Milk-Alkali Syndrome
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Milk-alkali syndrome is caused by the ingestion of large amounts of calcium and absorbable alkali, with resulting hypercalcemia. If unrecognized and untreated, milk-alkali syndrome can lead to metastatic calcification and renal failure. This syndrome was originally recognized in the 1920s during administration of the Sippy regimen, consisting of milk and bicarbonate, for treatment of peptic ulcer disease. (See Pathophysiology, Etiology, Prognosis, Presentation, and Workup.) [1]
With the development of nonabsorbable alkali and histamine-2 blockers for treatment of peptic ulcer disease, milk-alkali syndrome became a rare cause of hypercalcemia; however, with the increased use and promotion of calcium carbonate for dyspepsia and for calcium supplementation, a resurgence of milk-alkali syndrome has occurred. (See Etiology and Epidemiology.)
A few authors recommend changing the name of milk-alkali syndrome to calcium-alkali syndrome, since this name reflects the changing epidemiology. Calcium-alkali syndrome is now more common in postmenopausal women with the use of over-the counter (OTC) calcium and vitamin D supplements. Calcium- or milk-alkali syndrome is now the third most common cause of hypercalcemia in hospitalized patients. [2] The name milk-alkali syndrome was first used by Fuller Albright (one of the most important figures in endocrinology in the 20th century) and his colleagues in the 1949 New England Journal of Medicine article describing chronic renal disease in milk alkali syndrome. [3] This is the most cited article published about the condition with 251 citations in Web of Science as of June 2017 showing that the name milk-alkali syndrome has historical importance even if it does not reflect current pathogenesis.
Milk-alkali syndrome can have an acute course with rapid induction of hypercalcemia and acute renal failure soon (within a week) after excess calcium carbonate is begun. A more chronic course also is observed. In this form, irreversible renal failure may ensue, but many patients have partial recovery with a timely diagnosis. (See Prognosis, Presentation, and Workup.)
Wide variations in symptoms occur among individuals with hypercalcemia, even among patients with similar levels of serum calcium. Some patients may be completely asymptomatic, with hypercalcemia found incidentally after a multiple chemistry panel.
Patients may have severe mental status changes that include obtundation and coma, especially as serum calcium levels rise higher than 15 mg/dL. (See Presentation and Workup.)
Hypercalcemia may produce EKG changes such as shortened QT/QTc interval and nonhypothermic J (or Osborn) waves. [4]
The proper dose and the potentially harmful dose of calcium carbonate need to be discussed with the patient. Attention to ingredients in all medications should be stressed, because multiple over-the-counter (OTC) medications contain calcium carbonate. (See Treatment.)
Cases of calcium-alkali syndrome have been reported from calcium carbonate intake with 2-9 grams of elemental calcium per day. Comorbid illnesses like chronic kidney disease and/or use of diuretics can be predisposing factors. [5]
How oral intake of more than 2 g/day of elemental calcium with absorbable alkali results in hypercalcemia and alkalosis is not completely understood. Adaptation of intestinal calcium absorption to oral intake may play a role and help to explain individual variability in the development of milk-alkali syndrome. Some persons maintain a high fractional absorption of calcium even with a high intake, while other persons decrease fractional absorption with a high intake. The former are likely at risk of developing milk-alkali syndrome.
Calcium absorption is completed within 4 hours of intake. Avid absorption of large doses may lead to suppression of parathyroid hormone (PTH), which then leads to enhanced bicarbonate retention by the kidney. (The data are clear that PTH is suppressed in milk-alkali syndrome.) Continuing ingestion of calcium carbonate and bicarbonate retention leads to alkalosis, which causes increased calcium resorption in the distal collecting system of the kidney. Also, hypercalcemia produces a renal concentrating defect that can be considered a form of nephrogenic diabetes insipidus.
Resultant dehydration and volume depletion may worsen the hypercalcemia. PTH is further suppressed by hypercalcemia. This cyclic pathophysiology maintains hypercalcemia and alkalosis as long as calcium and alkali are taken in by mouth.
A low PTH level impairs gastrointestinal (GI) absorption of phosphate. Therefore, low PTH levels may be part of the mechanism by which phosphate levels either remain normal or rise abnormally high in many patients.
The milk-alkali syndrome from Sippy diet often was associated with hyperphosphatemia due to high phosphate content of milk with cream. However, in the new era of calcium-alkali syndrome, low or low normal serum phosphorus levels due to phosphate-binding properties of calcium carbonate are the norm. Low serum phosphate may be more prominent in elderly and patients with eating disorders with low intake of protein and phosphorus. [2]
Chronic milk-alkali syndrome can result in metastatic calcification due to high serum calcium levels and relatively high phosphate levels (calcium × phosphate). Irreversible renal failure may result. However, even severe renal failure may be completely reversible if milk-alkali syndrome is diagnosed early.
The cause of milk-alkali syndrome is ingestion of an inappropriately high amount of calcium carbonate. Ingestion of large amounts of milk or milk products is no longer a common feature of milk-alkali syndrome, and ingestion of milk and bicarbonate is now rare. One patient was reported to have developed milk-alkali syndrome during prolonged enteral tube feedings delivering 2.1 g of calcium daily. [6] Certainly more than 4 g/d of supplemental calcium can predispose to milk-alkali syndrome.
A myriad of OTC medicines have calcium carbonate as an ingredient. [7, 8] Patients may be acquiring it from more than 1 source. For example, a woman might take a 600 mg calcium carbonate tablet twice daily for calcium supplementation and additionally take 200 mg tablets marketed for dyspepsia treatment.
Thiazide diuretics can cause volume depletion and contraction alkalosis increasing renal calcium absorption. Angiotensin-converting enzyme inhibitors and NSAIDs decrease renal calcium excretion by decreasing GFR. [2]
While perhaps counterintuitive, the therapeutic index of calcium carbonate is small. The usual prescribed dose is 1200-1500 mg of elemental calcium for postmenopausal supplementation, while 2500-3000 mg of elemental calcium as the carbonate salt can produce milk-alkali syndrome.
A case report described a 64-year-old woman with recurrent hypercalcemia and milk-alkali syndrome with nicotine replacement gum and carbonated water as the source of excessive calcium intake. [9]
Milk-alkali syndrome has been reported in pregnancy. Pregnant women absorb calcium from the GI tract more avidly than do nonpregnant women. The serum level of PTH-RP is increased in pregnancy. Furthermore, pregnant women are prescribed calcium supplements and frequently have GI symptoms for which calcium carbonate–containing OTC preparations may be taken. (Milk-alkali syndrome has been treated with dialysis during pregnancy.) [10]
In one patient, milk-alkali syndrome was induced by ingestion of large amounts of calcium carbonate during hyperemesis gravidarum. The newborn of a pregnant woman with milk-alkali syndrome had hypocalcemia in the neonatal period, according to a report.
The author has reported iatrogenic milk-alkali syndrome in a patient with sepsis and acute renal failure who was given large doses of calcium carbonate as a phosphate-absorption blocker. As the renal failure resolved, calcium carbonate was continued and hypercalcemia developed. [11]
One older study indicated that milk-alkali syndrome causes less than 1% of hypercalcemia. However, a number of case reports over the last several years have suggested that milk-alkali syndrome is more common than previously observed or appreciated.
Moreover, in a study of patients hospitalized for emergent hypercalcemia, milk-alkali syndrome was the underlying cause in 6 (12%) of 49 of patients admitted over a 4-year period. [12] The syndrome was third behind hyperparathyroidism and solid malignancy as a cause of hypercalcemia requiring hospitalization and more common than multiple myeloma.
Another study, of patients hospitalized between 1998-2003 with hypercalcemia, found similar results. [13] Of 125 patients without end-stage renal disease, 11 (8.8%) had milk-alkali syndrome. Among 25 patients in the study with severely elevated calcium (serum calcium >14 mg/dL), milk-alkali syndrome was second only to malignancy, being present in 9 (25.7%) of these individuals.
International frequency is not known to be different than that observed in the United States. Occurrence should be related to the number of persons ingesting calcium carbonate. Areas of the world in which betel nut chewing is common may have an increased incidence of milk-alkali syndrome. Betel nut is a recreational drug used in Southeast Asia and India by an estimated 600 million persons daily. The meat of the betel nut is made into a paste (or quid) with dried oyster shell, wrapped in a betel nut leaf, and placed in the lateral buccal pouch. Because the paste contains calcium carbonate from oyster shell, milk-alkali syndrome can result from heavy use. [14]
Betel nut is addictive and causes oral cancer. Betel nut and related ingredients are available in areas of the West with large immigrant populations from Asia and India. The lips, tongue, and oral mucosa are stained a characteristic red in long-term users of betel nut.
No race predilection is recognized for milk-alkali syndrome, although Southeast Asians and Indians are potential users of betel nut, which can cause the syndrome.
In the era of calcium carbonate ingestion as the cause of milk-alkali syndrome, the average age among 65 patients with milk-alkali syndrome was 50.3 years, with a range of 24-95 years. Women are affected by milk-alkali syndrome more commonly than men and make up approximately 60% of patients. Older, postmenopausal women taking calcium supplementation may be at particularly high risk for the condition. Milk-alkali syndrome has been reported in children.
In the era of milk and bicarbonate as the etiology, milk-alkali syndrome was common in men with peptic ulcer disease. However, modern era calcium-alkali syndrome is more common in postmenopausal women, pregnant women, transplant recipients, dialysis patients, and patients with eating disorders like bulimia. [2]
The prognosis in milk-alkali syndrome usually is good, although this diagnosis is frequently missed. Reports indicate that some patients have been admitted with hypercalcemia several times before the diagnosis was made. A complete history of all medication use, including OTC medications, should prevent milk-alkali syndrome from escaping detection.
Once calcium carbonate is no longer being ingested and hypercalcemia has been treated acutely, further care specifically directed at the milk-alkali syndrome is not necessary.
Milk-alkali syndrome almost never results in death, but a significant number of patients may be left with permanent renal impairment. That is, chronic renal disease may result from milk-alkali syndrome. In reports from the last several years, 20 of 57 patients studied had a follow-up serum creatinine level of more than 1.5 mg/dL (see the Table below). Patients may have severe mental status changes that include obtundation and coma, especially as serum calcium levels rise higher than 15 mg/dL.
Table. Summary of 78 Consecutively Reported Adult Patients With Milk-Alkali Syndrome* (Open Table in a new window)
Mean Age
59.8 Years (Range, 24-95 y)
Sex
35 men and 43 women
Calcium source
Calcium carbonate in all but 1
Ingestion of bicarbonate
In 7 patients
Ingestion of milk
In 20 patients (plus one who ate yogurt)
Mean serum calcium
17. 2mg/dL (4.30mmol/L) (range, 11.1-27.5mg/dL)
High serum phosphorus
In 12 patients
Permanent renal insufficiency
In 20 of 57 patients eligible for evaluation
Parathyroid exploration
In 3 patients
Hypocalcemia with treatment
In 16 patients
*These data are derived from the 7 patients reported, plus the 28 reviewed in Beall and Scofield, 1995, [12] as well as additional patients reported by Gibbs and Lee, 1992; [15] Nakanishi et al, 1992 [16] ; Brandwein and Sigman, 1994 [17] ; Campbell et al, 1994 [18] ; Duthie et al, 1995 [19] ; Spital and Freedman, 1995 [20] ; Fiorino, 1996 [21] ; Lin et al, 1996 [22] ; Muldowney and Mazbar, 1996 [23] ; Sulkin and Krentz, 1999 [24] ; Camidge and Peaston, 2000 [25] ; George and Clark, 2000 [26] ; Vanpee et al, 2000 [27] ; Liu et al, 2002 [28] ; Robertson, 2002 [29] ; Morton, 2002 [30] ; Kleinig and Torpy, 2004 [6] ; Picolos et al, 2005 [13] ; Gordon et al, 2005 [31] ; Addington et al, 2006 [10] ; Verburg et al, 2006 [32] ; Ennen and Magann, 2006 [33] ; Caruso et al, 2007 [34] ; Dinnerstein et al, 2007 [35] ; Javid et al, 2007; Kaklamanos and Perros, 2007 [36] ; Shah et al, 2007 [37] ; Irtiza-Ali et al, 2008 [7] ; and Jousten and Guffens, 2008. [8]
Two of the patients were pregnant.
Medarov BI. Milk-alkali syndrome. Mayo Clin Proc. 2009 Mar. 84(3):261-7. [Medline]. [Full Text].
Patel AM, Goldfarb S. Got calcium? Welcome to the calcium-alkali syndrome. J Am Soc Nephrol. 2010 Sep. 21(9):1440-3. [Medline].
BURNETT CH, COMMONS RR. Hypercalcemia without hypercalcuria or hypophosphatemia, calcinosis and renal insufficiency; a syndrome following prolonged intake of milk and alkali. N Engl J Med. 1949 May 19. 240 (20):787-94. [Medline].
Chhabra L, Spodick DH. Milk Alkali syndrome: an electrocardiographic masquerader for non-hypothermic Osborn phenomenon. Heart. 2013 Sep. 99(17):1302-3. [Medline].
Neupane S. Incidence of milk alkali syndrome in the Women’s Health Initiative clinical trial and cohort study. Osteoporos Int. 2014 Mar. 25(3):1193. [Medline].
Kleinig TJ, Torpy DJ. Milk-Alkali syndrome: broadening the spectrum of causes to allow early recognition. Intern Med J. 2004 Jun. 34(6):366-7. [Medline].
Irtiza-Ali A, Waldek S, Lamerton E, Pennell A, Kalra PA. Milk alkali syndrome associated with excessive ingestion of Rennie: case reports. J Ren Care. 2008 Jun. 34(2):64-7. [Medline].
Jousten E, Guffens P. Milk-alkali syndrome caused by ingestion of antacid tablets. Acta Clin Belg. 2008 Mar-Apr. 63(2):103-6. [Medline].
Swanson CM, Mackey PA, Westphal SA, Argueta R. Nicotine-substitute gum-induced milk alkali syndrome: a look at unexpected sources of calcium. Endocr Pract. 2013 Nov-Dec. 19(6):142-4. [Medline].
Addington S, Larson N, Scofield RH. Milk-alkali syndrome in pre-eclamptic pregnancy: report of a patient and evaluation of albumin-corrected calcium in pre-eclamptic pregnancies. J Okla State Med Assoc. 2006 Sep. 99(9):480-4. [Medline].
Fayyaz A, Scofield RH. Iatrogenic Milk Alkali Syndrome in a Patient Recovering from Acute Renal Failure. J Endocrinol Diab. 2016. 3(3):1-3.
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(2):89-96. [Medline].
Picolos MK, Lavis VR, Orlander PR. Milk-alkali syndrome is a major cause of hypercalcaemia among non-end-stage renal disease (non-ESRD) inpatients. Clin Endocrinol (Oxf). 2005 Nov. 63(5):566-76. [Medline].
Wu KD, Chuang RB, Wu FL, Hsu WA, Jan IS, Tsai KS. The milk-alkali syndrome caused by betelnuts in oyster shell paste. J Toxicol Clin Toxicol. 1996. 34(6):741-5. [Medline].
Gibbs CJ, Lee HA. Milk-alkali syndrome due to Caved-S. J R Soc Med. 1992 Aug. 85(8):498-9. [Medline]. [Full Text].
Nakanishi T, Uyama O, Yamada T, Sugita M. Sustained metabolic alkalosis associated with development of the milk-alkali syndrome. Nephron. 1992. 60(2):251. [Medline].
Brandwein SL, Sigman KM. Case report: milk-alkali syndrome and pancreatitis. Am J Med Sci. 1994 Sep. 308(3):173-6. [Medline].
Campbell SB, Macfarlane DJ, Fleming SJ, Khafagi FA. Increased skeletal uptake of Tc-99m methylene diphosphonate in milk-alkali syndrome. Clin Nucl Med. 1994 Mar. 19(3):207-11. [Medline].
Duthie JS, Solanki HP, Krishnamurthy M, Chertow BS. Milk-alkali syndrome with metastatic calcification. Am J Med. 1995 Jul. 99(1):102-3. [Medline].
Spital A, Freedman Z. Severe hypercalcemia in a woman with renal failure. Am J Kidney Dis. 1995 Oct. 26(4):674-7. [Medline].
Fiorino AS. Hypercalcemia and alkalosis due to the milk-alkali syndrome: a case report and review. Yale J Biol Med. 1996 Nov-Dec. 69(6):517-23. [Medline]. [Full Text].
Lin SH, Lin YF, Shieh SD. Milk-alkali syndrome in an aged patient with osteoporosis and fractures. Nephron. 1996. 73(3):496-7. [Medline].
Muldowney WP, Mazbar SA. Rolaids-yogurt syndrome: a 1990s version of milk-alkali syndrome. Am J Kidney Dis. 1996 Feb. 27(2):270-2. [Medline].
Sulkin T, Krentz AJ. Iatrogenic recurrent severe hypercalcaemia and renal impairment. Postgrad Med J. 2000 Dec. 76(902):800, 807. [Medline]. [Full Text].
Camidge R, Peaston R. Recommended dose antacids and severe hypercalcaemia. Br J Clin Pharmacol. 2001 Sep. 52(3):341-2. [Medline]. [Full Text].
George S, Clark JD. Milk alkali syndrome-an unusual syndrome causing an unusual complication. Postgrad Med J. 2000 Jul. 76(897):422-3. [Medline]. [Full Text].
Vanpee D, Delgrange E, Gillet JB, Donckier J. Ingestion of antacid tablets (Rennie) and acute confusion. J Emerg Med. 2000 Aug. 19(2):169-71. [Medline].
Liu SW, Kumar AM, Nadel ES, Brown DF. A young woman with altered mental status. J Emerg Med. 2002 May. 22(4):405-8. [Medline].
Robertson WC Jr. Calcium carbonate consumption during pregnancy: an unusual cause of neonatal hypocalcemia. J Child Neurol. 2002 Nov. 17(11):853-5. [Medline].
Morton A. Milk-alkali syndrome in pregnancy, associated with elevated levels of parathyroid hormone-related protein. Intern Med J. 2002 Sep-Oct. 32(9-10):492-3. [Medline].
Gordon MV, McMahon LP, Hamblin PS. Life-threatening milk-alkali syndrome resulting from antacid ingestion during pregnancy. Med J Aust. 2005 Apr 4. 182(7):350-1. [Medline].
Verburg FA, van Zanten RA, Brouwer RM, Woittiez AJ, Veneman TF. [A man with a classic serious milk-alkali syndrome and a carcinoma of the stomach]. Ned Tijdschr Geneeskd. 2006 Jul 22. 150(29):1624-7. [Medline].
Ennen CS, Magann EF. Milk-alkali syndrome presenting as acute renal insufficiency during pregnancy. Obstet Gynecol. 2006 Sep. 108(3 Pt 2):785-6. [Medline].
Caruso JB, Patel RM, Julka K, Parish DC. Health-behavior induced disease: return of the milk-alkali syndrome. J Gen Intern Med. 2007 Jul. 22(7):1053-5. [Medline]. [Full Text].
Dinnerstein E, McDonald BC, Cleavinger HB, Thadani VM, Jobst BC. Mesial temporal sclerosis after status epilepticus due to milk alkali syndrome. Seizure. 2008 Apr. 17(3):292-5. [Medline].
Kaklamanos M, Perros P. Milk alkali syndrome without the milk. BMJ. 2007 Aug 25. 335(7616):397-8. [Medline]. [Full Text].
Shah BK, Gowda S, Prabhu H, Vieira J, Mahaseth HC. Modern milk alkali syndrome–a preventable serious condition. N Z Med J. 2007 Sep 21. 120(1262):U2734. [Medline].
Beall DP, Henslee HB, Webb HR, Scofield RH. Milk-alkali syndrome: a historical review and description of the modern version of the syndrome. Am J Med Sci. 2006 May. 331 (5):233-42. [Medline].
Patel AM, Adeseun GA, Goldfarb S. Calcium-alkali syndrome in the modern era. Nutrients. 2013 Nov 27. 5(12):4880-93. [Medline]. [Full Text].
Miller PD. Vitamin D, calcium, and cardiovascular mortality: a perspective from a plenary lecture given at the annual meeting of the American Association of Clinical Endocrinologists. Endocr Pract. 2011 Sep 1. 17(5):798-806. [Medline].
Papworth K, Grankvist K, Ljungberg B, Rasmuson T. Parathyroid hormone-related protein and serum calcium in patients with renal cell carcinoma. Tumour Biol. 2005 Jul-Aug. 26(4):201-6. [Medline].
Kifor O, Moore FD Jr, Delaney M, Garber J, Hendy GN, Butters R, et al. A syndrome of hypocalciuric hypercalcemia caused by autoantibodies directed at the calcium-sensing receptor. J Clin Endocrinol Metab. 2003 Jan. 88 (1):60-72. [Medline].
Pallais JC, Kifor O, Chen YB, Slovik D, Brown EM. Acquired hypocalciuric hypercalcemia due to autoantibodies against the calcium-sensing receptor. N Engl J Med. 2004 Jul 22. 351 (4):362-9. [Medline].
Soyfoo MS, Brenner K, Paesmans M, Body JJ. Non-malignant causes of hypercalcemia in cancer patients: a frequent and neglected occurrence. Support Care Cancer. 2013 May. 21(5):1415-9. [Medline].
LeGrand SB, Leskuski D, Zama I. Narrative review: furosemide for hypercalcemia: an unproven yet common practice. Ann Intern Med. 2008 Aug 19. 149(4):259-63. [Medline].
Mean Age
59.8 Years (Range, 24-95 y)
Sex
35 men and 43 women
Calcium source
Calcium carbonate in all but 1
Ingestion of bicarbonate
In 7 patients
Ingestion of milk
In 20 patients (plus one who ate yogurt)
Mean serum calcium
17. 2mg/dL (4.30mmol/L) (range, 11.1-27.5mg/dL)
High serum phosphorus
In 12 patients
Permanent renal insufficiency
In 20 of 57 patients eligible for evaluation
Parathyroid exploration
In 3 patients
Hypocalcemia with treatment
In 16 patients
*These data are derived from the 7 patients reported, plus the 28 reviewed in Beall and Scofield, 1995, [12] as well as additional patients reported by Gibbs and Lee, 1992; [15] Nakanishi et al, 1992 [16] ; Brandwein and Sigman, 1994 [17] ; Campbell et al, 1994 [18] ; Duthie et al, 1995 [19] ; Spital and Freedman, 1995 [20] ; Fiorino, 1996 [21] ; Lin et al, 1996 [22] ; Muldowney and Mazbar, 1996 [23] ; Sulkin and Krentz, 1999 [24] ; Camidge and Peaston, 2000 [25] ; George and Clark, 2000 [26] ; Vanpee et al, 2000 [27] ; Liu et al, 2002 [28] ; Robertson, 2002 [29] ; Morton, 2002 [30] ; Kleinig and Torpy, 2004 [6] ; Picolos et al, 2005 [13] ; Gordon et al, 2005 [31] ; Addington et al, 2006 [10] ; Verburg et al, 2006 [32] ; Ennen and Magann, 2006 [33] ; Caruso et al, 2007 [34] ; Dinnerstein et al, 2007 [35] ; Javid et al, 2007; Kaklamanos and Perros, 2007 [36] ; Shah et al, 2007 [37] ; Irtiza-Ali et al, 2008 [7] ; and Jousten and Guffens, 2008. [8]
Two of the patients were pregnant.
R Hal Scofield, MD Professor, Department of Medicine, Section of Endocrinology, University of Oklahoma College of Medicine; Associate Member, Arthritis and Immunology Program, Oklahoma Medical Research Foundation; Staff Physician, Oklahoma City Department of Veterans Affairs Medical Center
R Hal Scofield, MD is a member of the following medical societies: American Association of Immunologists, American College of Physicians, American College of Rheumatology, American Federation for Medical Research
Disclosure: Nothing to disclose.
Anum Fayyaz, MD Resident Physician, Departments of Internal Medicine and Pediatrics, University of Oklahoma Health Sciences Center
Disclosure: Nothing to disclose.
Rohan Sharma, MBBS Graduate Research Assistant, Oklahoma Medical Research Foundation
Disclosure: Nothing to disclose.
George T Griffing, MD Professor Emeritus of Medicine, St Louis University School of Medicine
George T Griffing, MD is a member of the following medical societies: American Association for the Advancement of Science, International Society for Clinical Densitometry, Southern Society for Clinical Investigation, American College of Medical Practice Executives, American Association for Physician Leadership, American College of Physicians, American Diabetes Association, American Federation for Medical Research, American Heart Association, Central Society for Clinical and Translational Research, Endocrine Society
Disclosure: Nothing to disclose.
Thuy-Trang Nguyen University of Louisville School of Medicine
Disclosure: Nothing to disclose.
Shabreen Abdul Sharief, MD Physician, Select Specialty Hospital
Shabreen Abdul Sharief, MD is a member of the following medical societies: American Medical Association, Indian Medical Association
Disclosure: Nothing to disclose.
Romesh Khardori, MD, PhD, FACP Former Professor, Department of Medicine, Former Chief, Division of Endocrinology, Metabolism, and Molecular Medicine, Southern Illinois University School of Medicine
Romesh Khardori, MD, PhD, FACP is a member of the following medical societies: American Association of Clinical Endocrinologists, American College of Physicians, American Diabetes Association, and Endocrine Society
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Medscape Salary Employment
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