Prolonged Use Of Non-steroidal Anti-inflammatory Drugs Research Articles

Anti-inflammatory and antinociceptive activities of Salvia halophila and Salvia virgata from Turkey

Chronic inflammatory diseases remain one of the world's major health problems (1). Currently, both steroidal and nonsteroidal anti-inflammatory drugs (NSAIDs) are used in the treatment of inflammatory disorders. Steroids have an obvious role in the treatment of inflammatory diseases, but due to rate limiting toxicities, can only be prescribed over short periods except in very severe cases where the risks are acceptable. Prolonged use of NSAIDs also associated with severe side effects, notably gastrointestinal haemorrhage (2). The recently developed cyclooxygenase-2 (COX- 2) selective drugs introduced into therapy, however, do not seem to be free of risk (3). Consequently, there is a need to develop new anti-inflammatory agents with minimum side effects. Turkey is an important country for Salvia species. The flora of Turkey includes 88 species of the genus Salvia. The aerial parts of S. halophila and S. virgata were used in Soxhlet extraction with different solvents such as n-hexane, ethylacetate, methanol and aqueous methanol (50%). Plants were also extracted with water under reflux. In the present study, the potential effects of the extracts from the aerial parts of S. halophila and S. virgata were studied in p-benzoquinone- induced writhing reflex for the assessment of antinociceptive activity and carrageenan-induced hind paw edema and 12-O-tetradecanoyl-13-acetate (TPA)-induced ear edema models in mice for the anti-inflammatory activity. Results have shown that methanol extract of S. virgata significantly inhibited carrageenan-induced paw edema and p-benzoquinone-induced writhing reflex at 100mg/kg dose, while this extract showed no effect in the TPA-induced ear edema. On the other hand, the other exracts did not show any inhibitory antinociceptive and anti-inflammatory activities in these in vivo models.

Enfermedad diafragmática intestinal asociada a AINE con histología de hamartoma neuromuscular y vascular. Presentación de un caso y revisión de la bibliografía

Diaphragm disease (DD) induced by non-steroidal anti-inflammatory drugs (NSAIDs) and neuromuscular and vascular hamartoma (NMVH) are rare entities that can be difficult to recognize clinically, radiologically and pathologically. Both may cause small bowel obstruction and both reveal annular constrictions macroscopically. However, the 2 entities differ in that the constrictions are purely fibrous in DD whereas they have a hamartomatous histopathology in NMVH. We describe the case of a 76-year-old woman with a history of prolonged NSAID use who developed clinical features and gross pathology consistent with DD and histopathology of NMVH.

DIAGNOSIS AND TREATMENT OF NONSTEROIDAL ANTI-INFLAMMATORY DRUG-ASSOCIATED UPPER GASTROINTESTINAL TOXICITY

Nonsteroidal anti-inflammatory drugs (NSAIDs) are widely prescribed in the United States to treat pain and reduce inflammation from chronic inflammatory disorders such as rheumatoid arthritis and osteoarthritis. Approximately 40% of older Americans take NSAIDs. Chronic NSAID use carries a risk of peptic ulcer and other gastrointestinal disturbances. This article reviews the diagnosis of medication-induced ulcers based on clinical presentation, laboratory tests, and endoscopic findings to assist the clinician in early diagnosis and appropriate therapy. Risk factors for NSAID-induced ulcers include old age, poor medical status, prior ulcer, alcoholism, smoking, high NSAID dosage, prolonged NSAID use, and concomitant use of other drugs that are gastric irritants, such as alendronate, a bone resorption inhibitor prescribed for osteoporosis. Appropriate treatment options for patients with medication-induced ulcers include dosage reduction, medication substitution, medication withdrawal, antiulcer therapy, and discontinuation of other gastrotoxic drugs.

Influence of anti-rheumatic drugs on gut permeability and on the gut associated lymphoid tissue

There is great interest in the association between intestinal inflammation and the various arthropathies. However, most studies assessing intestinal function in these diseases are confounded by the fact that non-steroidal anti-inflammatory drugs (NSAIDs) have profound effects on the small intestine. Hence NSAIDs cause quite distinct and severe biochemical damage during drug absorption (uncoupling of mitochondrial oxidative phosphorylation proving to be most important) which results in increased intestinal permeability. All commonly used NSAIDs, apart from aspirin and nalbumetone, are associated with increased intestinal permeability in man. Whilst reversible in the short term, it may take months to improve following prolonged NSAID use. Increased intestinal permeability appears to be the central mechanism of converting the biochemical damage to an inflammatory tissue reaction (NSAID enteropathy). The inflammatory enteropathy is not, however, unique to NSAIDs but similar changes are found with other permeability breakers. In intestinal infections and in diseases associated with reduced mucosal defence, suggesting that the small intestinal inflammation represents a common final pathway for a number of intestinal injuries. Spondylarthropathies are associated with a high prevalence of terminal ileitis, but as most patients have been receiving NSAIDs it has been difficult to dissociate the effects of NSAIDs on intestinal function from that of the ileitis itself. Nevertheless, two studies suggest that increased intestinal permeability in spondylarthropathies occur independently of NSAID ingestion. Whilst these findings may have implications for the development of arthritis, the permeability changes in spondylarthropathy do not differ quantitatively or qualitatively from that of NSAIDs or other permeability breakers. NSAID enteropathy can be differentiated from spondylarthropathic enteropathy by differences in location of disease and lack of predilection of certain HLA types. However, as the two may coexist both enteroscopy and ileocolonoscopy may be necessary for this distinction.

Influence of anti-rheumatic drugs on gut permeability and on the gut associated lymphoid tissue

There is great interest in the association between intestinal inflammation and the various arthropathies. However, most studies assessing intestinal function in these diseases are confounded by the fact that non-steroidal anti-inflammatory drugs (NSAIDs) have profound effects on the small intestine. Hence NSAIDs cause quite distinct and severe biochemical damage during drug absorption (uncoupling of mitochondrial oxidative phosphorylation proving to be most important) which results in increased intestinal permeability. All commonly used NSAIDs, apart from aspirin and nabumetone, are associated with increased intestinal permeability in man. Whilst reversible in the short term, it may take months to improve following prolonged NSAID use. Increased intestinal permeability appears to be the central mechanism of converting the biochemical damage to an inflammatory tissue reaction (NSAID enteropathy). The inflammatory enteropathy is not, however, unique to NSAIDs but similar changes are found with other permeability breakers. In intestinal infections and in diseases associated with reduced mucosal defence, suggesting that the small intestinal inflammation represents a common final pathway for a number of intestinal injuries. Spondylarthropathies are associated with a high prevalence of terminal ileitis, but as most patients have been receiving NSAIDs it has been difficult to dissociate the effects of NSAIDs on intestinal function from that of the ileitis itself. Nevertheless, two studies suggest that increased intestinal permeability in spondylarthropathies occur independently of NSAID ingestion. Whilst these findings may have implications for the development of arthritis, the permeability changes in spondylarthropathy do not differ quantitatively or qualitatively from that of NSAIDs or other permeability breakers. NSAID enteropathy can be differentiated from spondylarthropathic enteropathy by differences in location of disease and lack of predilection of certain HLA types. However, as the two may coexist both enteroscopy and ileocolonoscopy may be necessary for this distinction.