Plé:Diclofenac

Ón Vicipéid, an chiclipéid shaor.
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In the United Kingdom, India, Brazil and the United States, it may be supplied as either the sodium or potassium salt, in China most often as the sodium salt, while in some other countries only as the potassium salt. Diclofenac is available as a generic drug in a number of formulations. Over-the-counter (OTC) use is approved in some countries for minor aches and pains and fever associated with common infections.


Diclofenac is used to treat pain, inflammatory disorders, and dysmenorrhea.[1]


Voltaren (diclofenac) 50 mg enteric coated tablets Inflammatory disorder may include musculoskeletal complaints, especially arthritis, rheumatoid arthritis, polymyositis, dermatomyositis, osteoarthritis, dental pain, TMJ, spondylarthritis, ankylosing spondylitis, gout attacks,[2] and pain management in cases of kidney stones and gallstones.

As long-term use of diclofenac and similar NSAIDs predisposes for peptic ulcer, many patients at risk for this complication are prescribed a combination (Arthrotec) of diclofenac and misoprostol, a synthetic prostaglandin (PGE1) analogue, to protect the gastric mucosa.[citation needed]


Diclofenac is often used to treat chronic pain associated with cancer, in particular if inflammation is also present (Step I of the World Health Organization (WHO) Scheme for treatment of chronic pain). Good results (sometimes better than those with opioids) have been seen in female breast cancer and in the pain associated with bony metastases.[citation needed]

[edit]Contraindications

Hypersensitivity against diclofenac History of allergic reactions (bronchospasm, shock, rhinitis, urticaria) following the use of aspirin or another NSAID Third-trimester pregnancy Active stomach and/or duodenal ulceration or gastrointestinal bleeding Inflammatory intestinal disorders such as Crohn's disease or ulcerative colitis Severe insufficiency of the heart (NYHA III/IV) Recently,[when?] a warning has been issued by the FDA not to use for the treatment of patients recovering from heart surgery Severe liver insufficiency (Child-Pugh Class C) Severe renal insufficiency (creatinine clearance <30 ml/min) Caution in patients with preexisting hepatic porphyria, as diclofenac may trigger attacks Caution in patients with severe, active bleeding such as cerebral hemorrhage NSAIDs in general should be avoided during dengue fever, as it induces (often severe) capillary leakage and subsequent heart failure. In animals which when dead may be scavenged by vultures [edit]Side-effects

Diclofenac is among the better tolerated NSAIDs. Though 20% of patients on long-term treatment experience side-effects, only 2% have to discontinue the drug, mostly due to gastrointestinal complaints. And see #Ecological effects below.

[edit]Cardiac Following the identification of increased risks of heart attacks with the selective COX-2 inhibitor rofecoxib in 2004, attention has focused on all the other members of the NSAIDs group, including diclofenac. Research results are mixed with a meta-analysis of papers and reports up to April 2006 suggesting a relative increased rate of heart disease of 1.63 compared to non-users.[8] Professor Peter Weissberg, Medical Director of the British Heart Foundation said, "However, the increased risk is small, and many patients with chronic debilitating pain may well feel that this small risk is worth taking to relieve their symptoms". Only aspirin was found not to increase the risk of heart disease; however, this is known to have a higher rate of gastric ulceration than diclofenac. A subsequent large study of 74,838 users of NSAIDs or coxibs, published in May 2006, found no additional cardiovascular risk from diclofenac use.[9] A very large study of 1,028,437 Danish users of various NSAIDs or coxibs, published online on June 8, 2010, found that "Use of the nonselective NSAID diclofenac and the selective cyclooxygenase-2 inhibitor rofecoxib was associated with an increased risk of cardiovascular death (odds ratio, 1.91; 95% confidence interval, 1.62 to 2.42; and odds ratio, 1.66; 95% confidence interval, 1.06 to 2.59, respectively), with a dose-dependent increase in risk." .[10] Diclofenac has similar COX-2 selectivity to celecoxib.[11] A review by FDA Medical Officer David Graham concluded in September, 2006 that diclofenac does increase the risk of myocardial infarction.[12] [edit]Gastrointestinal Gastrointestinal complaints are most often noted (see above). The development of ulceration and/or bleeding requires immediate termination of treatment with diclofenac. Most patients receive an ulcer-protective drug as prophylaxis during long-term treatment (misoprostol, ranitidine 150 mg at bedtime or omeprazole 20 mg at bedtime). [edit]Hepatic Liver damage occurs infrequently, and is usually reversible. Hepatitis may occur rarely without any warning symptoms and may be fatal. Patients with osteoarthritis more often develop symptomatic liver disease than patients with rheumatoid arthritis. Liver function should be monitored regularly during long-term treatment. If used for the short-term treatment of pain or fever, diclofenac has not been found to be more hepatotoxic than other NSAIDs. As of 12/2009 Endo, Novartis and FDA notified healthcare professionals to add new warnings and precautions about the potential for elevation in liver function tests during treatment with all products containing diclofenac sodium.[13] Cases of drug-induced hepatotoxicity have been reported in the first month, but can occur at any time during treatment with diclofenac. Postmarketing surveillance has reported cases of severe hepatic reactions, including liver necrosis, jaundice, fulminant hepatitis with and without jaundice, and liver failure. Some of these reported cases resulted in fatalities or liver transplantation. Physicians should measure transaminases periodically in patients receiving long-term therapy with diclofenac. Based on clinical trial data and postmarketing experiences, transaminases should be monitored within 4 to 8 weeks after initiating treatment with diclofenac. [edit]Renal Studies in Pakistan showed that diclofenac caused acute kidney failure in vultures when they ate the carcasses of animals that had recently been treated with it (see below at ecological problems). Species and individual humans that are drug sensitive are initially assumed to lack genes expressing specific drug detoxification enzymes. NSAIDs "are associated with adverse renal [kidney] effects caused by the reduction in synthesis of renal prostaglandins"[14] in sensitive persons or animal species, and potentially during long-term use in non-sensitive persons if resistance to side-effects decreases with age. However, this side-effect cannot be avoided merely by using a COX-2 selective inhibitor because, "Both isoforms of COX, COX-1 and COX-2, are expressed in the kidney... Consequently, the same precautions regarding renal risk that are followed for nonselective NSAIDs should be used when selective COX-2 inhibitors are administered."[14] However, diclofenac appears to have a different mechanism of renal toxicity.[7] [edit]Mental health Mental health side effects have been reported; these symptoms are rare but exist in significant enough numbers to be included as potential side effects. These effects include: depression, anxiety, irritability, nightmares, and psychotic reactions.[15] [edit]Other Bone marrow depression is noted infrequently (leukopenia, agranulocytosis, thrombopenia with/without purpura, aplastic anemia). These conditions may be life-threatening and/or irreversible, if detected too late. All patients should be monitored closely. Diclofenac is a weak and reversible inhibitor of thrombocytic aggregation needed for normal coagulation. Induces warm antibody hemolytic anemia by inducing antibodies to Rh antigens, ibuprofen also does this.[16] Diclofenac may disrupt the normal menstrual cycle. [edit]Mechanism of action

The exact mechanism of action is not entirely known, but it is thought that the primary mechanism responsible for its anti-inflammatory, antipyretic, and analgesic action is inhibition of prostaglandin synthesis by inhibition of cyclooxygenase (COX). It also appears to exhibit bacteriostatic activity by inhibiting bacterial DNA synthesis.[17]


The action of one single dose is much longer (6 to 8 hours) than the very short half-life that the drug indicates.[citation needed] This could be partly because it persists for over 11 hours in synovial fluids.[18]