Hypercalcemia, treatment

Massagli TL, Cardenas DD. Immobilization hypercalcemia treatment with pamidronate disodium after spinal cord injury. Arch Phys Med Rehabil 1999 80(9) 998-1000. 

Exposure to all forms of vitamin D should be stopped. Treatment should be supportive and symptomatic. Hypercalcemia treatment should include a low-calcium diet and prednisone as necessary. 

In patients with hypercalcemia, treatment with a loop diuretic plus saline promotes calcium excretion and helps lower serum calcium. In patients with intact regulatory function, increases in calcium resorption promoted by thiazides have minor impact on serum calcium due to buffering in bone and gut. However, thiazides can unmask hypercalcemia that occurs in diseases that disrupt normal calcium regulation (eg, hyperparathyroidism, sarcoidosis, carcinoma). 

Vitamin D withdrawal is an obvious treatment for D toxicity (219). However, because of the 5—7 d half-life of plasma vitamin D and 20—30 d half-life of 25-hydroxy vitamin D, it may not be immediately successful. A prompt reduction in dietary calcium is also indicated to reduce hypercalcemia. Sodium phytate can aid in reducing intestinal calcium transport. Calcitonin glucagon and glucocorticoid therapy have also been reported to reduce semm calcium resulting from D intoxication (210). 

Diuretics are one of the dmg categories most frequendy prescribed. The principal uses of diuretics are for the treatment of hypertension, congestive heart failure, and mobilization of edema fluid in renal failure, fiver cirrhosis, and ascites. Other applications include the treatment of glaucoma and hypercalcemia, as well as the alkafinization of urine to prevent cystine and uric acid kidney stones. 

Use calcium metabolism regulator (treatment of Paget s disease, hypercalcemia of malignancy)... 

One of the major problems In the treatment of patients with vitamin D compounds (l.e., patients with hypoparathyroidism) has been the unpredictable development of hypercalcemia and the syndrome of vitamin D Intoxication. Although this problem may become less serious when some of the faster-acting metabolites and analogues of metabolites of vitamin D become available for clinical use. It Is likely that monitoring of serum levels of... 

TABLE 24-9. Selected Treatment Options for the Management of Hypercalcemia... 

The primary goal of treatment for hypercalcemia is to control the underlying malignancy. Therapies directed at lowering the calcium level are temporary measures that are useful until anticancer therapy begins to work. 

Therapeutic options for the treatment of hypercalcemia should be directed toward the level of corrected serum calcium and the presence of symptoms. Adequate treatment of mild or asymptomatic hypercalcemia may be achieved on an outpatient basis with nonpharmacologic measures. Moderate to severe or symptomatic hypercalcemia almost always requires pharmacologic intervention. 

What treatment plan would you outline to manage LP s hypercalcemia based on the calcium level and his signs and symptoms ... 

Therapeutic options for the treatment of hypercalcemia should be directed toward the level of corrected serum calcium and the presence of symptoms (Fig. 96-5). Hypercalcemia may be classified as mild [corrected calcium equal to 10.5-11.9 g/dL (2.6-3 mmol/L)], moderate [12-13.9 g/dL (3-3.5 mmol/L)], and severe [greater than 14 g/dL (3.5 mmol/L)].26 Adequate treatment of mild or asymptomatic hypercalcemia may be achieved on an outpatient basis with nonpharmacologic measures. Moderate to severe or symptomatic hypercalcemia almost always requires pharmacologic intervention. 

Calciuric therapy in the form of hydration is a key component of the treatment of hypercalcemia, regardless of severity or presence of symptoms.28 Mild or asymptomatic patients may be encouraged to increase oral fluid intake (3-4 L/day). Patients with moderate to severe or symptomatic hypercalcemia should receive normal saline at 200 to 500 mL/hour according to dehydration and cardiovascular status. Patients should be encouraged to ambulate as much as possible because immobility enhances... 

Multiple pharmacologic interventions are available for the treatment of hypercalcemia (Table 96-10). Furosemide 20 to 40 mg/day may be added to hydration once rehydration has been achieved to avoid fluid overload and enhance renal excretion of calcium. Although effective in relieving symptoms, hydration and diuretics are temporary measures that are useful until the onset of antiresorptive therapy thus hydration and antiresorptive therapy should be initiated simultaneously. 

The long-term success of therapy for hypercalcemia is determined primarily by the success of treatment of the underlying malignancy. In the short term, monitor patients for relief of... 

Although not as common as hypercalcemia, tumor lysis syndrome may cause significant morbidity and mortality if adequate prophylaxis and treatment are not instituted. Tumor lysis syndrome is the result of rapid destruction of malignant cells with subsequent release of intracellular contents into the circulation. 

I 12. The answer is b. (Hardman, pp 1264-1265J Dactinomycin s major toxicities include stomatitis, alopecia, and bone marrow depression. Bleomycin s toxicities include edema of the hands, alopecia, and stomatitis. Mitomycin causes marked bone marrow depression, renal toxicity, and interstitial pneumonitis. Plicamycin causes thrombocytopenia, leukopenia, liver toxicity, and hypocalcemia. The latter may be of use in the treatment of hypercalcemia. Doxorubicin causes cardiotoxicity, as well as alopecia and bone marrow depression. The cardiotoxicity has been linked to a lipid peroxidation within cardiac cells. 

Hypercalcemic crisis and symptomatic hypercalcemia are medical emergencies requiring immediate treatment. Rehydration with normal saline followed by loop diuretics can be used in patients with normal to moderately impaired renal function. Initiate treatment with calcitonin in patients in whom saline hydration is contraindicated (Table 78-3). 

Interleukin 1 (IL-1) is produced mainly by activated monocytes-macropha-ges, and its principal action is to stimulate thymocytes. A pleiotropic cytokine, IL-1 induces the expression of a large diversity of cytokines such as IL-6, leukaemia inhibitory factor (LIF), and other proinflammatory molecules (Di-marello 1994). IL-1 and TNF-a carry out as part of their function increasing the expression of NF-/cB and JNK (c-Jun N-terminal kinase). The importance of IL-1 in OCS is demonstrated because the IL-1-receptor-deficient mouse is resistant to ovariectomy (OVX)-induced bone loss (Lorenzo et al. 1998). The importance in pathological bone loss is also illustrated by the fact that treatment with IL-1 receptor antagonist slows down bone erosion for patients affected with rheumatoid arthritis (Kwan et al. 2004). IL-1 increases osteoclast differentiation rather than mature osteoclast activity, and infusion of IL-1 into mice induces hypercalcemia and bone resorption. Finally, IL-1 and TNF-a... 

Hypercalcemia of malignancy (HCM) For the treatment of FICM (zoledronic acid) in conjunction with adequate hydration for the treatment of moderate or severe hypercalcemia associated with malignancy, with or without bone metastases (pamidronate patients with epidermoid or nonepidermoid tumors respond to pamidronate) for FICM that persists after adequate hydration has been restored (zoledronic acid). 

---