Iron malabsorption is an important cause of irondeficiency anaemia (IDA). Coeliac disease-induced malabsorption in the small intestine also causes IDA. Furthermore, severe IDA may be the only sign of coeliac disease without any gastrointestinal symptoms. Eightyfive percent of patients with IDA recover from anaemia after iron-replacement therapy (1-3).
In 15-30% of patients with IDA, the underlying pathology is not known. We present here two cases of coeliac disease who had a 3-year history of unexplained severe iron-deficiency anaemia
Case 1. A 41-year old female with complaints of weakness, pallor, and palpitation was admitted to the internal medicine clinic of Turgut Ozal Medical Center, Malatya, for 3 years of regular oral iron treatment of refractory anaemia. Physical examination revealed pallor and systolic murmur on the cardiac apex. A complete blood count showed: haemoglobin of 4.6 g/dl, white blood cell count of 5.500/mm, platelet count of 367.000/ mm, mean corpuscular volume of 56 fl, and mean corpuscular haemoglobin of 16 pg. Serum iron was 22 ìg/dl, serum transferrin 508 mg/dl, and ferritin 11 ng/ dl. A blood-smear examination revealed hypochromia, anisocytosis, poikilocytosis, and microcytosis. Antigliadin IgA antibody was 18.25 U (normal value: 0-10 U) and anti-gliadin IgG antibody was 31.0 U (normal value: 0-24 U).
Case 2. A 34-year-old female with complaints of weakness for 3 and a half years was admitted to the clinic with refractory anaemia to oral iron treatment. She was regularly taking iron-containing drugs for the last 3 and a half years. She was pale, and had finger clubbing. Physical examination was otherwise normal. A complete blood count showed: haemoglobin of 5.2 g/dl, white blood cell count of 6.700/mm, platelet count of 287.000/ mm, mean corpuscular volume of 62 fl, and mean corpuscular haemoglobin of 17 pg. Serum iron was 16 ìg/dl, serum transferrin 520 mg/dl, and ferritin 9 ng/dl. A blood-smear examination revealed hypochromia, anisocytosis, poikilocytosis, and microcytosis. Antigliadin IgA antibody was 21.10 U, and anti-gliadin IgG antibody was 29.5 U.
Both the patients had no symptoms of malabsorption, such as diarrhoea, abdominal pain, and steatorrhea, but both had normal menstruation. They also did not have a history of operation on gastrointestinal, gynaecologic or pulmonary system. Biochemical tests, including serum potassium, sodium, calcium, phosphorus, creatinine, alkaline phosphatase, cholesterol, partial thromboplastin time, immunoglobulin A, G, M, tumor markers, folic acid, vitamin B12, haptoglobulin, acid haemolysis test (Ham's test), and thyroid function tests, were within normal limits. Serum protein level and protein electrophoresis were also normal. The erythrocyte sedimentation rates were 12 and 15 mm/h respectively. No parasite was detected in faeces; the test was repeated 3 times in both the patients, and the lipid tests of faeces were negative in both the patients. An endoscopical examination of the stomach, small bowel, and large bowel revealed no focus of bleeding, but there were subtotal atrophy in the duodenal mucosas and flattening and loss of villi in the biopsy specimens. Only gluten-free diet with no iron supplementation was given as treatment, and no antibiotic was used. An examination of both the patients after 7 months showed an improvement in the haemoglobin levels (12.2 and 13.1 g/dl respectively), and endoscopical and pathological examinations of the small intestine were found to be normal.
Coeliac disease (gluten-induced enteropathy) is a chronic, probably hereditary, illness of unknown aetiology, occurring in both children and adults, and is manifested clinically by steatorrhoea and deficiencies produced by intestinal malabsorption. The metabolites of gluten are thought to trigger an immunological reaction that leads to the damage of enterocytes and finally to malabsorption (4). …