F

Intestinal epithelium

Calcium-binding protein _

Calcium-stimulated ATPase t t

Alkaline phosphatase

Inhibition

Intestinal absorption of calcium

Plasma calcium ion concentration

Figure 35-9 Pathway for conversion of vitamin D3 into its active form (1,25-dihydroxycholecalciferol) and the role vitamin D plays in control of plasma calcium concentration. (From Haii JE. Parathyroid hormone, calcitonin, calcium and phosphate metabolism, vitamin D, bone, and teeth. In Guyton AC, Haii JE [eds]. Textbook of Medical Physiology, 12th ed. Philadelphia, Saunders-Eisevier, 2011.)

Box 35-12 Differential Diagnosis of Hypercalcemia

Primary hyperparathyroidism Parathyroid carcinoma Hypercalcemia of malignancy Nonparathyroid endocrine causes Thyrotoxicosis Pheochromocytoma Addison's disease Islet cell tumors Drug-related hypercalcemia Vitamin D Vitamin A Thiazide diuretics Lithium

Estrogen and antiestrogens Familial hypocalciuric hypercalcemia Miscellaneous Immobilization Milk-alkali syndrome Parenteral nutrition

From Silverberg SJ, Bilezikian JP. Primary hyperparathyroidism. In DeGroot LJ, Jameson JL (eds). Endocrinology, 5th ed, vol 2. Philadelphia, Elsevier-Saunders, 2006.

monitored and prescribed, can result in hypercalcemia. It is also important to inquire about nonprescription (OTC) medications because excess vitamin D (intoxication) can be a cause. If a patient is taking any of these substances and is asymptomatic, with serum calcium level less than 14 mg/ dL, the approach is to discontinue the medication and repeat the calcium level in a week. If the serum calcium is stable or declining, continue to monitor until it returns to normal.

Occasionally, adrenal insufficiency and hyperthyroidism are uncovered in the evaluation of a patient with an elevated serum calcium level.

Patients who have symptoms consistent with hypercalcemia or serum calcium levels in excess of 13.5 mg/dL may require more aggressive treatment. These patients will almost always be volume depleted as a result of hypercalciuria with resultant polyuria. Treatment is aimed initially at aggressive rehydration. Isotonic saline at 2 to 4 L/day until calcium level returns to normal is appropriate. Furosemide (loop diuretic) can be used with fluid replacement in older patients and those with renal or cardiac disorders to prevent fluid overload. Careful fluid management must be maintained to prevent inadvertent fluid overload or depletion (Table 35-11). Other treatments include IV bisphosphonate, calcitonin, and gallium nitrate or plicamycin (Table 35-12).

If the patient is determined to have a parathyroid adenoma, the only currently available option for cure is para-thyroidectomy. For asymptomatic patients, patients who have failed surgery, and those who do not meet surgical criteria, medical treatment includes moderate calcium intake,

Table 35-11 Summary of Most Generally Useful Medical Therapies for Hypercalcemia

Treatment

Onset of Action

Duration of Action

Advantages

Disadvantages

Rehydration

Hours

Rehydration invariably needed

None

Forced saline diuresis (with or without loop diuretics)

Hours

During treatment

Rapid action

Modest calcium-lowering effect Potential for volume overload Electrolyte disturbance Transient efficacy Inconvenient for patients

Calcitonin

Hours

1-2 days

Rapid onset of action

Modest calcium-lowering effect Tachyphylaxis develops in a few days

Bisphosphonates

Etidronate

1-3 days

5-7 days

First-generation bisphosphonate Well tolerated

3-day infusion protocol

Less effective than other bisphosphonates

Pamidronate

1-2 days

Weeks to months

Second-generation bisphosphonate Normalizes calcium levels in many patients

Fever

Occasional hypocalcemia, hypophosphatemia, and hypomagnesemia

Zoledronate

1-2 days

Weeks to months

Third-generation bisphosphonate More potent than second-generation bisphosphonates Normalizes calcium levels in 90% of patients

Hypophosphatemia

Hypocalcemia

Renal toxicity occasional

From Finkelstein JS, Potts JT. Medical management of hypercalcemia. In DeGroot LJ, Jameson JL (eds). Endocrinology, 5th ed, v

/ol 2. Philadelphia, Elsevier-Saunders, 2006.

Table 35-10 Biochemical Profile in Primary Hyperparathyroidism

Patients (mean +/- SEM)

Normal Range

Serum calcium

10.7 ±mg/dL

8.2-10.2 mg/dL

Serum phosphorus

2.8 ±0.1 mg/dL

2.5-4.5 mg/dL

Total alkaline phosphatase

114 ±5 IU/L

<100 IU/L

Serum magnesium

2.0 ±0.1 mg/dL

1.8-2.4 mg/dL

PTH (IRMA)

119 ±7 pg/mL

10-65 pg/mL

25(OH) vitamin D

19 ±1 ng/mL

9-52 ng/mL

1,25(OH)2 vitamin D

54 ±2 pg/mL

15-60 pg/mL

Urinary calcium

240 ±11 mg/g creatinine

Urine DPD

17.6 ± nmol/L/ mmol/L creatinine

<14.6 nmol/L/mmol/ L creatinine

Urine PYD

46.8 ±2.7 nmol/L/ mmol/L creatinine

<51.8 nmol/L/mmol/ L creatinine

From Silverberg SJ, Bilezikian JP. Primary hyperparathyroidism. In DeGroot LJ, Jameson JL (eds). Endocrinology, 5th ed, vol 2. Philadelphia, Elsevier-Saunders, 2006.

Table 35-12 Summary of Therapies for Hypercalcemia Useful in Special Circumstances

Treatment

Onset of Action

Duration of Action

Advantages

Disadvantages

Gallium nitrate

S days

7-10 days

May normalize calcium in patients resistant to bisphosphonates

Must be infused continuously over 5 days Occasional nephrotoxicity or hypophosphatemia

Glucocorticoids

Days

Days to weeks

Oral administration

Effective in granulomatous disorders and certain types of malignancies, especially hematologic

Dialysis

Hours

During use and for 24-48 hours afterward

Rapid onset of action Useful in patients with renal failure and heart failure Useful to treat life-threatening hypercalcemia

Complex procedure Reserved for extreme or special circumstances

Oral phosphate

24 hours

During use

Minimal toxicity if serum phosphate low Oral administration

Modest calcium-lowering effect Diarrhea

From Finkelstein JS, Potts JT. Medical management of hypercalcemia. In DeGroot LJ, Jameson JL (eds). Endocrinology, 5th ed, vc

)l 2. Philadelphia, Elsevier-Saunders, 2006.

estrogen replacement (when applicable), bisphosphonates, and selective estrogen receptor modulators (SERMs).

For the patient with PHPT not caused by malignancy, determining if there is one adenoma or multiple functioning adenomas and the location(s) is important in minimizing both duration and extent of surgery. It is possible to determine preoperatively which parathyroid gland(s) may be the source of the PTH utilizing ultrasound, CT, or MRI. If none of these provides definitive results, technetium-labeled (Tc-99m) sestamibi nuclear scan may localize the adenoma (Silverberg and Bilezikian, 2006).

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