Chapter 047. Hypercalcemia and Hypocalcemia (Part 2)

Table 47-1 Causes of HypercalcemiaExcessive PTH productionPrimary hyperparathyroidism (adenoma, hyperplasia, rarely carcinoma)Tertiary hyperparathyroidism (long-term stimulation of PTH secretion in renal insufficiency)Ectopic PTH secretion (very rare)Inactivating mutations in the CaSR (FHH)Alterations in CaSR function (lithium therapy)Hypercalcemia of malignancyOverproduction of PTHrP (many solid tumors)Lytic skeletal metastases (breast, myeloma)Excessive 1,25(OH)2D productionGranulomatous diseases (sarcoidosis, tuberculosis, silicosis)LymphomasVitamin D intoxicationPrimary increase in bone resorptionHyperthyroidismImmobilizationExcessive calcium intakeMilk-alkali syndromeTotal parenteral nutritionOther causesEndocrine disorders (adrenal insufficiency, pheochromocytoma, VIPoma)Medications (thiazides, vitamin A, antiestrogens) ...
Nội dung trích xuất từ tài liệu:
Chapter 047. Hypercalcemia and Hypocalcemia (Part 2) Chapter 047. Hypercalcemia and Hypocalcemia (Part 2) Table 47-1 Causes of Hypercalcemia Excessive PTH production Primary hyperparathyroidism (adenoma, hyperplasia, rarely carcinoma) Tertiary hyperparathyroidism (long-term stimulation of PTH secretion inrenal insufficiency) Ectopic PTH secretion (very rare) Inactivating mutations in the CaSR (FHH) Alterations in CaSR function (lithium therapy)Hypercalcemia of malignancy Overproduction of PTHrP (many solid tumors) Lytic skeletal metastases (breast, myeloma)Excessive 1,25(OH)2D production Granulomatous diseases (sarcoidosis, tuberculosis, silicosis) Lymphomas Vitamin D intoxicationPrimary increase in bone resorption Hyperthyroidism Immobilization Excessive calcium intake Milk-alkali syndrome Total parenteral nutrition Other causes Endocrine disorders (adrenal insufficiency, pheochromocytoma, VIPoma) Medications (thiazides, vitamin A, antiestrogens) Note: CaSR, calcium sensor receptor; FHH, familial hypocalciurichypercalcemia; PTH, parathyroid hormone; PTHrP, PTH-related peptide. Clinical Manifestations Mild hypercalcemia (up to 11–11.5 mg/dL) is usually asymptomatic andrecognized only on routine calcium measurements. Some patients may complainof vague neuropsychiatric symptoms, including trouble concentrating, personalitychanges, or depression. Other presenting symptoms may include peptic ulcerdisease or nephrolithiasis, and fracture risk may be increased. More severehypercalcemia (>12–13 mg/dL), particularly if it develops acutely, may result inlethargy, stupor, or coma, as well as gastrointestinal symptoms (nausea, anorexia,constipation, or pancreatitis). Hypercalcemia decreases renal concentrating ability,which may cause polyuria and polydipsia. With long-standinghyperparathyroidism, patients may present with bone pain or pathologic fractures.Finally, hypercalcemia can result in significant electrocardiographic changes,including bradycardia, AV block, and short QT interval; changes in serum calciumcan be monitored by following the QT interval (Fig. 221-16). Diagnostic Approach The first step in the diagnostic evaluation of hyper- or hypocalcemia is toensure that the alteration in serum calcium levels is not due to abnormal albuminconcentrations. About 50% of total calcium is ionized, and the rest is boundprincipally to albumin. Although direct measurements of ionized calcium arepossible, they are easily influenced by collection methods and other artifacts; thus,it is generally preferable to measure total calcium and albumin to correct theserum calcium. When serum albumin concentrations are reduced, a correctedcalcium concentration is calculated by adding 0.2 mM (0.8 mg/dL) to the totalcalcium level for every decrement in serum albumin of 1.0 g/dL below thereference value of 4.1 g/dL for albumin, and conversely for elevations in serumalbumin.