CHRONIC GASTRITIS CLINICAL FEATURES AND STOMACH FUNCTIONAL STATE DURING NONSTEROIDAL ANTI-INFLAMMATORY DRUGS ADMINISTRATION IN PATIENTS WITH OSTEOARTHRITIS

  • Maxim Zak Kharkiv national medical University, Ukraine
  • Lyudmila Pasiyeshvili Kharkiv national medical University, Ukraine
Keywords: chronic gastritis, osteoarthritis, nonsteroidal anti-inflammatory drugs

Abstract

Aim. Determination of chronic gastritis clinical features and stomach functional state during nonsteroidal anti-inflammatory drugs (NSAID) administration in patients with osteoarthritis (OA).

Materials and methods. 122 patients with OA and verified chronic gastritis (CG) (50 males and 72 females) aged 42 to 64 years (mean age – 49.65±3.51) were observed. Depending on gastritis morphological form, patients were divided into 2 groups: 54 patients with OA in combination with non-atrophic gastritis (NAG) were included into the group I, 68 patients with OA in combination with atrophic gastritis (AG) – into group II. 40 patients with OA without concomitant gastroduodenal pathology in anamnesis were included into the group III. All patients obtained selective NSAID for OA treatment: Meloxicam 15 mg daily or Nimesulide 200 mg daily. The control group was formed by 20 persons, which were found to be healthy after a complex examination. Stomach acid-forming function was investigated using esophageal pH monitoring. In the gastric contents, which obtained by aspiration, concentration of sialic acids glycoproteins, fucose, and hexosamines was determined.

Results. Clinical picture of NSAID gastropathy at NAG characterized by abdominal pain of varying intensity and not associated with eating, but in patients with AG severity and discomfort symptoms dominated over weakly expressed pain syndrome. As a result of NSAID, in the group I dyspepsia developed in 31 (57.4 %), and erosive gastropathy developed in 9 (16.7 %) patients. In the group II, erosive gastropathy and dyspepsia were observed in 15 (22.1%) and in 35 (51.5 %) patients, respectively. In the group III, erosive gastropathy was observed 3.3 times (c2=84.33;  р=0.009) and 4.4 times (c2=36.78; р=0.002) less than in groups I and II, respectively. In 25% patients of the group I after NSAID therapy intragastric pH increased from normacid to hyperacid status. In the group II, NSAID administration led to stomach mucosal (SM) protective factors depletion, which was observed in 73.3 % and in 28.6 % of patients with erosive gastropathy and NSAID-associated dyspepsia, respectively. At AG with erosive gastropathy, unlike NAG, several protective factors simultaneous reduction was observed.

Coonclusion. In anamnesis, CG factor at selective NSAID administration (Meloxicam and Nimesulide) in relation to OA significantly increases the risk of erosive gastropathy, compared with patients without CG in anamnesis. At OA NSAID administration in patients with NAG led to gastric contents acidification and in patients with AG – to SM protective factors depletion (glycoprotein, fucose, and hexosamine).

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Author Biographies

Maxim Zak, Kharkiv national medical University

Department of General Practice Family Medicine

Lyudmila Pasiyeshvili, Kharkiv national medical University

Department of General Practice Family Medicine

References

Kuryata, A. V., Grechanik, M. M. (2014). Problema lecheniya sustavnoy boli: focus na bezopasnost’. Health of Ukraine, 6, 43–44.

Kovalenko, V. M., Bortkiewicz, O. P. (2010). Osteoartroz: practichna nastanova. Kyiv: Morіon, 607.

McCarberg, B. H., Cryer, B. (2015). Evolving Therapeutic Strategies to Improve Nonsteroidal Anti-inflammatory Drug Safety. American Journal of Therapeutics, 22 (6), e167–e178. doi: 10.1097/mjt.0000000000000123

Zak, M. Y., Mosіychuk, L. M. (2011). Hronіchniygastrit i peredrakshlunka: practichniyposіbnik. Dnipropetrovs'k: Siaprint, 71.

Hochberg, M. C., Altman, R. D., April, K. T., Benkhalti, M., Guyatt, G., McGowan, J. et. al. (2012). American College of Rheumatology 2012 recommendations for the use of nonpharmacologic and pharmacologic therapies in osteoarthritis of the hand, hip, and knee. Arthritis Care & Research, 64 (4), 465–474. doi: 10.1002/acr.21596

Courties, A., Gualillo, O., Berenbaum, F., Sellam, J. (2015). Metabolic stress-induced joint inflammation and osteoarthritis. Osteoarthritis and Cartilage, 23 (11), 1955–1965. doi: 10.1016/j.joca.2015.05.016

Narouze, S., Souzdalnitski, D. (2015). Obesity and chronic pain: opportunities for better patient care. Pain Management, 5 (4), 217–219. doi: 10.2217/pmt.15.16

Matsui, H., Shimokawa, O., Kaneko, T., Nagano, Y., Rai, K., Hyodo, I. (2011). The pathophysiology of non-steroidal anti-inflammatory drug (NSAID)-induced mucosal injuries in stomach and small intestine. Journal of Clinical Biochemistry and Nutrition, 48 (2), 107–111. doi: 10.3164/jcbn.10-79

Boltin, D., Niv, Y. (2014). Pharmacological and alimentary alteration of the gastric barrier. Best Practice & Research Clinical Gastroenterology, 28 (6), 981–994. doi: 10.1016/j.bpg.2014.09.001

Sinha, M., Gautam, L., Shukla, P. K., Kaur, P., Sharma, S., Singh, T. P. (2013). Current Perspectives in NSAID-Induced Gastropathy. Mediators of Inflammation, 2013, 1–11. doi: 10.1155/2013/258209

Uyanikoglu, A., Danalioglu, A., Akyuz, F., Ermis, F., Gulluoglu, M., Kapran, Y. et. al. (2012). Etiological factors of duodenal and gastric ulcers. The Turkish Journal of Gastroenterology, 23 (2), 99–103. doi: 10.4318/tjg.2012.0435

Kayacetin, S., & Guresci, S. (2014). What is gastritis? What is gastropathy? How is it classified? The Turkish Journal of Gastroenterology, 25 (3), 233–247. doi: 10.5152/tjg.2014.7906

Dixon, M. F., Genta, R. M., Yardley, J. H., Correa, P. (1996). Classification and Grading of Gastritis. The American Journal of Surgical Pathology, 20 (10), 1161–1181. doi: 10.1097/00000478-199610000-00001

Blackler, R. W., De Palma, G., Manko, A., Da Silva, G. J., Flannigan, K. L., Bercik, P. et. al. (2015). Deciphering the pathogenesis of NSAID enteropathy using proton pump inhibitors and a hydrogen sulfide-releasing NSAID. American Journal of Physiology – Gastrointestinal and Liver Physiology, 308 (12), G994–G1003. doi: 10.1152/ajpgi.00066.2015

Kwiecień, S., Magierowska, K., Śliwowski, Z., Wójcik, D., Magierowski, M., Brzozowski, T. (2015). New insight into the mechanisms of gastroduodenal injury induced by nonsteroidal anti-inflammatory drugs: practical implications. Polskie Archiwum Medycyny Wewnetrznej, 125 (3), 191–198.

Maguilnik, I., Neumann, W. L., Sonnenberg, A., Genta, R. M. (2012). Reactive gastropathy is associated with inflammatory conditions throughout the gastrointestinal tract. Alimentary Pharmacology & Therapeutics, 36 (8), 736–743. doi: 10.1111/apt.12031

Roth, S. H. (2012). Coming to Terms with Nonsteroidal Anti-Inflammatory Drug Gastropathy. Drugs, 72 (7), 873–879. doi: 10.2165/11633740-000000000-00000

O’Connor, A., O’Moráin, C. (2014). Digestive Function of the Stomach. Digestive Diseases, 32 (3), 186–191. doi: 10.1159/000357848

Arismendi-Morillo, G., Hernández, I., Mengual, E., Abreu, N., Molero, N., Fuenmayor, A. et. al. (2013). Estimación de riesgo de cáncer gástrico en pacientes con gastritis crónica asociada a la infección por Helicobacter pylori en un escenario clínico. Revista de Gastroenterología de México, 78 (3), 135–143. doi: 10.1016/j.rgmx.2013.01.004

Rugge, M., de Boni, G., Pennelli, M. (2010). Gastritis OLGA – staging & gastric cancer risk: a twelve year clinico-pathological follow-up study (England) Minerva Gastroenterol. Dietol., 56 (1), 13–17.


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Published
2016-09-30
How to Cite
Zak, M., & Pasiyeshvili, L. (2016). CHRONIC GASTRITIS CLINICAL FEATURES AND STOMACH FUNCTIONAL STATE DURING NONSTEROIDAL ANTI-INFLAMMATORY DRUGS ADMINISTRATION IN PATIENTS WITH OSTEOARTHRITIS. EUREKA: Health Sciences, (5), 17-22. https://doi.org/10.21303/2504-5679.2016.00178
Section
Medicine and Dentistry