Bone Metabolism in Inflammatory Bowel Diseases 2

Czech version

Authors: Tomáš Kupka; Pavel Svoboda; Martina Bojková; Martin Blaho; Adam Vašura; Vladimír Hrabovský; Petr Dítě
Authors‘ workplace: Oddělení gastroenterologie Interní klinika LF OU a FN Ostrava
Published in: Vnitř Lék 2020; 66(7): 432-436
Category:

Overview

Inflammatory Bowel Disease encompasses Crohn’s Disease, which is capable of affecting the entire GI tract, although usually favors the ileocolonic and perianal areas, and Ulcerative Colitis, which is limited to the colon. The pathophysiology is not fully understood but is thought to be caused by a complex interplay among gut microbiota, dysregulation of the host’s immune system, genetic susceptibility and environmental factors. Osteopenia and osteoporosis are considered to be extraintestinal manifestations of inflammatory bowel disease. Osteoporosis is usually diagnosed by dual-energy X-ray absortiometry. Early interventions to treat active CD and preventative treatment strategies to reduce excessive bone loss might prevent long term consequences of bone loss, including fractures. The immune response in IBD includes increased production of variety of proinflammatory cytokines such as IL1β, TNFα, IL6 a IL1 from T cells and macrophages. These have both direct and indirect effects on bone turnover. Vitamin D is vital in mantenance of bone strenght, mineralisation and fracture prevention. Vitamin D’s physiological importance has also been implicated in a number of inflammatory diseases, mainly asthma, atherosclerosis and autoimmune disease.

Keywords:

bone mineral density (BDM) – inflammatory bowel disease – osteoporosis – vitamin D

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