LAUSR

A 31yearold woman was admitted to the emergency department due to an accidental injury to her left thumb. Hemoglobin level was found to be very low in routine examinations. Her medical history was unremarkable except for occasional weakness. She had no history of chronic disease, operation, history of gastrointestinal blood loss, drug use, or bone fractures. On physical examination, arterial blood pressure was 100/60 mm Hg, HR 98 beats/min, RR 22/min, temperature 36.4°C. Bilateral sclera were seen to be distinctly blue. (Figure 1) Lymphadenopathy and organomegaly were not detected. Hemoglobin level was 4.6 g/dl, RBC 2.85 × 106, hematocrit 17.8%, WBC 5.97 × 109/L, platelets 484 × 109/L, MCV 62.5 fL, MCH 16.1 pg, INR 1.13, and other biochemical findings were normal. Anisocytosis, poikilocytosis, hypochromia, and microcytosis were observed in the blood peripheral smear. (Figure 2) Iron deficiency anemia (IDA) was considered in the patient whose ferritin 1.31 ng/ml, total ironbinding capacity 466 μg/dL, iron 12 μg/dL, RDW 31.8%, reticulocyte index 0.14%, Mentzer index 23, and folate and Vit B12 levels were in the normal range. Abdominal ultrasonography was normal. Intravenous ferric carboxymaltose 500 mg × 2 was administered, and blood transfusion was performed. Gynecological disorder was considered as the etiological factor in the patient who had excessive menstrual bleeding, and she was directed to gynecology by arranging oral iron replacement. Meanwhile, other pathologies that could potentially cause blue sclera were evaluated. Osteogenesis imperfecta was excluded. Homocysteine level was 7 μmol/L (N), Rf 10 IU/ mL (N), ESR 20 mm/h, Anti CCP, and hepatitis markers were negative. The patient came to the outpatient clinic 1 month later. The blue sclera sign was ongoing, but she later discontinued followup. Ocular involvement in the course of IDA may present as conjunctival paleness, papilledema, and pseudotumor cerebri. Also, the blue sclera that can be seen in the course of IDA was first defined by von Ammon in the 19th century, and Osler found that it can be seen in patients with IDA anemia in 1908. It is thought that it may be due to deterioration in collagen structure, decrease in scleral thickness and so an increase in light transmission. It can be seen