Thyroid and parathyroid pathologies frequently manifest as complex, comorbid clinical conditions; however, the precise pathogenetic intersection between autoimmune thyroiditis (AIT) and secondary hyperparathyroidism remains insufficiently characterised in current literature. This observational study assessed the structural and functional interrelationship between these two endocrine entities in a cohort of 112 patients. Biochemical marker analysis — encompassing thyroid-stimulating hormone (TSH), parathyroid hormone (PTH), and ionised calcium — in conjunction with high-resolution ultrasonography, revealed profound disturbances in calcium-phosphorus metabolism initiated by primary hypothyroidism. Patients with uncompensated AIT demonstrated a statistically significant PTH elevation averaging 66.7% above baseline control values, which correlated directly with reactive parathyroid gland hyperplasia (r = 0.55; p < 0.05). Conversely, the thyrotoxic phase of subacute thyroiditis was characterised by transient hypercalcaemia accompanied by concurrent physiological PTH suppression. Echographic assessment identified hyperplastic parathyroid changes in 22.6% of the hypothyroid cohort. These metabolic disturbances necessitate timely, targeted intervention — specifically optimised cholecalciferol and calcium supplementation — to prevent irreversible osteological complications, including diminished bone mineral density. Incorporating routine PTH and ionised calcium monitoring into the diagnostic protocol for patients presenting with TSH levels exceeding 10 mcIU/ml substantially enhances therapeutic outcomes. This study provides evidence for a critical algorithmic transition in clinical endocrinology, advancing from isolated thyroid management towards a comprehensive, multi-glandular metabolic rehabilitation strategy.

Autoimmune thyroiditis, parathyroid glands, secondary hyperparathyroidism

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