Background: A 50-year-old female with a history of inflammatory bowel disease (IBD) with Crohn’s disease and ankylosing spondylitis diagnosed radiologically (untreated) presented with a cerebral venous thrombosis (CVT) of unknown etiology. She had multiple hospitalizations for abdominal pain and worsening pancolitis, with diffuse bowel wall thickening consistent with Crohn’s colitis. The patient had no family history of clotting disorders and was not on oral contraceptives. She managed with a heparin drip and transitioned to Eliquis 5 mg BID. The patient presented with persistent homonymous hemianopsia, and brain imaging showed hypoattenuation in the right cerebral hemisphere, more prominent than the left, with T2 flare hyperintensity. Notably, the patient had been receiving gesulkumab every eight weeks for Crohn’s disease, with the last dose administered three days prior to this episode. She has a history of seizures of unknown etiology, for which she was on Keppra 1000 mg BID. There was no recent febrile illness. The patient was transferred to Brigham and Women’s for further neurology evaluation due to concerns about venous sinus thrombosis raised by brain MRI and CT findings.

Case presentation: Lab values :

White blood cell count: 8.2

Hemoglobin: 15.2

Platelets: 214

Sodium: 135

Potassium: 4.1

Creatinine: normal

Electrolytes: within normal limits

UDS: positive for amphetamines and opiates

ESR: 34 (elevated), CRP: 0.8 (normal)

Serum workup: Elevated ANA titer (2560), normal TSH, negative SSA/SSB and HCV. Vitamin B12, folate, and HIV tests were normal.

Imaging : An MRI angiogram of the brain revealed non-occlusive venous sinus thrombosis involving the right transverse sinus, sigmoid sinus, and proximal jugular vein. T2 flare imaging showed non-occlusive VST, with hyperdensity and diffusion restriction in the right parietal-occipital lobe (right > left), right thalamus, and left temporal lobe.

Learning points for clinical practice: The patient’s venous thrombosis is likely multifactorial, including recent gesulkumab exposure, Crohn’s disease as a hypercoagulable state, and previous mesenteric ischemia from small emboli. The autoimmune process likely contributed to her thromboembolic event, which aggravated her seizures. Although the clot was not amenable to intervention, her symptoms were resolved by discharge. Mechanisms for clotting in Crohn’s disease include endothelial dysfunction and elevated procoagulant factors. Steroid use, concurrent with gesulkumab, may have also contributed to thrombosis. The patient was chronically bedbound due to severe abdominal pain, which may have further contributed to the thrombosis. No known vascular conditions were identified. The patient’s fibrinogen levels were not tested, but factors such as elevated fibrinogen, Factor V, and Factor VIII are known in inflammatory bowel disease.

REFERENCES: NIL.

Acknowledgements: NIL.

Disclosure of Interests: None declared.

© The Authors 2025. This abstract is an open access article published in Annals of Rheumatic Diseases under the CC BY-NC-ND license ( http://creativecommons.org/licenses/by-nc-nd/4.0/ ). Neither EULAR nor the publisher make any representation as to the accuracy of the content. The authors are solely responsible for the content in their abstract including accuracy of the facts, statements, results, conclusion, citing resources etc.