Primary hypoparathyroidism and non-functioning pituitary adenoma: An incidental coexistence? / Journal of the ASEAN Federation of Endocrine Societies

@#Primary hypoparathyroidism is caused by a group of heterogeneous conditions in which hypocalcemia and hyperphosphatemia occur as a result of deficient parathyroid hormone (PTH) secretion. The most common cause is surgical excision and damage to the parathyroid gland(s). Nonetheless, autoimmune endocrine disorder of primary hypothyroidism has been well-described in polyglandular autoimmune syndromes (PAS).1 Its association with pituitary lesion may be autoimmune lymphocytic hypophysitis as the cause for pituitary disorder. In this report, we encountered a patient with primary hypoparathyroidism who had a non-functioning pituitary tumour. It was confirmed as pituitary adenoma rather than lymphocytic hypophysitis from the histopathological examination. To our knowledge, this is the first reported case of non-functioning pituitary macroadenoma and primary hypoparathyroidism.

Hipoparatiroidismo primario asociado a convulsiones / Primary hypoparathyroidism associated with seizures

Resumen Se presenta el caso de un hombre de 31 años, sano hasta hace cuatro años, cuando inicia episodios de convulsiones tonicoclónicas generalizadas con episodios de tetania, espasmo carpo pedal, mialgias, pérdida progresiva de la agudeza visual bilateral y cambios del comportamiento con mutismo y apatía. Al examen físico con cataratas bilaterales subcapsulares posteriores grado III, hiperplasia gingival, con actitud perpleja, mutista, posturas catatoniformes, signo de Chvostek y espasmo carpo pedal positivos. El calcio inicial fue de 3.9 mg/dL (8.2-10.2), el fósforo de 10.1 mg/dL (2.5-4.5) y los niveles de parathormona de 0.2 pg/mL (15-68.3). La tomografía de cráneo mostró calcificaciones en los ganglios basales. Con estos hallazgos se realiza diagnóstico de hipoparatiroidismo primario idiopático, con marcada mejoría clínica y paraclínica con calcitriol y carbonato de calcio. Este caso invita a tener en mente la hipocalcemia como causa metabólica de convulsiones, las cuales son totalmente reversibles al mejorar la hipocalcemia. (Acta Med Colomb 2013; 38: 186-192).

Abstract We report the case of a 31 years old man healthy until four years ago, when he started to present episodes of generalized tonic-clonic seizures with episodes of tetany, carpal pedal spasm, myalgia, bilateral progressive loss of visual acuity and behavioral changes with mutism and apathy. Physical examination showed bilateral posterior subcapsular cataracts grade III, gingival hyperplasia, with perplexed attitude, mutism, catatonic postures and positive Chvostek sign and carpal pedal spasm. Initial calcium was 3.9 mg/dL (8.2-10.2), Phosphorus 10.1 mg/dL (2.5-4.5) and parathyroid hormone levels 0.2 pg/mL (15-68.3). The brain computed tomography showed basal ganglia calcifications. With these findings we made the diagnosis of primary idiopathic hypoparathyroidism, with marked clinical and paraclinical improvement with calcitriol and calcium carbonate. This case shows the importance of considering hypocalcemia as a metabolic cause of seizures, which are fully reversible by improving hypocalcemia. (Acta Med Colomb 2013; 38: 186-192).

Polyglandular Autoimmune Syndrome Type III with Primary Hypoparathyroidism

Polyglandular autoimmune syndrome is defined as multiple endocrine gland insufficiencies accompanied by autoimmune diseases of the endocrine and nonendocrine system. After Schmidt introduced a case of nontuberculosis adrenal gland dysfunction with thyroiditis in 1926, Neufeld defined polyglandular autoimmune syndrome by I, II, and III subtypes in 1980 by their presentation of occurrence age, heredity methods, relationship with human leukocyte antigen, and accompanying diseases. We report a case of a 32-year-old female with polyglandular autoimmune syndrome III accompanied by type 1 diabetes mellitus that was treated with insulin (36 units per day) for 11 years. She had insulin deficiency and Hashimoto thyroiditis as an autoimmune disorder. In addition, she had several features similar to Albright's hereditary osteodystrophy including short stature, truncal obesity, round face, short neck, low intelligence (full IQ 84), and decreased memory. Although Albright's hereditary osteodystrophy is morphological evidence of pseudohypoparathyroidism or pseudopseudohypoparathyroidism, she had primary hypoparathyroidism on laboratory results. Here, we report a case of polyglandular autoimmune syndrome III with type 1 diabetes mellitus, autoimmune thyroiditis, and primary hypoparathyroidism, accompanied by clinical features similar to Albright's hereditary osteodystrophy.