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      Hypercalcemia and Upper GI Symptoms

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      Canadian Journal of General Internal Medicine
      Dougmar Publishing Group, Inc.

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          Abstract

          Hypercalcemia is a common clinical presentation encountered in day to day practice. The most common causes of hypercalcemia have been shown to be primary hyperparathyroidism and hypercalcemia of malignancy accounting for around 90% of all cases. We present the case of a 78 year old male admitted to hospital with delirium and an uncommon cause of hypercalcemia, milk alkali syndrome (MAS) in the context of Peptic ulcer disease (PUD). MAS, caused by excessive intake of calcium based antacids, was first identified in the 1920’s when the Sippy regimen, consisting of milk or cream and calcium salts was used to treat peptic ulcers. With the advent of proton pump inhibitors and histamine-2 blockers, it had become a rare cause of hypercalcemia responsible for <1% of the cases. However, there has been a re-emergence of MAS due to the increased use of calcium supplements for osteoporosis prevention and over-the-counter preparations for dyspepsia. Interestingly, apart from the well-known classic symptoms of hypercalcemia, chronic hypercalcemia also increases gastric acid production and worsens PUD which in this case, could likely have lead to increased calcium–based antacid ingestion, worsening the hypercalcemia and creating a vicious cycle. This case report explores the physiology of the connection between hypercalcemia and PUD and emphasizes the need to keep MAS on the differential diagnosis for hypercalcemia.

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          Most cited references4

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          Milk alkali syndrome and the dynamics of calcium homeostasis.

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            Calcium-Alkali Syndrome in the Modern Era

            The ingestion of calcium, along with alkali, results in a well-described triad of hypercalcemia, metabolic alkalosis, and renal insufficiency. Over time, the epidemiology and root cause of the syndrome have shifted, such that the disorder, originally called the milk-alkali syndrome, is now better described as the calcium-alkali syndrome. The calcium-alkali syndrome is an important cause of morbidity that may be on the rise, an unintended consequence of shifts in calcium and vitamin D intake in segments of the population. We review the pathophysiology of the calcium-alkali syndrome.
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              Activation of the calcium sensing receptor stimulates gastrin and gastric acid secretion in healthy participants.

              In 17 adults on a fixed metabolic diet, an 11-day course of cinacalcet increased serum gastrin and basal gastric acid output, but not maximal gastric acid output, compared with a placebo. These findings indicate that the calcium sensor receptor plays a role in the regulation of gastric acid. Gastric acid secretion is a complex process regulated by neuronal and hormonal pathways. Ex vivo studies in human gastric tissues indicate that the calcium sensing receptor (CaR), expressed on the surface of G and parietal cells, may be involved in this regulation. We sought to determine whether cinacalcet, a CaR allosteric agonist, increases serum gastrin and gastric acid secretion. Seventeen healthy adults with normal gastric acid output were placed on an 18-day metabolic diet. On day 8 (baseline), participants were given cinacalcet (15 then 30 mg/day) or placebo for 11 days. Changes in gastric acid output, serum gastrin, and other measures were compared in the two groups. Changes in serum gastrin and basal acid output (adjusted for baseline body weight) were significantly more positive in the cinacalcet group compared with placebo (P = 0.004 and P = 0.039 respectively). Change in maximal acid output was similar in the two groups (P = 0.995). As expected, cinacalcet produced significant decreases in serum PTH (P < 0.001) and ionized calcium levels (P = 0.032), and increases in serum phosphorus levels (P = 0.001) and urinary calcium (P = 0.023). This study provides in vivo evidence that activation of the CaR increases serum gastrin levels and basal gastric acid secretion in healthy adults.
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                Author and article information

                Journal
                Canadian Journal of General Internal Medicine
                Can Journ Gen Int Med
                Dougmar Publishing Group, Inc.
                2369-1778
                1911-1606
                June 25 2018
                June 25 2018
                : 13
                : 2
                Article
                10.22374/cjgim.v13i2.224
                539d534b-ced2-40f5-8cf4-328af4fc75c7
                © 2018

                Copyright of articles published in all DPG titles is retained by the author. The author grants DPG the rights to publish the article and identify itself as the original publisher. The author grants DPG exclusive commercial rights to the article. The author grants any non-commercial third party the rights to use the article freely provided original author(s) and citation details are cited. To view a copy of this license, visit https://creativecommons.org/licenses/by-nc/4.0/


                General medicine,Geriatric medicine,Neurology,Internal medicine
                General medicine, Geriatric medicine, Neurology, Internal medicine

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