Parathyroid Physiology and Primary Hyperparathyroidism

Habener, Joel F.; Potts, John T.

doi:10.1016/b978-0-12-068702-2.50007-6

Cited by 12 publications

(13 citation statements)

References 398 publications

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“…The possible role of the stimulating effect of PTH and PTH-RP in the physiological regulation of the human adrenal gland remains to be demonstrated. It is interesting that the secretagogue effect on aldosterone and cortisol of PTH and PTH-RP could, in part, explain the mild hypertension frequently associated with primary hyperparathyroidism [25]. Elevated serum concentrations of PTH and PTH-RP were observed in several patients bearing benign or malignant pheochromocytomas [26], and the association of secreting pheochromocytomas with adrenal tumors and idiopathic hypercorticism has been described [27].…”

Section: Discussionmentioning

confidence: 99%

Adrenal effects of teriparatide in the treatment of severe postmenopausal osteoporosis

et al. 2010

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Section: Discussionmentioning

confidence: 99%

Adrenal effects of teriparatide in the treatment of severe postmenopausal osteoporosis

et al. 2010

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“…Normally, plasma calcium levels are maintained within narrow limits by the parathyroid hormone (PTH) and 1,25-dihydroxyvitamin D. Hypocalcemia triggers PTH release, which (1) stimulates 1,25-dihydroxyvitamin D synthesis by the kidney and leads to increased intestinal calcium absorption, (2) directly stimulates osteoclastic bone resorption, and (3) increases calcium reabsorption in the distal tubules of the kidney. Hypercalcemia occurs when increased bone resorption or gut absorption of calcium leads to an influx of calcium into the extracellular fluid, which overwhelms the compensatory homeostatic mechanisms that maintain the serum calcium in the normal range.…”

Section: Pathogenesismentioning

confidence: 99%

“…Hypersecretion of PTH by the parathyroid glands may be caused by a single adenoma, hyperplasia of all parathyroid glands, or carcinoma. More than 80% of sporadic cases are due to single adenomas [2], which are possibly caused by x-irradiation of the head and neck. A history of radiation exposure has been identified in 15 to 37% of patients with primary hyperparathyroidism in three series, whereas 4 to 10% of x-irradiated persons are at risk of primary hyperparathyroidism [3].…”

Section: Underlying Causes Of Hypercalcemiamentioning

confidence: 99%

Hypercalcemia in the Critically Ill Patient

Reasner

Mundy

1986

J Intensive Care Med

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Hypercalcemia is now frequently recognized in hospitalized patients, including those who are critically ill. Hypercalcemia in critically ill patients may be life threatening or an indication of an underlying but unsuspected disease process. All of the common causes of hypercalcemia can occur in the critically ill patient and are reviewed here. As in the general patient population, the two most common causes are probably malignant disease and primary hyperparathyroidism. Hypercalcemia is now readily reversible in most patients, particularly when the underlying pathophysiologic mechanisms responsible are recognized, and it should be treated actively.In the initial evaluation of hypercalcemia in a critically ill patient, the physician must decide if the elevated serum calcium level is responsible for the patient's condition or is merely an incidental finding that poses no immediate danger. Patients in the former category are said to be in hypercalcemic crisis, and they require immediate treatment to lower their serum calcium levels, which are life threatening. In the intensive care setting, hypercalcemic crisis is most commonly associated with primary hyperparathyroidism or malignancy. With the advent of automated screening procedures, asymptomatic hypercalcemia is frequently seen in hospitalized patients as well as outpatients [1], and mild hypercalcemia is at least as common in intensive care patients as in other patient populations. In this article we review the pathogenesis and treatment of the various conditions associated with hypercalcemia, particularly those diseases that are more likely to be seen in a critically ill patient. PathogenesisNormally, plasma calcium levels are maintained within narrow limits by the parathyroid hormone (PTH) and 1,25-dihydroxyvitamin D. Hypocalcemia triggers PTH release, which (1) stimulates 1,25-dihydroxyvitamin D synthesis by the kidney and leads to increased intestinal calcium absorption, (2) directly stimulates osteoclastic bone resorption, and (3) increases calcium reabsorption in the distal tubules of the kidney. Hypercalcemia occurs when increased bone resorption or gut absorption of calcium leads to an influx of calcium into the extracellular fluid, which overwhelms the compensatory homeostatic mechanisms that maintain the serum calcium in the normal range. Hypercalcemia itself may cause vomiting and a decrease in the renal concentrating mechanism. This leads to dehydration and further increases in plasma calcium levels.

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“…Primary hyperparathyroidism is found in the general population with a prevalence that ranges from 0.03 to 0.1%. 3,4,86 The most common causes of primary hyperparathyroidism are a single adenoma (81 to 86%), hyperplasia (13 to 18%), or carcinoma (1 to 4%) of the parathyroid glands. Hypercalcemia in this condition results from the effects of both increased PTH and 1,25(OH) 2 D on intestine, bone, and kidney.…”

Section: Hyperparathyroidismmentioning

confidence: 99%

“…Hypercalcemia (10 to 20%) and hypercalciuria (30 to 50%) are commonly seen in patients with sarcoidosis. 86 Most hypercalcemic sarcoid patients have an abnormal chest radiograph; however, on rare occasions chest radiographic changes may be minimal or absent. Sarcoid patients usually have abnormal pulmonary function studies and demonstrate increased bone turnover and gastrointestinal absorption of Ca compared with controls.…”

Section: Granulomatous Diseasementioning

confidence: 99%