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Clinico-endoscopic characteristic of gastropathy due to non-steroid anti-inflammatory drugs...
Atabaeva Saodat Muzaffarovna, senior researcher,
Department of Gastroenterology and Physiotherapy, Tashkent Institute of the Postgraduate Education for Doctors
E-mail: doctorcaodat@mail.ru Khamrabaeva Feruza Inbragimovna, doctor of medicine, professor, Head of Department of Gastroenterology and Physiotherapy, Tashkent Institute of the Postgraduate Education for Doctors
Clinico-endoscopic characteristic of gastropathy due to non-steroid anti-inflammatory drugs in the patients with ischemic heart disease
Abstract: The retrospective analysis of the history of the ischemic heart disease in the patients with gastropathy, induced by non-steroid anti-inflammatory drugs, has allowed revealing the high degree of correlation (R2 = 0.95) between the frequency of non-steroidal anti-inflammatory drug-gastropathies and duration of application of these drugs. The algorithm of treatment and prophylactic measures for non-steroid anti-inflammatory drug-gastropathies in patients with ischemic heart disease should include usage of proton pump inhibitors and nonabsorbable antacids. When detecting infection H.pylori it is necessary to conduct basic eradication therapy during 10 days.
Keywords: Non-steroid anti-inflammatory agents — gastropathies, antisecretory therapy, IHD, H. pylori infection.
Introduction
The algorithm of therapeutic-preventive measures of nonsteroid anti-inflammatory drug-gastropathies in the patients with ischemic heart disease (IHD) provides application of the proton pump inhibitors and of non-absorbable antacids. At revealing of the infection H. pylori it is necessary to perform 10-day basis eradication therapy.
Ischemic heart disease (IHD) is characterized by developing and progressing disturbances of the homeostasis, that dictates necessity in use of persistent anti-aggregate therapy. The preparations made on the basis of acetylsalicylic acid (ASA) seem to be the "gold" standard for this purpose [1].
Representative researches showed that the use of ASA and nonsteroid anti-inflammatory preparations (NSAID) induces statistically significant decrease in risk of development of myocardial infarction and stroke as well as lethal outcome in one third ofpatients with high risk of coronary artery occlusion [2]. However, despite of high efficiency, the application of ASA in 25 % of cases was accompanied by development of adverse effects. The most significant of them are the gastropathies induced by NSAID [3]. Potentially the development of gastropathy threatens to any patient receiving ASA for a long time [4].
NSAID-gastropathy is a collective notion including ulcers and erosion of the mucosa of gastroduodenal zone (GDZM) and the special form of gastritis — "chemical", according to the Sydney classification [5].
NSAID have property to penetrate directly into the cells of mucosa in the gastric acid medium. Change of mucous-bicarbonate barrier and reversal diffusion of hydrogen ions result in "contact" damage of the superficial endothelium. The processes of oxidizing phosphorylation, developing as a result of blocking of mitochondrial epithe-liocyte enzymatic systems promote to reduction of cell resistance to aggressive effect of the hydrochloric acid and pepsin, formation of necrobiotic processes, appearance of erosive-ulcerative processes, disturbance of the regeneration processes in the mucosa [6].
The risk factors of NSAID-gastropathy include gastroduo-denal ulcer in the medical history of the patient; high doses of the NSAID; their combined receiving preparations of ASA,
antiaggregates, steroids, anticoagulants; age above 65 years; smoking; presence of Helicobacter pylori infection; activity of the chronic gastritis in the anthral part according to the findings of the morphological investigation [7].
NSAID-gastropathies have a latent clinical course approximately in 50 % ofpatients. Frequently, only bleedings can be a single sign of the erosive-ulcerative damages of the gastroduodenal mucosa. Only in a part of patients there is observed dyspepsia, pain and discomfort in the epigastral area. As a rule, only the gastroduodenal complications at the receiving of NSAIDS are manifested without previous dyspepsia [8].
The criteria of the diagnosis of NSAID-gastropathy in the patients with IHD [9] are as follows:
- Appearance, on the basis of NSAID usage, of acute, usually multiple gastroduodenal erosions and/or ulcers with predominant localization in the anthral site of stomach;
- absence of local inflammation and histological signs of gastritis;
- few symptoms or asymptomatic clinical picture;
- frequent manifestation of complications;
- ulcer tendency to healing at stopping of NSAID receiving.
The majority of patients with gastrointestinal risk factors, receiving NSAIDS or ASA for a short or long periods should receive prophylactically every day the antisecretory drugs of the group of proton pump inhibitors (PPI), that decreases dyspepsia and improves the quality of life of the patients [8].
Developing for a long time the asymptomatic NSAID-gastrop-athy is frequently complicated by gastroduodenal bleeding or ulcer perforation, that appears to be the cause of lethal outcome. In this connection the questions of early diagnosis and adequate therapy of NSAID-gastropathy in the patients with IHD seems to be very actual.
Purpose of the research was to study clinical and endoscopic events of gastropathies induced by receiving of non-steroid antiinflammatory drugs in the patients with IHD.
Material and methods. Under supervision there were 121 patients with the various forms of IHD, receiving the common treatment in the Republican clinical hospital № 1 of the Ministry of Health of the Republic of Uzbekistan, during the period
Section 5. Medical science
from 2012 to 2014. The gastroduodenal pathology was related to usage of NSAIDS and ASA (cardiomagnil, thromboass, aspirin-cardio) and was found in 101 (83.5 %) cases. The mean age of the patients accounted for 67.7 ± 3.5 years. Males were 78 (65.5 %), females — 43 (34.5 %).
The examination of the patients included assessment of the main disease, frequency and structure of NSAID-gastropathy and its complications, clinical (dyspeptic and pain) and objective (localization and intensity of the abdominal pain) gastroenterological symptoms, details of the medical history (duration of NSAIDS receiving, age, sex, "ulcerative anamnesis").
There were analyzed conclusions of the fibroesophagogas-troduodenoscopy (FEGDS): character, intensity, localization of the inflammatory and erosive-ulcerative changes in the gastroduodenal mucosa. Endoscopic investigations were performed in patients with IHD according to the following indications: presence of gastroenterological symptoms; before performance of coronarography, operation of aorta-coronary bypass, stenting of the coronary arteries.
Results of research and their discussion
At the analysis of the complaints it was appeared, that the most often symptoms in the patients were heartburn in 18 (14.9 %) and periodical weak abdominal pains — in 22 (18.2 %) patients. Dyspeptic symptoms, nausea and vomiting were noted only in 6.5 % and 3.9 % of case, respectively. In the majority of patients (74.8 %) with erosive-ulcerative lesions of the gastroduodenal mucosa the clinical symptoms of dyspepsia and abdominal pains were absent.
The signs of gastroduodenal bleeding — coffee-ground vomiting and tarry stool were noted in 7 (9.1 %) patients
The erosive-ulcerative lesions of gastroduodenal mucosa were observed predominantly in the patients with acute or repeated myocardial infarction. In all the cases the performed conservative haemostatic therapy (quamatel 40 mg. in 200 ml. of isotonic solution of NaCl intravenously by drops in the system, etamzilat 40 mg. intravenously) allowed stopping of bleeding. The lethal outcome due to severe bleeding lost was not observed.
It the patients receiving NSAIDS or ASA there was performed search for gastroenterological risk factors. For this purpose the "ulcerative" anamnesis was studied and it was determined whether there was complication (bleeding, penetration or perforation). At absence of "ulcerative" anamnesis the other risk factors were evaluated.
Analysis of the risk factors showed that in the patients with IHD with NSAID-gastropathy mainly there were two factors prevailed, that is, age above 65 years (82.5 %) and prolonged receiving of preparations ASA or NSAIDS (70 %). The "ulcerative" anamnesis was revealed only in 6.5 % of cases.
Detailed study of anamnesis data has allowed establishment that during increase in period of disease development and, consequently, duration in using NSAIDS or ASA, as preventive antiaggregate therapy, there was noted direct proportional dependence of the increase in frequency of gastropathy.
The basic mass consisted of the patients receiving NSAIDS and ASA preparations during the period from 10 till 15 years (26.0 %) and more than 15 years (39.0 %). The patients using these medicinal preparations about 1 year (3.9 %) were least of all.
The analysis of nosological forms of IHD has shown, that the greatest specific weight was made by the patients with progressing stenocardia (49.4 %) and acute myocardial infarction (26.0 %). The patients with a repeated heart attack accounted for 13.0 %, with the primary arisen stenocardia — 6.5 %. The detailed elaboration of the data of anamnesis has allowed establishment, that the patients with primary arisen stenocardia were also prescribed
ASA preparations due to present arterial hypertension of various severity degree for some years.
The clinical picture at NSAID-induced gastropathies was characterized by disbalance between symptoms and endoscopic changes. So, in a number of the patients having pains or others dyspeptic disorders, at PEGDS there were revealed minimal changes in the gastroduodenal mucosa. On the contrary at presence of multiple erosion and ulcers the NSAID-gastropathies were progressing frequently without symptoms. At PEGDS in the patients with IHD there were revealed various changes in the gastroduodenal mucosa (table 1).
Table 1. - Endoscopic signs of the NSAID-gastropathy
N Endoscopic changes abs %
1 Chronic superficial gastritis 68 56.2
2. Duodenogastric reflux 28 23.2
3. Acute gastric erosion 24 19.9
4. Acute gastric ulcers 22 18.2
5. Acute duodenal erosion 19 5.7
6. Acute duodenal ulcers 15 12.4
7. Chronic gastric erosion 15 12.4
8. Chronic gastric ulcer 14 11.6
9. Chronic gastroduodenal ulcer 13 10.8
10. Mellory Weiss syndrome 8 6.7
The analysis of results of endoscopic researches allowed to ascertain, that in the patients, receiving preparations ASA or NSAID for a long time, the changes were mainly observed as chronic gastritis (56.2 %). On the second place by frequency there was observed duodenogastric reflux (23.2 %). The acute erosion and ulcers were located mainly in a stomach, accounting for 18.2 % and 15.7 %, in the duodenum they were in 12.4 % and 10.8 %, respectively. The chronic erosion and ulcer of a stomach (respectively, 12.4 % and 11.6 % of cases), chronic duodenal ulcer (10.8 %), Mellory-Weiss's syndrome (6.7 %) cases were revealed too.
In the clinical practice it is difficult to determine a clear border between NSAID-gastropathies and «stressful» erosions and ulcers arising in the patients with acute myocardial infarction and other heavy pathology or operative interventions. Only carefully detailed anamnesis, indicating about duration of receiving of preparations of ASA and NSAIDS allows identification of these damages in the top departments of a digestive tract. It was established, that all patients used various preparations ofASA or NSAIDS for a long time. Therefore, all presented cases of GDP in the patients with IHD revealed at careful examinations of the studied patients, allow us to believe about presence of NSAID-gastropathy in them.
According to the results of the researches performed the algorithm of treatment of NSAID-gastropathies included the following notions: prescription of a medical diet (Table 1); at all patients with erosion-ulcerative lesions in the gastroduodenal mucosa there was solved the problem on an opportunity of a cancellation or decrease of a doze of NSAID and antiaggregants; proton pump inhibitors were nominated in standard dozes and modes.
To the patients with ulcerative anamnesis and also at detection of an infection Helicobacter pylori (H. pylori) with the help of immu-nofermentative analysis (IFA) or urease respiratory test, the 10-days eradication therapy was prescribed which included: omeprazole 20 mg. 1tab. x 2 times a day, + amoxicillin1000 mg. 2 tab. x 2 times a day + clarythromicin 500 mg. in 2 tab. x 2 times a day.
At detection of H.pylori the eradication should be performed before application of NSAIDS or ASA. Eradication of the presenting infection is rationalized also in a case of prospective long preventive application of PPI. At absence of ulcerative anamnesis and
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under the conditions of continuing therapy with NSAID or ASA the eradication therapy should be also performed. It is necessary to take into account, that in all situations the successful eradication of an infection H. pylori does not exclude necessity of the subsequent preventive application of PPI [12].
As symptomatic treatment the patients were prescribed the widely used in the gastroenterological practice non-absorbable antacids (almagel, Maalox or other). They, absorbing the hydrochloric acid, reduce proteolytic activity of gastric juice (by means of pepsin absorbtion, increase in pH of the environment), therefore pepsin has become inactive. Antacides have enveloping properties, binds lizoleci-tin and bilious acids having unfavoutable effect on the gastroduodenal mucosa. Last years in the experimental and clinical researches it has been established, that cytoprotective effect of antacides is caused by increase in prostaglandins contents in the gastric wall, increase in bicarbonate secretion, and increase in glycoproteins in the gastric mucus. Their application has shown sufficient therapeutic efficiency as medical means for elimination of dyspeptic syndrome [10; 11].
Erosive changes in the gastroduodenal mucosa at absence of the symptoms of hemorrhage did not require stopping receiving of NSAID or ASA. In a case of identification of the ulcerative damages at any stage of NSAID-therapy their cancellation and prescription
of PPI appeared to be the most rational tactics. The same means were applied in the cases when it was impossible to stop receiving of NSAID because of high risk of thromboembolic complications of the ischemic heart diseases. The patients were recommended continuing treatment with PPI during 4 to 8 weeks with subsequent endoscopic control.
Conclusions:
1. The clinical features of NSAID-gastropathy and revealed at endoscopic examinations changes in the gastroduodenal mucosa in the patients with IHD do not meet, so endoscopic control, particularly at early time of treatment (the first 1-2 months) is an obligatory and adequate method of prevention of heavy complications.
2. At the patients with IHD at presence of gastroduodenal ulcers and erosion with a bleeding or its threat it is recommended to cancel NSAID, if this is impossible, it is necessary to lower a doze of a preparation and to prescribe PPI + antacids.
3. Strategy of treatment and prevention of NSAID-gastropa-thies should include prescription of gastroprotectors at presence of risk factors and symptoms of dyspepsia.
4. At revealing of H. pylori, according to the recommendations of Maastricht IV Consensus (2011) it is necessary to perform 10-day basic eradication therapy.
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Ahmadaliev Rustam Umaraliyevich, Fergana branch of Tashkent medical academy E-mail: arsif@mail.ru
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Abstract:
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