Case Reports in Medicine exposure to excessive calcium and alkali ingestion can cause marked increases in serum Ca and bicarbonate in rare cases, mild intermittent hypercalcemia can be seen in a signiﬁcant number of patients. Renal vasoconstriction secondary to hypercalcemia leads to a fall in glomerular ﬁltration rate, and hypercalcemia directly stimulates tubular hydrogen ion secretion and, therefore, bicarbonate reabsorption leading to metabolic alkalosis. The alkalosis helps to maintain hypercalcemia and volume depletion by enhancing the activity of the CaSR and by increasing calcium reabsorption in the distal tubule via the pH-sensitive calcium channel, the transient receptor potential vanilloid member 5 [TRPV5] [17–19]. Volume contraction due to vomiting, diuretics, or the natriuretic eﬀects of hypercalcemia further aggravates hypercalcemia and alkalosis. Marked hypercalcemia can lead to the patient presenting with acute toxicity (nausea, vomiting, weakness, and mental changes with psychosis or depressed sensorium). After extensive clinical and laboratory evaluation, no evi- dence of malignant disease or primary hyperparathyroidism was seen in our patient. No cause of hypercalcemia could be identiﬁed other than the ingestion of large amount of CaCO3 (calcium carbonate) with concurrent use of thiazide diuretic. Along with the pathophysiology of hypercalcemia secondary to large calcium intake and absorption as mentioned above, thiazide diuretics are known to reduce urinary calcium excretion and produce mild hypercalcemia [16, 17]. In the kidney, distal convoluted tubule reabsorbs about 8% of the ﬁltered Ca load. This occurs via epithelial Ca2+ channels. In the steady state, the cell must extrude all penetrating Ca, which occurs via a Ca2+ ATPase and through Na+/Ca2+ exchanger located on the basolateral surface of the cells of the distal tubule. Thiazides inhibit the Na+/Cl− symport in the early distal convoluted tubule, thus causing a decrease in intracellular Na. This, in turn, enhances the activity of the Na+/Ca2+ exchanger, creating an increased driving for Ca resorption through the epithelial Ca2+ channels. The ﬁnal eﬀects increased Ca reabsorption leading to hypercalcemia. In a novel study, Nijenhuis et al. showed that mice that lacked active distal Ca2+ reabsorption (TRVP5-knockout) developed hypercalcemia with hydrochlorothiazide (HCTZ) treatment and that enhanced passive Ca2+ transport in the proximal tubule rather than active Ca2+ transport in distal convolution explains thiazide-induced hypocalciuria [20]. In conclusion, the ingestion of absorbable calcium, metabolic alkalosis, and concomitant use of thiazide diuretic can produce severe hypercalcemia which can be potentially more life threatening than is generally observed with either agent alone. This must be taken into account while prescrib- ing thiazide diuretics for hypertension to patient with gastric reﬂux disease due to the ready availability of nonprescription medication containing CaCO3. Conﬂict of Interests The authors declare that there is no conﬂict of interests. Authors’ Contribution B. Parvez and C. Emuwa contributed equally to the paper. 3 References [1] B. W. Sippy, “Landmark article May 15, 1915: gastric and duodenal ulcer. Medical cure by an eﬃcient removal of gastric juice corrosion. By Bertram W. Sippy,” Journal of the American Medical Association, vol. 250, no. 16, pp. 2192–2197, 1983. [2] J. B. Kirsner and W. L. 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