Parathyroid hormone functions

Barzel US. 1975. The effect of chronic ammonium chloride ingestion on parathyroid hormone function. Nephron 14 339-346. 

Pseudohypoparathyroidism is characterized by end-organ resistance to parathyroid hormone (98,108). This disease takes various forms, including Albright s hereditary osteodystrophy, which has unusual physical features and a generalized resistance to G-protein-linked hormones that function through cAMP as a second messenger. This defect is associated with a deficiency in the levels of the a-subunit of (109). Because this defect may be generalized, such patients also have olfactory dysfunction (110). 

Although it is being found that vitamin D metaboUtes play a role ia many different biological functions, metaboHsm primarily occurs to maintain the calcium homeostasis of the body. When calcium semm levels fall below the normal range, 1 a,25-dihydroxy-vitainin is made when calcium levels are at or above this level, 24,25-dihydroxycholecalciferol is made, and 1 a-hydroxylase activity is discontiaued. The calcium homeostasis mechanism iavolves a hypocalcemic stimulus, which iaduces the secretion of parathyroid hormone. This causes phosphate diuresis ia the kidney, which stimulates the 1 a-hydroxylase activity and causes the hydroxylation of 25-hydroxy-vitamin D to 1 a,25-dihydroxycholecalciferol. Parathyroid hormone and 1,25-dihydroxycholecalciferol act at the bone site cooperatively to stimulate calcium mobilization from the bone (see Hormones). Calcium blood levels are also iafluenced by the effects of the metaboUte on intestinal absorption and renal resorption. 

Systemic regulators of osteoblast, osteocyte and osteoclast functions, and therefore of bone metabolism. The major bone-seeking hormones are parathyroid hormone (PIH), 1,25-dihydroxy vitamin D3 (calcitriol) and the various ex hormones. 

Increases in parathyroid hormone (PTH) occur early as renal function begins to decline. The actions of PTH on bone... 

Secondary hyperparathyroidism Increased secretion of parathyroid hormone from the parathyroid glands caused by hyperphosphatemia, hypocalcemia, and vitamin D deficiency that result from decreased kidney function. It can lead to bone disease (renal osteodystrophy). 

Discuss functions and factors regulating release of the following hormones thyroid hormones, calcitonin, parathyroid hormone, catecholamines, aldosterone, cortisol, adrenal androgens, insulin, and glucagon... 

Human parathyroid hormone (hPTH) is an 84 amino acid polypeptide that functions as a primary regulator of calcium and phosphate metabolism in bones. It stimulates bone formation by osteoblasts, which display high-affinity cell surface receptors for the hormone. PTH also increases intestinal absorption of calcium. 

Parathyroid hormone (PTH) produces CNS effects in normal subjects and neuropsychiatric symptoms are frequently encountered in patients with primary hyperparathyroidism, where EEG changes resemble those described in acute renal failure. Circulating PTH is not removed by hemodialysis. In uremic patients both EEG changes and neuropsychiatric symptoms are improved by either parathyroidectomy or medical suppression of PTH. The mechanism whereby PTH causes disturbances of CNS function is not well understood, but it has been suggested that increased PTH might facilitate the entry of Ca2+ into the cell resulting in cell death. 

Calcium-phosphorus balance is mediated through a complex interplay of hormones and their effects on bone, GI tract, kidney, and parathyroid gland. As kidney disease progresses, renal activation of vitamin D is impaired, which reduces gut absorption of calcium. Low blood calcium concentration stimulates secretion of parathyroid hormone (PTH). As renal function declines, serum calcium balance can be maintained only at the expense of increased bone resorption, ultimately resulting in renal osteodystrophy (ROD) (Fig. 76-7). 

The parathyroid hormone content of blood has not been studied sufficiently to yield any data with regard to variation. The functioning of the glands is so closely related to other factors which regulate calcium and phosphorus metabolism that it is impossible to assign differences in these areas to variation in parathyroid function. The variation of the calcium (and phosphorus) in the blood has been noted (p. 55), and this variation, of course, may be due in a substantial degree to differences in parathyroid functioning. 

Keywords FoUide-stimulating hormone gain of function gonadotropin-releasing hormone (GnRHR) G protein-coupled receptor loss of function luteinizing hormone melanocortin monogenic disease parathyroid hormone rhodopsin thyrotropin. 

Estrogens have a number of important metabolic and cardiovascular effects. They seem to be partially responsible for maintenance of the normal structure and function of the skin and blood vessels in women. Estrogens also decrease the rate of resorption of bone by promoting the apoptosis of osteoclasts and by antagonizing the osteoclastogenic and pro-osteoclastic effects of parathyroid hormone and interleukin-... 

Such observations have led to the idea that depression may be a pseudomonoamine deficiency due to a deficiency in signal transduction from the monoamine neurotransmitter to its postsynaptic neuron in the presence of normal amounts of neurotransmitter and receptor. If there is a deficiency in the molecular events that cascade from receptor occupancy by neurotransmitter, it could lead to a deficient cellular response and thus be a form of pseudomonoamine deficiency (i.e., the receptor and the neurotransmitter are normal, but the transduction of the signal from neurotransmitter to its receptor is somehow flawed). Such a deficiency in molecular functioning has been described for certain endocrine diseases such as hypoparathyroidism (parathyroid hormone deficiency), pseudohypoparathyroidism (parathyroid receptors deficient but parathyroid hormone levels normal), and pseudo-pseudohypoparathyroidism (signal transduction deficiency leading to hypoparathyroid clinical state despite normal levels of hormone and receptor). 

Uptake of Ca2+ from the intestine is stimulated by vitamin D.447 Vitamin D3 is converted to the 25-hydroxy derivative in the liver (equation 11) by a two component mixed-function hydroxylase.448 The metabolically active 1,25-dihydroxy form is synthesized by further hydroxylation in the kidney. This latter stage involves the renal 25-hydroxyvitamin D3- 1-hydroxylase in a reaction which is controlled by Ca2+, parathyroid hormone and phosphate. This renal hydroxylase contains a flavoprotein, an iron-sulfur protein (with an Fe2S2 cluster) and cytochrome P-450.447... 

Chorev, M. 2002. Parathyroid hormone 1 receptor insights into structure and function. Receptors Channels 8 219-242. Fukugawa, M. and K. Kurokawa. 2002. Calcium homeostasis and imbalance. Nephron 92 (Suppl. 1) 41—45. 

According to Jonxis and Huisman (J6, J9, J12), hyperamino aciduria may be observed among the other members of the family of a patient with common rachitis and may sometimes (but not always) be corrected by vitamin D administration. There are presumably different grades of hereditary vitamin sensitiveness of the renal tubular function to vitamin D. The regulation does not take place through the mediation of the parathyroid hormone. 

---