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Anti-infammatory treatment o acute gouty arthritis

Acute gouty arthritis is characterised by acute and severe episodes triggered by

the precipitation of monosodium urate (MSU) crystals in the synovium of usually

peripheral joints. The most common joint aected is the rst meta!tarsal

phalangeal joint. This deposition and precipitation event causes an acute

in"ammatory reaction involving chemo#ines and the recruitment of neutrophils

to the synovium ($hanna % &it'gerald *+). The treatment of acute gouty

arthritis typically involves ade,uate treatment of pain and anti!in"ammatory

therapy. The choice of anti!in"ammatory therapy -ill be discussed here.

 The follo-ing anti!in"ammatory treatments are available for the treatment of 

acute gout /SA01s2 corticosteroids and colchicine. The purpose of these

medications is to reduce the in"ammatory reaction that results in pain and joint

deformity. The recommendations of the American 3ollege of 4heumatology and

5ritish Society of 4heumatology both state that /SA01s2 corticosteroids and oral

colchicine are all similarly eective in the treatment of acute gout. 6o-ever2 The

7uropean 8eague against 4heumatism (7U8A4) recommends oral colchicine

and9or /SA01s as rst!line treatments for the treatment of acute attac#s over

oral corticosteroids ($hanna % &it'gerald *+). The results of a recent

systematic revie- concluded that there is e,uivalent e:cacy of /SA01s and

corticosteroids -ith no head!to!head study comparing these -ith colchicine

($hanna et. al. *;).

 The most commonly used /SA01 in the treatment of acute gout is indomethacinand dosing is usually +mg orally every < hours until pain scores fall to an

acceptable level. /SA01s are not advised for use in patients -ith previous history

of coronary artery disease2 cerebrovascular disease2 gastrointestinal bleeding2

and hepatic9renal impairment ($hanna et. al. *;).

3orticosteroids2 as previously mentioned2 have similar e:cacy to /SA01s and

oral colchicine ho-ever should only be administered if septic arthritis has been

e=cluded. 0t may be delivered orally2 intra!muscularly or intra!articularly in the

case of large joints. 3ommonly prescribed doses vary from !;mg oral daily ina tapered dosing pattern ($hanna et. al. *;).

0t is recommended to begin colchicine at the lo-est possible dose (*.mg

follo-ed by .>mg * hour later) and increasing until desired eect or restricted

by adverse eects (?0 disturbance2 thrombocytopaenia2 leu#opaenia2

granulocytopaenia etc.). A study comparing lo- dose colchicine -ith placebo

found no statistically signicant dierence in adverse eects and a signicantly

decreased adverse eects prole compared to high!dose colchicine -hilst

maintaining similar e:cacy (Ter#eltaub et. al. *). 3olchicine is not

recommended for patients -ith renal9hepatic impairment due to the ris# of acute

to=icity (Turner % 3ooper *+).

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0n the case of Mr 4?2 he -as given an /SA01 for his pain -ith prednisolone @mg

orally. This is appropriate in the conte=t of the available evidence. There is

currently no reliable trial data comparing the use of /SA01s9corticosteroids and

colchicine. 0n clinical practice it remains that there is relative freedom in thechoice of anti!in"ammatory medications for acute gout. ith similar e:cacy

bet-een the three choices it is usual practice to delay more to=ic medications

(colchicine) after others have proven inade,uate. 3are must also be ta#en in

considering the patientBs co!morbidities in choosing the most appropriate

therapy.

Reerences$hanna2 C % &it'?erald2 D *+2 E7volution of management of gout a comparisonof recent guidelinesB2 Current Opinion – Rheumatology 2 vol. ;2 no. 2 pg. *@F!*;>.

$hanna2 C2 ?ladue2 62 Singh2 M2 &it'?erald2 D2 5ae2 S2 Cra#ash2 S2 $aldas2 M2?ogia2 M2 5errocal2 G2 To-nsend2 2 Ter#eltaub2 4 % $hanna2 1 *;2 ETreatmentof acute gout a systematic revie-B2 Seminars in Arthritis and Rheumatism2 vol.;;2 no. *2 pg. @*!@