Can you take Calcipotriene / dimethicone topical with Calcium phosphate, tribasic?

Calcium phosphate, tribasic has a major potential interaction with Achlorhydria.

Calcium is absorbed from the intestinal tract by active transport and passive diffusion. Malabsorption syndromes (celiac disease, GI resection), deficiency of vitamin D, parathyroid hormone, or calcitonin, or an alkaline gastric pH (achlorhydria, carbonate or phosphate salts) can decrease the absorption of oral formulations of calcium. Calcium is available in oral and parenteral formulations.

Calcium phosphate, tribasic has a major potential interaction with Arrhythmia.

Calcium is involved in cardiac muscle contraction and electrical impulse conduction. Therapy with calcium salt formulations (particularly IV) should be administered cautiously to patients with cardiac disease. Patients receiving cardiac glycosides and concomitant IV calcium may experience arrhythmias. Therapy with IV calcium should be administered slowly and at reduced dosages in patients with cardiac disease.

The calcipotriene topical in calcipotriene / dimethicone topical has a major potential interaction with Hypercalcemia.

The use of calcipotriene topical preparations is contraindicated in patients with demonstrated hypercalcemia or evidence of vitamin D toxicity. Calcipotriene is a synthetic vitamin D3 analog. Systemic absorption of topically applied calcipotriene ranges from less than 1% for the scalp solution to 5% to 6% for the ointment. Calcipotriene has been reported to be 100 to 200 times less potent in its effects on calcium utilization than natural vitamin D, which facilitates the absorption of calcium in the intestine. Transient, rapidly reversible elevation of serum calcium has been reported following the topical administration of calcipotriene. If elevation in serum calcium outside the normal range occurs, treatment should be discontinued until normal calcium levels are restored. Patients should be advised to contact their physician if they experience early symptoms of hypercalcemia such as weakness, fatigue, somnolence, headache, anorexia, dry mouth, metallic taste, nausea, vomiting, abdominal cramps, constipation, diarrhea, vertigo, tinnitus, ataxia, exanthema, muscle pain, bone pain, and irritability.

Calcium phosphate, tribasic has a major potential interaction with Malabsorption Syndrome.

Calcium is absorbed from the intestinal tract by active transport and passive diffusion. Malabsorption syndromes (celiac disease, GI resection), deficiency of vitamin D, parathyroid hormone, or calcitonin, or an alkaline gastric pH (achlorhydria, carbonate or phosphate salts) can decrease the absorption of oral formulations of calcium. Calcium is available in oral and parenteral formulations.

Calcium phosphate, tribasic has a major potential interaction with Phosphate Imbalance.

Elevated serum concentrations of calcium and phosphate can exceed the solubility level and result in calcium- phosphate precipitates that deposit in vascular and renal systems as well as other soft tissues of the body. Therapy with calcium should be administered with extreme caution in patients with hyperphosphatemia (hypoparathyroidism or severe renal impairment). Administration of oral calcium acetate or calcium carbonate, in addition to providing calcium, complexes phosphates within the GI tract. These complexes are eliminated in the feces. Clinical monitoring of serum calcium and phosphate concentrations is necessary.

The calcipotriene topical in calcipotriene / dimethicone topical has a major potential interaction with Poisoning by Vitamins.

The use of calcipotriene topical preparations is contraindicated in patients with demonstrated hypercalcemia or evidence of vitamin D toxicity. Calcipotriene is a synthetic vitamin D3 analog. Systemic absorption of topically applied calcipotriene ranges from less than 1% for the scalp solution to 5% to 6% for the ointment. Calcipotriene has been reported to be 100 to 200 times less potent in its effects on calcium utilization than natural vitamin D, which facilitates the absorption of calcium in the intestine. Transient, rapidly reversible elevation of serum calcium has been reported following the topical administration of calcipotriene. If elevation in serum calcium outside the normal range occurs, treatment should be discontinued until normal calcium levels are restored. Patients should be advised to contact their physician if they experience early symptoms of hypercalcemia such as weakness, fatigue, somnolence, headache, anorexia, dry mouth, metallic taste, nausea, vomiting, abdominal cramps, constipation, diarrhea, vertigo, tinnitus, ataxia, exanthema, muscle pain, bone pain, and irritability.

Calcium phosphate, tribasic has a major potential interaction with Renal Dysfunction.

Absorption of oral calcium formulations may be altered and elimination of calcium by the kidney decreased with renal impairment. Hyperphosphatemia occurs during renal failure. Calcium acetate or calcium carbonate, in addition to providing calcium, complexes phosphates within the GI tract. Calcium carbonate can partially correct metabolic acidosis associated with chronic renal failure. Clinical monitoring of renal function and serum calcium and phosphate concentrations is necessary.

Calcium phosphate, tribasic has a major potential interaction with Sarcoidosis.

Hypercalciuria, with or without hypercalcemia, may occasionally occur in patients with sarcoidosis. Elevated calcium levels may result from increased intestinal absorption of calcium, which is related to the extrarenal production of vitamin D by mononuclear phagocytes present within the sarcoid granuloma. Therapy with calcium salts should be administered cautiously and only if necessary in patients with sarcoidosis.