Parathyroid hormone 294 Subject

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. 

Typical changes in bone mineral density with time after the onset of menopause, with and without treatment. In the untreated condition, bone is lost during aging in both men and women. Fluoride, strontium (Sr2+), and parathyroid hormone (PTH) promote new bone formation and can increase bone mineral density in subjects who respond to it throughout the period of treatment, although PTH also activates bone resorption. In contrast, estrogen, calcitonin, and bisphosphonates block bone resorption. This leads to a transient increase in bone mineral density because bone formation is not initially decreased. However, with time, both bone formation and bone resorption are decreased with these pure antiresorptive agents, and bone mineral density reaches a new plateau. 

Prank, K., Harms, H., Dammig, M., Brabant, G., Mitschke, F., and Hesch, R., Is there low-dimensional chaos in pulsatile secretion of parathyroid hormone in normal human subjects American Journal of Physiology Endocrinology and Matabolism, Vol. 266, No. 4, 1994, pp. E653-E658. 

In lithium treated subjects, there is no evidence of reduced bone mass at any of the measured sites in relation to that of control subjects. The mechanism responsible for the maintenance of bone mass despite biochemical evidence of hyperparathyroidism is not clear [45]. We suspect that it is due to renal calcium retention. Indeed, in dogs lithium administration for only 3 days causes a striking decrease in urinary calcium excretion which is independent of the presence of parathyroid hormone and occurs despite the concurrent development of metabolic acidosis [Batlle D, Arruda J, and Kurtzman NA 1981 unpublished observations]. 

Figure 49-15 Midregion (A) and intact (B) PTH in normal subjects and patients with primary hyperparathyroidism, hypercalcemia associated with malignancy, and hypoparathyroidism. (From Endres DB, Viifanueva R, Sharp CF jr. Singer FR. /Vleasurement of parathyroid hormone. Endocrinol Metab Clin North Am 1989 18 611-29.)...

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.)...

The capacity of the tubules to reabsorb or secrete a substance is subject to several variables. Thus, the expansion of extracellular fluid volume inhibits the reabsorption of sodium, bicarbonate, and phosphate and depresses the secretion of PAH. The tubular reabsorption of phosphate is inhibited by increased circulating levels of parathyroid hormone. The reabsorption of phosphate and bicarbonate by the tubules is directly related to the glomerular filtration rate. The reabsorption of bicarbonate by the tubule is also directly related to the pC02 level. 

As discussed above, lithium inhibits the synthesis of thyroid hormone and its release from the thyroid, and stimulates the formation of antithyroid antibodies in susceptible subjects [112]. Lithium-induced hypothyroidism responds to thyroxine therapy. Lithium can increase the secretion of parathyroid hormone and therefore can increase serum calcium concentrations, but symptomatic hypercalcemia is rare (see hormonal effects). 

A wide range of plasma phosphorus concentration has been observed by other workers in primary hyperparathyroidism (C7) and explained in terms of diet and renal excretion. Unlike the calcium concentration, which is normally very constant regardless of dietary intake and urinary excretion, the concentration of inorganic phosphate in plasma is the resultant of the rate of phosphorus absorption from the gut and protein catabolism, on the one hand, and of renal excretion, on the other. Although the parathyroid hormone promotes phosphorus excretion, this is only one of the factors governing plasma phosphate concentration. Plasma phosphate in cases of hyperparathyroidism on a relatively high phosphorus intake may therefore not be distinguishable from that in normal subjects on a lower intake. 

The consumption of a diet sufficient in phosphorus, in the form of phosphate salts or organophosphate molecules, is critical for the support of human metabolic functions. Too much phosphorus, in relation to too little dietary calcium, may contribute to bone loss, and too little phosphorus along with too little dietary calcium may not adequately maintain bone mass, especially in the elderly. Therefore, under normal dietary conditions, dietary phosphorus is used for numerous functions without any concern it is only when too much or too little phosphorus is ingested that skeletal problems may arise. Certainly, elderly subjects need to consume sufficient amounts of phosphorus, like calcium, to maintain bone mass and density, but too much phosphorus may contribute to inappropriate elevations of parathyroid hormone (PTH) and bone loss. It is not clear where most elderly subjects fall along this continuum of intake patterns. This article discusses the mechanisms by which phosphate ions impact on calcium and also on bone tissue. 

Both hypo- and hyperparathyroidism have been observed in human beings, and, if the principle of genetic gradients (p. 13) is valid, various intermediate levels of hormone activity will be found in the general population. Although the data on the subject, with the exception of that concerning anatomy, are not definitive, there would seem to be little doubt as to the existence of several-fold variation in the parathyroid activities of "normal" individuals. 

---