Chronic iron deficiency anaemia after Roux-en-Y gastric bypass leading to Plummer Vinson syndrome.

Plummer-Vinson Syndrome (PVS) is a rare condition that classically presents as a triad of dysphagia, proximal esophageal webs, and iron deficiency anemia. The prevalence of PVS has rapidly declined since it was first described by Henry Plummer and Stanley Vinson in the early 1900’s due to improved nutritional status and subsequent resolution of iron deficiency . To our knowledge, only one prior case of PVS has been reported following gastric bypass surgery. PVS is most commonly observed among middle-aged Caucasian females, and only rarely is present among those of African descent. We report a unique case of PVS diagnosed during a workup for chronic iron deficiency anemia in an African-American patient with a prior history of gastric bypass surgery.
A 31-year-old African-American female status post Roux-en-Y gastric bypass surgery for morbid obesity in 2010 presented to the hospital in August 2016 with dysphagia of three to four weeks duration. She noted more discomfort with solid than liquid substances as well as epigastric pain. She reported often having to massage her anterior neck to help with passage of food. On review of systems she endorsed progressive burning sensation around her mouth and tongue, discoloration of her tongue, and worsening fatigue. She denied fever, chills, nausea, vomiting, diarrhea, chest pain, shortness of breath, melena, hematochezia, easy bruising, or rash. She was not taking any medications although she reported a history of previous iron supplementation more than two years ago which was selfdiscontinued due to constipation and dyspepsia. Treatment for PVS includes iron supplementation initiation as well as dilation of esophageal webs as was done in our patient. These patients need additional surveillance after diagnosis due to an increase risk of squamous cell carcinoma of the pharynx and esophagus. Although the pathophysiology and etiology of PVS development among patients with chronic