Hypomagnesemia in a Patient With an Eating Disorder

Abstract

A 39-year-old woman presented for evaluation of severe hypomagnesemia of more than 10 years' duration (average serum magnesium concentration, 1.1; range, 0.5-2.8 mg/dL). She has a history of psychiatric disorders, including major depression, attention-deficit/ hyperactivity disorder, anorexia nervosa, and past laxative abuse. Hypokalemia has rarely accompanied the hypomagnesemia (average serum potassium concentration, 4.0; range, 3.4-4.8 mEq/L). There is no family history of renal or electrolyte disorders. She does not use tobacco, alcohol, or illicit substances. Based on psychiatric history, hypomagnesemia had previously been attributed to suspected surreptitious diuretic use. She denies vomiting, diuretic or laxative abuse, recent weight change, or diarrhea despite high-dose oral magnesium supplementation. Her concerns were diffuse myalgia and parasthesias of the upper extremities, upper back, neck, and thighs.

Effects of Magnesium Deficiency on Mechanisms of Insulin Resistance in Type 2 Diabetes: Focusing on the Processes of Insulin Secretion and Signaling

“…The causes of Mg 2+ loss through the kidneys are elucidated in detail during the recent years and may involve various damage of the transport systems located in the thick ascending limb (TAL) of Henle’s loop and distal convoluted tubules [6,12]. Inherited tubular disorders that result in urinary Mg 2+ waste are Gitelman syndrome, Bartter syndrome, familial hypomagnesemia with hypercalciuria and nephrocalcinosis (FHHNC), autosomal-dominant hypocalcemia with hypercalciuria (ADHH), isolated dominant hypomagnesemia (IDH) with hypocalciuria, isolated recessive hypomagnesemia (IRH) with normocalcemia, and hypomagnesemia with secondary hypocalcemia (HSH) [9,65,66]. Recent findings in obese diabetic rats found that TRPM6 was down regulated, explaining renal Mg 2+ waste.…”

Diagnostic Dilemma in an Adolescent Girl with an Eating Disorder, Intellectual Disability, and Hypomagnesemia

“…Hypomagnesemia, classified as decreased serum Mg 2+ concentrations (<0.7 mmol/L), is most commonly caused by either excessive gastrointestinal or renal losses. Gastrointestinal causes include those caused by short bowel and gastric bypass surgeries, malabsorption syndromes, and medications such as laxatives and proton pump inhibitors [1]. Renal magnesium wasting can be caused by an array of medications, most notably thiazide and loop diuretics, as well as aminoglycosides, amphotericin, pentamidine, cisplatin, calcineurin inhibitors, and antibodies targeting epidermal growth factors (EGFs) or EGF receptor [1].…”

“…Gastrointestinal causes include those caused by short bowel and gastric bypass surgeries, malabsorption syndromes, and medications such as laxatives and proton pump inhibitors [1]. Renal magnesium wasting can be caused by an array of medications, most notably thiazide and loop diuretics, as well as aminoglycosides, amphotericin, pentamidine, cisplatin, calcineurin inhibitors, and antibodies targeting epidermal growth factors (EGFs) or EGF receptor [1]. Additionally, over a dozen genetic diseases in children are associated with renal magnesium losses, including Bartter and Gitelman syndromes [2].…”