ДИФФЕРЕНЦИАЛЬНАЯ ДИАГНОСТИКА НОРМОКАЛЬЦИЕМИЧЕСКОГО ВАРИАНТА ГИПЕРПАРАТИРЕОЗА

Abstract

Objective: to describe a case of normocalcemic hyperparathyroidism. Materials and methods. A female patient aged 51 years sought medical advice for complaints of spinal column and bone pains, periodic dizziness, and hand numbness. The patient underwent clinical and biochemical blood tests, determination of the blood levels of calcium, phosphorus, parathyroid hormone, concentrations of total vitamin D, calciuria, electrocardiography, thyroid ultrasonography, and neck computed tomography. Results. Based on her complaints, examination evidence, evaluation of the clinical presentations of the disease, and objective and instrumental examination findings, the patient was diagnosed with left parathyroid adenoma and primary hyperparathyroidism; stage II hypertensive disease, grade I, a moderate risk; retinal angiopathy of both eyes; stage I dyscirculatory encephalopathy with liquor and venous dyscirculation and moderate vestibular ataxia; urolithiasis; kidney stones; and spondylosis mainly involving the lumbar spine. The diagnostic determinants for verifying the diagnosis were the results of neck computed tomography, namely: the signs of space-occupying lesion in the projection of the left parathyroid gland; the blood level of parathyroid hormone 118.6 pg/ml (normal value (N) 9.5–75.0 pg/ml); total vitamin D 21.64 nmol/l (N 75–250 nmol/l); and calcium 2.48 mmol/l (N 2.15–2.50 mmol/l). The history of urolithiasis, repeated lithotripsy, as well as spondylosis with lumboischalgia was an absolute indication for surgical treatment. Conclusion. The practical interest in this case is due to the complexity of diagnosing normocalcemic hyperparathyroidism after vitamin D deficiency. The early stages of primary hyperparathyroidism are asymptomatic and frequently give rise to irreversible renal complications, causing renal failure and, as a consequence, disability. This clinical case demonstrates the importance of routinely determining vitamin D concentrations, which in turn triggers parathyroid adenomas.