Non-steroidal anti-inflammatory drugs – the potential risks and benefits for the gastrointestinal tract
Non-steroidal anti-inflammatory drugs (NSAIDs) are a group of compounds with analgesic, antipyretic and anti-inflammatory and, in most cases able to suppress platelet aggregation. Their main mechanism of action is inhibition of the activity of enzymes involved in the metabolism of arachidonic acid. In this paper also discusses the different mechanisms of action of NSAIDs. Presents the indications and contraindications for the use of this group of drugs. It also discusses the use of NSAIDs side effects resulting from their influence on the synthesis of prostaglandins.
Toxicity of non-steroidal anti-inflammatory drugs (NSAIDs) in relation to the upper gastrointestinal tract is well documented. However, they may also cause damage to the duodenum distal to the – in the small intestine and intestine, and / or other organs of the digestive system. Non-steroidal anti-inflammatory drugs cause perforations, ulcerations and narrowing of the small intestine, which require surgical treatment of inflammation and loss of blood and protein, called enteropathy. May reinforce the primary symptoms of bowel diseases (e.g. ulcerative colitis, diverticular disease), enhance secondary or inactive disease activity induce primary episode of inflammatory bowel diseases, with rapid disappearance of symptoms after discontinuation of the drug. This suggests their participation in the development of microscopic colitis. In clinical practice, the toxicity of the NSAID in the small and large intestines increasingly recognized due to the availability of increasingly common endoscopic procedures. Liver damage is a rare but potentially fatal complication. It could occur after using any NSAIDs, but the most common problem cause diclofenac, meloxicam and sulindac. Non-steroidal anti-inflammatory drugs may be involved in acute fatty liver in pregnant women. The hepatotoxicity may be a result of idiosyncratic response of the immune response or metabolic disorders. The most important benefits of NSAID therapy reports have shown a possible prophylaxis, delayed or regression of cancer in the colon, esophagus, stomach, and cancer of the breast, lung, prostate and skin. Despite these findings recommendations for the prevention and treatment of NSAID in the course of any of these cancers are not yet formulated. Risk-benefit resulting from such treatment must be assessed in studies in the respective groups.
Infection with Helicobacter pylori (Hp), as well as use of non-steroidal anti-inflammatory drugs (NSAIDs) is considered major next smoking, the factors leading to the development of gastritis and mucosal lesions and peptic ulcers. However, there is controversy whether the simultaneous operation of Hp and NSAIDs on the stomach resulting in an increased risk of ulcer development, and whether, therefore, should be the people infected with Hp and at the same time taking NSAIDs expose Hp eradication or vice versa – Hp infection is beneficial for NSAID-induced ulcers and eradication of Hp misses with the target.
Unlike Hp infection usually leads to the development of gastritis type B (B gastritis), the use of NSAIDs causes inflammation of the stomach chemical type (gastritis C), covering and the core, and antrum, often leading to bleeding, especially at the beginning of therapy with these drugs . Histologically, there is no clear distinction between the Hepatitis B, Hepatitis C, and biochemically, in the first case is the increased expression of cyclooxygenase-2 (COX-2) and an increased activity of this enzyme together with a protective release abundant mucosal cells operating on prostaglandins, especially type E (PGE). In the second case, although the increased expression of COX-2 is maintained, however, the enzyme activity is inhibited the production of PGE. There are two opposing gastrological schools in assessing the effects of simultaneous action of Hp and NSAID on the mucosa of the stomach and duodenum.