Case Presentation: A 66-year-old male with history of type 1 Von Willebrand disease, colonic polyps, and gastric ulcer from naproxen use due to osteoarthritis presented with a 3-week history of lethargy and fatigue with walking short distances. He denied melena or hematemesis but did report consistent ibuprofen use for his osteoarthritis over the past few months. Routine blood work was notable for a hemoglobin of 5.5 g/dl and a mean corpuscular volume (MCV) of 115 fL. He was hemodynamically stable without tachycardia. He had mildly diffuse abdominal tenderness but more so over the left lower quadrant without rebound tenderness or guarding. A rectal exam was notable for brown stool. The patient was started on a proton pump inhibitor (PPI) intravenously and an esophagogastroduodenoscopy (EGD) and possible colonoscopy were strongly considered. Iron studies revealed an elevated serum iron level (221 ug/dl) and a normal ferritin level (216 ng/ml), which raised the suspicion that the etiology of his anemia was not due to an acute gastrointestinal bleed. Further workup revealed spherocytes on the peripheral smear and a haptoglobin level of less than 15 mg/dl, along with an elevated LDH (493 IU/L), indirect bilirubin (3.0 mg/dl) with direct bilirubin (0.3 mg/dl), reticulocyte percentage (29%) and count (0.65 x 10e6/ul), and a positive direct antibody test for warm IgG antibodies. These results were consistent with a diagnosis of warm autoimmune hemolytic anemia (AIHA) and the patient was started on corticosteroids prior to discharge. On outpatient follow up a few months later, the patient was found to have low levels of IgG and IgM which were greater than two standard deviations below the mean for his age. This finding suggested a possible diagnosis of common variable immunodeficiency (CVID). 

Discussion: While this patient’s initial presentation was suspicious for anemia secondary to a gastrointestinal bleed, careful interpretation and follow up of laboratory tests eventually led to a much less common underlying etiology that was effectively treated. Anchoring on a possible gastrointestinal bleed as a cause of his anemia could have caused unwarranted exposure to invasive procedures. Cognitive biases such as anchoring predispose clinicians to focus on certain diagnoses irrespective of incongruent data. Regardless of a patient’s initial presentation, clinicians should factor unexpected results into clinical decision making to prevent exposure to unwarranted studies and procedures.

Conclusions: Although an unusual cause of anemia, 2.8-6.4% of cases of CVID have been associated with AIHA. This case serves as a reminder that the differential for anemia should include autoimmune causes even if there are is a possible alternate etiology.