In PHP type 1, cyclic AMP is not synthesized in response to PTH, because of a deficiency of the coupling protein Gαs. As a result, little cyclic AMP is produced…

PTH produces its effects on target cells by stimulating the synthesis of second messengers, most notably cyclic adenosine monophosphate (cyclic AMP) by the enzyme adenylate cyclase (see Plate 3-9). This…

PTH activates its target cells by increasing the activity of adenylyl cyclase, thereby increasing cellular levels of cyclic AMP. Cyclic AMP activates a cascade of proteins that produces the physiologic…

More typically, patients with hypocalcemia may be asymptomatic or experience milder symptoms such as muscle cramps and paresthesias. The paresthesias, described as “pins and needles” sensations in the hands, feet,…

Despite the hypocalcemia, soft tissue calcifications may develop in patients with hypoparathyroidism when elevated serum phosphorus levels lead to an elevated (i.e., >70 mg2/dL2) calcium × phosphorus solubility product. A…

Deletions within two nonoverlapping regions of 10p can lead to a phenotype similar to DiGeorge sequence, namely, the hypoparathyroidism, sensorineural deafness, and renal dysplasia (HDR) syndrome. Unlike patients with the…

The serum level of PTH distinguishes primary hyperparathyroidism from other disorders causing hypercalcemia, because it is the only hypercalcemic disorder resulting from excessive production of PTH. Serum phosphate levels are…

Hyperparathyroidism causes hypercalcemia as a result of increased resorption of bone, reabsorption of calcium in the renal tubule, and absorption of calcium from the gut. PTH also decreases reabsorption of…

In severe hypercalcemia, precipitates can occur in the renal interstitium and incite an inflammatory reaction (nephrocalcinosis). By the time interstitial calcium deposits are visible on radiography, renal function is already…