{"title":"结核病患者维生素B6反应性铁母细胞贫血1例。","authors":"H Demiroglu, S Dündar","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>A 39-year-old woman was admitted with fatigue, weight loss, and fever. Nothing, except skin pallor could be found on physical examination. Her haemoglobin (Hb) was 6.3 g/dl. The blood picture showed dimorphic red cell changes and there were dyserythropoiesis and ring sideroblasts in the bone marrow. After detailed investigations, she was diagnosed with tuberculosis, and anaemia was assigned to chronic disease. With anti-tuberculosis therapy (including isoniazid), her Hb and bone marrow findings returned to normal. After cessation of therapy, Hb fell to 8.9 g/dl. Bone marrow examination again showed dyserythropoietic morphologic abnormalities and ring sideroblasts. No reason could be identified to explain the recurrence of anaemia. When we realised that preparations of isoniazid included vitamin B6 to prevent the development of sideroblastic anaemia, we challenged with pyridoxin 200 mg daily. Her Hb rose to 14.6 g/dl. We suggest that in any cases with sideroblastic anaemia, if no cause can be identified, or anaemia persists or recurs despite therapy, pyridoxine therapy should be instituted.</p>","PeriodicalId":22312,"journal":{"name":"The British journal of clinical practice","volume":"51 1","pages":"51-2"},"PeriodicalIF":0.0000,"publicationDate":"1997-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Vitamin B6 responsive sideroblastic anaemia in a patient with tuberculosis.\",\"authors\":\"H Demiroglu, S Dündar\",\"doi\":\"\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>A 39-year-old woman was admitted with fatigue, weight loss, and fever. Nothing, except skin pallor could be found on physical examination. Her haemoglobin (Hb) was 6.3 g/dl. The blood picture showed dimorphic red cell changes and there were dyserythropoiesis and ring sideroblasts in the bone marrow. After detailed investigations, she was diagnosed with tuberculosis, and anaemia was assigned to chronic disease. With anti-tuberculosis therapy (including isoniazid), her Hb and bone marrow findings returned to normal. After cessation of therapy, Hb fell to 8.9 g/dl. Bone marrow examination again showed dyserythropoietic morphologic abnormalities and ring sideroblasts. No reason could be identified to explain the recurrence of anaemia. When we realised that preparations of isoniazid included vitamin B6 to prevent the development of sideroblastic anaemia, we challenged with pyridoxin 200 mg daily. Her Hb rose to 14.6 g/dl. We suggest that in any cases with sideroblastic anaemia, if no cause can be identified, or anaemia persists or recurs despite therapy, pyridoxine therapy should be instituted.</p>\",\"PeriodicalId\":22312,\"journal\":{\"name\":\"The British journal of clinical practice\",\"volume\":\"51 1\",\"pages\":\"51-2\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"1997-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"The British journal of clinical practice\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"The British journal of clinical practice","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Vitamin B6 responsive sideroblastic anaemia in a patient with tuberculosis.
A 39-year-old woman was admitted with fatigue, weight loss, and fever. Nothing, except skin pallor could be found on physical examination. Her haemoglobin (Hb) was 6.3 g/dl. The blood picture showed dimorphic red cell changes and there were dyserythropoiesis and ring sideroblasts in the bone marrow. After detailed investigations, she was diagnosed with tuberculosis, and anaemia was assigned to chronic disease. With anti-tuberculosis therapy (including isoniazid), her Hb and bone marrow findings returned to normal. After cessation of therapy, Hb fell to 8.9 g/dl. Bone marrow examination again showed dyserythropoietic morphologic abnormalities and ring sideroblasts. No reason could be identified to explain the recurrence of anaemia. When we realised that preparations of isoniazid included vitamin B6 to prevent the development of sideroblastic anaemia, we challenged with pyridoxin 200 mg daily. Her Hb rose to 14.6 g/dl. We suggest that in any cases with sideroblastic anaemia, if no cause can be identified, or anaemia persists or recurs despite therapy, pyridoxine therapy should be instituted.