higher than their healthy peers. In conclusion, it can be said that Cys-C may be a factor in the etiopathogenesis of autoimmune thyroiditis, and even small changes in TSH values affect Cys-C levels.
Funding source: Manufacturer company “Roche Diagnostics, Mannheim, Germany” by means of Turkey distributor by supplying the cystatin C (CysC) test kit free of charge
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Research funding: This study was supported by manufacturer company “Roche Diagnostics, Mannheim, Germany” by means of Turkey distributor by supplying the cystatin C (CysC) test kit free of charge. The funding company played no role in the study design, the collection, analysis, and interpretation of data, in the writing or submission of the manuscript. 
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Author contributions: All authors have accepted responsibility for the entire content of this manuscript and approved its submission. 
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Competing interests: Authors state no conflict of interest. 
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Informed consent: Informed consent was obtained from all individuals included in this study. 
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Ethical approval: The local Institutional Review Board deemed the study exempt from review. 
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© 2022 Walter de Gruyter GmbH, Berlin/Boston
Articles in the same Issue
- Frontmatter
- Editorial
- Disorders of sex development – biologic, genetic, cultural, societal, and psychologic diversity of the human nature
- Review
- Diagnostic approach in 46, XY DSD: an endocrine society of bengal (ESB) consensus statement
- Original Articles
- Penile diameter during puberty in boys: a retrospective analysis of longitudinally obtained data
- Evaluation of bladder dysfunction in children and adolescents with type 1 diabetes mellitus by uroflowmetry
- All aspects of galactosemia: a single center experience
- The evolution of pituitary cysts in growth hormone-treated children
- Phototherapy-induced hypocalcemia and hypoparathyroidism in icteric term newborns
- Clinical and laboratory evaluation of children with congenital hyperinsulinism: a single center experience
- Does cystatin C have an immunomodulatory role in Hashimoto’s thyroiditis?
- Molecular genetic etiology by whole exome sequence analysis in cases with familial type 1 diabetes mellitus without HLA haplotype predisposition or incomplete predisposition
- Features of BSCL2 related congenital generalized lipodystrophy in China: long-term follow-up of three patients and literature review
- Case Reports
- Congenital adrenal hyperplasia with a CYP21A2 deletion overlapping the tenascin-X gene: an atypical presentation
- The smallest dislocated microduplication of Xq27.1 harboring SOX3 gene associated with XX male phenotype
- Rare PHEX intron variant causes complete and severe phenotype in a family with hypophosphatemic rickets: a case report
- Human chorionic gonadotrophin secreting adrenocortical neoplasm presenting with peripheral precocious puberty in an infant
- Atypical familial diabetes associated with a novel NEUROD1 nonsense variant
Articles in the same Issue
- Frontmatter
- Editorial
- Disorders of sex development – biologic, genetic, cultural, societal, and psychologic diversity of the human nature
- Review
- Diagnostic approach in 46, XY DSD: an endocrine society of bengal (ESB) consensus statement
- Original Articles
- Penile diameter during puberty in boys: a retrospective analysis of longitudinally obtained data
- Evaluation of bladder dysfunction in children and adolescents with type 1 diabetes mellitus by uroflowmetry
- All aspects of galactosemia: a single center experience
- The evolution of pituitary cysts in growth hormone-treated children
- Phototherapy-induced hypocalcemia and hypoparathyroidism in icteric term newborns
- Clinical and laboratory evaluation of children with congenital hyperinsulinism: a single center experience
- Does cystatin C have an immunomodulatory role in Hashimoto’s thyroiditis?
- Molecular genetic etiology by whole exome sequence analysis in cases with familial type 1 diabetes mellitus without HLA haplotype predisposition or incomplete predisposition
- Features of BSCL2 related congenital generalized lipodystrophy in China: long-term follow-up of three patients and literature review
- Case Reports
- Congenital adrenal hyperplasia with a CYP21A2 deletion overlapping the tenascin-X gene: an atypical presentation
- The smallest dislocated microduplication of Xq27.1 harboring SOX3 gene associated with XX male phenotype
- Rare PHEX intron variant causes complete and severe phenotype in a family with hypophosphatemic rickets: a case report
- Human chorionic gonadotrophin secreting adrenocortical neoplasm presenting with peripheral precocious puberty in an infant
- Atypical familial diabetes associated with a novel NEUROD1 nonsense variant