Parathyroid disorders

Other Inflammatory Muscle Disorders Endocrine Myopathies Thyroid Disorders Adrenal Disorders Pituitary Disorders Parathyroid Disorders Pancreatic Disorders Drug-Induced and Toxic Myopathies Management of Muscle Disease... 

Endocrine disorders Hypothyroidism Parathyroid disorders Adrenal disorders Therapeutic dose replacement or adjustment... 

Endres DB. Hypercalcemia and parathyroid disorders. Curr Opin Rheumatol 1992 4 383-8. 

R. S. Flueck, J. A. "The Interrelationships Between Vitamin D and Parathyroid Hormone in Disorders of Mineral Metabolism in Man" (Proceedings of 2nd Vitamin D Symposium), Weisbaden, West Germany, Oct., 1974, In Press. 

The suppression of PTH secretion from the parathyroid gland that accompanies the constitutive activation of the CASR makes the disorder difficult to recognize and treat. In some cases, it has been reported that seizures can be intractable. The abnormal set point of calcium regulation complicates treatment with calcitriol and dietary calcium supplementation because the CASR expressed in the kidney controls calcium excretion. The constitutively activated CASR mutant induces hypercalciuria, which may compound the hypocalcemia (42). 

Endocrine disorders Adrenal Addison s disease and Cushing s disease Diabetes mellitus Parathyroid hyper-/hypo-Reproductive ovary/testicle failure Thyroid hyper-/hypo-... 

Renal osteodystrophy is a complex disorder with several pathogenic factors. Histological evidence of bone disease is common in early renal failure and deficits in calcitriol synthesis seems to be an important factor in the pathogenesis of secondary hyperparathyroidism in early CRF. The most common component is osteitis fibrosa manifested as subperiosteal resorption of bone. This is due to decreased excretion as well as increased secretion of parathyroid hormone. In CRF small increments of serum phosphorus cause small decreases in serum calcium. 

The controlled deposition of calcium salts is essential for the development of extracellular structures such as bones, teeth and shell. The process begins with uptake of calcium in the intestine, followed by transport, and then the laying down of structures. A complex system is necessary for the control of all these stages, and involves, for example, vitamin D, parathyroid hormone, calcium-binding proteins for transport, and a range of other proteins and polysaccharides for ordered deposition. Precipitation of calcium salts in the incorrect location can result in stone formation, osteoarthritis, cataracts and arterial disorders. 

CaR expression is greatest in the parathyroid glands, calcitonin-secreting C-cells of the thyroid gland, and kidney, but the CaR is also found in the two other key organs that participate in calcium homeostasis gut and bone (Brown and MacLeod, 2001). This review will focus on the structure and function of the CaR, its role in normal physiology and in various disorders of Ca -sensing, and the development of CaR-based therapeutics. 

Not all calcium present in the diet is absorbed by the small intestine and mechanisms are present to ensure only amounts appropriate to body needs are absorbed. These processes are complex and involve the interaction of special transport protein, vitamin D and parathormone. Thus, abnormalities of calcium metabolism may result from many different disease processes. Diseases affecting the bowel may prevent normal absorption, diseases of the parathyroid gland may result in inappropriate levels of parathormone for calcium requirement and a nutritionally inadequate diet may cause vitamin D deficiency with consequent disordered calcium absorption. 

Calcitonin is a 32-amino-acid polypeptide hormone that was hrst purihed in 1962 by Copp and Cheney (121). It was originally thought as a product from parathyroid glands, but later it was discovered to be made by the C cells of the thyroid gland. Calcitonin participates in calcium and phosphorus metabolism, lowers plasma calcium and phosphate levels, and it has been used as a drug for bone and mineral disorders for a long time. 

Saxe AW, Gibson G, Silvera E. Effects of long-term lithium infusion on normal parathyroid. Surgery 1995 117 577-580. McHenry CR, Lee K Lithium therapy and disorders of the parathyroid glands. Endocr Pract 2 103-109,1996. 

Determination of PTH is useful in the differential diagnosis of both hypercalcemia and hypocalcemia for assessing parathyroid function in renal failure and for evaluating parathyroid function in bone and mineral disorders (see Calcium, Clinical Significance, Hypocalcemia, and Hypercalcemia Metabohc Bone Diseases and Interpretation of PTH Results). 

Figure 49-22 PTHrP in normal subjects and patients with malignancies and other disorders. Hatched area indicates the normal reference interval. (Adapted from Pandian AIR, Morgan CH, Carlton E, Segre GV. Modified /mmunorod/ometr/c ossoy of parathyroid hormone-related protein clinical app/icatfon in the differential diagnosis of hypercalcemia. Clin Chem 1992 38 282 SS.)...

PHP, a rare heterogeneous genetic disorder characterized by end-organ resistance to parathyroid hormone, is discussed further in Chapter 8. Heterozygous inactivating GNAS mutations lead to PHP type la (PHP-Ia) when maternally inherited, or pseudopseudohypoparathyroidism (PPHP), if paternally derived [48]. To date, only variants of the Ga- and Gp-subunits of the G protein have been implicated in human disease—no Gy-subunit disruptions have been identified. 

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