Calcium therapy with

Patients with asymptomatic left ventricular systolic dysfunction and hypertension should be treated with P-blockers and ACE inhibitors. Those with heart failure secondary to left ventricular dysfunction and hypertension should be treated with drugs proven to also reduce the morbidity and mortality of heart failure, including P-blockers, ACE inhibitors, ARBs, aldosterone antagonists, and diuretics for symptom control as well as antihypertensive effect. In African-Americans with heart failure and left ventricular systolic dysfunction, combination therapy with nitrates and hydralazine not only affords a morbidity and mortality benefit, but may also be useful as antihypertensive therapy if needed.66 The dihydropyridine calcium channel blockers amlodipine or felodipine may also be used in patients with heart failure and left ventricular systolic dysfunction for uncontrolled blood pressure, although they have no effect on heart failure morbidity and mortality in these patients.49 For patients with heart failure and preserved ejection fraction, antihypertensive therapies that should be considered include P-blockers, ACE inhibitors, ARBs, calcium channel blockers (including nondihydropyridine agents), diuretics, and others as needed to control blood pressure.2,49... 

Pharmacologic therapy with sodium bicarbonate or citrate/citric acid preparations maybe needed in patients with stage 3 CKD or higher to replenish body stores of bicarbonate. Calcium carbonate and calcium acetate, used to bind phosphorus in sHPT, also aid in increasing serum bicarbonate levels, in conjunction with other agents. 

Dextrose and insulin (with or without sodium bicarbonate) are typically given at the time of calcium therapy in order to redistribute potassium into the intracellular space. Dextrose 50% (25 g in 50 mL) can be given by slow IV push over 5 minutes or dextrose 10% with 20 units of regular insulin can be given by continuous TV infusion over 1 to 2 hours. The onset of action for this combination is 30 minutes and the duration of clinical effects... 

Applications of cation and anion resins are varied and include purification of sugar, identification of drugs and biomacromolecules, concentration of uranium, calcium therapy to help increase the amount of calcium in our bones (i.e., increase the bone density), and use as therapeutic agents for the control of bile acid and gastric acidity. In the latter use, a solid polyamide (Colestid) is diluted and taken with orange juice, which facilitates removal of bile acids from the body. This removal helps the body to produce more bile acid from cholesterol, thus effectively reducing the cholesterol level. 

Fracture In Paget patients, treatment regimens of etidronate exceeding the recommended daily maximum dose of 20 mg/kg or continuous administration for periods greater than 6 months may be associated with an increased risk of fracture. Hypocalcemia Hypocalcemia has occurred with pamidronate therapy. Rare cases of symptomatic hypocalcemia (including tetany) occurred during pamidronate treatment. If hypocalcemia occurs, consider short-term calcium therapy. Hypocalcemia must be corrected before therapy initiation with alendronate and risedronate. Also effectively treat other disturbances of mineral metabolism (eg, vitamin D deficiency). 

J.D. Ringe, A. Dorst, C. Kipshoeven, L.C. Rovati, I. Setnikar, Avoidance of vertebral fractures in men with idiopathic osteoporosis by a three year therapy with calcium and low-dose intermittent monofluorophosphate, Osteoporos. Int. 8 (1998) 47-52. 

Carbamazepine produces complex effects in a variety of neurotransmitters, receptors, and second messenger and neuropeptide systems (Post et al. 1992, 1994a). Determining which of these effects is most closely associated with its psychotropic properties in bipolar disorder and which of these or other effects may be responsible for the augmentation response in combination therapy with dihydropyridine L-type CCBs remains to be further evaluated. However, discussion of two possibilities might be beneficial. One possibility, of course, is that actions of carbamazepine unrelated to calcium dynamics account for its augmenting effects with nimodipine. The plethora of these other... 

Approximately two thirds of kidney stones contain Ca2+ phosphate or Ca2+ oxalate. Many patients with such stones exhibit a defect in proximal tubular Ca2+ reabsorption that causes hypercalciuria. This can be treated with thiazide diuretics, which enhance Ca2+ reabsorption in the distal convoluted tubule and thus reduce the urinary Ca2+ concentration. Salt intake must be reduced in this setting, since excess dietary NaCI will overwhelm the hypocalciuric effect of thiazides. Calcium stones may also be caused by increased intestinal absorption of Ca2+, or they may be idiopathic. In these situations, thiazides are also effective, but should be used as adjunctive therapy with other measures. 

Therapy with hydrochlorothiazide, up to 50 mg twice daily, or chlorthalidone, 50-100 mg daily, is recommended. Loop diuretics such as furosemide and ethacrynic acid should not be used because they increase urinary calcium excretion. The major toxicity of thiazide diuretics, besides hypokalemia, hypomagnesemia, and hyperglycemia, is hypercalcemia. This is seldom more than a biochemical observation unless the patient has a disease such as hyperparathyroidism in which bone turnover is accelerated. Accordingly, one should screen patients for such disorders before starting thiazide therapy and monitor serum and urine calcium when therapy has begun. 

Collings WCJ, Cullen MJ, Feely J. The effect of therapy with dihydropyridine calcium channel blockers on glucose tolerance in non-insulin dependent diabetes. Br J Clin Pharmacol 1986 21 568. 

On the other hand, therapy of essential arterial hypertension with dihydropyridine or calcium channel antagonists (felodipine, amlodipine or lercanidipine) for 10 weeks led to a significant increase of blood plasma TAC (by 42%) (D5). Therapy with gliclazide, a sulfonylurea hypoglycemic drug, enhanced blood plasma TAC (Ol). 

Long-term anticonvulsive therapy with diphenylhydantoin or phenobarbital is known to cause osteomalacia by influencing calcium metabolism (24,25). Alteration in the metabolism of vitamin D, presumably secondary to induction of hepatic microsomal enzymes, leads to the calcium and bone abnormalities (26). Patients on anticonvulsive therapy with phenytoin exhibit a decrease in serum 25-hydroxyvitamin D (27). Adequate dietary amounts of vitamin precursors or microsomal enzyme stimulators might prevent these effects of long-term therapy. 

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