Tumor suppressor Parkin induces p53-mediated cell cycle arrest in human lung and colorectal cancer cells.

INTRODUCTION

Thyroid dysfunctions in the paediatric population can present with atypical and nonspecific systemic manifestations, making diagnosis particularly challenging. Viral infections, including severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), have increasingly been implicated in the onset or exacerbation of autoimmune thyroid diseases both in children and adults. This report describes a case of autoimmune thyroiditis with a transient hyperthyroid phase (hashitoxicosis) following prior exposure to SARS-CoV-2, highlighting the possible immune-mediated mechanisms of viral-induced endocrine autoimmunity that may extend to paediatric populations.

CASE REPORT: A previously healthy 13-year-old boy presented with fever, asthenia, bicytopenia, and hepatic cytolysis. Extensive infectious workup, including tests for hepatitis viruses, Epstein-Barr virus, cytomegalovirus, Leptospira spp., and Coxiella burnetii, was negative, except for rhinovirus detection by reverse transcription-polymerase chain reaction. Thyroid function testing revealed elevated thyroid-stimulating hormone (11.9 μIU/ml) and positive anti-thyroid antibodies (anti-thyroid peroxidase >1000 IU/ml, anti-thyroglobulin, 2108 IU/ml). Anti-SARS-CoV-2 neutralizing antibodies were markedly increased, consistent with previous infection. Thyroid ultrasound showed diffuse inhomogeneous echotexture with a pseudonodular pattern and increased vascularity, consistent with autoimmune thyroiditis. Corticosteroid therapy led to fever resolution and normalization of laboratory parameters, followed by a transient hyperthyroid phase (hashitoxicosis) and subsequent progression to subclinical hypothyroidism.

CONCLUSION

This case underscores the importance of thyroid function evaluation in paediatric or adult patients presenting with unexplained systemic inflammation or cytolysis following viral infections. The overlapping effects of SARS-CoV-2 and other respiratory viruses may unmask or accelerate autoimmune thyroid disorders.

LEARNING POINTS: Post-viral thyroid dysfunction, including autoimmune thyroiditis, may occur after severe acute respiratory syndrome coronavirus 2 infection even in children and should be considered in the differential diagnosis of prolonged febrile or inflammatory syndromes.Hashitoxicosis represents a transient destructive phase of autoimmune thyroiditis and can mimic subacute thyroiditis or other causes of thyrotoxicosis; ultrasound vascularity and antibody profile help differentiate them.Systemic inflammation with hepatic cytolysis or cytopenias may accompany autoimmune thyroid involvement, reflecting multi-organ immune activation rather than isolated endocrine disease.Thyroid function testing (thyroid-stimulating hormone, free thyroxine, antibodies) should be included in the evaluation of patients, children or adults, with unexplained post-viral symptoms or abnormal inflammatory profiles.