Osteologie 2009; 18(03): 209-216
DOI: 10.1055/s-0037-1619894
Original and review articles
Schattauer GmbH

Erythrocyte sedimentation rate as an osteoporosis risk factor in patients with active Crohn’s disease

Blutsenkungsgeschwindigkeit als ein Risikofaktor für Osteoporose in Patienten mit aktivem Morbus Crohn
H. Siggelkow
1   Department of Gastroenterology and Endocrinology, University Clinic of Goettingen, Goettingen, Germany
2   Endokrinologikum Gö ttingen, Goettingen, Germany
,
J. Cortis
1   Department of Gastroenterology and Endocrinology, University Clinic of Goettingen, Goettingen, Germany
,
Ch. Claus
1   Department of Gastroenterology and Endocrinology, University Clinic of Goettingen, Goettingen, Germany
,
M. Funke
3   Department of Radiology, University Clinic of Gö ttingen, Goettingen, Germany
,
W. Nolte
1   Department of Gastroenterology and Endocrinology, University Clinic of Goettingen, Goettingen, Germany
,
M. Hü fner
1   Department of Gastroenterology and Endocrinology, University Clinic of Goettingen, Goettingen, Germany
,
D. Raddatz
1   Department of Gastroenterology and Endocrinology, University Clinic of Goettingen, Goettingen, Germany
› Institutsangaben
Weitere Informationen

Publikationsverlauf

received: 06. November 2008

accepted after revision: 02. Februar 2009

Publikationsdatum:
28. Dezember 2017 (online)

Summary

Crohn’s disease (CD) is associated with reduced bone mineral density and increased fracture risk. To assess the effects of the inflammatory process itself on bone parameters, we investigated patients with active CD and in remission without glucocorticoid treatment four weeks prior to analysis. Patients with active CD were compared to age-and sex-matched healthy volunteers and osteoporosis patients. Bone mineral density, bone formation and resorption markers were assessed, in addition to simple inflammatory markers and cytokines. Out of seven patients with active disease, three had osteopenia and one osteoporosis (WHO definition). The erythrocyte sedimentation rate (ESR) was associated with BMD at the femoral neck (R2 = 0.853, p < 0.01) and the spine (R2 = 0.772, p < 0.05). ESR seems to influence bone formation, as shown by lower bone alkaline phosphatase with high ESR (R2 = 0.725, R = – 0.852, p < 0.05). The clinical disease activity score was not useful in determining patients’ risk of acquiring bone disease. In conclusion, in patients with Crohn’s disease, the degree of the inflammatory process as assessed by ESR indicates bone loss and might be of value in identifying patients at risk of developing osteoporosis.

Zusammenfassung

Bei Patienten mit Morbus Crohn (MC) besteht hä ufig eine erniedrigte Knochendichte (BMD) und ein erhö htes Risiko fü r Frakturen. In dieser Studie untersuchten wir Patienten im akuten Schub eines MC und in Remission ohne Steroidtherapie vier Wochen vor der Untersuchung hinsichtlich Knochenstoffwechsel, Knochendichte, Entzü ndungsmarkern sowie Zykotinen. Als Vergleich dienten alters-und geschlechtsadaptierte gesunde Probanden sowie Osteoporosepatienten. Von sieben Patienten mit akutem Schub des MC hatten vier eine Osteopenie oder Osteoporose nach WHO-Kriterien. Die Blutsenkung (BSG) war mit der BMD am Femurhals (R2 = 0.853, p < 0.01) und an der Wirbelsä ule assoziiert (R2 = 0.772, p < 0.05). Die BSG korrelierte weiterhin negativ zur Knochenformation gemessen an der knochenspezifischen alkalischen Phosphatase (R2 = 0.725, R = – 0.852, p < 0.05). Der klinische Aktivitä tsindex CDAI war nicht in der Lage, das Risiko fü r die Knochenbeteiligung vorherzusagen. Bei Patienten mit MC scheint der Entzü ndungsprozess, charakterisiert durch die hohe BSG, Knochenverlust anzuzeigen und kann fü r die Bestimmung des Osteoporoserisikos bei MC-Patienten wertvoll sein.

 
  • References

  • 1 Bernstein CN, Blanchard JF, Leslie W. et al. The incidence of fracture among patients with inflammatory bowel disease. A population-based cohort study. Ann Intern Med 2000; 133 (10) 795-799.
  • 2 Vestergaard P, Krogh K, Rejnmark L. et al. Fracture risk is increased in Crohn’s disease, but not in ulcerative colitis. Gut 2000; 46 (02) 176-181.
  • 3 Vestergaard P, Mosekilde L. Fracture risk in patients with celiac Disease, Crohn’s disease, and ulcerative colitis: a nationwide follow-up study of 16,416 patients in Denmark. Am J Epidemiol 2002; 156 (01) 1-10.
  • 4 Van Staa TP, Leufkens HG, Abenhaim L. et al. Use of oral corticosteroids and risk of fractures. J Bone Miner Res 2000; 15 (06) 993-1000.
  • 5 Klaus J, Armbrecht G, Steinkamp M. et al. High prevalence of osteoporotic vertebral fractures in patients with Crohn’s disease. Gut 2002; 51 (05) 654-658.
  • 6 Siffledeen JS, Siminoski K, Jen H, Fedorak RN. Vertebral fractures and role of low bone mineral density in Crohn’s disease. Clin Gastroenterol Hepatol 2007; 05 (06) 721-728.
  • 7 Heijckmann AC, Huijberts MS, Schoon EJ. et al. High prevalence of morphometric vertebral deformities in patients with inflammatory bowel disease. Eur J Gastroenterol Hepatol 2008; 20 (08) 740-747.
  • 8 Lamb EJ, Wong T, Smith DJ. et al. Metabolic bone disease is present at diagnosis in patients with inflammatory bowel disease. Aliment Pharmacol Ther 2002; 16 (11) 1895-1902.
  • 9 Andreassen H, Rungby J, Dahlerup JF, Mosekilde L. Inflammatory bowel disease and osteoporosis. Scand J Gastroenterol 1997; 32 (12) 1247-1255.
  • 10 Croucher PI, Vedi S, Motley RJ. et al. Reduced bone formation in patients with osteoporosis associated with inflammatory bowel disease. Osteoporos Int 1993; 03 (05) 236-241.
  • 11 Stevens C, Walz G, Singaram C. et al. Tumor necrosis factor-alpha, interleukin-1 beta, and interleukin-6 expression in inflammatory bowel disease. Dig Dis Sci 1992; 37 (06) 818-826.
  • 12 Reinecker HC, Steffen M, Witthoeft T. et al. Enhanced secretion of tumour necrosis factor-alpha, IL-6, and IL-1 beta by isolated lamina propria mononuclear cells from patients with ulcerative colitis and Crohn’s disease. Clin Exp Immunol 1993; 94 (01) 174-181.
  • 13 Pacifici R. Estrogen, cytokines, and pathogenesis of postmenopausal osteoporosis. J Bone Miner Res 1996; 11 (08) 1043-1051.
  • 14 van Staa TP, Cooper C, Brusse LS. et al. Inflammatory bowel disease and the risk of fracture. Gastroenterology 2003; 125 (06) 1591-1597.
  • 15 Best WR, Becktel JM, Singleton JW, Kern Jr F. Development of a Crohn’s disease activity index. National Cooperative Crohn’s Disease Study. Gastroenterology 1976; 70 (03) 439-444.
  • 16 Bartram SA, Peaston RT, Rawlings DJ. et al. Mutifactorial analysis of risk factors for reduced bone mineral density in patients with Crohn’s disease. World J Gastroenterol 2006; 12 (35) 5680-5686.
  • 17 Habtezion A, Silverberg MS, Parkes R. et al. Risk factors for low bone density in Crohn’s disease. Inflamm Bowel Dis 2002; 08 (02) 87-92.
  • 18 Espallargues M, Sampietro-Colom L, Estrada MD. et al. Identifying bone-mass-related risk factors for fracture to guide bone densitometry measurements: a systematic review of the literature. Osteoporos Int 2001; 12 (10) 811-822.
  • 19 Wardlaw GM. Putting body weight and osteoporosis into perspective. Am J Clin Nutr 1996; 63 (03) Suppl 433S-436S.
  • 20 Reid IR. Relationships among body mass, its components, and bone. Bone 2002; 31 (05) 547-555.
  • 21 Bernstein CN, Blanchard JF, Metge C, Yogendran M. The association between corticosteroid use and development of fractures among IBD patients in a population-based database. Am J Gastroenterol 2003; 98 (08) 1797-1801.
  • 22 Bernstein CN, Leslie WD. Review article: Osteoporosis and inflammatory bowel disease. Aliment Pharmacol Ther 2004; 19 (09) 941-952.
  • 23 Kirschner BS, DeFavaro MV, Jensen W. Lactose malabsorption in children and adolescents with inflammatory bowel disease. Gastroenterology 1981; 81 (05) 829-832.
  • 24 von Tirpitz C, Kohn C, Steinkamp M. et al. Lactose intolerance in active Crohn’s disease: clinical value of duodenal lactase analysis. J Clin Gastroenterol 2002; 34 (01) 49-53.
  • 25 Eivindson M, Gronbaek H, Flyvbjerg A. et al. The insulin-like growth factor (IGF)-system in active ulcerative colitis and Crohn’s disease: relations to disease activity and corticosteroid treatment. Growth Horm IGF Res 2007; 17 (01) 33-40.
  • 26 Gilman J, Shanahan F, Cashman KD. Altered levels of biochemical indices of bone turnover and bonerelated vitamins in patients with Crohn’s disease and ulcerative colitis. Aliment Pharmacol Ther 2006; 23 (07) 1007-1016.
  • 27 Vihinen MK, Kolho KL, Ashorn M. et al. Bone turnover and metabolism in paediatric patients with inflammatory bowel disease treated with systemic glucocorticoids. European Journal of Endocrinology 2008; 159 (06) 693-698.
  • 28 Leslie WD, Miller N, Rogala L, Bernstein CN. Vitamin D status and bone density in recently diagnosed inflammatory bowel disease: the Manitoba IBD Cohort Study. Am J Gastroenterol 2008; 103 (06) 1451-1459.
  • 29 Abreu MT, Kantorovich V, Vasiliauskas EA. et al. Measurement of vitamin D levels in inflammatory bowel disease patients reveals a subset of Crohn’s disease patients with elevated 1,25-dihydroxyvitamin D and low bone mineral density. Gut 2004; 53 (08) 1129-1136.
  • 30 Scharla SH, Minne HW, Lempert UG. et al. Bone mineral density and calcium regulating hormones in patients with inflammatory bowel disease (Crohn’s disease and ulcerative colitis). Exp Clin Endocrinol 1994; 102 (01) 44-49.
  • 31 Sostegni R, Daperno M, Scaglione N. et al. Review article: Crohn’s disease: monitoring disease activity. Aliment Pharmacol Ther 2003; 17 (Suppl. 02) 11-17.
  • 32 Trebble TM, Wootton SA, Stroud MA. et al. Laboratory markers predict bone loss in Crohn’s disease: relationship to blood mononuclear cell function and nutritional status. Aliment Pharmacol Ther 2004; 19 (10) 1063-1071.
  • 33 Brignola C, Campieri M, Bazzocchi G. et al. A laboratory index for predicting relapse in asymptomatic patients with Crohn’s disease. Gastroenterology 1986; 91 (06) 1490-1494.
  • 34 Trebble TM. Bone turnover and nutritional status in Crohn’s disease: relationship to circulating mononuclear cell function and response to fish oil and antioxidants. Proc Nutr Soc 2005; 64 (02) 183-191.
  • 35 Lin CL, Moniz C, Chambers TJ, Chow JW. Colitis causes bone loss in rats through suppression of bone formation. Gastroenterology 1996; 111 (05) 1263-1271.
  • 36 Hyams JS, Wyzga N, Kreutzer DL. et al. Alterations in bone metabolism in children with inflammatory bowel disease: an in vitro study. J Pediatr Gastroenterol Nutr 1997; 24 (03) 289-295.
  • 37 Sylvester FA, Wyzga N, Hyams JS, Gronowicz GA. Effect of Crohn’s disease on bone metabolism in vitro: a role for interleukin-6. J Bone Miner Res 2002; 17 (04) 695-702.
  • 38 Varghese S, Wyzga N, Griffiths AM, Sylvester FA. Effects of serum from children with newly diagnosed Crohn disease on primary cultures of rat osteoblasts. J Pediatr Gastroenterol Nutr 2002; 35 (05) 641-648.
  • 39 Sylvester FA, Davis PM, Wyzga N. et al. Are activated T cells regulators of bone metabolism in children with Crohn disease?. J Pediatr 2006; 148 (04) 461-466.