Chronic Gastritis Clinical Features and Stomach Functional State during Nonsteroidal Anti-inflammatory Drugs Administration in Patients with Osteoarthritis

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).