Prevalence of hyperhomocysteinaemia, activated protein C resistance and prothrombin gene mutation in inflammatory bowel disease.
BACKGROUND
Thromboembolic disease is a significant cause of morbidity and mortality in patients with inflammatory bowel disease (IBD). A hypercoagulable state exists in IBD that may involve many components of haemostasis and is closely linked to the disease pathogenesis. It has been proposed that microvascular thrombosis and infarction may trigger the underlying inflammatory process.


OBJECTIVE
To determine the prevalence of prothrombotic factors including hyperhomocysteinaemia, activated protein C (APC) resistance and prothrombin gene mutations as well as vitamin levels in the local IBD population.


METHODS
A total of 68 patients (37 men and 31 women) attending the IBD clinic were enrolled into the study. Citrated and ethylenediamine tetraacetic acid blood samples were collected from all patients as well as from 30 controls. Homocysteine levels were measured using the IMX immunoassay. APC resistance was measured using an unmodified activated partial thromboplastin time-based clotting assay. Prothrombin mutations were determined using polymerase chain reaction with the HB-gene factor II detection system.


RESULTS
Mean homocysteine levels were significantly higher and APC resistance ratios significantly lower in IBD patients compared with controls. No significant difference was detected between patients with ulcerative colitis or Crohn's disease. There was no significant increase in the incidence of prothrombin mutation in IBD patients. IBD patients had lower vitamin B12 and higher serum folate levels than controls.


CONCLUSIONS
High homocysteine and high serum folate may be associated with low vitamin B12 levels in IBD patients. We did not find any association between a low APC ratio and the factor V Leiden mutation or high factor VIII levels. Both hyperhomocysteinaemia and a low APC ratio may contribute to an increased risk of thromboembolic disease in IBD patients.
Mahmood
Asif
A
North Hampshire Hospital, Basingstoke, UK.
Needham
Jane
J
Prosser
Jeanne
J
Mainwaring
Jason
J
Trebble
Tim
T
Mahy
Gillian
G
Ramage
John
J
D020016:Activated Protein C Resistance / Q000097:blood* / Q000150:complications / Q000235:genetics; D000328:Adult; D003093:Colitis, Ulcerative / Q000097:blood / Q000150:complications / Q000235:genetics; D003424:Crohn Disease / Q000097:blood / Q000150:complications / Q000235:genetics; D005165:Factor V / Q000235:genetics; D005169:Factor VIII / Q000032:analysis; D005260:Female; D005492:Folic Acid / Q000097:blood; D006710:Homocysteine / Q000097:blood; D006801:Humans; D020138:Hyperhomocysteinemia / Q000097:blood* / Q000150:complications / Q000235:genetics; D015212:Inflammatory Bowel Diseases / Q000097:blood* / Q000150:complications / Q000235:genetics; D008297:Male; D008875:Middle Aged; D009154:Mutation; D011486:Protein C / Q000032:analysis; D011516:Prothrombin / Q000235:genetics*; D014805:Vitamin B 12 / Q000097:blood
D011486:Protein C; C095381:factor V Leiden; D006710:Homocysteine; D005165:Factor V; D011516:Prothrombin; D005169:Factor VIII; D005492:Folic Acid; D014805:Vitamin B 12