Case report reveals that vitamin K deficiency can cause coagulopathy in quiescent Crohn’s disease, highlighting potential risks.
Background: Vitamin K serves as a critical coenzyme in the gamma-carboxylation of clotting factors II, VII, IX, and X, underscoring its essential role in the coagulation cascade. Deficiency of this fat-soluble vitamin is frequently observed in individuals with chronic gastrointestinal disorders, particularly those affecting nutrient absorption. If left untreated, long-term vitamin K deficiency can lead to serious complications, including an increased risk of bleeding, intracranial haemorrhage, and impaired bone mineralization. Given the potential severity of these outcomes, prompt recognition and treatment are imperative. Case report: An 87-year-old male with a history of Crohn’s disease and bowel resection 30 years ago, in sustained remission, presented with cutaneous purpura and elevated prothrombin time (PT) and activated partial thromboplastin time (aPTT). Laboratory evaluation revealed low serum vitamin K levels and decreased activity of vitamin K-dependent coagulation factors, which were corrected with vitamin K supplementation. Conclusion: This case highlights that acquired vitamin K deficiency should be considered a potential cause of coagulopathy, even in patients with quiescent Crohn’s disease and no active gastrointestinal symptoms. Our patient developed clinically significant bleeding decades after bowel resection, emphasizing that long-term nutritional consequences of gastrointestinal surgery may persist silently. Vigilance for vitamin K and other micronutrient deficiencies is essential in this population. Early recognition and supplementation can reverse coagulopathy, prevent haemorrhagic complications, and improve outcomes through regular monitoring and timely intervention.
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Patel et al. (2025) studied this question.
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