Format

Send to

Choose Destination
See comment in PubMed Commons below
Osteoporos Int. 2009 Jun;20(6):935-42. doi: 10.1007/s00198-008-0764-2. Epub 2008 Sep 30.

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

Author information

1
Department of Food and Nutrition, Kyoto Women's University, 35, Imakumano-kitahiyoshicho, Higashiyama, Kyoto 605-8501, Japan.

Abstract

SUMMARY:

Vitamin K and D deficiency and decreased bone mineral density (BMD) were highly prevalent in patients with inflammatory bowel disease (IBD), especially Crohn's disease (CD). Dietary intakes of these vitamins, however, were above the Japanese adequate intakes in IBD patients, suggesting that malabsorption is the basis for hypovitaminosis K and D and decreased BMD.

INTRODUCTION:

We have studied the possible involvement of vitamin K and D deficiency in the pathogenesis of decreased BMD in IBD.

METHODS:

Seventy patients with IBD were evaluated for their BMD; plasma levels of vitamin K; phylloquinone (PK), menaquinone-7 (MK-7), and 25OH-D; serum PTH, protein induced by vitamin K absence (PIVKA-II), and undercarboxylated osteocalcin (ucOC) levels; and their food intake.

RESULTS:

Compared with ulcerative colitis (UC) patients, CD patients had significantly lower plasma vitamin K and 25OH-D concentrations; significantly higher serum levels of PTH, PIVKA-II, and ucOC; and significantly lower BMD scores at almost all measurement sites. More IBD patients were vitamin K deficient in bone than in liver. Multiple regression analyses revealed that low plasma concentrations of vitamin K and 25OH-D were independent risk factors for low BMD and that they were associated with the patients' fat intake, but not with their intake of these vitamins.

CONCLUSION:

IBD patients have high prevalence of decreased BMD and vitamin K and D deficiency probably caused by malabsorption of these vitamins.

PMID:
18825300
DOI:
10.1007/s00198-008-0764-2
[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Springer
    Loading ...
    Support Center