Parathyroid hyperplasia low mag.<unk>  is almost always related to end stage kidney disease and a secondary hyperparathyroidism. Physiological changes due to the kidney damage adversely affect feedback loops that control secretion of parathyroid hormone. Renal management of phosphate is impaired in secondary hyperparathyroidism which results in hyperphosphatemia. Primary hyperplasia of the parathyroid gland, results from both hypocalcaemia and increased phosphate levels by decreasing expression of calcium sensing receptors and vitamin D receptors at the parathyroid gland. These decreases in receptor expression lead to hyperfunctioning of the parathyroid. Hyperfunction of the parathyroid gland is thought to exacerbate primary hyperplasia which evolves further to a secondary more aggressive hyperplasia. Histologically, these hyperplasic glands can be either diffuse or nodular. Primary hyperplasia, usually resulting in diffuse polyclonal growth is manly related to reversible secondary hyperparathyroidism. Secondary hyperplasia of the parathyroid gland is more often a nodular, monoclonal growth that sustains secondary hyperparathyroidism and is the catalyst in the progression to<unk> . Nodular hyperplastic glands in<unk>  are distinctly larger in both absolute size and weight up to 20-40-fold increases have been reported. Parathyroid hyperplasia medium mag. Parathyroid glands are normally composed of chief cells, adipocytes and scattered oxyphil cells. Chief cells are thought to be responsible for the production, storage and secretion of parathyroid hormone. These cells appear light and dark with a prominent Golgi body and endoplasmic reticulum. In electron micrographs, secretory vesicles can be seen in and around the Golgi and at the cell membrane. These cells also contain prominent cytoplasmic adipose. Upon onset of hyperplasia these cells are described as having a nodular pattern with enlargement of protein synthesis machinery such as the endoplasmic reticulum and Golgi. Increased secretory vesicles are seen and decreased intercellular fat is characteristic. Oxyphil cells also appear hyperplasic however, these cells are much less prominent. Parathyroid hyperplasia high mag. Biochemically, there are changes in function between normal and nodular hyperplastic parathyroid glands. These changes involve proto-oncogene expression and activation of proliferative pathways while inactivating apoptotic pathways. In nodular parathyroid tissue increased expression of TGF-a, a growth factor, and EGFR, its receptor, results in aggressive proliferation and further downregulation of vitamin D receptors, which act to suppress hormone secretions. Furthermore, the proliferative marker, Ki67 is seen to be highly expressed in the secondary nodular hyperplastic state. Tumour suppressor genes have also been highlighted as being silenced or degraded in nodular hyperplastic parathyroid tissue. One such gene, p53, has been shown to regulate multiple tumour suppressor pathways and in tumorigenesis can be degraded by b-catenin. This pathway, in some aspect, is mediated by CACYBP, which is highly expressed in nodular parathyroid hyperplasia.
Tertiary hyperparathyroidism
Primary hyperparathyroidism
Secondary hyperparathyroidism
Familial hypocalciuric hypercalcemia
Normophosphatemic familial tumoral calcinosis
Parathyroid adenoma
Pseudohypoparathyroidism
Pseudopseudohypoparathyroidism