[MedicalConspiracies] Phillips Milk of Magnesia Oral has a caution for aluminum

Med Watch Has this info for their doctors for Milk of magnesia
It seems this is old information since it was changed years ago, Milk of magnesia is considered an aluminum antacid you can call the company and see.
Thank you Dr Powers for this info.
http://www.medscape.com/druginfo/monograph?cid=med&drugid=9415&drugname=Phillips+Milk+of+Magnesia+Oral&monotype=monograph&monographid=382762&secid=9

Phillips Milk of Magnesia Oral Monograph - Antacids Class: ANTACIDS AND ADSORBENTS(56:04) Sections: Introduction | Uses | Dosage and Administration | Cautions | Drug Interactions |Pharmacology | Chemistry and Stability | Preparations Cautions Pending revision, the material in this section should be considered in light of more recently available information in the MedWatch notification at the beginning of this monograph. Most antacids contain sodium as an impurity, and antacid products must be labeled with their sodium content if they contain more than 0.2 mEq of sodium per dose. Sodium bicarbonate is contraindicated and use of other sodium-containing antacids should be restricted in patients on low-sodium diets and in those with congestive heart failure, renal failure, edema, or cirrhosis. Antacid products containing more than 25 mEq of potassium in the recommended daily dosage should be used cautiously in patients with renal disease and only under the supervision of a physician. Since antacids may alter the absorption of certain concomitantly administered oral drugs, patients taking oral drugs should be advised to consult their physician or other health professional before taking concomitant antacids. (See Drug Interactions.) The most common adverse effects associated with prolonged administration of antacids are constipation and diarrhea. Although fixed-combination antacid products are frequently administered to balance the laxative and cathartic effects of each, bowel function must often be regulated by administering supplemental doses of an antacid with constipating (i.e., aluminum salt) or laxative (i.e., magnesium salt) action. Some commercially available antacids contain the dye tartrazine (FD&C yellow No. 5), which may cause allergic reactions including bronchial asthma in susceptible individuals. Although the incidence of tartrazine sensitivity is low, it frequently occurs in patients who are sensitive to aspirin. Individuals with phenylketonuria (i.e., homozygous genetic deficiency of phenylalanine hydroxylase) and other individuals who must restrict their intake of phenylalanine should be warned that Maalox® Quick Dissolve® Chewables and Maalox® Quick Dissolve® Chewables Maximum Strength contain aspartame which is metabolized in the GI tract to phenylalanine following oral administration. •Aluminum Antacids  The most frequent adverse effect of aluminum antacids is constipation. Decreased bowel motility, dehydration, or fluid restriction may predispose patients to intestinal obstruction. Hemorrhoids and fissures, or fecal impaction may occur. Long-term administration of aluminum antacids in patients with renal failure or chronic renal failure may result in hyperaluminemia since small amounts of aluminum are absorbed from the GI tract and excretion of aluminum is decreased in patients with renal failure. Absorbed aluminum becomes bound to serum proteins (e.g., albumin, transferrin) and therefore is not easily dialyzed; aluminum may then accumulate in bones, lungs, and nerve tissue. Aluminum accumulation in the CNS may be the cause of dialysis encephalopathy, while aluminum accumulation in the bones may result in or worsen dialysis osteomalacia. Dialysis dementia also may occur in patients with renal failure receiving long-term aluminum antacid therapy for hyperphosphatemia. Several cases of dialysis encephalopathy have been associated with increased aluminum concentrations in the dialysate water. Aluminum intoxication with severe osteomalacia and extensive aluminum deposition at the junction between calcified and noncalcified bone has been reported in several young children who were receiving large dosages of aluminum hydroxide for the management of hyperphosphatemia associated with azotemia; the children were not undergoing hemodialysis during aluminum hydroxide therapy. Aluminum salts may cause phosphorus depletion which is generally negligible. However, with prolonged administration or large doses, hypophosphatemia may occur, especially in patients with inadequate dietary intake of phosphorus; hypercalciuria secondary to bone resorption and increased intestinal absorption of calcium results. This phosphorus depletion syndrome is characterized by anorexia, malaise, and muscle weakness, and prolonged aluminum antacid therapy may cause urinary calculi, osteomalacia, and osteoporosis. A low-phosphorus diet, diarrhea, excessive phosphorus losses from malabsorption, and restoration of renal function after a kidney transplant increase the likelihood of the syndrome. Serum phosphate concentrations should be monitored at monthly or bimonthly intervals in patients on maintenance hemodialysis who are receiving chronic aluminum antacid therapy.