Gout medical therapy: Difference between revisions
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Another possibility is use of [[acetazolamide]], one of the first diuretics discovered. This drug inhibits the action of carbonic anhydrase on the proximal convoluted tubules within the kidneys, which effectively inhibits reabsorption of [[bicarbonate]], thus alkalinizing the urine. After two to three days of usage, the diuretic effects of this drug decline because of increased downstream reabsorption of ions and water by the renal tubules; however, the alkalinization of urine persists, and this basic urine attracts weak acids such as '''uric acid''' and cystine into the urine, thus increasing their urinary excretion.<sup>35</sup> | Another possibility is use of [[acetazolamide]], one of the first diuretics discovered. This drug inhibits the action of carbonic anhydrase on the proximal convoluted tubules within the kidneys, which effectively inhibits reabsorption of [[bicarbonate]], thus alkalinizing the urine. After two to three days of usage, the diuretic effects of this drug decline because of increased downstream reabsorption of ions and water by the renal tubules; however, the alkalinization of urine persists, and this basic urine attracts weak acids such as '''uric acid''' and cystine into the urine, thus increasing their urinary excretion.<sup>35</sup> | ||
===Prevention=== | |||
[[Allopurinol]] can reduce frequency of attacks.: | |||
* According to a small [[randomized controlled trial]], allopurinol can be initiated at the time acute therapy is initiated for a flare without increasing complications among patients also started on indomethacin 50 mg 3 times per day for 10 days and colchicine 0.6 mg twice per day.<ref name="pmid23098865">{{cite journal| author=Taylor TH, Mecchella JN, Larson RJ, Kerin KD, Mackenzie TA| title=Initiation of allopurinol at first medical contact for acute attacks of gout: a randomized clinical trial. | journal=Am J Med | year= 2012 | volume= 125 | issue= 11 | pages= 1126-1134.e7 | pmid=23098865 | doi=10.1016/j.amjmed.2012.05.025 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23098865 }} </ref> Previously, allopurinol was delayed till resolution of the acute attack. | |||
* [[Colchicine]] 0.6 mg twice daily should also be used to prevent a flare. In a [[randomized controlled trial]], co-treatment with colchicine 0.6 mg twice daily while allopurinol was tapered up from 100 mg/day until 3 months after the serum urate concentration < 6.5 mg/dl, reduced flares of gout from 77% in the placebo broup to 33% with colchicine prophylaxis. Most of these patients had tophi.<ref name="pmid15570646">{{cite journal |author=Borstad GC, Bryant LR, Abel MP, Scroggie DA, Harris MD, Alloway JA |title=Colchicine for prophylaxis of acute flares when initiating allopurinol for chronic gouty arthritis |journal=J. Rheumatol. |volume=31 |issue=12 |pages=2429–32 |year=2004 |pmid=15570646 |doi=}}</ref> One third of the patients had diarrhea and many reduced the medication to once per day. | |||
[[Allopurinol]] should be increased as possible to achieve a goal serum urate of <u><</u>6 mg/dl (360 micromoles/liter).<ref name="pmid17907217">{{cite journal |author=Perez-Ruiz F, Lioté F |title=Lowering serum uric acid levels: What is the optimal target for improving clinical outcomes in gout? |journal=Arthritis Rheum. |volume=57 |issue=7 |pages=1324–8 |year=2007 |pmid=17907217 |doi=10.1002/art.23007}}</ref> | |||
[[Febuxostat]], a non-purine inhibitor, is equally effective as allopurinol when compared in a [[randomized controlled trial]].<ref name="pmid16339094">{{cite journal| author=Becker MA, Schumacher HR, Wortmann RL, MacDonald PA, Eustace D, Palo WA et al.| title=Febuxostat compared with allopurinol in patients with hyperuricemia and gout. | journal=N Engl J Med | year= 2005 | volume= 353 | issue= 23 | pages= 2450-61 | pmid=16339094 | doi=10.1056/NEJMoa050373 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16339094 }} </ref><ref name="pmid20370912">{{cite journal| author=Becker MA, Schumacher HR, Espinoza LR, Wells AF, MacDonald P, Lloyd E et al.| title=The urate-lowering efficacy and safety of febuxostat in the treatment of the hyperuricemia of gout: the CONFIRMS trial. | journal=Arthritis Res Ther | year= 2010 | volume= 12 | issue= 2 | pages= R63 | pmid=20370912 | doi=10.1186/ar2978 | pmc=PMC2888216 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20370912 }} </ref> | |||
== References == | == References == | ||
Revision as of 14:00, 6 December 2012
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Overview
The first goal of therapy when treating gout, is pain relief. This can be acheived with NSAIDs, and oral or intra-articular glucocorticoids. If colchicine is given, it should be taken within the first 12 hours of the attack. Other, less standard methods of treatment include the use of hemorrhoidal ointment, ice, increasing mobility, and acetazolamide.
Medical Therapy
Acute Attacks
The first line of treatment should be pain relief. Once the diagnosis has been confirmed, the drugs of choice are indomethacin, other nonsteroidal anti-inflammatory drugs (NSAIDs), oral glucocorticoids, or intra-articular glucocorticoids administered via a joint injection.
Colchicine was previously the drug of choice in acute attacks of gout, as it impairs the motility of granulocytes and can prevent the inflammatory phenomena that initiate an attack. Colchicine should be taken within the first 12 hours of the attack and usually relieves the pain within 48 hours, although side effects (gastrointestinal upset such as diarrhea and nausea) can complicate its use. NSAIDs are the preferred form of analgesia for patients with gout.
A randomized controlled trial found similar benefit from nonsteroidal anti-inflammatory drugs and oral glucocorticoids; however, less adverse drug reactions occurred in the glucocorticoids group.[1] In the nonsteroidal anti inflammatory drugs group, each patient initially received diclofenac (75 mg) intramuscularly, indomethacin 50 mg orally, and acetaminophen 1 g orally. The patient was received a 5-days of indomethacin (50 mg orally every 8 hours for 2 days, followed by indomethacin 25 mg every 8 hours for 3 days), and acetaminophen 1 g every 6 hours as needed. The glucocorticoids patients received prednisolone 30 mg orally, and acetaminophen 1 g orally. The patient was then given prednisolone 30 mg orally once per day for five days.
Before medical help is available, some over-the-counter medications can provide temporary relief from pain and swelling. NSAIDs such as ibuprofen can reduce the pain and inflammation slightly, although aspirin should not be used as it can worsen the condition. Preparation H hemorrhoidal ointment can be applied to the swollen skin to reduce the swelling temporarily. Professional medical care is needed for long-term management of gout.
Ice may be applied for 20–30 minutes several times a day, and a randomized controlled trial found that patients who used ice packs had better relief of pain without side effects.[2] Keeping the affected area elevated above the level of the heart also may help.
Due to swelling around affected joints for prolonged periods, shedding of skin may occur. This is particularly evident when small toes are affected and may promote fungal infection in the web region if dampness occurs, and treatment is similar to that for common athlete's foot.
Some sufferers of Gout report an aggravation of the condition in the knees and toes associated with long periods of immobility, such as when sitting at a computer desk for long hours. This can be particularly unfortunate if the sufferer is searching for work as the aggravation can interefere with mobility. Sufferers who notice early swelling or early pain may appear to be able to arrest the aggravation when medical treatment is applied before the condition gets worse. Where this is the case, a medically prescribed anti-inflammatory oral treatment taken with food and bed rest may provide relief within 6-8 hours.
Another possibility is use of acetazolamide, one of the first diuretics discovered. This drug inhibits the action of carbonic anhydrase on the proximal convoluted tubules within the kidneys, which effectively inhibits reabsorption of bicarbonate, thus alkalinizing the urine. After two to three days of usage, the diuretic effects of this drug decline because of increased downstream reabsorption of ions and water by the renal tubules; however, the alkalinization of urine persists, and this basic urine attracts weak acids such as uric acid and cystine into the urine, thus increasing their urinary excretion.35
Prevention
Allopurinol can reduce frequency of attacks.:
- According to a small randomized controlled trial, allopurinol can be initiated at the time acute therapy is initiated for a flare without increasing complications among patients also started on indomethacin 50 mg 3 times per day for 10 days and colchicine 0.6 mg twice per day.[3] Previously, allopurinol was delayed till resolution of the acute attack.
- Colchicine 0.6 mg twice daily should also be used to prevent a flare. In a randomized controlled trial, co-treatment with colchicine 0.6 mg twice daily while allopurinol was tapered up from 100 mg/day until 3 months after the serum urate concentration < 6.5 mg/dl, reduced flares of gout from 77% in the placebo broup to 33% with colchicine prophylaxis. Most of these patients had tophi.[4] One third of the patients had diarrhea and many reduced the medication to once per day.
Allopurinol should be increased as possible to achieve a goal serum urate of <6 mg/dl (360 micromoles/liter).[5]
Febuxostat, a non-purine inhibitor, is equally effective as allopurinol when compared in a randomized controlled trial.[6][7]
References
- ↑ Man CY, Cheung IT, Cameron PA, Rainer TH (2007). "Comparison of oral prednisolone/paracetamol and oral indomethacin/paracetamol combination therapy in the treatment of acute goutlike arthritis: a double-blind, randomized, controlled trial". Annals of emergency medicine. 49 (5): 670–7. doi:10.1016/j.annemergmed.2006.11.014. PMID 17276548.
- ↑ Schlesinger N, Detry MA, Holland BK; et al. (2002). "Local ice therapy during bouts of acute gouty arthritis". J. Rheumatol. 29 (2): 331–4. PMID 11838852.
- ↑ Taylor TH, Mecchella JN, Larson RJ, Kerin KD, Mackenzie TA (2012). "Initiation of allopurinol at first medical contact for acute attacks of gout: a randomized clinical trial". Am J Med. 125 (11): 1126–1134.e7. doi:10.1016/j.amjmed.2012.05.025. PMID 23098865.
- ↑ Borstad GC, Bryant LR, Abel MP, Scroggie DA, Harris MD, Alloway JA (2004). "Colchicine for prophylaxis of acute flares when initiating allopurinol for chronic gouty arthritis". J. Rheumatol. 31 (12): 2429–32. PMID 15570646.
- ↑ Perez-Ruiz F, Lioté F (2007). "Lowering serum uric acid levels: What is the optimal target for improving clinical outcomes in gout?". Arthritis Rheum. 57 (7): 1324–8. doi:10.1002/art.23007. PMID 17907217.
- ↑ Becker MA, Schumacher HR, Wortmann RL, MacDonald PA, Eustace D, Palo WA; et al. (2005). "Febuxostat compared with allopurinol in patients with hyperuricemia and gout". N Engl J Med. 353 (23): 2450–61. doi:10.1056/NEJMoa050373. PMID 16339094.
- ↑ Becker MA, Schumacher HR, Espinoza LR, Wells AF, MacDonald P, Lloyd E; et al. (2010). "The urate-lowering efficacy and safety of febuxostat in the treatment of the hyperuricemia of gout: the CONFIRMS trial". Arthritis Res Ther. 12 (2): R63. doi:10.1186/ar2978. PMC 2888216. PMID 20370912.