Keywords
How to Cite
Abstract views: 241 PDF Downloads: 144
Abstract
Exocrine pancreatic insufficiency (EPI) is a polyetiological pathogenetic syndrome associated with numerous diseases of the pancreas and other organs (of gastroduodenal and hepatobiliary systems, etc.). Recent studies indicate a developing interest in osteoarthritis (OA) comorbidities. However, the pathogenetic mechanisms of the risk of developing EPI in comorbid diseases among OA patients have not been adequately investigated.
The aim of the study is to analyze the influence of comorbid pathology on the onset and development of EPI in patients with primary OA.
Materials and methods. We examined 304 patients with primary OA who had comorbid EPI-associated diseases without exacerbation. According to the type of comorbid pathology associated with EPI, all patients were divided into five categories that were analogous in terms of clinical and gender criteria, the severity of primary OA, and the treatment received: Group 1 (n=62) — patients with OA without comorbid pathology; Group 2 (n=59) — patients with OA in comorbidity with chronic pancreatitis; Group 3 (n=60) — patients with OA in comorbidity with diseases of the biliary system with EPI; Group 4 (n=61) — patients with OA and chronic gastritis and duodenitis; Group 5 (n=62) — patients with OA and diabetes mellitus type 2.
Results. The percentage differences in the content of fecal α-elastase in the experimental groups of patients with primary OA were compared to that in the control group: the value of the percentage difference in the content of fecal α-elastase was 5.47% lower in Group 2 compared to Group 5, 4.35% lower in Group 5 compared to Group 3, 9.63% lower in Group 3 compared to Group 4, and 12.82% lower in Group 4 compared to Group 1. Group 1 of patients with primary OA without comorbid pathology had a significantly lower level of fecal α-elastase compared to the control group, indicating a mild degree of EPI, which may have resulted from long-term treatment of OA with nonsteroidal anti-inflammatory drugs, glucocorticoids, chondroprotectors, chondrostimulants, etc., which had a toxic effect on the organs of the gastrointestinal tract and contributed to the development of gastroenterological pathology, specifically diseases associated with EPI.
Conclusion. According to the level of fecal α-elastase and the level of the total final score of the PEI-Q questionnaire, the following ranking of the influence of the most significant comorbid pathology on the state of EPI in patients with primary OA was presented, starting with the greatest: chronic pancreatitis ˃ diabetes mellitus type 2 ˃ chronic non-stone cholecystitis and functional diseases of the gallbladder and biliary system ˃ chronic gastritis and duodenitis (p˂0.05).
References
American College of Rheumatology. Osteoarthritis guideline recommendations for the use of nonpharmacologic and pharmacologic therapies in osteoarthritis of the hand, hip, and knee. 2020. URL: https://www.rheumatology.org/Practice-Quality/Clinical-Support/Clinical-Practice-Guidelines (last accessed: 30.09.2023).
Babinets L. S., Halabitska I. M. Characteristics of joint pain in patients with primary osteoarthritis and comorbid conditions with exocrine pancreatic insufficiency. Lek. Obz. 2021. Vol. 70, No 2. P. 62–64.
Babinets L. S., Halabitska I. M., Kotsaba Y. Y., Borovyk I. O., Migenko B. O., Ryabokon S. S., Tsybulska L. S. The effect of the proteolisis’ system activity for the trophological status of patients with osteoarthrosis and excretory insufficiency of pancreas. Wiad. Lek. 2018. Vol. 71, No 2. P. 273–276.
Bannuru R. R., Osani M. C., Vaysbrot E. E. OARSI Guidelines for the non-surgical management of knee, hip, and polyarticular osteoarthritis Osteoarthritis and Cartilage. 2019. Vol. 27, No 11. P. 1578–1589.
Cai X., Yuan S., Zeng Y., Wang C., Yu N., Ding C. New trends in pharmacological treatments for osteoarthritis. Front. Pharmacol. 2021. Vol. 12. P. 645842.
Cisternas M. G., Murphy L., Sacks J. J., Solomon D. H., Pasta D. J., Helmick C. G. Alternative methods for defining osteoarthritis and the impact on estimating prevalence in a US population-based survey. Arthritis Care Res. (Hoboken). 2016. Vol. 68. P. 574–580.
GBD 2015 DALYs and HALE Collaborators. Global, regional, and national disability-adjusted life-years (DALYs) for 315 diseases and injuries and healthy life expectancy (HALE), 1990–2015: a systematic analysis for the Global Burden of Disease Study 2015. Lancet. 2016. Vol. 388. P. 1603–1658.
Gleason B., Chisari E., Parvizi J. Osteoarthritis can also start in the gut: the gut ― joint axis. Indian J. Orthop. 2022. Vol. 56, No 7. P. 1150–1155.
Halabitska I. M., Babinets L. S. Different consequences of the treatment of osteoarthritis in gastrointestinal comorbidity with exocrine pancreatic insufficiency. Fam. Med. Prim. Care Rev. 2021. Vol. 23, No 4. P. 422–428.
Hunter D. J., Bierma-Zeinstra S. Osteoarthritis. Lancet. 2019. Vol. 393, No 10182. P. 1745–1759.
Kwon D. G., Kim M. K., Jeon Y. S., Nam Y. C., Park J. S., Ryu D. J. State of the art: the immunomodulatory role of MSCs for osteoarthritis. Int. J. Mol. Sci. 2022. Vol. 23, No 3. P. 1618.
Murphy L., Schwartz T. A., Helmick C. G., Renner J. B., Tudor G., Koch G., Dragomir A., Kalsbeek W. D., Luta G., Jordan J. M. Lifetime risk of symptomatic knee osteoarthritis. Arthritis Care Res. 2008. Vol. 59. P. 1207–1213.
Qin J., Barbour K. E., Murphy L. B., Nelson A. E., Schwartz T. A., Helmick C. G., Allen K. D., Renner J. B., Baker N. A., Jordan J. M. Lifetime risk of symptomatic hand osteoarthritis: the Johnston County Osteoarthritis Project. Arthritis Rheumatol. 2017. Vol. 69, No 6. P. 1204–1212.
Robinson W. H., Lepus C. M., Wang Q., Raghu H., Mao R., Lindstrom T. M., Sokolove J. Low-grade inflammation as a key mediator of the pathogenesis of osteoarthritis. Nat. Rev. Rheumatol. 2016. Vol. 12, No 10. P. 580–592.
Sakellariou G., Conaghan P. G., Zhang W., Bijlsma J. W., Boyesen P., D’Agostino M. A., Doherty M., Fodor D., Kloppenburg M., Miese F., Naredo E. EULAR recommendations for the use of imaging in the clinical management of peripheral joint osteoarthritis. Ann. Rheum. Dis. 2017. Vol. 76. P. 1484–1494.
Tan T. C., Chong T. K. Y., Low A. H. L., Leung Y. Y. Microbiome and osteoarthritis: new insights from animal and human studies. Int. J. Rheum. Dis. 2021. Vol. 24, No 8. P. 984–1003.