The hepatotoxic potential of diclofenac, a commonly used non-steroidal anti-inflammatory agent, is well established in literature. However, cases of diclofenac-induced liver disease have occurred almost exclusively with the oral formulation of this medication. We report the case of an elderly man with Paget’s disease and osteoarthritis who developed acute hepatotoxicity, as evidenced by laboratory diagnostics, four months after use of topical diclofenac 1% gel. Once diclofenac gel was discontinued, repeat blood work three weeks after discharge demonstrated return of liver function tests to baseline. Given the temporal relationship between the initiation and escalation of topical diclofenac and the changes in liver function tests, the likelihood of diclofenac-induced liver injury was deemed possible using a well-recognized causality assessment tool. Further research on topically administered non-steroidal anti-inflammatory agents is needed to identify monitoring intervals for early detection and avoidance of adverse effects in patients using topical diclofenac.

Case Description/Methods: Patient is a 26-year-old female with a past medical history significant for poorly controlled Crohn's disease who presented due to abdominal pain and hematochezia. Physical exam was notable for pain in the right upper quadrant. CT abdomen and pelvis with contrast showed high-grade small bowel obstruction with tethering of small bowel centrally concerning for active Crohn's disease. Colorectal surgery was consulted and performed laparotomy with ileocecectomy and end ileostomy formation. The terminal ileum and cecum were sent to pathology for further analysis. The pathology report showed "wall thickening with extensive neural hyperplasia (ganglioneuromatosis) and plexiform neurofibromas. The features seen in the resection favor intestinal neurofibromatous proliferations with secondary chronic mucosal changes. There is no transmural inflammation, granulomas or other features typically seen in Crohn's disease." (Figure) Discussion: This patient was initially thought to have SBO due to Crohn's disease flare, but pathology report showed that the underlying cause was secondary to plexiform neurofibromas. A systematic review of the literature shows that this is a rare finding as only 25 cases were identified from 1972 to 2013 of NF1 patients who underwent laparotomy for SBO [2]. SBO is a rare but possible manifestation of NF1.[3481] Figure 1. CT Abdomen / Pelvis showing high grade small bowel obstruction.

Figure 1. Peripherally enhancing fluid collection in the left upper quadrant/gastric wall. There is a communication between this collection with the gastric lumen.