Normal Paratiroid Dokusu ve Paratiroid Patolojisine Giriş

Yazarlar

Yazgı Köy
https://orcid.org/0000-0002-3413-0837

Özet

Paratiroid bezleri, kalsiyum homeostazında kritik rol oynayan endodermal kökenli organlardır. Normalde yetişkinlerde toplam ağırlığı 140-160 mg olan dört bez bulunur ve ana epitelyal bileşenlerini esas ile oksifil hücreler oluşturur. Gelişimsel anomaliler arasında sayıca fazlalık, ektopik doku, paratiromatozis, kistler ve DiGeorge sendromu gibi aplazi/hipoplazi durumları yer alır. Primer hiperparatiroidizm; kalsiyum ve PTH artışıyla karakterize olup en sık paratiroid adenomundan (%80-85), ardından hiperplazi (%10-15) ve nadiren karsinomdan (%1'den az) kaynaklanır. Ailesel geçişli sendromlar (MEN1, MEN2A, HPT-JT, FHH) ve lityum tedavisi bu patolojilerle ilişkilidir. Sekonder hiperparatiroidizm, hipokalsemiye adaptif bir yanıt iken; uzun sürdüğünde otonom nodül gelişimiyle tersiyer forma dönüşebilir. Otoimmün veya enfeksiyöz paratiroiditler ile cerrahi/konjenital nedenli hipoparatiroidizm de bezin işlevsel bozukluklarındandır. Cerrahi eksizyon sırasında patolojik doku tipinin doğrulanmasında intraoperatif frozen kesit ve sitolojik "touch imprint" incelemeleri hayati öneme sahiptir.

The parathyroid glands are endodermal organs playing a critical role in calcium homeostasis. Adults typically possess four glands with a combined weight of 140-160 mg, primarily composed of chief and oxyphil cells. Developmental anomalies include supernumerary glands, ectopic tissue, parathyromatosis, cysts, and aplasia/hypoplasia like DiGeorge syndrome. Primary hyperparathyroidism, characterized by elevated serum calcium and PTH, is most commonly caused by parathyroid adenoma (80-85%), followed by hyperplasia (10-15%) and rarely carcinoma (<1%). Familial syndromes (MEN1, MEN2A, HPT-JT, FHH) and lithium therapy are associated with these pathologies. Secondary hyperparathyroidism is an adaptive response to hypocalcemia, which can progress into autonomous tertiary hyperparathyroidism over time. Functional disorders also include autoimmune or infectious parathyroiditis and surgery- or congenital-induced hypoparathyroidism. Intraoperative frozen section evaluation and cytological touch imprint analysis are essential during surgery to accurately verify parathyroid tissue presence and identify specific lesions.

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