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Enhanced risk of thrombotic disease in patients with acquired vitamin B 12 and/or folate deficiency: role of hyperhomocysteinemia

Enhanced risk of thrombotic disease in patients with acquired vitamin B 12 and/or folate... A number of studies have identified elevated levels of homocysteine (Hcy) as a risk factor for thrombosis. Given the relationship between Hcy and thrombosis, a high prevalence of thrombosis would be expected in patients with megaloblastic anemia. The aim of our study was to determine whether an acquired vitamin B 12 /folate deficiency is a risk factor for thrombosis. A retrospective case and control study was performed that included 193 cases with reduced levels of vitamin B 12 /folate. The cases were divided initially into two groups (105 with serum vitamin B 12 ≤150 pmol/l and/or low red cell folate ≤450 nmol/l and 88 with serum vitamin B 12 between 150 and 200 pmol/l and/or red cell folate between 450 and 590 nmol/l). The control group consisted of 87 additional patients who had normal levels of serum vitamin B 12 , red cell folate, and normal renal function. Serum Hcy, thrombotic events, and risk factors were evaluated in all participants. Eight patients (9%) in the control group had had previous vascular events although only three of these events (37.5%) were observed between the vitamin study and 2 years prior to the study. In the case group, 20% of the patients had a history of thrombosis. In contrast with controls, 85% of cases suffered thrombosis between the time they were diagnosed and 2 years prior to the time they were diagnosed as showing a vitamin deficiency. Multivariate analysis demonstrated that vitamin deficiency was a significant risk factor for arterial thrombosis (adjusted odds ratio (OR) 3.3, confidence interval (CI) 1.1–10.2). However, when hyperhomocysteinemia was included in the analysis, vitamin deficiency was no longer a risk factor, suggesting that hyperhomocysteinemia was responsible for arterial thrombotic risk in these patients (adjusted OR 2.5, CI 1.1–5.8). As a consequence of hyperhomocysteinemia, patients with acquired vitamin deficiency of vitamin B 12 /folate had a high risk of thrombosis. However, a more extensive study that controls risk variables and genetic factors is needed to sort out the various contributing factors. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Annals of Hematology Springer Journals

Enhanced risk of thrombotic disease in patients with acquired vitamin B 12 and/or folate deficiency: role of hyperhomocysteinemia

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References (29)

Publisher
Springer Journals
Copyright
Copyright © 2002 by Springer-Verlag
Subject
Legacy
ISSN
0939-5555
eISSN
1432-0584
DOI
10.1007/s00277-002-0560-6
pmid
12454698
Publisher site
See Article on Publisher Site

Abstract

A number of studies have identified elevated levels of homocysteine (Hcy) as a risk factor for thrombosis. Given the relationship between Hcy and thrombosis, a high prevalence of thrombosis would be expected in patients with megaloblastic anemia. The aim of our study was to determine whether an acquired vitamin B 12 /folate deficiency is a risk factor for thrombosis. A retrospective case and control study was performed that included 193 cases with reduced levels of vitamin B 12 /folate. The cases were divided initially into two groups (105 with serum vitamin B 12 ≤150 pmol/l and/or low red cell folate ≤450 nmol/l and 88 with serum vitamin B 12 between 150 and 200 pmol/l and/or red cell folate between 450 and 590 nmol/l). The control group consisted of 87 additional patients who had normal levels of serum vitamin B 12 , red cell folate, and normal renal function. Serum Hcy, thrombotic events, and risk factors were evaluated in all participants. Eight patients (9%) in the control group had had previous vascular events although only three of these events (37.5%) were observed between the vitamin study and 2 years prior to the study. In the case group, 20% of the patients had a history of thrombosis. In contrast with controls, 85% of cases suffered thrombosis between the time they were diagnosed and 2 years prior to the time they were diagnosed as showing a vitamin deficiency. Multivariate analysis demonstrated that vitamin deficiency was a significant risk factor for arterial thrombosis (adjusted odds ratio (OR) 3.3, confidence interval (CI) 1.1–10.2). However, when hyperhomocysteinemia was included in the analysis, vitamin deficiency was no longer a risk factor, suggesting that hyperhomocysteinemia was responsible for arterial thrombotic risk in these patients (adjusted OR 2.5, CI 1.1–5.8). As a consequence of hyperhomocysteinemia, patients with acquired vitamin deficiency of vitamin B 12 /folate had a high risk of thrombosis. However, a more extensive study that controls risk variables and genetic factors is needed to sort out the various contributing factors.

Journal

Annals of HematologySpringer Journals

Published: Nov 1, 2002

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