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Agarwal et al. CVT in UC relapse

for MTHFR mutation. Furthermore, he was also found vein thrombosis is clinically suspected, so that the
to have serum homocysteine level of 20.5 μmol/L. early diagnosis is not missed. MRI and MRV are
His levels of anti-nuclear antibody, anti-double considered the best tools for diagnosis and follow-up.
strand deoxyribonucleic acid, lupus anticoagulants, The anticoagulation therapy for patients with CVT is
antiphospholipid antibodies, anticardiolipin antibodies, similar in both with active and chronic UC, and has
and anticyclic citrullinated peptides were negative. been associated with lower incidence of mortality, if
started at appropriate time.
The patient clinically improved in a period of five to
seven days with the treatment. His symptoms had In patients with cerebral venous thrombosis,
gradually subsided. He was then discharged. favourable results are possible with earlier diagnosis
and appropriate treatment plan. If patients remain
DISCUSSION untreated, the mortality rate can be very high.
Therefore, the present report highlights the value of
Extensive thrombosis of venous sinuses is a serious considering the diagnosis of CVT, in patients with IBD,
complication of ulcerative colitis. Venous thrombosis especially when the disease is in its relapse phase.
is known to occur with a greater frequency than
general population in patients with ulcerative colitis. In conclusion, it is necessary to suspect CVT in a patient
Incidence of thrombosis is about 6.5% in patients with with relapse of UC, who presents with recent, unusual
active IBD. The relationship between thrombosis and severe headache, stroke like features, seizures, or
[4]
UC has not been well defined. But recent evidence any other brain syndrome. The physician, neurologist
suggests that UC is an important factor for thrombotic or the gastroenterologist should be well aware of the
complications. The exact cause for the increased increased risk of CVT in patients with relapse of UC.
[7]
rate of thrombotic events in patients with IBD is still The gastroenterologists treating UC should be wise
uncertain. However, it is most likely related to the enough to suspect CVT, especially in genetically
interaction between acquired and inherited genetic predisposed and immediately seek a neurologist’s
risk factors. Also, the recent research has suggested opinion for proper management. Also, it would be
it to be an interaction between the coagulation useful to investigate for genetic hypercoaguable state
cascade in the body and cytokine mediators of chronic in patients of UC, in order to find out the at-risk group
inflammation and also the inflammatory process can of UC patients.

itself activate coagulation cascade. The inflammatory
[8]
process initiates clotting, impairs the fibrinolytic system Financial support and sponsorship
and decreases the activity of natural anticoagulation Nil.
mechanisms. Depression of anticoagulation mechanisms
not only increases thrombosis, but also potentiates Conflicts of interest
the inflammatory process. That is why, the majority There are no conflicts of interest.
of thrombotic events occur during the active phase Patient consent
of disease. Abnormalities in coagulation cascade
such as elevated fibrinogen level, factor V, factor VIII, Patient consent was obtained from the patient.
and increase in circulating thrombin-antithrombin Ethics approval
complexes, decreased antithrombin III, thrombocytosis Ethics approval was obtained prior to the
and increased platelet aggregation have been commencement of the study.
documented. However, there is no significant
[9]
evidence to associate hematological and coagulation REFERENCES
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