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DOI 10.1007/s12022-018-9524-9

Медицинская библиотека · Endocrine pathology · 2018

Clinical Impact of p27Kip1 and CaSR Expression on Primary Hyperparathyroidism.

Sengul Aycicek Gozde, Aydogan Berna Imge, Sahin Mustafa, Cansız Ersoz Cevriye, Sak Serpil Dizbay, Baskal Nilgun

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Аннотация

We aimed to investigate the expressions of p27 kinase inhibitory protein 1 (p27Kip1) and calcium sensing receptor (CaSR) in adenomas and normal parathyroid tissue and to evaluate the relationship of these molecules with clinical and biochemical parameters in primary hyperparathyroidism (PHPT). Fifty-one patients with histopathologically confirmed parathyroid adenomas and 20 patients with normal parathyroid glands (which were removed incidentally during thyroid resection) were included. Immunohistochemical stainings of CaSR and p27Kip1 were performed in surgical specimens. Clinical features, biochemical parameters, and BMD measurements of patients with PHPT were evaluated retrospectively. Expressions of p27Kip1 and CaSR were decreased in parathyroid adenomas, compared to normal glands (p < 0.05). High intensity of CaSR staining (3+) was more frequent in normal parathyroid tissue (75%) than adenomas (12%) (p < 0.01). Hypertension was not observed in patients with high staining intensity of CaSR (p = 0.032). There was a negative association between CaSR expression and body mass index (BMI) (p = 0.027, r = - 0.313). There was no significant relationship between p27Kip1 and CaSR expressions, serum calcium, plasma parathormone, 25-hydroxy vitamin D levels, and bone density (p > 0.05). The expressions of p27Kip1 and CaSR were decreased in PHPT patients. This reduction may play an important role in the pathogenesis of PHPT. However, neither p27Kip1 nor CaSR expression was found to be useful in predicting prognosis or severity of disease.

Для цитирования: Sengul Aycicek Gozde, Aydogan Berna Imge, Sahin Mustafa, Cansız Ersoz Cevriye, Sak Serpil Dizbay, Baskal Nilgun. Clinical Impact of p27Kip1 and CaSR Expression on Primary Hyperparathyroidism.. Endocrine pathology. 2018. DOI: 10.1007/s12022-018-9524-9.

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