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This page has moved. Click here to view. HyperparathyroidismPrimary Hyperparathyroidism. Primary hyperparathyroidism is characterized by excessive production of PTH and hypercalcemia.27,2~ In 80 percent of cases, it is caused by a benign solitary parathyroid adenoma. Surgical reports suggest multiple adenomas are present in 2 to 4 percent of cases. About 15 percent of patients have diffuse hyperplasia of all four parathyroid glands, a condition that is frequently hereditary. Parathyroid carcinoma accounts for less than hyperparathyroidism, hypercalcemia, high calcium, parathyroid Hyperparathyroidism is seen two to four times more commonly in women than men, and its incidence increases with age; 60 to 65 percent of cases occur in Secondary Hyperparathyroidism. Secondary hyperparathyroidism occurs as a result of low serum calcium levels. Most cases have hyperplasia in all four parathyroid glands. It is most often seen in chronic renal disease, but can also occur with disorders of vitamin D metabolism The physician should consider the many causes of hypercalcemia (Table I0). More than two-thirds of patients with hyperparathyroidism are asymptomatic; a biochemical panel will reveal elevated serum calcium levels. The remaining patients present with complaints of nonspecific symptoms ranging from fatigue, mild "aches and pains," constipation, Manifestations of Parathyroid Adenomas. Calcium oxalate or phosphate stones may develop. Polydipsia and polyuria are often reported and are secondary to hypercalcemia. Eventually, renal failure and nephrocalcinosis may result. Although mild hypercalcemia is often asymptomatic, more severe cases can cause nausea, vomiting, thirst, and anorexia. A history of peptic ulcer disease or hypertension is not uncommon, and there may be accompanying constipation, anemia, and weight loss. Some patients present with a neuromuscular disorder, such as paresthesias, Evaluation and Diagnosis. The hallmark of primary hyperparathyroidism is hypercalcemia (a corrected serum calcium level greater than 10.5 mg per dL). Serum PTH should be determined by measuring intact PTH using the newer two-site immunoassay. An elevated PTH level in the presence of hypercalcemia confirms the diagnosis of primary Table 10 Causes of Hypercalcemia Approximate Cause Disease incidence Endocrine Hyperparathyroidism, 46 percent disorders hyperthyroidism, Addison's disease, pheochromocytoma, hypothyroidism, vipoma Cancer Breast, metastatic, parathyroid 45 percent hormone-related peptide secreting (lung, kidney cancer), multiple myeloma, leukemias, others Increased Milk alkali syndrome, vitamin A 4 percent intake or D intoxication, drugs (e.g., thiazides, lithium, aluminum) Granulomatous Sarcoidosis, tuberculosis, etc 3 percent diseases Benign familial Paget's disease, immobilization, 2 percent hypocalciuric idiopathic hypercalcemia of hypercalcemia, infancy, aluminum intoxication, others dysproteinemias, rhabdomyolysis, measurement artifact A benign autosomal dominant disorder known as familial hypocalciuric hypercalcemia also deserves mention. This disorder is characterized by hypocalciuria (usually greater than 50 mg per 24 hours), hypermagnesemia, and normal Treatment. Hospitalization is necessary when hypercalcemia is symptomatic and severe (generally defined as a serum level greater than 14 mg per dL). Vigorous hydration and correction of underlying hyponatremia and hypokalemia should be undertaken. Restoration of blood volume with saline followed by administration of a loop diuretic, such as furosemide, causes increased calcium excretion with a resulting decline in serum calcium levels. In addition, any milk A National Institutes of Health Consensus Development Conference on Diagnosis and Management of Asymptomatic Primary Hyperparathyroidism addressed the diagnosis and management of hyperparathyroidism (Table i 3J.3E Some experts think that surgical management of primary hyperparathyroidism is the only viable treatment option. In Management of Hypercalcemia Therapy Drug regimen Comments Hydration Normal saline, 150 to 300 Mainstay of acute treatment to increase mL per hour calcium excretion Base hydration rate on patient's fluid and cardiovascular status: Diuresis Furosemide (Lasix®), Use only with adequate hydration 40 to 80 mg intravenously Monitor electrolytes every one to four hours Calcitonin-salmon 4 IU per kg intramuscularly or Acute, use only for rapid reduction while (Calcimar®, Osteocalcin®, subcutaneously every 12 hours awaiting response to other therapies Salmonine®) or Rapid onset, but degree of calcium (Miacalcin®) 2 to 18 IU per kg infusion reduction is unpredictable and often small Calcitonin-human intravenously every 12 hours (Cibacalcin®) Plicamycin 25 mcg per ~ infusion Use a~er hydration and diuresis [mithramycin] intravenously over three to Peak drop in calcium levels seen within (Mithracin®) six hours in saline solution 48 to 96 hours or over three to four days in dextrose solution Glucocorticoids 40 to 80 mg per day Not for acute situations Prednisone or Most effective in multiple myeloma, Hydrocoisone 200 to 300 mg per day sarcoidosis, leukemia/lymphoma, for three to five days hype~imminosis A and D Not effective in primary hyperparathyroidism Bisphosphonams 7.5 mg per ~ per day Inhibits osteoclast function Etidronate (Didronel®) intravenously over threeHighly effective in controlling hypercalcemia hours associated with malignancy Pamidronate (Aredia®) 60- to 90-mg infusion intravenously over 24 hours Gallium nitrate 200 mg per m~ per day Indicated for symptomatic hypercalcemia of (Ganite®) intravenously for five days malignancy not responsive to hydration Oral phosphorus [lemental phosphorus, Especially effective with chronic hypercalcemia (K-Phos Neutral®, I to 3 g per day due to hyperparathyroidism and malignancy Uro-KP-Neutral®)
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