Genetic determinants of IL-6 expression levels do not influence bone loss in inflammatory Bowel disease

• Published in: Digestive diseases and sciences 2001-11, Vol.46 (11), p.2521-2528
• Main Authors: SCHULTE, Claudia M. S, GOEBELL, Harald, RÖHER, Hans-Dietrich, SCHULTE, Klaus-Martin
• Format: Article
• Language: English
• Subjects: Adult; Biological and medical sciences; Bone and Bones - metabolism; Bone Density; Case-Control Studies; Digestive system; Female; Follow-Up Studies; Genotype; Haplotypes; Humans; Inflammatory bowel disease; Inflammatory Bowel Diseases - complications; Inflammatory Bowel Diseases - genetics; Inflammatory Bowel Diseases - metabolism; Interleukin-6 - blood; Interleukin-6 - genetics; Investigative techniques, diagnostic techniques (general aspects); Male; Medical sciences; Osteoporosis - etiology; Osteoporosis - genetics; Osteoporosis - metabolism; Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques; Polymorphism, Genetic; Time Factors
• ISSN: 0163-2116; 1573-2568
• DOI: 10.1023/A:1012300609279

Bone loss in inflammatory bowel disease (IBD) is presumed to be mediated by inflammation. Increased levels of the multifunctional cytokine IL-6 in inflammatory diseases have been proposed to be the link in such "inflammation-mediated osteopenia." A recently described G/C polymorphism with an effect on transcription rate and plasma levels of IL-6 suggests a genetically determined difference in the degree of the IL-6 response to stressful stimuli between individuals. This study aimed to assess the frequency of genotypes and haplotypes of the G/C polymorphism of IL-6 in IBD patients. A further aim was to assess whether carriage of the potentially protective CC genotype is favorable with respect to the development of bone disease in IBD. The IL-6 polymorphism was typed in 105 IBD patients and 113 healthy controls. Bone mineral density was evaluated at baseline and after a prospective 2-year-follow-up. The favorable CC genotype with decreased IL-6 release was not underrepresented in IBD patients compared to healthy controls. Carriage of this genotype was not protective with respect to the development of bone disease, either for the bone mineral density at baseline or for the prospectively observed bone loss. Within the subgroup of patients who did not receive steroids during follow-up, the prospectively observed bone loss was even slightly higher in CC carriers, but differences did not reach significance. Genetically determined differences in the degree of the IL-6 response to stressful stimuli are no major predictors for the degree of bone disease in IBD patients.