S6126 Incidental Discovery of Celiac Disease in a Patient With Mycosis Fungoides

Introduction: In asymptomatic patients with underlying Celiac disease (CD), the clue to the initial diagnosis can be through laboratory detection of vitamin malabsorption. We describe a patient whose CD was diagnosed after her vitamin A malabsorption was unmasked during treatment for an unrelated disease. Case Description/Methods: A 66-year-old woman was referred for evaluation of vitamin A malabsorption. She had a 15-year history of chronic skin rashes and was diagnosed with stage III folliculotropic mycosis fungoides 7 years prior. Her past medical history includes hypertension and ANA-positive inflammatory arthritis managed with losartan, hydroxychloroquine and low-dose prednisone, as well as surgical resection of an ovarian adenofibroma. Her mycosis fungoides had been treated with multiple modalities including ultraviolet B therapy (discontinued due to lack of response), bexarotene (discontinued due to hypertriglyceridemia), mogamulizumab (discontinued due to lack of response) and Acitretin with topical tretinoin cream. During Acitretin therapy, a low serum vitamin A level (298 mcg/L) was noted. Oral vitamin A supplementation produced inadequate response. Parenteral vitamin A injections raised her level to 477 mcg/L, but levels declined again upon cessation (377, 313 mcg/L). Workup for malabsorption revealed normal pancreatic elastase (>800), normal CFTR gene expression and slightly elevated fecal calprotectin (142 mcg/g). Vitamin E and K levels were at the low-normal range; iron, B12 and folate were normal. Notably, serum tissue transglutaminase IgA was significantly elevated (400.5 FLU), strongly suggesting CD as a possible cause of her vitamin A malabsorption. The patient is waiting for an endoscopic evaluation with biopsies for confirmation. Discussion: Micronutrient deficiencies are a common manifestation of CD and may precede gastrointestinal symptoms. Iron, vitamin D, and zinc deficiencies are most frequently reported, though vitamin A deficiency is seen in up to 7.5% cases. In this patient, vitamin A deficiency—identified during acitretin therapy—was the initial clue to CD. The vitamin A deficiency was incidentally found after treatment with acitretin during routine monitoring of vitamin A levels. Inadequate response to oral vitamin A supplementation suggests ongoing malabsorption. This case highlights the importance of considering CD in patients with unexplained vitamin deficiencies, even in the absence of gastrointestinal complaints.