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Clozapine-induced constipation is an increasingly recognized adverse reaction that frequently impairs optimal management of treatment-resistant schizophrenia. The Food and Drug Administration recently strengthened an existing warning for clozapine, citing constipation as an adverse effect that can progress to serious bowel complications. Evidence-based guidelines for laxatives in the management of clozapine-induced constipation remain scarce, and there is a general need for improved algorithms in the management of this common condition. Lubiprostone is a relatively new laxative that has labeled indications for opioid-induced constipation, irritable bowel syndrome with constipation, and chronic idiopathic constipation. This case series describes clinical pearls associated with four cases of treatment-resistant schizophrenia who underwent treatment of clozapine-induced constipation with lubiprostone. The findings of this case series suggest that there may be significant therapeutic potential in the utilization of lubiprostone for the management of clozapine-induced constipation with a low risk of adverse reactions. The study of lubiprostone benefit (i.e., without coadministration of other laxatives) continues to be of prominent interest in understanding its ability to manage clozapine-induced constipation.

BACKGROUND: Hypermagnesemia can be a fatal condition and should be diagnosed early on. Most reports of hypermagnesemia have been of adults with impaired renal function. We describe the case of a pediatric patient without renal dysfunction who developed severe hypermagnesemia.
METHODS: A healthy 20-month-old Asian girl presented to our emergency department with episodes of vomiting and a reduced level of consciousness. The neurological examination showed a symmetric decrease in muscle tone, and the deep tendon reflexes were decreased. On admission, her magnesium (Mg) level was 11.0 mg/dL after receiving magnesium oxide for 4 days because of constipation. She was immediately administered calcium gluconate infusion (3.9 mEq), and then was continuously infused with it (0.23 mEq/h) as a Mg antagonist to cardiac side effects. She was kept hydrated with 0.9% sodium chloride to maintain good urine output to excrete the Mg. The level of the serum Mg decreased to 2.4 mg/dL, enabling her to regain consciousness. During 5 years of follow-up, she was neurologically well, without the recurrence of hypermagnesemia.
CONCLUSIONS: Even in the absence of significant renal dysfunction, the prescription of a laxative containing Mg for constipation can result in severe hypermagnesemia. In addition, the symptoms of hypermagnesemia are nonspecific, and early diagnosis is difficult unless it is actively suspected.

OBJECTIVE: The imbalance in serum potassium caused by laxatives can negatively affect the cardiovascular system, leading to life-threatening consequences. Our objective was to evaluate the reported evidence of adverse events related to the cardiac system due to laxative-induced hypokalaemia from case reports.
METHODS: A systematic electronic literature search of PubMed, Embase, the Cochrane Library and Science Direct was conducted for the period 1995-2019. In these databases, search terms describing hypokalaemia and cardiotoxicity were combined with the term laxative use.
CONCLUSIONS: Over the 23 years, 27 incidents were identified in 12 countries. There were 19 female and eight male patients, with ages ranging from 1 month to 93 years. The frequency of reported cases according to severity was the following: severe hypokalaemia 48%, moderate hypokalaemia 44.4% and mild hypokalaemia 7.4%. In 70% of patients, the effect of laxative on the heart was typical hypokalaemic electrographic changes, 7.4% showed abnormal changes in cardiac rhythm, whereas in 18.5%, the cardiotoxicity observed was a very serious kind. Two patients died due to severe cardiac effects.
CONCLUSIONS: The laxatives-along with the involvement of some other contributing factors-caused mild-to-severe hypokalaemic cardiotoxicity. These factors were non-adherence of the patient to the recommended dosage, laxative abuse, drug-drug and drug-disease interactions, non-potassium electrolyte imbalances and the use of herbal laxatives. We recommend that laxatives and aggravating factors should be taken into account in the assessment of patients with suspected hypokalaemic cardiotoxicity.

We report a fatal case of hypermagnesemia caused by oral ingestion of milk containing magnesium chloride as a folk remedy. The autopsy of the 75-year-old woman showed no injury or illness as the cause of death. Neither alcohol nor controlled drugs were found by the toxicological analysis. Her posthumous serum magnesium concentration was 10.2 mg/dL. The concentration of magnesium in serum was higher than that of the previous reports. Therefore, the cause of death was considered to be hypermagnesemia. Recently, the prescription drugs, over-the-counter drugs, and health foods containing magnesium are consumed as supplements in the world, and their potential toxicity should be recognized.