Case Presentation: A 51 year old woman with lichen planus presented with dysphagia to solids and liquids, excess oral secretions, and globus sensation for three days. Her history included hypothyroidism, GERD, and episodic dysphagia for two years. Surgical history included a prior endoscopy revealing nonspecific esophagitis. The patient had no toxic habits and family history was noncontributory.  Pertinent findings included gray-white patchiness of her lateral tongue, buccal mucosal ulceration, and hyperpigmented patchy lesions over her arms, legs, and back. Routine studies including CBC, CMP, PT/INR, TSH as well as chest x-ray were non-diagnostic.  Our patient was started on IV solumedrol, IV pantoprazole, and nystatin solution. Endoscopy revealed upper third food impaction, two separate proximal esophageal stenoses, esophagitis with diffuse desquamation and highly friable mucosa with multiple bullae. Perforation risk from the degree of mucosal friability precluded endoscopic dilation. Our patient improved on day three of IV steroid therapy and tolerated an oral diet. Esophageal biopsy showed nonspecific chronic inflammation that was negative for metaplasia. She was discharged on a long term oral steroid taper, carafate and protonix for esophageal lichen planus.

Discussion: Our case is significant because it illustrates an exceedingly rare cause of a common presenting inpatient complaint of dysphagia. Lichen planus itself is an infrequent, multifaceted disease; <1% have esophageal involvement, and only about 80 cases have ever been reported. Patients usually present with episodic dysphagia or odynophagia. Endoscopic findings include pseudomembranes, friable inflamed mucosa, submucosal papules, lacy white plaques, erosions, strictures, and bullae, all of which spare the lower third of the esophagus. Histologic findings include saw-tooth epidermis with “Civatte Bodies”, or apoptotic keratinocytes at the dermoepidermal junction. Our patient’s history and endoscopic findings included many classic findings associated with the disease; however, biopsy results were nonspecific. The presumptive diagnosis was strongly supported by the degree of mucosal friability in a patient with known cutaneous and oral lichen planus. Our diagnosis was further strengthened by the localization of findings to the upper two thirds of the esophagus, highly characteristic of esophageal lichen planus. Of note, limited case series have shown typical Civatte bodies in only ~10-15% suspected cases.

Conclusions: Esophageal lichen planus is a rare entity with the potential for significant morbidity.  A paucity of literature and standardized diagnostic criteria underscores the need for clinical diagnosis, as biopsy alone is insufficient. Esophageal dilation carries a risk of perforation and management relies on empiric steroid therapy.