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Manfred Hauben, Hypokalemia associated with infliximab: A pharmacovigilance perspective, Inflammatory Bowel Diseases, Volume 13, Issue 7, 1 July 2007, Pages 935–936, https://doi.org/10.1002/ibd.20117
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To the Editor:
I read with interest the case report by Karamanolis et al1 describing symptomatic hypokalemia associated with infliximab. The authors identify infliximab as the most likely etiological suspect based on the absence of prior hypokalemic episodes, a normal pretreatment level of serum potassium, and the development of hypokalemia “just after infliximab infusion.”
A possible role of intravenous hydrocortisone (given as premedication2) merits discussion. Hypokalemia secondary to the mineralocorticoid actions of hydrocortisone infusion is documented in a variety of settings, including inflammatory bowel disease, although often after multiple doses.3,–5 Both mineralocorticoid and glucocorticoid actions are primarily genomic effects requiring several hours to become fully operational, although more rapid effects may occur via nongenomic mechanisms.6,7 The reported time interval spanning premedication, infliximab infusion (minimum duration of 2 hours2), and observation of the adverse event (AE) several hours after the infliximab infusion is consistent with a genomically mediated mineralocorticoid effect of hydrocortisone. Therefore, the timing after infliximab infusion, cited by the authors as evidence of infliximab as the etiology, does not exclude hydrocortisone as a suspect drug, especially given the potential for preexisting subclinical potassium depletion due to gastrointestinal losses. However, the apparent offset of the clinical effect may possibly have more differential diagnostic value.
