The Most Effective Preventative Medicine For Gout

To prevent gout, it is necessary to reduce uric acid, because elevated uric acid levels are the most fundamental factor in gout attacks. Patients can try to reduce uric acid through diet control, increased exercise, and weight loss. If the effect is not good, oral uric acid-lowering drugs can be used to reduce uric acid levels. If the patient has high uric acid, it is necessary to avoid excessive exercise and cold, because these factors may be the factors that induce gout on the basis of high uric acid level. Non-steroidal anti-inflammatory drugs (NSAIDs) are used to treat acute gout attacks and are the first choice of preventative medicine for gout. NSAIDs are a class does not contain the structure of the steroidal anti-inflammatory drugs, and this preventative medicine for gout, including aspirin, acetaminophen, indomethacin, naproxen, naphthalene, ketone, diclofenac, ibuprofen, beauty nimesulide, ever had cloth, celecoxib, etc., These drugs have anti-inflammatory, anti-rheumatism, analgesic, antipyretic and anticoagulant effects, and are widely used in clinical osteoarthritis, rheumatoid arthritis, a variety of fever and pain symptoms relief, quick effect, good effect.

Pharmacological action

NSAIDs have different chemical structures, but all exert their antipyretic, analgesic and anti-inflammatory effects by inhibiting the synthesis of prostaglandins.

Antipyretic effect

NSAIDs play an antipyretic effect by inhibiting the synthesis of central prostaglandins. These drugs can only reduce the body temperature of those with fever, but have no effect on normal body temperature. Antipyretic drugs are only symptomatic treatment, and the body temperature will rise again after the elimination of drugs in the body. Therefore, patients with fever should focus on the etiological treatment and only be used when the fever is high.

Analgesic effect

NSAIDs produce moderate analgesic effects, mainly in the periphery. Ineffective for severe pain and visceral smooth muscle colic caused by various traumas. It is effective for chronic pain such as headache, joint muscle pain, toothache, etc. During tissue damage or inflammation, pain-causing substances are locally produced and released, while the synthesis of prostaglandins is increased. Prostaglandins increase the sensitivity of pain receptors to pain-causing substances and amplify inflammatory pain. The analgesic mechanisms of NSAIDs are: ① Inhibit prostaglandin synthesis; ② Inhibit lymphocyte activity and activation of T lymphocyte differentiation, reduce the stimulation of afferent nerve endings; ③ It directly acts on nociceptive receptors and prevents the formation and release of pain-causing substances.

Anti-inflammatory effect

Most NSAIDs have anti-inflammatory properties. NSAIDs exert anti-inflammatory effects by inhibiting the synthesis of prostaglandins, inhibiting the aggregation of leukocytes, reducing the formation of bradykinin, and inhibiting platelet aggregation. It is effective in controlling the symptoms of rheumatoid and rheumatoid arthritis.

Preventive effect on tumor

NSAIDs have inhibitory effects on the occurrence, development and metastasis of tumors, and have synergistic effects with other anti-tumor drugs. Its mechanism of action is to inhibit the production of PGS and induce apoptosis of tumor cells. The COX-1RNA in the colon tumor tissue induced by oxyazomethane in rats was equivalent in intensity between the tumor and the normal tissue, and the COX-2RNA in the early tumor was significantly higher than that in the normal mucosa. In ulcerative colitis with early stage tumors, increased COX-2 expression was detected at the tumor site by in situ hybridization and immunohistochemistry. These studies suggest that COX-2 may be a target for early diagnosis and prevention of colorectal cancer. COX inhibitors and selective COX-2 inhibitors with low response in digestive system are valuable for the prevention of at least one type of colon tumor and rectal cancer.

Adverse reactions

Gastrointestinal tract: abdominal discomfort, dull pain, nausea, vomiting, fullness, belching, loss of appetite and other indigestion symptoms may occur. About 10% to 25% of patients taking long-term oral NSAIDs develop peptic ulcers, and less than 1% of them develop serious complications such as bleeding or perforation.

Liver: at therapeutic doses, biochemical abnormalities with mild liver damage occurred in 10% of patients, but marked elevations in alanine aminotransferase occurred in less than 2%.

Nervous system: headache, dizziness, tinnitus, deafness, amblyopia, drowsiness, insomnia, paresthesia, numbness, etc. may occur. Some symptoms are uncommon, such as hyperactivity, excitement, hallucinations, tremors, etc., and the incidence is generally less than 5%.

Urinary system: it can cause proteinuria, casts, red and white blood cells in the urine, and severe cases can cause interstitial nephritis. In a multicenter clinical study, long-term oral NSAIDs patients had a 2.1-fold higher risk of developing kidney disease than the general population.

Blood system: some NSAIDs can cause neutropenia, aplastic anemia, and coagulation disorders.

Allergy: idiopathic people may have allergic reactions such as rash, angioedema, and asthma.

Conclusion

In short, only when doctors, pharmacists, patients and the society pay attention to the issue of safe preventative medicine for gout use, adhere to rational drug use, and try to avoid and reduce the harm of adverse preventative medicine for gout reactions, can a barrier to safe preventative medicine for gout use be truly built.