Paradoxical hypomagnesemia caused by excessive ingestion of magnesium hydroxide

Excessive ingestion of magnesium may lead to hypermagnesemia even without kidney dysfunction. Several cases of development of hypermagnesemia after overdose of magnesium hydroxide have been reported. Although magnesium hydroxide is widely used as laxative, its overdose may induce diarrhea, which is followed by excessive magnesium loss. I report a case of paradoxical hypomagnesemia developed after excessive ingestion of magnesium hydroxide. A 39-year-old woman was presented to the emergency department complaining of severe watery diarrhea and carpopedal spasm after ingesting a handful of magnesium hydroxide tablets. The laboratory tests detected hypomagnesemia, hypocalcemia, and normokalemia. Calcium gluconate was given to the patient, but her symptom did not improve shortly. The symptom disappeared spontaneously 2 days after the watery diarrhea subsided. This case shows that overdose of magnesium hydroxide, which leads to massive diarrhea, might induce hypomagnesemia unexpectedly. This case also suggests that it should be treated, as well as typical magnesium deficiency. Hypomagnesemia is associated with defect in absorption, excretion, or poor intake of magnesium. In general, it is known that excessive intake of magnesium leads to hypermagnesemia. Several cases of hypermagnesemia associated with excessive intake of magnesium hydroxide have been reported [1,2]. Meanwhile, magnesium hydroxide is used as laxative, and overdose of magnesium hydroxide may induce severe diarrhea, which may lead to magnesium deficiency. I report a case of paradoxical hypomagnesemia after overdose of magnesium hydroxide. A 39-year-old woman was presented to the emergency department (ED) complaining of vomiting and massive watery diarrhea. Her medical history revealed that she had ingested a handful of magnesium hydroxide tablets for a suicidal attempt 4 hours before she was taken to the ED. At least 20 tablets, each of which contains 500 mg of magnesium hydroxide, were estimated to be ingested. Her vital signs were stable, and initial physical examination revealed no specific symptoms or signs but watery diarrhea and carpopedal spasm. The results of initial laboratory tests showed potassium concentration of 3.5 mEq/L, ionized calcium concentration of 1.15 mmol/L, and magnesium concentration of 1.9 mg/dL, which is close to the lower limit of reference range. An arterial blood gas analysis showed arterial blood pH, 7.454; partial pressure of arterial carbon dioxide, 31.8 mm Hg; partial pressure of arterial oxygen, 79.4 mm Hg; bicarbonate concentration, 22 mmol/L; and arterial oxygen saturation, 96.7%, which is far from hyperventilation syndrome. Eight hours after the patient's admission, tingling sensation and muscle spasm of upper extremities were aggravated. At that moment, Chvostek sign and Trousseau sign were positive. The follow-up laboratory tests revealed potassium concentration of 4 mEq/L, ionized calcium concentration of 0.87 mmol/L, and magnesium concentration of 1.6 mg/dL, which indicate hypocalcemia, hypomagnesemia, and normokalemia. Electrocardiography was obtained, and it showed normal sinus rhythm. Calcium gluconate 1 g was given intravenously, but she still complained of the symptoms until the next day. Trousseau sign and Chvostek sign did not subside either, but watery diarrhea was improved. The next follow-up laboratory evaluation revealed potassium concentration of 3.7 mEq/L, ionized calcium concentration of 1.05 mmol/L, and magnesium concentration of 1.6 mg/dL, still showing mild hypocalcemia and hypomagnesemia. On the third day, the patient was asymptomatic. The laboratory findings revealed potassium concentration of 3.9 mEq/L, total calcium concentration of 8.7 mg/dL, ionized calcium concentration of 1.23 mmol/L, phosphorus concentration of 2.2 mg/dL, and magnesium concentration of 2.0 mg/dL, showing normalized electrolyte levels. Chvostek sign and Trousseau sign disappeared. Therefore, she was discharged. It is counterintuitive that hypomagnesemia was developed after overdose of magnesium hydroxide. Although magnesium deficiency has various etiologies, the patient did not have relevancy except diarrhea. She did not have history of malnutrition and malabsorption syndrome or surgical resection of small intestine, which may lead to decreased uptake of magnesium. Although evaluation of urine magnesium was not performed, there was no other evidence of endocrine or kidney disease which might induce excessive urinary loss of magnesium. She was not alcoholic. No miscellaneous disease possibly responsible for hypomagnesemia such as acute pancreatitis or malignancy was present. Therefore, it is plausible to assume that excessive loss of gastrointestinal fluid due to severe vomiting and watery diarrhea may have been the cause of hypomagnesemia. She also presented hypocalcemia, which is well known to be often associated with hypomagnesemia. Although parathormone study was not performed, it was presumed that secondary hypocalcemia was developed due to hypomagnesemia. Despite hypomagnesemia, I hesitated to supplement magnesium because I was concerned about magnesium toxicity. Only calcium was administered, but the symptoms did not improve shortly. As the watery diarrhea stopped and the magnesium level was restored spontaneously, the calcium level came back to normal and the symptoms improved. Similar case report about hypomagnesemia after overdose of magnesium was searched in the literature, but it has never been reported. In conclusion, this case shows that overdose of magnesium-containing laxatives may possibly induce severe diarrhea, which, in turn, may develop paradoxical hypomagnesemia. This case also suggests that supplement of magnesium should be done in the same way as treating typical magnesium deficiency. Although it has not been studied whether magnesium should be given parenterally or orally in the case of paradoxical hypomagnesemia, it seems that it is reasonable to administer intravenously to prevent exacerbating diarrhea.