Vnitřní lékařství 7/2020

PŘEHLEDOVÉ ČLÁNKY Kostní metabolismus u idiopatických střevních zánětů 1 E6 | VNITŘNÍ LÉKAŘSTVÍ / Vnitř Lék 2020; 66(7): e3–e7 /  www.casopisvnitrnilekarstvi.cz Nedávné studie poukázaly na asociaci mezi použitím inhibitorů protonové pumpy a zlomeninami kyčle. I když ne všechny studie ukazují jasné spojení (57), většina důkazů ukazuje mírné zvýšení prevalence osteoporózy a zlomenin u dlouhodobých uživatelů inhibitorů proto- nové pumpy (58). Běžně předpokládaný mechanismus, tedy snížená absorpce vápníku v důsledku nedostatečné tvorby žaludeční kyseliny, pravděpodobně není správný (59) a mechanismus tak zůstává nejasný. Zdá se, že anti-TNF zlepšuje BMD u pacientů s IBD jak přímým příznivým účinkem na kostní metabolismus, tak zlepšením základního zánětlivého procesu ve střevě. Je potřeba určit, zda jiné přípravky biolo- gické léčby, které jsou nyní k dispozici pro léčbu IBD, jako je vedolizumab nebo ustekinumab, mají nějaký vliv na metabolismus kostí (60). Práce byla podpořena grantem LF OU SGS02/LF/2018-2019. LITERATURA 1. Loftus EV. Clinical epidemiology of inflammatory bowel disease: incidence, prevalence, and environmental issues. Gastroenterology 2004; 126: 1504–1517. 2. Molodecky NA, Soon IS, Rabi DM, et al. Increasing incidence and prevalence of the in- flammatory bowel diseases with time, based on systematic review. Gastroenterology 2012; 142: 46–54. 3. Khor B, Gardet A, Xavier RJ. Genetics and pathogenesis of inflammatory bowel disea- se. Nature 2011; 474: 307–317. 4. Lennard-Jones JE. Classification of inflammatory bowel disease. Scand J Gastroente- rol Suppl 1989; 170: 2–6. 5. Loftus jr. EV. Osteoporosis and Inflammatory Bowel Disease. Healio Rheumatolo- gy 2017. Availalble from WWW: < https://www.healio.com/rheumatology/osteoarthri- tis-and-bone-disorders/news/print/healio-rheumatology/%7B9391f09f-6b83-40dc-a- 913-080747d434e0%7D/osteoporosis-and-inflammatory-bowel-disease> 6. Katz S, Weinerman S. Osteoporosis and gastrointestinal disease. Gastroenter Hepatol 2010; 6: 506–517. 7. Bischoff SC, Herrmann A, Göke M, et al. Altered bone metabolism in inflammatory bowel disease. Am J Gastroenterol 1997; 92: 1157–1163. 8. Bernstein CN, Benchimol EI, Bitton A, et al. The Impact of Inflammatory Bowel Disea- se in Canada 2018: Extra-intestinal Diseases in IBD. J Can Assoc Gastroenterol 2019; 2: (Suppl. 1): S73–S80. 9. Sugimoto K, Ikeya K, et al. An increased serumN-terminal telopeptide of type I collagen, a biochemical marker of increased bone resorption, is association with infliximab therapy in patients with Crohn’s disease. Dig Dis Sci 2016; 61: 99–106 10. Metzger CE, Narayanan A, Zawieja DC, et al. Inflammatory Bowel Disease in a Rodent Model Alters Osteocyte Protein Levels Controlling Bone Turnover. J Bone Miner Res 2017; 32: 802–813. 11. Tilg H, Moschen AR, Kaser A, et al. Gut, inflammation and osteoporosis: basic and cli- nical concepts. Gut 2008; 57: 684–694. 12. Targownik LE, Leslie WD, Carr R, et al. Longitudinal change in bone mineral density in a population-based cohort of patients with inflammatory bowel disease. Calcif Tissue Int 2012; 91: 356–363. 13. Hidalgo DF, Boonpheng B, Phemister J, et al. Inflammatory Bowel Disease and Risk of Osteoporotic Fractures: A Meta-Analysis. Cureus 2019; 11: e5810. 14. Lewiecki EM, Borges JL. Bone density testing in clinical practice. Arq Bras Endocrinol Metabol 2006; 50: 586–595. 15. NIH Consensus Development Panel on Osteoporosis Prevention. Diagnosis, and thera- py. Osteoporosis prevention, diagnosis, and therapy. JAMA 2001; 285: 785–795. 16. Couttenye MM, D’Haese PC, Van Hoof VO, et al. Low serum levels of alkaline phos- phatase of bone origin: a good marker of adynamic bone disease in haemodialysis pati- ents. Nephrol Dial Transpl 1996; 11: 1065–1072. 17. Eastell R, Mallinak N, Weiss S, et al. Biological variability of serum and urinary N-telopep- tides of type I collagen in postmenopausal women. J Bone Miner Res 2000; 15: 594-598. 18. Szulc P, Meunier PJ. Is vitamin K deficiency a risk factor for osteoporosis in Crohn’s di- sease? Lancet 2001; 357: 1995–1996. 19. Miheller P, Muzes G, Hritz I, et al. Comparison of the effects of 1,25 dihydroxyvitamin D and 25 hydroxyvitamin D on bone pathology and disease activity in Crohn’s disease patients. Inflamm Bowel Dis 2009; 15: 1656–1662. 20. Leichtmann GA, Bengoa JM, Bolt MJ, et al. Intestinal absorption of cholecalciferol and 25-hydroxycholecalciferol in patients with both Crohn’s disease and intestinal resection. Am J Clin Nutr 1991; 54: 548–552. 21. Compston JE, Judd D, Crawley EO, et al. Osteoporosis in patients with inflammatory bowel disease. Gut 1987; 28: 410–415. 22. Bjarnason I, Macpherson A, Mackintosh C, et al. Reduced bone density in patients with inflammatory bowel disease. Gut 1997; 40: 228–233. 23. van Bodegraven AA, et al. Treatment of bone loss in osteopenic patients with Cro- hn’s disease: a double-blind, randomised trial of oral risedronate 35 mg once weekly or pla- cebo, concomitant with calcium and vitamin D supplementation. Gut 2014; 63: 1424–1430. 24. Melek J, Sakuraba A. Efficacy and safety of medical therapy for low bone mineral density in patients with inflammatory bowel disease: a meta-analysis and systematic review. Clin Gastroenterol Hepatol 2014; 12: 32–44. 25. Redlich K, Smolen J. Inflammatory bone loss: pathogenesis and therapeutic interven- tion. Nat Rev Drug Discov 2012; 11: 234–250. 26. Katz S, Weinerman S. The elderly inflammatory bowel disease patient and osteopo- rosis. Aging Health 2012; 8: 31–42. 27. Nielsen OH, Vainer B, Madsen SM, et al. Established and emerging biological activity markers of inflammatory bowel disease. Am J Gastroenterol 2000; 95: 359–367. 28. Thearle M, Horlick M, Bilezikian JP, et al. Osteoporosis: an unusual presentation of child- hood Crohn’s disease. J Clin Endocrinol Metab 2000; 85: 2122–2126. 29. Gilbert L, He X, Farmer P, et al. Inhibition of osteoblast differentiation by tumor necro- sis factor-alpha. Endocrinology 2000; 141: 3956–3964. 30. Azuma Y, Kaji K, Katogi R, et al. Tumor necrosis factor-alpha induces differentiation of and bone resorption by osteoclasts. J Biol Chem 2000; 275: 4858–4864. 31. Kaji K, Katogi R, Azuma Y, et al. Tumor necrosis factor alpha-induced osteoclastoge- nesis requires tumor necrosis factor receptor-associated factor 6. J Bone Miner Res 2001; 16: 1593–1599. 32. Bertolini DR, Nedwin GE, Bringman TS, et al. Stimulation of bone resorption and inhibiti- on of bone formation in vitro by human tumor necrosis factors. Nature 1986; 319: 516–518. 33. Tsuboi M, Kawakami A, Nakashima T, et al. Tumor necrosis factor-alpha and interle- ukin-1beta increase the Fas-mediated apoptosis of human osteoblasts. J Lab Clin Med 1999; 134: 222–231. 34. Fernandez-Martin JL, Kurian S, Farmer P, et al. Tumor necrosis factor activates a nuc- lear inhibitor of vitamin D and retinoid-X receptors. Mol Cell Endocrinol 1998; 141: 65–72. 35. Horwood NJ, Elliott J, Martin TJ, et al. IL-12 alone and in synergy with IL-18 inhibits os- teoclasts formation in vitro. J Immunol 2001; 166: 4915–4921. 36. Monteleone G, Trapasso F, Parrello T, et al. Bioactive IL-18 expression is up-regulated in Crohn’s disease. J Immunol 1999; 163: 143–147. 37. Quinn JM, Itoh K, Udagawa N, et al. Transforming growth factor beta affects osteoc- last differentiation via direct and indirect actions. J Bone Miner Res 2001; 16: 1787–1794. 38. Tauseef A, Lam D, Bronze M, et al. Osteoporosis in inflammatory bowel disease. Am J Med 2009; 122: 599–604. 39. Łodyga M, Eder P, Bartnik W, et al. Guidelines for the management of Crohn’s disease. Recommendations of the Working Group of the Polish National Consultant in Gastroen- terology and the Polish Society of Gastroenterology. Prz Gastroenterol 2012; 7: 317–338. 40. Krela-Kaźmierczak I, Wysocka E, Szymczak A, et al. Osteoprotegerin, s-RANKL, and se- lected interleukins in the pathology of bone metabolism in patients with Crohn’s disea- se. Prz Gastroenterol 2016; 11: 30–34. 41. Moschen AR, Kaser A, Enrich B, et al. The RANKL/OPG system is activated in inflamma- tory bowel disease and relates to the state of bone loss. Gut 2005; 54: 479–487. 42. Agrawal M, Arora S, Li J, et al. Bone, inflammation, and inflammatory bowel disease. Curr Osteoporos Rep 2011; 9: 251–257. 43. Geginat J, Larghi P, Paroni M, et al. The light and the dark sides of Interleukin – 10 in immune – mediated diseases and cancer. Cytokine Growth Factor Rev 2016; 30: 87–93. 44. Evans KE, Fox SW. Interleukin – 10 inhibits osteoclastogenesis by reducing NFATc1 ex- pression and preventing its translocation to the nucleus. BMC Cell Biol 2007; 8: 4. 45. Bonewald LF. The amazing osteocyte. J Bone Miner Res 2011; 26: 229–238. 46. Baek K, Hwang HR, Park HJ, et al. TNF-α upregulates sclerostin expression in obese mice fed a high – fat diet. Cell Physiol 2014; 229: 640–650. 47. Ghishan FK, Kiela P. Advances in the understanding of mineral and bone metabolism in inflammatory bowel diseases. Am J Physiol Gastrointest Liver Physiol 2011; 300: G191-G201. 48. DiStefano M, Veneto G, Malserervis S, et al. Lactose malabsorption and intolerance and peak bone mass. Gastroenterology 2002; 122: 1793–1799. 49. Razzaque MS. The FGF23-Klotho axis endocrine regulation of phosphate homeosta- sis. Nat Rev Endocrinol 2009; 5: 611–619. 50. Booth SL. Roles for vitamin K beyond coagulation. Ann Rev Nutr 2009; 28: 88–110. 51. Nakajima S, Iijima H, Egawa S, et al. Association of vitamin K deficiency with bonemetabo- lismand clinical disease activity in inflammatory bowel disease. Nutrition 2011; 27: 1023–1028. 52. Stevenson M, Lloyd-Jones M, Papaioannou D. Vitamin K to prevent fractures in older women: systematic review and economic evaluation. Health Technol Assess 2009; 13: 1–134. 53. Mazziotti G, Canalis E, Giustina A. Drug-induced osteoporosis: mechanisms and clini- cal implications. Am J Med 2010; 123: 877–884.