Читать книгу Parathyroid Disorders - Группа авторов - Страница 30

Asymptomatic PHPT is caused by inappropriate secretion or oversecretion of parathyroid hormone (PTH) [10]. Solitary parathyroid adenomas cause PHPT 80–85% of the time, whereas multigland hyperplasia is found in 15–20% of cases, and parathyroid cancer is noted in less than 0.5% of cases [11]. As with other endocrine tumors, pathologic diagnosis of parathyroid carcinoma is difficult and is usually based on the examination of local tissue, presence of vascular invasion, or detection of metastatic disease [12]. Most single adenomas are due to sporadic disease, whereas 4-gland hyperplasia implies a familial disorder, most commonly MEN1 or 2A, or familial isolated PHPT [13].

The causes of asymptomatic sporadic PHPT are not well understood. It is presumed that causes of asymptomatic PHPT are similar to those causing symptomatic PHPT. Previous exposure to neck irradiation contributes in a minority of cases, typically 20–30 years after such exposure [14]. More commonly, adenomas represent clonal expansion of a single or several abnormal cells, attributable to a genetic abnormality that results in either stimulation of cell proliferation or loss of inhibition of cell proliferation [15].

Normocalcemic, or “incipient,” hyperparathyroidism occurs when serum calcium is normal but PTH is increased, without evidence of vitamin D deficiency, hypercalciuria, or other causes of hyperparathyroidism [16]. This condition requires documentation of normal serum 25-hydroxyvitamin D and 24-h urine calcium levels to rule out other causes of physiological hyperparathyroidism. It may be due to an early stage of evolving PHPT or very mild PHPT, with more complications than expected for asymptomatic PHPT [17].

Most current patients with PHPT in Europe and the USA are asymptomatic, typically with serum calcium levels <1.0 mg/dL above the upper end of the normal range [18]. Most of these cases lack classical skeletal features, including osteitis fibrosa cystica or osteoporosis. Bone disease is currently diagnosed in <5% of patients with PHPT [19, 20]. Bone density of the 1/3 distal radius increases the detection rate of osteoporosis in patients with PHPT by 11% [21]. Renal disease, including nephrocalcinosis, calcium-containing nephrolithiasis, or renal insufficiency, may be found in up to 20% of patients [22]. Hypercalciuria is reported in up to 30% of patients [23].

Asymptomatic patients do not complain of mild fatigue, weakness, or subtle cognitive impairment [24]. Other classical abnormalities of PHPT, such as gout or pseudogout, anemia, band keratopathy, or loosened teeth due to lamina densa resorption, are rarely seen in patients with asymptomatic PHPT.