A lot of patients with a history of gout disease have a normal lab in acute attack . What should we do?
A normal uric acid level is frequently seen in acute flares of gouty arthritis. so if the clinical diagnosis is clear I would give the patients colchicin (0.5 TID) and either NSAIDs (if GFR is >45 ml/min) or steroids if impaired renal function is known. Xanthinoxidase Inhibitors should be halted and only started after a couple of weeks at a low dose or under prophylaxis with colchicin.
In acute podagra attack the medication of choice is colchicine independently from the level of uric acid. It works.
Dr. Omar, you are right. Allopurinol does not work adequately in acute gouty attack.
Regards
Dr Sunil Kumar- Middlemore Hospital New Zealand
In Acute gout it is not uncommon to see a normal serum uric acid level as the acute inflammatory process drives the uric acid into the joints and the seum levels are falsely low. Treatment can be provided with NSAIDS if no contrindications, or colchicine or corticosteroids. If patient is already on allopurinol then we suggest continuing on the same dose. If they are not, then check uric acid level in 2-4 weeks and commence allopurinol at a small dose and escalate treatment to achieve a target urate level of less than 0.36mmol/l. Patient should be on prophylactic treatment with colchicine during this period and until they are free of acute attacks for at least 3-6 months
Safety Profile of Anti-gout Agents: An Update
Lisa K. Stamp
The management of gout is two-fold: firstly, adequate treatment of acute gouty episodes and secondly sustained reduction of serum urate to below 0.36 mmol/l (6 mg/dl), or lower in some cases, to prevent recurrent attacks and promote resorption of tophi. Non-steroidal anti-inflammatory drugs, colchicine and corticosteroids, are all therapeutic options for acute gout.[1] The choice of agent is dictated by the patient's concomitant medications and comorbidities, particularly renal function, as well as previous response. Colchicine appropriate first-line treatment for acute gout unless there are contraindications.Colchicine has a narrow therapeutic index, and low doses are effective with less gastrointestinal toxicity. The Acute Gout Flare Receiving Colchicine Evaluation (AGREE) study demonstrated that low-dose colchicine (1.8 mg total) is as effective as high-dose colchicine (4.8 mg total), but has significantly fewer gastrointestinal adverse effects. Myotoxicity is a particular problem in both renal[6–8] and cardiac transplant recipients. Whereas NSAIDs and corticosteroids may contribute to cardiovascular risk, there is a suggestion from recent studies that colchicine may have a role in secondary prevention of cardiovascular disease. In a retrospective review of 1288 gout patients, use of colchicine was associated with a significantly lower prevalence of myocardial infarction.
This all was a citing from above. I prefer as follows: aspiration (dereases the pressure, can be used for diagnostic reasons), than inject using the same in place staying canule cortison/ LA (fastest recovery effect.) followed by dressing.
Determining uric acid level in acute gouty arthritis does not add any information about decision-making. Amdiminister the treatment according to your protocol.
Agree with all who say that the uric acid level may be normal in an acute attack of gout, so the acute attack should be treated as clinically warranted. I do not measure serum uric acid in an acute attack. Colchicine regularly is useful in an acute attack, as well as prophylactically during allopurinol therapy. Allopurinol is not indicated to be started at an acute attack, but it is important to note that if the patient is already on allopurinol, it should not be stopped when he/she has an acute attack.
Agree with above. Whether or not the patient will need a urate lowering agent later, especially if the patient suffered only one attack will depend on the level of hyperuricemia, measured a few weeks after the attack. The therapeutic target here is to achieve a serum uric acid of 6.0 mg/dl or less. For patients with mild hyperuricemia, say 7.2 mg/dl or less, normal renal function, and no co-morbidities, life-style modifications on occasions may suffice, i.e., no alcohol, less red meat and seafood, no soft drinks, etc. However, the most dietary modifications could achieve would be a reduction of 1-2 mg/dl of serum uric acid. If the baseline serum uric acid (not measured during an attack) is significant, e.g., 8.5 mg/dl, diet alone is unlikely to normalize it. The reason serum uric acid levels can be relatively normal during an acute attack has to do at least in part with the release of pro-inflammatory cytokines such as IL-1 and IL-6 that have uricosurc properties.
by diet the acchievable lowering of uric acid lies around 20%, by allopurinol around 30- 40%. But it all depends from the patient- heavy drinkers, heavy eaters, heavy smokers.... Just see what you got and whats is applicable.
A simple point is that the level at which urate ions can form monosodium urate crystals is actually within the 'normal range' - at about 0.4mmol/L. Whether crystals occur depends on a variety of local and general factors not fully understood. For some time I tried to persude our biochemistry lab to report results not as 'normal' i.e. 2 standard deviations from a mean or whatever, but as 'below crystallisation threshold' (or not). Of course they found this incomprehensible.
I am not sure it matters much whether there is an acute attack or not, in most men with gout the first attack occurs rather little above the crystallisation threshold and quite often in the 'normal range'. Most gout in women is diuretic induced and so is quite different with levels usually above 0.6mmol/L right from the start. As indicated above, I am not sure the level is that important in the average middle aged man with gout - it is the frequency of attacks. On the other hand high levels in, for instance, young women with one attack of gout may be an important danger signal for an atypical genetically based disorder of urate metabolism.