Anaemia in Crohn's Disease
N H Dyer, J. Anthony Child, David L. Mollin, A M Dawson
Abstract
N H Dyer, J. Anthony Child, David L. Mollin, A M Dawson
Abstract
Abstract Sixty-three patients admitted to hospital with an exacerbation of Crohn's disease were investigated. Anaemia was found in 79 per cent of males and 54 per cent of females. Low levels of serum iron (65 per cent), total iron-binding capacity (22 per cent), serum vitamin B12, (16 per cent), serum folate (64 per cent), and red-cell folate (35 per cent) were also present. With the exception of the serum vitamin B12, these levels were directly related to the severity of the disease and were less reduced in patients with post-operative recurrences. There was a poor correlation with the site of disease. The serum iron, iron-binding capacity, and transferrin saturation were unreliable in the diagnosis of iron deficiency. An increased TIBC usually indicated iron deficiency and a subnormal TIBC suggested chronic inflammation but did not exclude iron deficiency. Based on the examination of bone marrow iron stores, evidence of iron deficiency was found in 18 (39 per cent) of 46 patients. The incidence of iron deficiency may have been over emphasized in the past because bone marrow iron stores have not always been examined. Of the 46 patients who had bone marrow aspirated, 18 (39 per cent) were megaloblastic. Folate deficiency was implicated as the underlying cause in 11 and vitamin B12 deficiency in six patients; one patient had both deficiencies. Vitamin B12, deficiency was usually associated with ileal resection, while folate deficiency was probably due to dietary deficiency and/or increased folate requirements. Vitamin B12, or folate deficiency should not be implicated as the cause of anaemia on the basis of serum levels alone. Moreover, the finding of megaloblastic change in the marrow should not obscure the importance of coexisting iron deficiency or the effects of the inflammatory disease process on erythropoiesis. When there is clear evidence of iron, folate, or B12-deficiency anaemia this should be treated with appropriate haematinics, although the response may be suboptimal until the inflammatory process is suppressed. As the disease process itself aggravates the severity of the anaemia, there will probably be a partial response to any treatment which reduces the activity of the disease.
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Abstract Sixty-three patients admitted to hospital with an exacerbation of Crohn's disease were investigated. Anaemia was found in 79 per cent of males and 54 per cent of females. Low levels of serum iron (65 per cent), total iron-binding capacity (22 per cent), serum vitamin B12, (16 per cent), serum folate (64 per cent), and red-cell folate (35 per cent) were also present. With the exception of the serum vitamin B12, these levels were directly related to the severity of the disease and were less reduced in patients with post-operative recurrences. There was a poor correlation with the site of disease. The serum iron, iron-binding capacity, and transferrin saturation were unreliable in the diagnosis of iron deficiency. An increased TIBC usually indicated iron deficiency and a subnormal TIBC suggested chronic inflammation but did not exclude iron deficiency. Based on the examination of bone marrow iron stores, evidence of iron deficiency was found in 18 (39 per cent) of 46 patients. The incidence of iron deficiency may have been over emphasized in the past because bone marrow iron stores have not always been examined. Of the 46 patients who had bone marrow aspirated, 18 (39 per cent) were megaloblastic. Folate deficiency was implicated as the underlying cause in 11 and vitamin B12 deficiency in six patients; one patient had both deficiencies. Vitamin B12, deficiency was usually associated with ileal resection, while folate deficiency was probably due to dietary deficiency and/or increased folate requirements. Vitamin B12, or folate deficiency should not be implicated as the cause of anaemia on the basis of serum levels alone. Moreover, the finding of megaloblastic change in the marrow should not obscure the importance of coexisting iron deficiency or the effects of the inflammatory disease process on erythropoiesis. When there is clear evidence of iron, folate, or B12-deficiency anaemia this should be treated with appropriate haematinics, although the response may be suboptimal until the inflammatory process is suppressed. As the disease process itself aggravates the severity of the anaemia, there will probably be a partial response to any treatment which reduces the activity of the disease.
Key concepts: Iron deficiency, Medicine, Transferrin saturation, Serum iron, Vitamin B12, Total iron-binding capacity, Internal medicine, Gastroenterology