Date Published: August 29, 2019
Publisher: Wolters Kluwer
Author(s): Ramy Mansour, Pujyitha Mandiga, Derek Thigpin.
We present a 71-year-old white man with active ileocolonic Crohn’s disease, recently started on budesonide therapy, who presented with extreme weakness and muscle aches. He was diagnosed with hypokalemia-induced rhabdomyolysis, 3 weeks after starting budesonide therapy. His symptoms and laboratory values improved with budesonide discontinuation and appropriate fluid and electrolyte replacement. This is only the second case of hypokalemia-induced rhabdomyolysis secondary to budesonide.
Budesonide has long been accepted as induction therapy for mild to moderate Crohn’s disease (CD).1 Although budesonide is considered highly efficacious because of its anti-inflammatory properties, it can be offsetting because of its serious side effects.2 We present only the second reported case of hypokalemia-induced rhabdomyolysis secondary to budesonide.
A 71-year-old white man presented with hypertension and ileocolonic stricturing CD since 1974. He had undergone 3 surgeries including ileocecectomy and 2 small bowel resections in 1975, 1986, and 2007. Current medications include 6-mercaptopurine, amlodipine, metoprolol, vitamin D, calcium, and a multivitamin. He was previously treated with sulfasalazine and oral mesalamine. He sparingly required oral steroids throughout his life. In October 2018, he presented for a 5-month history of worsening watery diarrhea and unintentional weight loss. Stool studies, including Clostridium difficile, were negative. Colonoscopy to the neoterminal ileum revealed a Rutgeerts score of i3. He was started on oral budesonide as a bridge to biologic therapy.
Hypokalemia-induced rhabdomyolysis due to laxative abuse, chronic diarrhea, renal tubular acidosis, and diuretics use is well reported.3,4 Hypokalemia is a known side effect of budesonide; however, there has only been 1 case report of hypokalemia-induced rhabdomyolysis from budesonide therapy.1,5,6 Rhabdomyolysis is a syndrome which is characterized by muscle necrosis with creatine phosphokinase 4 times more than the upper limit of normal.4
Author contributions: All authors wrote the manuscript. D. Thigpin is the article guarantor.