Development of collagenous colitis in inflammatory bowel disease: two case reports and a review of the literature.

The occurrence of collagenous colitis (CC) in patients with pre-existing inflammatory bowel diseases (IBD) is rare, with only seven cases reported in the past. Herein, we report two IBD cases who developed CC after successful treatment of their IBD with two different tumor necrosis factor (TNF)-α inhibitors, which have been previously reported to successfully treat refractory CC. This report highlights the need to do random biopsies of the colon for CC diagnosis in IBD patients with symptoms of diarrhea after complete mucosal healing. The report also reviews plausible mechanisms as to how CC may develop, including the role of multiple medications.

Collagenous colitis development occurs after long standing mucosal healing in IBD with TNF-α inhibitors, and could be due to exaggerated healing response from excess TNF-α inhibition.

Collagenous colitis is a relatively rare disorder affecting mainly middle-aged women where they present with chronic non-bloody diarrhea. Both with lymphocytic colitis they compose microscopic colitis. The exact cause of collagenous colitis is still unknown however; many potential pathophysiologic mechanisms have been proposed but no convincing mechanism has been identified. Collagenous colitis has been linked to medications mainly NSAIDs, SSRIs, and PPIs. It is also believed that collagenous colitis is autoimmune disease and there are weak believe it could have some genetic inheritance. We reported before two cases of collagenous colitis developed in patients with Crohn's disease and ulcerative colitis while they were in complete mucosal remission after being treated with tumor necrosis factors-α inhibitors. In this article we will try to explain how collagenous colitis can develop in patients with inflammatory bowel disease especially those on tumor necrosis factors-α inhibitors.

A Rare Case of Esophageal Adenocarcinoma with Urinary Bladder Metastasis.

Metastatic esophageal adenocarcinoma to the urinary bladder is extremely rare. We describe a previously healthy 49-year-old female with recent diagnosis of adenocarcinoma of the gastroesophageal junction with metastatic disease to the liver. Biopsy was positive for human epidermal growth factor receptor 2 (HER2) by Fluorescence In Situ Hybridization (FISH). She received six cycles of Cisplatin, 5-Fluorouracil, and Herceptin and subsequently developed symptomatic anemia and hematuria. Cystoscopy with retroflexion was performed and she received a transurethral resection of bladder tumor with fulguration. Pathology of the bladder tumor revealed similar morphology to her liver metastasis and immunohistochemical stains were consistent with metastatic esophageal cancer. Three weeks after being diagnosed with metachronous urinary bladder metastasis from esophageal adenocarcinoma primary, she expired. She only received her first cycle of palliative chemotherapy with Ramucirumab and Paclitaxel.