2 with large soft tissue deposits of calcium. Renal insuﬃciency often improved but did not resolve completely. 2. Case Presentation Our patient is a 64-year-old Caucasian male who presented to the emergency room (ER) with a 2-week complaint of progressive weakness, dizziness on ambulation, nausea, and per accompanying family members, a deterioration in mental status. In the ER, he was hemodynamically stable, but serum analysis was signiﬁcant for hypercalcemia of 16.9 with corrected calcium per serum albumin 18.2 (normal 8.4–10.2 milligrams per deciliter (mg/dL), formula for corrected serum calcium = measured serum calcium + 0.8 ∗ (normal albumin – measured patient albumin)), alkalosis with bicarbonate 34.6 (normal 21.0–31.0 millimole per liter (mmol/L), renal insuﬃciency with BUN 30 (normal 6– 20 mg/dL) and creatinine 4.0 (normal 0.5–1.2 mg/dL), total protein 5.8 (normal 6.2–8.2 g/dL), albumin 3.0 (normal 3.2– 5.0 g/dL), phosphorus 3.1 (normal 2.5–4.6 mg/dL), WBC 11.5 (normal 4.5–10.0 K/cumm), hemoglobin 14.3 (normal 13.0–17.0 g/dL), hematocrit 40.9 (normal 39.0–52.0), and platelets 341 (normal 140–400 K/cumm). Electrocardiogram (ECG) showed sinus tachycardia at 106 beats per minute, normal PR, and QRS intervals with QT/QTc 304/400 msec. Arterial blood gas showed alkalemia: pH 7.48 (normal 7.35– 7.45), pCO2 46 (normal 35–45 mm/Hg), and O2 saturation 99% (normal 95–98). With this physical presentation, hypercalcemia with renal insuﬃciency and alkalosis, he was admitted to acute medicine ﬂoor. Management included aggressive ﬂuid resus- citation with normal saline, acute coronary syndrome rule out, telemetry placement for cardiac arrhythmia monitoring, and workup for the etiology of hypercalcemia. On thorough history and chart review, the patient admitted to taking large quantities of over-the-counter calcium supplementation in the form of TUMS for his chronic acid reﬂux spanning over 3 decades. Recently, over the past several weeks, due to worsening reﬂux symptoms, he had increased his daily TUMS from 5-6 tablets to as much as 20–30 tablets per day. He had previously been seen in a cardiology clinic (6 months prior to this presentation) for followup of hypertension (HTN) and was started on low-dose hydrochlorothiazide 12.5 mg per day. He was seen in a pulmonary clinic for followup of lung nodule (which had previously been worked up as benign) and in a gastrointestinal clinic 2 months after cardiology visit and was noted to have serum Ca of 11.6. He was counseled extensively on stopping over the counter acid suppression and given prescription of omeprazole 40 mg BID which he decided not to take. Etiology workup revealed ionized calcium (iCa) at 8.3 (normal 4.48–5.28 mg/dL), intact parathyroid hormone (iPTH) < 3.0 (normal 10–65 pg/mL) indicating non-PTH- mediated hypercalcemia, parathyroid-hormone-related pep- tide (PTHrp) at 0, Vit D 1,25 <8 (normal 18–64 pg/mL), and Vit D 25 at 23 (optimum level 25–80 ng/mL) ruling out malignancy and hypervitaminosis. Other causes were also ruled out with normal serum thyroid studies, serum protein electrophoresis, chest radiograph, and chest CT Case Reports in Medicine showing no new changes and renal ultrasound being benign. Gastroenterology and nephrology consults were obtained to conclude the diagnosis of milk-alkali syndrome and to formulate multidisciplinary plan. He underwent esopha- gogastroduodenoscopy (EGD) which showed grade IV reﬂux esophagitis, distal esophageal stricture, gastritis, and erosive duodenitis. Pathologic specimen was reported as benign squamous hyperplasia with negative stain for H. pylori. Initial ﬂuid resuscitation was supplemented with IV proton pump inhibitor twice a day and nutrition evaluation and recommendation; all of which resulted in impressive resolu- tion of hypercalcemia and restoration of renal functions to normal thus conﬁrming milk-alkali syndrome. Patient was later discharged home on omeprazole 40 mg twice a day (BID) and hydrochlorothiazide 12.5 mg. As followup, he was seen in internal medicine clinic 3 months after discharge with serum Ca of 10.6, albumin 4.3, improvement in reﬂux symptoms, and baseline functional status. 3. Discussion In the milk-alkali syndrome, hypercalcemia develops because the input of calcium (dietary intake and intestinal absorp- tion) exceeds the output (primarily renal excretion). About 4 to 60 g/d of calcium carbonate has been reported to induce the milk-alkali syndrome, indicating that factors besides calcium intake contribute to the development of the milk-alkali syndrome [9]. Factors that can increase calcium input include increased dietary calcium intake, ingestion of supplemental calcium, enhanced intestinal absorption of calcium usually resulting from stimulation by vitamin D that is present in some calcium supplements, and other dietary factors. Calcium-containing compounds have also been shown to directly increase gastric acid secretion by stim- ulating the CaSR (calcium-sensing receptor) when ingested orally, which in turn increases the availability of free calcium for absorption [10, 11]. It is likely that bone, the primary repository for calcium, increases calcium uptake but becomes saturated during high calcium exposure. The capacity of bone to increase calcium uptake per unit of bone changes with age as does the extent of bone remodeling [12, 13]. Randall et al. in 1961 gave insight into the time course of this syndrome after observing 40 men with peptic ulcer disease who were treated with milk and either aluminum hydroxide or calcium carbonate [8]. In the milk–carbonate group (12 grams of calcium per day), the mean plasma calcium concentration rose within 24 hours from 10 mg/dL to 11 mg/dL (2.5 to 2.75 mmol/L). In 9 of 20 patients treated for one week, the plasma calcium concentration reached or exceeded 11.3 mg/dL (2.8 mmol/L) and, in a few cases, exceeded 12 mg/dL (3 mmol/L). The mean plasma bicarbonate concentration rose slightly, but in three of the 20 patients exceeded 31.5 meq/L. The plasma creatinine concentration rose from 1.2 to 1.4 mg/dL (106 to 124 mmol/L) on the third day. The plasma phosphate concentration rose during the ﬁrst few days. One patient developed the acute milk-alkali syndrome with hypercal- cemia preceding the development of renal insuﬃciency and alkalosis. From this study, it can be concluded that although