Vitamin K

Why it happens in Crohn’s disease

Vitamin K comes from two sources and Crohn’s disease compromises both. Dietary K1 is fat-soluble and requires bile salts for absorption, so ileal disease, resection and bile acid depletion reduce uptake in the same way they do for vitamin D. Menaquinones (K2) are produced by colonic bacteria, and the dysbiosis characteristic of Crohn’s — compounded by the repeated antibiotic courses used for perianal and fistulising disease — cuts that supply as well. Vitamin K is the cofactor for gamma-carboxylation of osteocalcin, the protein that binds calcium into bone matrix. Undercarboxylated osteocalcin cannot do this, which is the mechanism linking vitamin K status to the osteopenia seen in Crohn’s independently of vitamin D.

Who is most at risk

• Ileal disease or resection with bile salt depletion
• Repeated antibiotic courses depleting menaquinone-producing colonic flora
• Cholestyramine or other bile acid sequestrants
• Fat malabsorption and steatorrhoea
• Prolonged corticosteroid exposure compounding bone loss

Symptoms of deficiency

• Usually silent — bone loss is asymptomatic until a fracture occurs
• Easy bruising and prolonged bleeding from minor cuts in severe deficiency
• Prolonged prothrombin time / raised INR without anticoagulant use
• Reduced bone mineral density on DXA, and fragility fracture
• Elevated undercarboxylated osteocalcin, the sensitive functional marker

Many of these overlap with Crohn’s disease itself, which is exactly why deficiencies are missed. Fatigue attributed to active disease is frequently anaemia, and neuropathy attributed to medication is sometimes B12.

How it is tested

There is no routine serum test that performs well. Prothrombin time/INR only becomes abnormal in severe deficiency, long after bone effects begin. Undercarboxylated osteocalcin and PIVKA-II are the sensitive functional markers but are not widely available outside research settings. In practice, vitamin K status is inferred from risk profile, and bone health is monitored directly with DXA — recommended in Crohn’s patients with prolonged steroid exposure, low body weight, prior fracture or postmenopausal status.

Replenishment protocols

There is no established IBD-specific replacement protocol, which is itself worth knowing. Dietary sources — leafy greens for K1, natto and fermented foods for K2 — are first-line. Where supplementation is used, K1 at 100–1,000 mcg/day or K2 (MK-7) at 90–200 mcg/day are the commonly used ranges, and K2 has the better evidence for bone outcomes in non-IBD populations. Vitamin K is best given alongside vitamin D and calcium as part of an overall bone protection strategy rather than in isolation, since the three act on the same pathway at different points.

Amounts reflect what gastroenterology literature and guidelines describe. The right dose for you depends on your test results, absorption and surgical history, so test first and work with your care team to personalise it.

Medication interactions

Vitamin K directly antagonises warfarin, and any change in intake must be discussed with whoever manages anticoagulation — relevant because IBD substantially raises venous thromboembolism risk. Direct oral anticoagulants are not affected. Cholestyramine and orlistat reduce absorption. Prednisone and other corticosteroids compound bone loss through separate mechanisms, making vitamin K, vitamin D and calcium status collectively more important during steroid courses.

Sources

1. 1

   Association of vitamin K deficiency with bone metabolism and clinical disease activity in inflammatory bowel disease

   Nakajima S, Iijima H, Egawa S, et al. · Nutrition · 2011 · PMID 21482072

2. 2

   High prevalence of vitamin K and D deficiency and decreased BMD in inflammatory bowel disease

   Kuwabara A, Tanaka K, Tsugawa N, et al. · Osteoporosis International · 2009

3. 3

   Prevalence and pathogenesis of osteoporosis in patients with inflammatory bowel disease

   Bernstein CN, Leslie WD. · Gastroenterology Clinics of North America · 2005 · PMID 15785432