Acute pancreatitis is caused by alcohol, gall stone disease, drugs, trauma, infections, and metabolic causes such as hypercalcemia and hyperlipidemia. Hypercalcemia-induced acute pancreatitis has been well documented but only rarely occurs due to over-the-counter calcium carbonate. In this article, we present a case of over-the-counter calcium carbonate-induced acute pancreatitis

Essrani, Rajesh

Lohana, Ajeet Kumar

Mehershahi, Shehriyar

Mehmood, Asif

Parvataneni, Swetha

English

eCommons@AKU

eCommons@AKU Section of Gastroenterology Department of Medicine 1-2020 Over-the-counter drug causing acute pancreatitis Swetha Parvataneni Geisinger Lewistown Hospital, Lewistown, PA, USA. Rajesh Essrani Geisinger Lewistown Hospital, Lewistown, PA, USA. Shehriyar Mehershahi Bronx-Lebanon Hospital Center, New York, NY, USA. Rajesh Essrani Bronx-Lebanon Hospital Center, New York, NY, USA. Ajeet Kumar Lohana Aga Khan University See next page for additional authors Follow this and additional works at: https://ecommons.aku.edu/pakistan_fhs_mc_med_gastroenterol  Part of the Gastroenterology Commons Recommended Citation Parvataneni, S., Essrani, R., Mehershahi, S., Essrani, R., Lohana, A. K., Mehmood, A. (2020). Over-the-counter drug causing acute pancreatitis. Journal of Investigative Medicine High Impact Case Reports, 8, 1-3. Available at: https://ecommons.aku.edu/pakistan_fhs_mc_med_gastroenterol/271 Authors Swetha Parvataneni, Rajesh Essrani, Shehriyar Mehershahi, Rajesh Essrani, Ajeet Kumar Lohana, and Asif Mehmood This report is available at eCommons@AKU: https://ecommons.aku.edu/pakistan_fhs_mc_med_gastroenterol/271 https://doi.org/10.1177/2324709620922724Journal of Investigative Medicine HighImpact Case ReportsVolume 8: 1–3© 2020 American Federation forMedical ResearchDOI  10.1177/232470962 227 4journals.sagepub.com/home/hicCreative Commons Non Commercial CC BY-NC: This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (https://creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage).Case ReportIntroductionAcute pancreatitis is defined as inflammation of the pancreas and is one of the common reasons for hospital admissions in the United States.1 It has multiple causes, with alcohol and gall stone disease contributing to 80% to 90% of cases.2 Other reported causes include drugs, common bile duct obstructions secondary to neoplasms and sphincter of Oddi dysfunction, and metabolic alterations such as hypercalce-mia or hypertriglyceridemia. Hypercalcemia associated with primary hyperparathyroidism contributes to 3.6% cases of pancreatitis cases, while pancreatitis induced by excess con-sumption of over-the-counter (OTC) calcium carbonate is rare and very seldom reported in the literature.3,4 In this arti-cle, we present the case of a young male with pancreatitis secondary to OTC calcium carbonate medications.Case DescriptionA 35-year-old male with no significant past medical history was admitted for epigastric pain with radiation to the back associated with nausea and vomiting. He complained of fatigue, poor appetite, and increased urination. He had a his-tory of gastroesophageal reflux disease for which he was tak-ing OTC medications. His vital signs were stable. On examination, he appeared slightly confused, with dry skin and generalized abdominal tenderness. Blood work: white blood cells 16 400/µL, sodium 139 mmol/L, blood urea nitro-gen 23 mg/dL, creatinine 2.6 mg/dL, aspartate aminotrans-ferase 34 U/L, alanine aminotransferase 26 U/L, bicarbonate 34 mmol/L, alkaline phosphatase 114 U/L, calcium 15.1 mg/dL, triglyceride level 79 mg/dL, low-density lipoprotein 110 mg/dL, lipase 560 U/L, albumin 3.9 g/dL, and negative for ethanol. Computed tomography scan of abdomen/pelvis showed pancreatitis with a normal biliary tract. He was treated with pain medications and ringer lactate fluid.Further investigation showed low parathyroid hormone (PTH) = 18 pg/mL, low vitamin D (25) = 17 ng/mL, along with normal PTH-related peptide, vitamin D (1,25), serum protein electrophoresis, urine protein electrophoresis, and free light chain. The patient admitted that he had been taking 7 to 8 tablets of 600 mg calcium carbonate per day over the past 3 weeks for acid reflux. His symptoms and calcium level gradually improved with ringer lactate, and he was dis-charged after 6 days. He was educated on the side effects of excessive OTC drug use.DiscussionMilk-alkali syndrome (MAS) is caused by increased con-sumption of calcium and alkali products. MAS is character-ized by the triad of hypercalcemia, renal failure, and metabolic alkalosis. Increased use of OTC drugs in patients 922724 HICXXX10.1177/2324709620922724Journal of Investigative Medicine High Impact Case ReportsParvataneni et alcase-report202020201Geisinger Lewistown Hospital, Lewistown, PA, USA2Geisinger Health System, Danville, PA, USA3Bronx-Lebanon Hospital Center, New York, NY, USA4Aga Khan University, Karachi, PakistanReceived February 6, 2020. Revised April 1, 2020. Accepted April 3, 2020.Corresponding Author:Swetha Parvataneni, MD, Internal Medicine, Geisinger Lewistown Hospital, 400 Highland Avenue, Lewistown, PA 17044-1198, USA. Email: swethaparvataneni88@gmail.comOver-the-Counter Drug Causing Acute PancreatitisSwetha Parvataneni, MD1 , Rajesh Essrani, MD2,  Shehriyar Mehershahi, MD3, Rajesh Essrani, MD3,  Ajeet Kumar Lohana, MBBS4, and Asif Mehmood, MD2AbstractAcute pancreatitis is caused by alcohol, gall stone disease, drugs, trauma, infections, and metabolic causes such as hypercalcemia and hyperlipidemia. Hypercalcemia-induced acute pancreatitis has been well documented but only rarely occurs due to over-the-counter calcium carbonate. In this article, we present a case of over-the-counter calcium carbonate–induced acute pancreatitis.KeywordsOTC, over the counter, CT, computed tomography, MAS, milk-alkali syndrome, PUD, peptic ulcer disease2 Journal of Investigative Medicine High Impact Case Reportswith osteoporosis and kidney failure can lead to a life-threat-ening illness. In the early days after its discovery, MAS was associated with an increased mortality rate of 4.4%.5 MAS was first described by Hardt and Rivers in 1923.6 They attrib-uted this syndrome to the Sippy regimen, which was devel-oped in 1915 for peptic ulcer disease. The Sippy regimen comprised the hourly consumption of milk, cream, and a mixture of alkaline powders. Prior to the discovery of H2 blockers and proton pump inhibitors, the Sippy regimen was commonly used in peptic ulcer disease.7 In the 1970s and 1980s, MAS contributed to less than 2% of hospitalized patients with hypercalcemia, but this incidence has increased to 12% in recent years.8 MAS is now considered to be the third most common cause of hypercalcemia, after hyperpara-thyroidism and malignant neoplasms. Some authors have suggested that this increased incidence is due to increased use of OTC drugs.9The pathophysiology of MAS is classified into 2 phases: a generation phase and a maintenance phase. Excess calcium consumption increases serum calcium levels; this results in volume depletion from diuresis and natriuresis by activation of the calcium sensing receptor (CaSR), which stimulates renal tubular absorption of bicarbonate and decreases glo-merular filtration rate. This decreased glomerular filtration rate reduces filtration of calcium, while volume depletion and metabolic alkalosis lead to increased renal absorption of calcium in order to maintain calcium homeostasis. The pathophysiology of hypercalcemia-induced pancreatitis is unclear, but high calcium levels are thought to lead to intra-cellular activation of proteases.10-13 In addition to OTC drugs as an inciting factor for MAS, other cyclic pathophysiologic pathways that promote alkalosis, hypercalcemia, and renal failure can mimic MAS. MAS has been reported with the consumption of more than 4 to 5 g of calcium carbonate per day.9 These cases present in 3 forms: acute, subacute (cope syndrome), and chronic (Burnett syndrome).14 In the acute phase, patients present with symptoms of toxemia, such as nausea, vomiting, anorexia, dizziness, vertigo, and confu-sion; and in chronic phase, they present with muscle aches, polyuria, polydipsia, psychosis, tremor, pruritis, and abnor-mal calcifications. Ocular calcification, renal calcinosis, and rarely breast calcifications have been reported.15 The diagno-sis is clinical, and a detailed history along with a physical can aid the diagnosis of MAS. Treatment is mostly supportive, with hydration and removal of the underlying causative agent.According to the evidence discussed above, we conclude that medications should be reconciled on every patient encounter, including OTC medications, and patients should be educated about the side effects of excessive use. Daily elemental calcium intake should not exceed 2 g per day. However, MAS has also been reported with a lower calcium intake in patients on thiazides and with preexisting renal fail-ure, as in our patient. Therefore, it is very important that all patients should be educated on various drug interactions in addition to information about daily calcium intake.Authors’ NoteThe work has been published previously as an abstract at the American College of Gastroenterology Annual Scientific Meeting on October 25, 2019, in San Antonio, Texas.Declaration of Conflicting InterestsThe author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.FundingThe author(s) received no financial support for the research, author-ship, and/or publication of this article.Ethics ApprovalOur institution does not require ethics approval for reporting indi-vidual cases.Informed consentVerbal consent was obtained from the patient(s) for their anony-mized information to be published in this article.ORCID iDSwetha Parvataneni  https://orcid.org/0000-0002-5932-2237References 1. Nadhem O, Salh O. Acute pancreatitis: an atypical presenta-tion. Case Rep Gastroenterol. 2017;11:359-363. 2. Tun-Abraham ME, Obregón-Guerrero G, Romero-Espinoza L, Valencia-Jiménez J. Acute pancreatitis associated with hyper-calcaemia. Cir Cir. 2015;83:227-231. 3. Diallo I, Fall CA, Ndiaye B, et al. Primary hyperparathyroid-ism and pancreatitis: a rare association with multiple facets. Int Sch Res Notices. 2016;2016:7294274. 4. Vassallo P, Green N, Courtney E. Hypercalcemia secondary to excessive self-medication with antacids causing acute pancre-atitis: a case report. Croat Med J. 2019;60:42-45. 5. Medarov BI. Milk-alkali syndrome. Mayo Clin Proc. 2009;84:261-267. 6. Hardt LL, Rivers AB. Toxic manifestations following the alka-line treatment of peptic ulcer. Arch Intern Med. 1923;31:171-180. 7. Sippy BW. Gastric and duodenal ulcer. Medical cure by an efficient removal of gastric juice corrosion. J Am Med Assoc. 1915;64:1625-1630. 8. Beall DP, Scofield RH. Milk-alkali syndrome associated with calcium carbonate consumption. Report of 7 patients with parathyroid hormone levels and an estimate of prevalence among patients hospitalized with hypercalcemia. Medicine (Baltimore). 1995;74:89-96. 9. Daniel NJ, Wadman MC, Branecki CE. Milk-alkali-induced pancreatitis in a chronically hypocalcemic patient with DiGeorge syndrome. J Emerg Med. 2015;48:e63-e66.Parvataneni et al 3 10. Felsenfeld AJ, Levine BS. Milk alkali syndrome and the dynamics of calcium homeostasis. Clin J Am Soc Nephrol. 2006;1:641-654. 11. Frick TW, Mithöfer K, Fernández-del Castillo C, et al. Hypercalcemia causes acute pancreatitis by pancreatic secre-tory block, intracellular zymogen accumulation, and acinar cell injury. Am J Surg. 1995;169:167-172. 12. Niederau C, Luthen R, Klonowski-Stumpe H, et al. The role of calcium in pancreatitis. Hepatogastroenterology. 1999;46:2723-2730. 13. Petersen OH, Gerasimenko OV, Gerasimenko JV. Pathobiology of acute pancreatitis: focus on intracellular calcium and calmodulin. F1000 Med Rep. 2011;3:15. 14. Punsar S, Somer T. The milk-alkali syndrome. A report of three illustrative cases and a review of the literature. Acta Med Scand. 1963;173:435-449. 15. Al-Hwiesh AK, Abdul-Rahman IS, Al-Oudah N, Al-Solami S, Al-Muhanna FA. Milk-alkali syndrome induced by H1N1 influenza vaccine. Saudi J Kidney Dis Transpl. 2017;28: 912-915.

Over-the-counter drug causing acute pancreatitis

Essrani, Rajesh, MD

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Over-the-Counter Drug Causing Acute Pancreatitis.

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Over-the-counter drug causing acute pancreatitis

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