scholarly journals The improvement of treatment efficacy of gastropathy associated with the use of nonsteroidal anti-inflammatory drugs in Helicobacter pylori-negative patients with osteoarthritis

2014 ◽  
Vol 27 (4) ◽  
pp. 237-239
Author(s):  
Antonina V. Antonenko ◽  
Tetyana V. Beregova
Keyword(s):  
Gastric Mucosa ◽  
Initial Step ◽  
Colon Tissue ◽  
Nsaid Enteropathy ◽  
Osteoarthritis Treatment ◽  
Direct Injury ◽  
Treatment Changes ◽  
Nsaid Gastropathy ◽  
Inflammatory Drugs ◽  
Gastric Mucous

Abstract Among the more common side effects of osteoarthritis treatment are NSAID-gastropathy and NSAID-enteropathy. NSAIDs can cause direct injury to colon tissue and also impair synthesis of prostaglandins, reduce mucosal integrity, increase permeability and promote an influx of bacteria and toxins. Alterations in gastrointestinal permeability are considered as an initial step in the development of lesions of the gastric mucosa such as erosions and ulcers. The mechanisms underlying the ability of NSAIDs to cause ulceration in the stomach and proximal duodenum are well understood and this injury can be largely be prevented through suppression of gastric acid secretion. However, our work showed that 28-day administration of the anti-secretory preparation pantoprazole (20 mg 2 times per day) resulted in a statistically significant increase of dysbiosis. Monitoring of patients with osteoarthritis who used NSAIDs for more than three months showed that, in comparison to the situation before the beginning of treatment, changes in colonic microbiota were present. Multiprobiotic “Symbiter® acidophilic concentrated” introduced simultaneously with pantoprazole during 20 days prevented formation of dysbiotic changes and led to the quicker healing of gastric mucous healing, in comparison with patients who used only pantoprazole alone. Moreover, it brought about total healing of the gastric mucosa within 4 weeks from the beginning of treatment.

scholarly journals NSAID enteropathy

2020 ◽  
Vol 92 (2) ◽  
pp. 85-92
Author(s):  
E. N. Kareva
Keyword(s):  
Small Intestine ◽  
Therapeutic Strategy ◽  
Intestinal Flora ◽  
Nsaid Enteropathy ◽  
The World ◽  
Prevention And Treatment ◽  
Nsaid Gastropathy ◽  
Inflammatory Drugs ◽  
Very High

Nonsteroidal anti-inflammatory drugs (NSAIDs) are one of the most commonly used drugs in the world, and their side effects are very high. First of all, these are NSAID gastropathy, but in the long term, 5070% of NSAIDs cause damage to the small intestine (NSAID enteropathy), sometimes with serious consequences. To date, no drugs have been proposed with proven effectiveness to prevent this side effect. Apparently, this is not due to the fully clarified mechanism of pathogenesis. The most promising is the hypothesis of the participation of individual representatives of microflora in the development of enteropathy. Therefore, modulating the intestinal flora with the help of probiotics can be the basic therapeutic strategy for the prevention and treatment of such damage.

scholarly journals Can Ultrasound Therapy Be an Environmental-Friendly Alternative to Non-Steroidal Anti-Inflammatory Drugs in Knee Osteoarthritis Treatment?

Materials ◽  
2021 ◽  
Vol 14 (11) ◽  
pp. 2715
Author(s):  
Rodica Ana Ungur ◽  
Viorela Mihaela Ciortea ◽  
Laszlo Irsay ◽  
Alina Deniza Ciubean ◽  
Bogdana Adriana Năsui ◽  
...  
Keyword(s):  
Ultrasound Therapy ◽  
Negative Effects ◽  
Beneficial Effects ◽  
Knee Oa ◽  
Environmental Friendly ◽  
Chemical Pollutants ◽  
Osteoarthritis Treatment ◽  
Inflammatory Drugs ◽  
Anti Inflammatory ◽  
And Function

The non-steroidal anti-inflammatory drugs (NSAIDs) are the most used drugs in knee OA (osteoarthritis) treatment. Despite their efficiency in pain and inflammation alleviation, NSAIDs accumulate in the environment as chemical pollutants and have numerous genetic, morphologic, and functional negative effects on plants and animals. Ultrasound (US) therapy can improve pain, inflammation, and function in knee OA, without impact on environment, and with supplementary metabolic beneficial effects on cartilage compared to NSAIDs. These features recommend US therapy as alternative for NSAIDs use in knee OA treatment.

Effect of nonsteroidal anti-inflammatory drugs on LFA-1 and ICAM-1 expression in gastric mucosa

1994 ◽  
Vol 266 (4) ◽  
pp. G657-G664 ◽  
Author(s):  
F. J. Andrews ◽  
C. Malcontenti-Wilson ◽  
P. E. O'Brien
Keyword(s):  
Gastric Mucosa ◽  
Blood Vessels ◽  
Adhesion Molecules ◽  
Leukocyte Adhesion ◽  
Mucosal Damage ◽  
Gastric Injury ◽  
Lymphocyte Function ◽  
Nsaid Treatment ◽  
Inflammatory Drugs ◽  
Anti Inflammatory

Leukocyte adhesion to the endothelium appears to play an important role in gastric injury. This study aimed to develop immunohistochemical staining techniques to investigate the distribution and sequence of expression of both leukocyte [lymphocyte function associated antigen 1 (LFA-1)] and endothelial [intracellular adhesion molecule 1 (ICAM-1)] adhesion molecules in the mucosa after treatment with nonsteroidal anti-inflammatory drugs (NSAIDs). In control rats there were 803 +/- 72 LFA-1-stained cells/mm2 in the deep mucosa, 134 +/- 32 cells/mm2 in the superficial mucosa, and 6.4 +/- 1.2 ICAM-1-stained blood vessels/mm2 in the total mucosa. The number of ICAM-1-stained blood vessels in the mucosa increased significantly after 30 min of treatment with intragastric aspirin (30 mM; 25.2 +/- 7.2/mm2, P < 0.01) and indomethacin (20 mg/kg; 20.7 +/- 4.4/mm2, P < 0.01) before any appreciable mucosal damage was evident. This increase was reversed by treatment with misoprostol (100 micrograms/kg) in both aspirin- (7.6 +/- 1.7/mm2, P < 0.01) and indomethacin-treated animals (10.7 +/- 2.6/mm2, P < 0.05). There was no significant increase in LFA-1-positive cells until 60 min of NSAID treatment. We conclude that the adhesion molecules LFA-1 and ICAM-1 are expressed in the normal gastric mucosa and that the number of ICAM-1-stained blood vessels increase rapidly after NSAID treatment. This increase in ICAM-1 expression may be associated with an inhibition of prostaglandin synthesis by NSAIDs. These results provide further support for the role of early vascular changes in NSAID gastropathy.

scholarly journals Effects of licofelone, a novel 5-LOX inhibitor, in comparison to celecoxib on gastric mucosa of dogs

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Aidin Shojaee Tabrizi ◽  
Mohammad Azizzadeh ◽  
Aidin Esfandiari
Keyword(s):  
Gastric Mucosa ◽  
Occult Blood ◽  
Fecal Occult Blood ◽  
Fecal Occult ◽  
Mixed Breed ◽  
Dual Inhibitors ◽  
Group 3 ◽  
Inflammatory Drugs ◽  
Cox 2 ◽  
Group 2

Despite the extensive application of nonsteroidal anti-inflammatory drugs (NSAIDs), the use of these drugs is limited due to their adverse effects especially on gastric mucosa. Dual inhibitors that inhibit both cyclooxygenase (COX) and lipoxygenase (LOX) metabolites are considered to have less gastric toxicity in comparison to non-selective and COX-2 selective inhibitors. In this study, fifteen mixed breed dogs were randomly divided into three groups: group 1 (n=5) received placebo, group 2 (n=5) licofelone, an inhibitor of COX- 1, COX-2, and 5-LOX (2.5 mg/kg; twice daily) and group 3 (n=5) celecoxib, a COX-2 selective inhibitor (3 mg/kg; twice daily) per os for 14 days. All dogs underwent blinded gastroscopies on days 0, 7, 14 and one week after cessation of treatment and gastric lesions were scored. Examinations to detect fecal occult blood were performed daily. Results showed that licofelone is significantly better tolerated than celecoxib in terms of gastric side effects (P=0.008). Therefore, it seems that licofelone can be an appropriate alternative in dogs when NSAID therapy is necessary. Occult blood was not detected in any dog during the study.

scholarly journals CHARACTERISTICS OF GASTRIC MUCOSA INJURY IN PATIENTS WITH NSAID-INDUCED GASTROPATHY AND CONCOMITANT ISCHEMIC HEART DISEASE, AND WAYS TO CORRECT THIS CONDITION

2020 ◽  
Vol 20 (2) ◽  
pp. 70-75
Author(s):  
V.V. Parkhomenko ◽  
І.М. Skrypnyk ◽  
І.І. Starchenko ◽  
O.F. Gopko
Keyword(s):  
Heart Disease ◽  
Gastric Mucosa ◽  
Ischemic Heart Disease ◽  
Proton Pump Inhibitors ◽  
Proton Pump ◽  
Morphological Changes ◽  
Ischemic Heart ◽  
Mucosal Barrier ◽  
Nsaid Gastropathy ◽  
H Pylori

The non-steroidal anti-inflammatory drugs (NSAIDs) in general clinical practice can provoke the development of NSAID-induced gastropathy, which can be complicated by bleeding. The aim of this article was to evaluate the effect of eupatilin on histological changes of the gastric mucosa in patients with NSAID-induced gastropathy and concomitant ischemic heart disease depending on the association with Helicobacter pylori. The study included 125 patients with NSAID-gastropathy and concomitant stable ischemic heart disease I-II functional class. Patients were divided into two groups: I (n=82) included individuals with NSAID-gastropathy, which was not associated with H. pylori, while II (n=43) included individuals with H. pylori-induced gastropathy. Depending on the prescribed treatment complexes, patients were subdivided as follows: I-A (n=44) included patients, who took proton pump inhibitors in standard doses and II-A group (n=23) included patients, who received antihelicobacter therapy according to Maastricht V (2016) guidelines. Patients of groups I-B (n=38) and II-B (n=20) were additionally prescribed 60 mg of eupatilin (1 tablet) 3 times a day for 28 days. The upper endoscopy with the gastric mucosa biopsy, followed by histological examination was done at the beginning of treatment and in 45±2 days. The severity of gastric mucosa erosive and ulcerative injury was assessed endoscopically using a modified Lanzascore scale; morphological changes were evaluated by a semi-quantitative method on a visual-analogue scale. H. pylori is an independent and significant factor determining the severity of endoscopic and morphological changes in NSAID-gastropathy patients with concomitant ischemic heart disease. Acid-suppressive and antihelicobacter therapy can reduce the intensity of the structural injury of the gastric mucosa, but the identified changes substantiate the feasibility of long-term proton pump inhibitors prescribed to the patients with NSAID-gastropathy. Prescribing eupatilin against the background of basic therapy can significantly reduce the severity of erosive-ulcerative gastric mucosa injury assessed by Lanzascore scale while histomorphological parameters by reducing the activity of neutrophilic inflammation, protective effect on mucosal barrier resistance and microcirculatory condition.

scholarly journals The cytoprotective effect of a nitric oxide donor drug on gastric mucous membrane of rats treated with ketoprofen, a non-steroidal anti-inflammatory drug

2006 ◽  
Vol 43 (3) ◽  
pp. 233-237 ◽  
Author(s):  
Afonso Luiz Villa ◽  
Ceneviva Reginaldo ◽  
Fernanda Viaro ◽  
Fernando Ramalho ◽  
Antonio Dorival Campos ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Isosorbide Dinitrate ◽  
Saline Solution ◽  
Isotonic Saline ◽  
Nitric Oxide Donor ◽  
Group Iii ◽  
Inflammatory Drugs ◽  
Anti Inflammatory ◽  
Gastric Mucous ◽  
Lesion Index

BACKGROUND: Non-steroidal anti-inflammatory drugs are considered today a very important group of medication, with a wide variety of therapeutic use, in different areas of modern medicine. Despite their beneficial effects on the patient, these drugs show a high incidence of side effects, mainly in the gastrointestinal tract. The physiopathological mechanisms of non-steroidal anti-inflammatory drugs induced lesions and the gastric mucosa defense mechanism became an important source for medical research, especially those which try to evaluate the role of nitric oxide as a cytoprotective agent. AIM: To define a possible cytoprotective effect of a nitric oxide donor, isosorbide dinitrate, on the gastric mucous of rats submitted to non-steroidal anti-inflammatory drugs ketoprofen treatment. METHODS: Adult male Wistar rats, previously submitted to starvation for 24 hours and divided in three groups: group I (standard): animals that received isotonic saline solution intragastric by gavage and intravenous. Group II (control-ketoprofen): animals that received isotonic saline solution intragastric by gavage and ketoprofen intravenous. Group III (nitrate/ketoprofen): animals that received 2mM solution of isosorbide dinitrate intragastric by gavage and ketoprofen intravenous. Later on, these animals were sacrificed and had their stomach removed and submitted to macroscopical, microscopical and biochemical studies. The evaluated parameters were: a) gastric lesion index; b) gastric mucous layer thickness; c) gastric tissue nitrate/nitrite (NOx) concentration and d) gastric tissue malondialdehyde concentration. RESULTS: a) Gastric lesion index evaluation showed a smaller statistically significant incidence on the animals of group III; b) group III showed a thicker mucous layer, which also was statistically significant, when compared to group II; c) the variation on tissue nitrate/nitrite concentration was similar in all three groups, without statistical significance when compared to each other. CONCLUSION: Isosorbide dinitrate has a cytoprotective activity on the gastric mucosa of rats submitted to ketoprofen action.

Gastric ulceration: critical events at the neutrophil–endothelium interface

1993 ◽  
Vol 71 (1) ◽  
pp. 98-102 ◽  
Author(s):  
John L. Wallace
Keyword(s):  
Vascular Endothelium ◽  
Proteolytic Enzymes ◽  
Mucosal Blood Flow ◽  
Mucosal Injury ◽  
Gastric Ulceration ◽  
Critical Event ◽  
Neutrophil Adherence ◽  
Nsaid Gastropathy ◽  
Inflammatory Drugs ◽  
Gastrointestinal Ulceration

Neutrophil adherence to the vascular endothelium and the subsequent release of oxygen-derived free radicals and proteolytic enzymes has been implicated as a critical event in the pathogenesis of various forms of gastrointestinal ulceration. This paper reviews the evidence that events at the neutrophil-endothelium interface are important in the pathogenesis of gastric ulceration induced by nonsteroidal anti-inflammatory drugs (NSAIDs). Endothelial injury occurs within minutes of NSAID administration and appears to be attributable to neutrophil adherence and activation. Neutrophil adherence in response to NSAIDs may occur as a consequence of inhibition of endothelial prostaglandin synthesis, but it appears to involve a lipoxygenase product, such as leukotriene B4. Prevention of neutrophil adherence to the vascular endothelium results in near-complete prevention of experimental NSAID gastropathy. Depletion of circulating neutrophils also results in reduced susceptibility to NSAID-induced mucosal injury. As prostaglandins are potent inhibitors of neutrophil adherence and activation, it is possible that the neutrophil–endothelium interface represents one of the most important targets of action of these compounds in terms of their ability to prevent or reduce the severity of NSAID-induced ulceration.Key words: ulcer, mucosal blood flow, prostaglandin, neutrophil, leukotriene.

scholarly journals NSAID Gastroenteropathy: Past, Present and Future

1996 ◽  
Vol 10 (7) ◽  
pp. 451-459 ◽  
Author(s):  
John L Wallace
Keyword(s):  
Gastrointestinal Tract ◽  
Inflammatory Disorders ◽  
The Past ◽  
Prostaglandin Synthase ◽  
Nsaid Enteropathy ◽  
The Future ◽  
Inflammatory Drugs ◽  
Anti Inflammatory ◽  
Identification And Characterization

The toxicity of nonsteroidal anti-inflammatory drugs (NSAIDs) in the gastrointestinal tract continues to be a major limitation to their use in the treatment of inflammatory disorders. Better understanding of the pathogenesis of NSAID enteropathy has facilitated the development of novel NSAIDs that spare the gastrointestinal tract. In particular, identification and characterization of the inducible form of prostaglandin synthase has led to the design of novel NSAIDs that specifically target that enzyme. The pathogenesis of NSAID gastroenteropathy is reviewed, as are the strategies that have been used in the past and are used now to develop NSAIDs that spare the gastrointestinal tract. Also reviewed are the strategies being employed to achieve this goal in the future.

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