Case Report Shortness of Breath: Anyone Consider the Gut?

Dyspnea is a common complaint that compels patients to seek medical care. Usual etiologies include asthma, chronic obstructive pulmonary disease, myocardial dysfunction and pulmonary embolus. In our case a patient was admitted to our hospital with dyspnea, fatigue and pleuritic chest pain for three weeks. Physical examination and imaging were unremarkable. Labs were only significant for severe microcytic anemia with hemoglobin 2.8 g/dL, hematocrit of 12%, MCV 56, iron <6 mcg/dL, and ferritin 13.9 ng/mL. All the usual causes of iron deficiency anemia were ruled out and patient was diagnosed with celiac disease. The incidence of celiac disease in patients with iron deficiency anemia has been reported to be from 6% to 12%. Among patients whose anemia does not respond to iron therapy the incidence increases to 20%. This case illustrates that when a patient with common complaints of dyspnea and anemia is evaluated celiac disease should always be considered in the differential.


Introduction
Dyspnea is a very common complaint for which patients seek medical care. In majority of the patients their dyspnea can be attributed to one of the following causes asthma, pneumonia, chronic obstructive pulmonary disease, myocardial dysfunction, pulmonary embolus and deconditioning [1]. Our case here presents an etiology representing a subtle cause of myocardial dysfunction.

Case Presentation
A 39 year old Caucasian male with no past medical history was admitted to an inpatient service for the complaint of dyspnea on exertion and fatigue for three weeks. His exertional capacity had progressively declined from 1000ft to 100ft. He also reported pleuritic chest pain and a dry cough. He denied fevers, chills, hemoptysis, hematemesis, melena, hematuria, hematochezia, decreased appetite, dysphagia, abdominal pain, diarrhea and PICA. He admitted to consuming a balanced diet and denied a surgical or traumatic history, foreign family heritage or history of blood disorders.
A celiac antibody panel performed to further evaluate the showed 124 Transglutaminase IgA Abs, 46 Gliadin IgG Abs, >30 Gliadin IgA Abs,   Quantitative IgA 344 mg/dL, 9 Transglutaminase IgG Abs. Levels of >30 are positive and suggest celiac disease. An EGD showed flattening of duodenal folds and distal esophagitis. Random biopsies were consistent with celiac disease (Figure1, Figure 2).

Discussion
The fundamental factor in determining this patient's cause of dyspnea is severe iron deficiency, which in the USA is mostly secondary to occult blood loss [2]. But more and more studies now are pointing towards celiac disease as a frequent cause of iron deficiency. One study reports that 12% of 93 patients with iron deficiency anemia had findings compatible with celiac disease on small bowel biopsy [3]. Another study reports the incidence as 6% (85 patients) and the incidence increases to 20% in the subset of anemic patients that are unresponsive to iron therapy [4]. It remains unclear whether a component of blood loss contributes to iron deficiency in celiac disease [5][6][7].
The diagnosis of celiac disease often requires serological testing and small bowel biopsy, both of which are recommended while patients are on a gluten-containing diet [5]. The exception to a small bowel biopsy is biopsy-proven dermatitis herpetiformis [6]. A positive IgA tissue transglutaminase or endomysial antibody test is considered highly specific, whereas standard antigliadin antibody tests have lower diagnostic accuracy and are falsely positive up to 20% of the time [5]. The hallmark histology of small bowel biopsy is the presence of villous atrophy. Several biopsies in the second and third portion of the duodenum should be obtained to maximize the likelihood of detecting villous atrophy [7].
As our case illustrates the differential for SOB is not just limited to pulmonary and cardiac disease processes but gastrointestinal diseases as well. Celiac disease should now be considered in all patients with iron deficiency anemia and may help us identify this disease process earlier on.