ISCHEMIC STROKE / ETIOPATHOGENESIS
Stroke and idiopathic inflammatory bowel diseases
Created 16/02/2023, last revision 24/06/2023
- idiopathic inflammatory bowel diseases (IBDs) are chronic, medically incurable inflammatory disorders of the gastrointestinal (GI) tract with unknown etiopathogenesis. In general, idiopathic IBDs include these forms:
- ulcerative colitis (UC) – transmural segmental involvement
- Crohn’s disease (CD) – superficial inflammation without T-cell activation, humoral mechanisms predominate
- IBD-unclassified (IBD-U)
- ulcerative colitis (UC) – transmural segmental involvement
- the incidence and prevalence of IBD are increasing around the world
- IBDs are associated with an increased risk of thromboembolic events (including stroke) (Sun, 2023)
- meta‐analysis indicates that IBD was associated with an increased risk of stroke (OR/RR = 1.21, 95% CI 1.08 to 1.34, I 2 = 83.6%, p < .001) (Chen, 2021)
- the study also showed that CD was more relevant to the risk of stroke than UC
- increased risk of stroke is probably related to inflammatory mechanisms (elevated CRP), as it is also associated with other systemic diseases such as psoriasis, systemic sclerosis, and systemic lupus erythematosus (SLE)
- diagnosis is based on the following:
- clinical presentation
- endoscopic and radiologic findings
- histology

Etiopathogenesis of complications
- systemic inflammation with the production of cytokines and free oxygen radicals
- the exact etiology of IBD remains unclear; epidemiologic data suggest that multiple risk factors are associated with IBD, including diet, smoking, and genetic factors
- probable mechanisms increasing the risk of stroke and other CV diseases include:
- systemic inflammation (inflammation‐mediated premature atherosclerosis)
- intestinal microflora has also been implicated as a potential contributor to CVD
- abnormalities of the coagulation system (→ hypercoagulable state)
- protein C and S deficiency
- high fibrinogen concentrations
- hyperhomocysteinemia [Romagnuolo, 2001]
- antiphospholipid syndrome [Mevorach, 1996]
Clinical presentation
Extraintestinal non-thrombotic symptoms
- non-neurological
- arthritis
- sclerosing cholangitis
- gluten-sensitive enteropathy
- neurological
- peripheral neuropathies
- myelopathy
- myasthenia gravis
Extraintestinal thrombotic symptoms
- deep vein thrombosis and/or pulmonary embolism (VTE)
- venous thrombosis of atypical localization (mesenteric, etc.)
- stroke and cerebral venous sinus thrombosis (CVST)
- mostly due to hypercoagulable state
- vasculitis is rare
Management
Acute stroke management
- recanalization therapy in eligible patients
- intravenous thrombolysis (IVT) may be associated with an increased risk of bleeding
- mechanical recanalization or local thrombolysis may be preferred [Brosch, 2012]
- antiplatelet therapy if recanalization therapy is not indicated
Stroke prevention
- the mainstay of prevention is the compensation for the inflammatory disease + treatment of traditional vascular risk factors
- low-dose anticoagulation or antiplatelet therapy reduces the risk of thromboembolism but increases the risk of bleeding
- start vitamin supplementation in case of hyperhomocysteinemia → see here