Endocarditis in Crohnʼs disease

To the Editor: Bacterial endocarditis is an uncommon cardiac complication of inflammatory bowel disease (IBD).1 It has been described in both Crohn's disease (CD) and ulcerative colitis (UC). We describe a patient with Enterococcus fecaelis endocarditis complicating Crohn's colitis. A 56-year-old female with a long history of steroid-dependent Crohn's pancolitis was poorly adherent to medical therapy and follow-up. She refused recommended evaluation, conversion to immunomodulator or biologic therapy, or total colectomy. She presented emergently with acute onset of pain in both feet. She had noticed recent onset of pain in the left lower quadrant as well. She had been on prednisone 40 mg/day for 6 weeks, and had not returned for follow-up to taper her dose. Physical exam revealed that both feet were cold, pale, and pulseless. There was tenderness in the left lower quadrant. Bowel sounds were present. Doppler ultrasound demonstrated emboli in both iliac arteries. Emergent embolectomy was performed. Gram stain revealed Gram-positive cocci within the emboli. Multiple blood cultures were positive for E. fecaelis. A 2D echocardiogram showed mitral valve vegetations and mitral regurgitation. Computed tomography of the abdomen and pelvis revealed a left lower quadrant walled off abscess in contiguity with the left colon (Fig. 1). She was treated with colectomy and diverting colostomy, 6 weeks of intravenous antibiotics, and ultimately, mitral valve replacement. Her corticosteroids were tapered and discontinued. CT scan showing abdominal abscess in contiguity with the left colon. Endocarditis can complicate IBD.1 In a study of 213 consecutive patients with bacterial endocarditis, there was a statistically significant 44-fold overrepresentation of IBD patients compared with expected based on prevalence data.1 Six of these 213 patients with endocarditis had IBD—3 with CD and 3 with UC. All of these 6 patients were on immunosuppressive medications. Three of these patients had surgical and/or endoscopic procedures, and 2 of these 3 patients also had central lines. Three of the 6 patients with endocarditis had preexisting valvular lesions as a risk factor for endocarditis, while 3 did not. Three patients without underlying valvular lesions had severe IBD activity. Three of the 6 patients with endocarditis were infected with fecal organisms; 2 with E. fecaelis and 1 with pepto-streptococcus. It was felt that a combination of immunosuppressive therapy together with IBD activity and/or instrumentation was required for endocarditis to occur. Our case highlights the risk of pyogenic complications of CD coupled with prolonged corticosteroid immunosuppression in the development of endocarditis. In addition, prolonged corticosteroid immunosuppression may have contributed to more aggressive complications of endocarditis (multiple septic emboli) as seen in this case. Another known but uncommon cardiac association with IBD is pericarditis.2 This may represent an autoimmune phenomenon, an incidental association, or a complication of therapy (mesalamine or sulfasalazine sensitivity or anti-tumor necrosis factor drug-induced lupus). Other rare cardiac associations include cardiac tamponade,3 myocarditis,4,5 cardiomyopathy,6 EKG abnormalities,7 heart block,8 2D echocardiographic abnormalities,8 aortic insufficiency—with and without9 ankylosing spondylitis,15 and aortitis.10 Anti-tumor necrosis factor therapy has also been associated with congestive heart failure11 and drug-induced lupus-related pericarditis12 in IBD. In summary, we report a patient with E. fecaelis endocarditis complicated by aggressive septic emboli in the setting of corticosteroid therapy and an abdominal abscess in Crohn's colitis. This emphasizes the importance of minimizing corticosteroid exposure and aggressively managing purulent complications of CD.