van Vonderen I K, Kooistra H S, Peeters M E, Rijnberk A, van den Ingh T S G A M
Department of Clinical Sciences of Companion Animals, Faculty of Veterianry Medicine, Utrecht University, P. O. Box 80.154, Yalelaan 8, 3508 TD, Utrecht, The Netherlands.
J Comp Pathol. 2003 Jul;129(1):61-9. doi: 10.1016/s0021-9975(03)00004-5.
In primary hyperparathyroidism, calcium homeostasis is disrupted by excessive synthesis and secretion of parathyroid hormone (PTH), which is usually caused by a solitary adenoma, or less often by nodular hyperplasia or carcinoma of the parathyroid glands. So far, the distinction between these forms of primary hyperparathyroidism has been made by histological examination. In this report clinical and histological findings, including PTH immunohistochemistry, are described in five dogs with primary hyperparathyroidism, three dogs with secondary hyperparathyroidism due to chronic renal failure, and eight control dogs. In the dogs with primary hyperparathyroidism, nodular adenomatous hyperplasia was found in two animals and parathyroid adenoma in three. The dogs with chronic renal failure had diffuse parathyroid gland hyperplasia. The parathyroid glands of the control dogs and the inactive cells surrounding the hyperplastic nodules showed slight to moderate, localized, paranuclear PTH immunolabelling. In the primary nodular and secondary diffuse hyperplasia, all parathyroid cells had a diffuse cytoplasmic PTH labelling pattern, sometimes in combination with localized paranuclear labelling. In parathyroid adenoma, areas with either paranuclear labelling or diffuse cytoplasmic labelling were observed. As both parathyroid adenoma and primary nodular parathyroid gland hyperplasia have characteristics of intrinsic autonomy (i.e., suppression of the remaining endocrine tissue), there would seem to be no functional difference between the two abnormalities. It is argued that primary (multi)nodular hyperplasia is a multiple form of parathyroid adenoma.
在原发性甲状旁腺功能亢进症中，甲状旁腺激素（PTH）的过度合成和分泌会破坏钙稳态，这通常由单个腺瘤引起，较少情况下由甲状旁腺的结节性增生或癌引起。到目前为止，这些原发性甲状旁腺功能亢进症形式之间的区别是通过组织学检查来确定的。在本报告中，描述了5只患有原发性甲状旁腺功能亢进症的犬、3只因慢性肾衰竭导致继发性甲状旁腺功能亢进症的犬以及8只对照犬的临床和组织学发现，包括PTH免疫组化。在患有原发性甲状旁腺功能亢进症的犬中，2只动物发现有结节性腺瘤样增生，3只发现有甲状旁腺腺瘤。患有慢性肾衰竭的犬有弥漫性甲状旁腺增生。对照犬的甲状旁腺以及增生结节周围的静止细胞显示出轻微至中度、局部的、核旁PTH免疫标记。在原发性结节性和继发性弥漫性增生中，所有甲状旁腺细胞都有弥漫性细胞质PTH标记模式，有时还伴有局部核旁标记。在甲状旁腺腺瘤中，观察到有核旁标记或弥漫性细胞质标记的区域。由于甲状旁腺腺瘤和原发性结节性甲状旁腺增生都具有内在自主性的特征（即对其余内分泌组织的抑制），这两种异常之间似乎没有功能差异。有人认为原发性（多）结节性增生是甲状旁腺腺瘤的一种多形式。
