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[Acquired protein C deficiency in ulcerative colitis. The cause of thromboembolic complications]
Insights
Acute exacerbation of ulcerative colitis can cause protein C deficiency. Rigorous treatment of the underlying colitis reversed this deficiency in three patients, highlighting a key link between inflammatory bowel disease and coagulation disorders.
Area of Science:
- Internal Medicine
- Hematology
- Gastroenterology
Background:
- Ulcerative colitis exacerbations are associated with significant morbidity.
- Thromboembolic events are a known complication of severe ulcerative colitis.
- Protein C deficiency is a prothrombotic state.
Observation:
- Three patients with acute ulcerative colitis presented with acquired protein C deficiency (32-48% activity).
- Two male patients developed severe thromboembolic complications (cavernous sinus thrombosis, pulmonary embolism) during heparin therapy.
- The female patient's protein C activity was measured early, before heparin, due to awareness of the other cases.
Findings:
- All patients received sulphasalazine, fluocortolone, and heparin.
- Protein C activity normalized in all three patients upon remission of ulcerative colitis.
- One patient required subtotal colectomy for colitis remission and protein C normalization.
Implications:
- Acquired protein C deficiency in ulcerative colitis is reversible.
- Aggressive management of the underlying inflammatory bowel disease is crucial.
- This suggests a direct link between ulcerative colitis activity and coagulation abnormalities.
Abstract:
Three patients with an acute exacerbation of ulcerative colitis (a 40-year-old and a 31-year-old man and a 30-year-old woman) developed a protein C deficiency (serum protein C activity between 32 and 48%). In the two men the protein C deficiency was diagnosed only after the onset of severe thromboembolic complications (cavernous sinus thrombosis; pulmonary embolism) during heparin treatment. But in the woman protein C activity was measured immediately after hospital admission (in the knowledge of the first two cases) even before heparin administration was started. All three patients received treatment with sulphasalazine (3 g daily) and fluocortolone (60 mg daily), as well as full heparinization (22,500-36,000 IU daily). Protein C activity returned to normal on remission of the ulcerative colitis (in one case only after subtotal colectomy). These case reports show that acquired protein C deficiency can be reversed by rigorous treatment of the underlying disease.