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Published in Samar Razaq, Difficult Cases in Primary Care, 2021
Acute salt loss in CF may lead to the gradual development of abnormally low serum electrolyte levels (hypochloraemia, hypokalaemia and hyponatraemia) and metabolic alkalosis with a failure to thrive. Weight gain resumes with replacement of the lost salts (Kennedy, et al., 1990). Excessive ingestion of milk or calcium carbonate as antacids may lead to hypercalcaemia, alkalosis and renal failure (milk-alkali syndrome). Undiagnosed diabetes, a recognised complication of CF, may result in metabolic acidosis in the form of diabetic ketoacidosis (rather than alkalosis). Pyloric stenosis may cause a similar alkalotic picture and has been discussed elsewhere. It is not a recognised complication of CF. Imerslund–Gräsbeck syndrome is another autosomal recessive disorder, resulting in an inability to absorb vitamin B12.
Calcium and Magnesium
Published in Luke R. Bucci, Nutrition Applied to Injury Rehabilitation and Sports Medicine, 2020
In general, daily doses of 1000 to 2500 mg of calcium are safe for long-term administration. Exceptions are persons with renal disease, sarcoidosis, or persons prone to kidney stone formation. Milk-alkali syndrome is possible after consumption of two or more quarts of milk daily along with large amounts of calcium carbonate antacids. Calcium deposition in soft tissues and formation of kidney stones are symptoms of milk-alkali syndrome. Intakes of calcium greater than 2 to 4 g daily have the potential to depress uptake of magnesium, iron, zinc, manganese, and other minerals.
The minerals
Published in Geoffrey P. Webb, Nutrition, 2019
Toxicity – At high doses gastrointestinal symptoms may occur and in those taking medicinal calcium supplements a milk alkali syndrome sometimes occurs and results in hypercalcaemia, calcification of tissues, alkalosis, hypertension, neurological symptoms and renal impairment.
Hypercalcemia and acute kidney injury induced by eldecalcitol in patients with osteoporosis: a case series of 32 patients at a single facility
Published in Renal Failure, 2019
Seishi Aihara, Shunsuke Yamada, Hideaki Oka, Taro Kamimura, Toshiaki Nakano, Kazuhiko Tsuruya, Atsumi Harada
Another potential risk factor for ELD-induced AKI is concomitant medications that patients may be taking that affect renal hemodynamics and renal calcium metabolism. NSAIDs cause spasm of renal afferent arteriole [18], and RAASIs have a vasodilatory effect on the efferent arteriole [19], which decreases glomerular filtration rate and leads to decreased urinary Ca excretion and an increased serum Ca level. Magnesium oxide is an absorbent alkaline and is associated with milk-alkali syndrome. Milk-alkali syndrome is characterized by the triad of hypercalcemia, metabolic alkalosis, and diminished kidney function [20]. Metabolic alkalosis, initiated by alkali ingestion, increases the affinity of Ca sensing receptor for Ca, thereby enhancing the inhibition of sodium and Ca reabsorption [21]. Even in our study, patients tended to exhibit metabolic alkalosis (hydrogen carbonate was 29.1 ± 4.3 mmol/L, Table 3). In such a mechanism, corrected serum Ca levels on admission might have been higher when magnesium oxide was used in our study.
An update on the latest chemical therapies for reflux esophagitis in children
Published in Expert Opinion on Pharmacotherapy, 2019
Marc Bardou, Kyle J. Fortinsky, Nicolas Chapelle, Maxime Luu, Alan Barkun
The effectiveness of antacids in children has been studied in two small trials. Both trials found that antacids are successful in treating GER in large doses. They were found to be equally effective to H2RAs in healing esophagitis as well as improving symptoms of GER [38,39]. While the benefit of antacids is their relative safety compared to other medications such as PPIs, H2RAs, and prokinetics, they still have some associated risks. There have been reports of aluminum toxicity in preparations containing aluminum hydroxide, leading to osteopenia, microcytic anemia, and neurotoxicity [40]. Moreover, other preparations containing calcium can lead to milk-alkali syndrome, a syndrome of hypercalcemia, alkalosis, and renal failure [41].
The patient with metabolic alkalosis
Published in Acta Clinica Belgica, 2019
Valentine Gillion, Michel Jadoul, Olivier Devuyst, Jean-Michel Pochet
The ingestion of calcium along with alkali (calcium carbonate, baking soda…) results in the classical triad of hypercalcemia, metabolic alkalosis, and renal insufficiency of the Milk-alkali syndrome. The syndrome was initially associated with the ingestion of large quantities of milk along with alkali to treat peptic ulcer disease. Vomiting is usually associated, which, in addition to the exogenous alkali, further contributes to the onset or worsening of metabolic alkalosis. In such cases, bicarbonate cannot be excreted because of the associated hypovolemia, reduced glomerular filtration rate (resulting from hypovolemia and hypercalcemia), and hypercalcemia itself (promoting hydrogen ion secretion) [8].