Inflammatory disorders of the parathyroid gland are poorly defined, and theories have always focused on diagnostic possibilities of probable autoimmune and non-infectious etiology.

Tuberculosis continues to be a major public health problem, including in developing and developed countries with high incidence of the disease.

Mycobacterial infection with chronic granulomatous inflammation could lead to mediators acting as paracrine regulators in germinal centers of the parathyroid chief cell mass, producing hyperplasia and increased glandular function.

Inflammatory disorders of the parathyroid gland are poorly defined. Only seven cases of granulomatous infection have been reported in the literature.

A 68-year-old woman presented with parathyroid hormone level at 277 pg/mL and calcium level at 10.8 mg/dL, considered as primary hyperparathyroidism. Parathyroidectomy was performed, normalizing analytical values.

Normal-size gland with chief cell hyperplasia, focal pseudofollicular changes, and presence of epithelioid granulomas with Langhans giant cells and caseous necrosis areas, and a positive PCR for M. tuberculosis complex was identified. Chronic granulomatous inflammation could provoke a cascade of immune system activation, resulting in hyperplasia with the consequent increase in parathyroid function, and therefore primary hyperparathyroidism.

In populations with a high incidence of tuberculosis, the coexistence of these pathologies must be kept in mind. This theory needs further biomolecular studies to be confirmed, but it provides a new perspective within the possible etiologies of hyperparathyroidism.

Hyperparathyroidism

Tuberculosis

Granulomatosis

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