Rheumatology & Family Medicine & Internal Medicine
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Gout is the most common form of inflammatory arthritis in adults—it results from the deposition of monosodium urate (MSU) crystals in joints, bursae, and soft tissues, following chronic hyperuricemia (serum uric acid >360 µmol/L, or 6 mg/dL). Uric acid is the end product of purine catabolism in humans—an evolutionary peculiarity linked to the loss of uricase during hominid evolution (unlike most mammals, which break down uric acid into water-soluble allantoin). Gout affects approximately 4% of the adult population in Canada, with a clear male predominance (a male-to-female ratio of 4:1 before menopause—which decreases afterward due to the loss of estrogen’s uricosuric effect). Its incidence has been steadily increasing for 50 years, correlated with the epidemic of obesity, metabolic syndrome, and chronic kidney disease. Gout typically progresses through four stages: asymptomatic hyperuricemia → first gout attack → intercritical period → chronic tophaceous gout. Its treatment is both symptomatic (management of acute attacks) and maintenance (long-term uric acid-lowering therapy to dissolve urate deposits and prevent recurrences), with a target serum uric acid level of <360 µmol/L (and <300 µmol/L in tophaceous forms).
Pathophysiology, risk factors and clinical presentation
- Uric Acid Metabolism and Mechanisms of Hyperuricemia: uric acid: end product of purine catabolism (adenine + guanine) — pathway: dietary purines + endogenous nucleotides → hypoxanthine → xanthine → uric acid (xanthine oxidase — XO — the target enzyme of allopurinol and febuxostat) — in humans: plasma urate = ionized form of uric acid at pH 7.4 — plasma solubility: saturation limit ≈ 420 µmol/L (7 mg/dL) → above this threshold: risk of crystallization (especially in cooled peripheral tissues — big toe + ankle + knee); Uric acid elimination: 70% via the kidneys (glomerular filtration → predominantly tubular reabsorption via URAT1 + tubular secretion via ABCG2) + 30% via the digestive tract (broken down by intestinal bacteria) — uricosuric drugs (losartan + benzbromarone + probenecid) → inhibit URAT1 → increase renal excretion → lower serum uric acid levels; mechanisms of hyperuricemia: renal under-excretion (90% of hyperuricemia cases): chronic kidney disease + hypertension + thiazide diuretics + cyclosporine + low-dose aspirin (paradoxical — inhibits tubular secretion at low doses) + alcohol (competition with lactic acid for tubular excretion) + dehydration + hypothyroidism + hyperparathyroidism — overproduction (10% of cases): Lesch-Nyhan syndrome (HPRT deficiency — X-linked) + PRPP synthase deficiency + chronic hemolysis + tumor lysis syndrome + psoriasis + purine-rich diet (red meat + organ meats + seafood — beer ++) + genetics: SLC22A12 (URAT1) polymorphisms + ABCG2 + SLC2A9 (GLUT9) → common variants associated with hyperuricemia; inflammatory mechanism of gout attacks: UMS crystals phagocytosed by synovial macrophages → activation of the NLRP3 inflammasome → secretion of caspase-1 → maturation of IL-1β → inflammatory cascade (IL-6 + TNF-α + IL-8 → massive recruitment of PNN) → acute hyperalgesic synovitis — IL-1β is the key cytokine in a gout attack (therapeutic target of anakinra and canakinumab)
- Risk factors and systemic associations: Non-modifiable risk factors: age (incidence increases with age—rare before age 30 except in cases of secondary hyperuricemia) + male gender (testosterone → reduced renal excretion of urate) + genetic predisposition (ABCG2 and URAT1 polymorphisms — variants common in Polynesian and Māori populations → very high prevalence of gout); modifiable risk factors: obesity and metabolic syndrome (insulin resistance → reduced renal excretion of urate + overproduction) + urate-raising diet: red meat + organ meats (liver + kidney + brain) + seafood + beer (maltose + alcohol + guanosine — triple hyperuricemic effect) + alcohol in general (conversion of ethanol → acetaldehyde → acetate → increased AMP → purine catabolism + lactate-urate competition for tubular excretion) + fructose and sugary drinks (fructose → activation of AMP kinase → increased purine catabolism — robust data for HFCS-sweetened drinks) + hyperuricemic medications: thiazide diuretics (+++), loop diuretics + low-dose aspirin + cyclosporine + tacrolimus + pyrazinamide + ethambutol + levodopa; protective factors: coffee (40–50% risk reduction — mechanism: non-caffeine — likely non-purine xanthines that compete with XO) + low-fat dairy products (casein + lactalbumin → uricosuric + anti-inflammatory effect) + vitamin C (>500 mg/day → slight reduction in serum uric acid — modest effect) + folic acid → weight loss + moderate physical exercise (caution: intense exercise → lactic acid production → competition → may transiently raise serum uric acid levels); comorbidities associated with gout (often present and should be systematically screened for): hypertension (75% of gout patients) + chronic kidney disease (uric acid nephropathy — urate deposits in the renal interstitium) + metabolic syndrome (abdominal obesity + dyslipidemia + hyperglycemia) + type 2 diabetes + atherosclerotic cardiovascular disease (independent CV risk associated with gout — inflammatory mediators)
- Clinical presentation by stage of development: Asymptomatic hyperuricemia: serum uric acid >360 µmol/L without joint symptoms or tophi → no routine uric acid-lowering treatment recommended (except in cases of: Lesch-Nyhan syndrome + chemotherapy + very high serum uric acid >600 µmol/L) → screening and treatment of comorbidities (hypertension + metabolic syndrome) + dietary measures; acute gout attack: typically nocturnal onset (low joint temperature promotes crystallization + nocturnal cortisol fluctuations) → acute hyperalgesic monoarthritis (pain reaching maximum intensity within a few hours — often unbearable — interfering with sleep + inability to tolerate contact with sheets) → erythema + heat + swelling + total functional limitation → systemic signs sometimes present: mild fever (38–38.5 °C) + chills — location: metatarsophalangeal joint of the big toe (MTP1 — podagra — 60–70% of first attacks) → ankle + tarsus + knee + wrist + fingers + olecranon bursa + prepatellar bursa → spontaneous course: resolution within 7–14 days without treatment — triggering factors: overeating (heavy meals + alcohol) + dehydration + local trauma + surgery + infection + initiation of uric acid-lowering therapy (mobilization of deposits) + uric acid-raising medications; intercritical period: asymptomatic + invisible microtophi + persistent hyperuricemia → variable duration (months to years between attacks) → shortening of the intercritical period over time → increasingly frequent and multisystemic attacks; chronic tophaceous gout: tophi (macroscopic deposits of uric acid crystals surrounded by a granulomatous reaction): helix of the ear + olecranon bursa + Achilles tendons + MTH1 + fingers + elbows + feet → bone erosions (X-rays: «punch-out» erosions with a sclerotic rim + prominent margin — distinct from rheumatoid erosions + chronic polyarthritis + joint deformities
Diagnosis, crisis management, and maintenance treatment
| Clinical situation | Diagnosis and assessment | Treatment and follow-up |
|---|---|---|
| Gout diagnosis Crystals — Uremia — ACR/EULAR criteria |
A definitive diagnosis of gout is based on the detection of uric acid monosodium urate (UMS) crystals in synovial fluid or in a tophus; joint aspiration and synovial fluid analysis: indications: first episode of atypical acute monoarthritis + diagnostic uncertainty + to rule out septic arthritis (emergency) — technique: aspiration of synovial fluid (yellow-greenish purulent fluid in gout — may resemble septic arthritis) + analysis under compensated polarized light: needle-shaped UMS crystals with negative birefringence (yellow when parallel to the polarizer’s vibration axis) → pathognomonic of gout + calcium pyrophosphate dihydrate (CPDD — pseudogout) crystals: rhomboid shapes with positive birefringence (blue) — synovial fluid culture: essential to rule out septic arthritis (serious diagnostic error); serum uric acid measurement: note: serum uric acid may be normal or even low during an acute attack (mobilization of deposits + inflammatory response) → do not rule out gout based on normal serum uric acid during an attack → measure serum uric acid after the attack has subsided (3–4 weeks) → serum uric acid >360 µmol/L (6 mg/dL) = saturation threshold → >420 µmol/L = overt hyperuricemia; 2015 ACR/EULAR classification criteria (if no joint aspiration performed): weighted scoring system — clinical signs (MTH1 involvement + erythema + hyperalgesia + swelling) + serum uric acid + imaging + history — score ≥8 = gout with high diagnostic probability; imaging: standard X-rays: normal at onset → «punch-out» erosions with prominent rim + peripheral sclerosis in chronic forms → distinct from rheumatoid erosions + joint ultrasound: double-contour sign (urate deposit on the surface of the articular cartilage — pathognomonic of gout if present) + hyperechoic intra-articular tophi + snow in the synovial fluid (crystals) → sensitivity 77% + specificity 96% for the double-contour sign + DECT (dual-energy CT): detection of urate deposits appearing green (differentiation of UMS crystals vs. calcium) → highly sensitive and specific + non-invasive + useful for assessing total urate burden + MRI: useful for deep tophi (spine + sacroiliac joint — rare) | Routine additional testing upon diagnosis of gout: laboratory tests: serum uric acid (between attacks) + creatinine + eGFR + urinalysis (associated uric acid stones—15–20% of gout patients) + blood glucose + HbA1c + lipid panel (associated metabolic syndrome) + complete blood count + liver function tests (prior to allopurinol or febuxostat) + TSH (hypothyroidism as a cause of hyperuricemia) + 24-hour uric acid (if deciding on uric acid-lowering therapy — distinguishes overproducer vs. under-excretor → >700 mg/day = overproduction → xanthine oxidase ++ → allopurinol/febuxostat); screening for comorbidities: BP + waist circumference + ECG (CV risk) + fundus examination if history of hypertension + screening for renal complications (proteinuria + microalbuminuria); differential diagnosis of acute monoarthritis: septic arthritis (emergency — aspiration + culture + Gram stain mandatory if in doubt) + pseudogout (CPDD — positive birefringent rhomboid crystals — knee++ + wrist) + reactive arthritis + psoriatic arthritis (mono- or oligoarthritis + history of psoriasis) + septic bursitis (heat + fluctuation + skin entry site) + traumatic hemarthrosis + aseptic osteonecrosis |
| Management of acute gout flare Colchicine — NSAIDs — Corticosteroids — IL-1 |
Treatment for a gout attack aims to quickly resolve inflammation—it is most effective if started within the first few hours of the attack (ideally within 12–24 hours); assessment of attack severity: mild to moderate (1–2 small or medium joints — EVA pain score <7) → outpatient oral treatment; severe (polyarthritis + large joint — knee + ankle + EVA pain score ≥7 + bedridden patient) → more aggressive treatment + consider hospitalization if comorbidities are present; colchicine (Colcrys — first-line treatment if initiated within 12–36 hours): mechanism: inhibition of tubulin polymerization → blocking the mobility of neutrophils + inhibition of the NLRP3 inflammasome → reduction in IL-1β secretion — recommended Canadian dosage (2020 ACR guidelines + SRC): low dose: 1.2 mg PO immediately + 0.6 mg PO 1 hour later (total 1.8 mg on Day 1) → as effective as high doses with fewer gastrointestinal side effects (AGREE trial — Terkeltaub 2010) — then colchicine 0.6 mg × 1–2/day until complete resolution of the attack (5–10 days) — precautions: CRF (GFR <30 → dose reduction or contraindication) + significant drug interactions: P-gp and CYP3A4 inhibitors (clarithromycin + cyclosporine + verapamil + ketoconazole) → risk of severe toxicity (pancytopenia + neuropathy + myopathy) → reduce dose by 50% 1–3 times daily + statins (myopathy rare but possible); NSAIDs (first- or second-line — highly effective if started early): indomethacin 50 mg × 3/day × 5–7 days (historically the most commonly used) or naproxen 500 mg × 2/day × 5–7 days or ibuprofen 800 mg × 3/day — concomitant esomeprazole or pantoprazole (gastroprotection) — Contraindications: chronic renal failure (GFR <45 → avoid) + peptic ulcer + heart failure + anticoagulation — use at maximum doses from the start + taper after 48–72 hours if improvement; corticosteroids (2nd or 3rd line — or 1st line if contraindicated for colchicine AND NSAIDs): prednisone 30–50 mg/day PO × 3–5 days followed by rapid tapering over 5–10 days — methylprednisolone IV or IM if oral administration is impossible or in severe flare-ups — intra-articular corticosteroid injection (triamcinolone — Kenalog — 10–40 mg IA): effective and rapid option if 1–2 accessible joints → resolution within 24–48 hours — Contraindications: septic arthritis must be definitively ruled out before injection | Anti-IL-1 (reserved for refractory forms or CI to standard treatments): anakinra (Kineret - IL-1 receptor antagonist): 100 mg SC/day x 3-5 days → off-label but highly effective (resolution in 24-48h) → used in refractory flares + gouty polyarthritis ± intensive care patients + canakinumab (Ilaris - anti-IL-1β - mAb): 150 mg SC x 1 injection → approved by EMA for refractory gout — not approved by Health Canada for this indication + very expensive → exceptional use; complementary measures during the flare: rest of the affected joint + local ice (reduction of heat and pain - 20 min x 3-4/day) + limb elevation + adequate hydration + avoid alcohol and purine-rich foods during the flare + DO NOT initiate or modify hypouricemic treatment during the acute flare (risk of prolonging or worsening the flare by mobilizing deposits) — if already on hypouricemic treatment: do not stop it either (risk of rebound); reassessment interval post-flare: consultation 2-4 weeks after complete resolution of the flare → uricemia measurement + decision to start long-term hypouricemic treatment + patient information on dietary measures and triggering factors |
| Long-term hypouricemic treatment Allopurinol — febuxostat — uricemia target |
Urate-lowering therapy (ULT) is the curative treatment for gout—it aims to dissolve urate deposits by maintaining serum uric acid levels below the solubility threshold for an extended period; indications for urate-lowering therapy: 2020 ACR + 2016 EULAR recommendations: any diagnosed gout with: ≥2 attacks per year + 1 attack + tophi OR 1 attack + stage ≥2 chronic kidney disease (CKD) OR 1 attack + uric acid stones OR 1 attack + serum uric acid >480 µmol/L (8 mg/dL) → treatment recommended after the first attack according to the new 2020 ACR guidelines (lowered threshold for indication) — no treatment recommended for asymptomatic hyperuricemia alone (except in cases of: serum uric acid >600 µmol/L + Lesch-Nyhan syndrome + chemotherapy); initiation of urate-lowering therapy: start after the acute attack has resolved (3–4 weeks after resolution) + simultaneously initiate attack prophylaxis (see below) → do not initiate during an active attack; allopurinol (Zyloprim — xanthine oxidase inhibitor — XOI): universal first-line treatment — mechanism: competitive inhibition of XO → reduction in uric acid production — initial dose: 100 mg/day PO → gradual increase in 100 mg increments every 2–4 weeks until target serum uric acid level is reached (maximum 900 mg/day — 300–600 mg/day is usually sufficient) — CAUTION: adjust the initial dose according to renal function: eGFR <60 → start at 50 mg/day + very gradual increase — febuxostat (Uloric — non-purine XO inhibitor): Second-line treatment if allergic or intolerant to allopurinol + often more effective than allopurinol in lowering serum uric acid levels (80 mg/day or 120 mg/day) → CONFIRMS trial (2010): febuxostat 80 mg superior to allopurinol 300 mg for achieving the serum uric acid target — CARDIOVASCULAR WARNING: CARES study (2018): febuxostat associated with a slightly higher risk of cardiovascular mortality than allopurinol → use with caution in patients at high CV risk + FAST study (2020 — Lancet): no significant difference in overall mortality — unresolved debate | Goals of uric acid-lowering treatment and follow-up: target serum uric acid level: <360 µmol/L (6 mg/dL) for all gout patients (UMS solubility threshold) + <300 µmol/L (5 mg/dL) for tophaceous gout or recurrent polyarthritis (faster dissolution of tophi) + monitoring of serum uric acid levels: 1 month after initiation + with each dose change + every 6 months once the target is reached → dose adjustment if necessary + duration of treatment: Lifelong for patients with tophi or recurrent polyarticular gout + possible discontinuation of treatment if: single attack + absence of tophi + normalized serum uric acid levels over several years + correction of triggering factors (weight loss + discontinuation of diuretics ++) → individualized decision + recommended minimum duration: 5 years; uricosuric agents (2nd-line — increase renal urate excretion): probenecid (not commonly available in Canada) + benzbromarone (not available in Canada — available in Europe) + losartan (ARB with modest uricosuric properties — 15–20% reduction in serum uric acid — useful in hypertensive gout patients requiring an ARA2) + practical tips: drink ≥2 L of water/day + alkalinize urine (sodium bicarbonate or Vichy water) if a uricosuric agent is used (reduces the risk of uric acid stones); rasburicase (Fasturtec — recombinant uricase): treatment of severe hyperuricemia in tumor lysis syndrome (hematology-oncology) → not used in chronic gout (neutralizing antibodies) + pegloticase (Krystexxa — pegylated uricase): not available in Canada — FDA-approved for severe refractory tophaceous gout (rapid reduction of tophi) → frequent infusion reactions + very high cost |
| Prophylaxis of attacks during the initiation of hypouricemic treatment Colchicine — NSAID — duration 3–6 months |
Starting urate-lowering therapy mobilizes urate deposits and can trigger paradoxical attacks within the first few weeks to months—this phenomenon is common (30–60% of patients within the first 6 months) and is the main reason patients discontinue urate-lowering therapy; Mechanism of paradoxical attacks: the gradual dissolution of UMS microcrystals releases small crystals into the joint → phagocytosis by macrophages → activation of the NLRP3 inflammasome → inflammatory attack—this phenomenon is evidence that the treatment is working and that the deposits are dissolving → essential information to convey to the patient to prevent premature discontinuation of treatment; Recommended prophylaxis (ACR 2020 + EULAR 2016): low-dose colchicine: 0.5–0.6 mg/day PO (first-line — best tolerated) → duration: 3–6 months after initiation of urate-lowering therapy (or until serum uric acid normalizes + absence of tophi + absence of attacks for ≥3 months) — if contraindicated or intolerant to colchicine: Low-dose NSAIDs (naproxen 250 mg × 2/day — ibuprofen 200–400 mg × 2/day) × 3–6 months + low-dose prednisone (5–10 mg/day) if contraindicated for both — interactions with prophylactic colchicine: same precautions as for treatment but at lower doses → reduced risk of interaction but requires monitoring (statins + CYP3A4/P-gp); laboratory monitoring during urate-lowering therapy: CBC + creatinine + transaminases (liver function tests): before initiation → at 1 month → every 6–12 months → allopurinol: rare risk of hepatic toxicity + DRESS syndrome (Drug Reaction with Eosinophilia and Systemic Symptoms): rare (1/1,000) but serious — risk factor: HLA-B*58:01 (high prevalence in Southeast Asian populations—Thailand, Korea, and China → genetic screening recommended before allopurinol in these populations—CPIC guidelines) + renal insufficiency (accumulation of oxypurinol) → initiation at 50–100 mg + slow titration | Patient education and information — key elements: explaining the chronic nature of the illness: gout is a curable disease if uricemia is maintained below the target level → hypouricemic treatment is not a treatment for crises but lifelong (or very long-term) foundational treatment → dissolution of deposits takes 1–2 years → crises can paradoxically increase in the first few months of treatment + explaining the target uricemia level: monitor uricemia every 3–6 months → target <360 µmol/L (<300 if tophi) → adjust dose until target is reached + dietary measures (modest but complementary effects): reduce red meat + offal + seafood (purines) + drastically reduce alcohol (especially beer) + reduce sugary drinks + fructose + increase low-fat dairy products + coffee + water (≥2 L/day) + gradual weight loss (rapid loss can trigger crises) + never stop hypouricemic treatment during a crisis (frequent mistake) + report any skin symptoms after starting allopurinol (DRESS) → urgent consultation if rash + fever occurs within the first 8 weeks; the role of the family doctor in gout: the vast majority of gout cases are managed by the family doctor → indications for rheumatology referral: severe tophaceous gout + treatment resistance + diagnostic difficulty (septic arthritis to rule out) + severe polyarticular forms + gout associated with complex systemic disease |
| Chronic tophaceous gout and special situations Tophus — IRC — transplantation — pregnancy |
Tophaceous gout: tophi = macroscopic deposits of uric acid monosodium salt (UMS) surrounded by a foreign-body granulomatous reaction — common sites: auricular helix + olecranon bursa + extensor tendons of the fingers + inner edge of the big toe + Achilles tendon + knees + bones (erosions) + spine (rare — may mimic spondylodiscitis) — complications of tophi: skin ulceration with discharge of chalky white material (MSU — macroscopically visible crystals) + local superinfection + nerve compression (carpal tunnel syndrome due to tophi) + extensive bone erosions → deformities + joint destruction; assessment of urate burden: DECT (dual-energy CT): non-invasive quantification of total urate burden → useful for monitoring response to treatment (reduction in urate burden under urate-lowering therapy) + ultrasound (intra-articular tophi + double contour); Therapeutic goal in tophaceous gout: target serum uric acid level <300 µmol/L (5 mg/dL) → faster dissolution of tophi (resorption within 1–3 years depending on size) + surgical treatment of tophi: exceptional — reserved for ulcerated + infected + compressive tophi (carpal tunnel syndrome) + functionally bothersome tophi + medical treatment alone allows for resolution in the vast majority of cases; Gout and chronic kidney disease (CKD): complex interactions — hyperuricemia worsens CKD (interstitial urate deposits + vasoconstriction + inflammation) + CKD increases serum uric acid levels (reduced excretion) → vicious cycle — treatment adjustments: colchicine: contraindicated if eGFR <15 + dose reduction if eGFR 15–59 (maximum 0.3 mg/day) + NSAIDs: avoid if eGFR <30 (risk of acute kidney injury + worsening of CKD) + allopurinol: start at 50 mg/day + very slow titration (50 mg every 4–8 weeks) — same serum uric acid target but more difficult to achieve + febuxostat: may be used at 40–80 mg/day even in moderate CKD (no renal accumulation of oxypurinol) — pharmacokinetic advantage over allopurinol in CKD + corticosteroids: often the only available option for acute attacks in severe CKD | Gout and solid organ transplantation: cyclosporine and tacrolimus (calcineurin inhibitors) → reduced renal urate excretion + post-transplant chronic kidney disease (CKD) → frequent severe hyperuricemia (40–80% of kidney transplant recipients) + accelerated tophaceous forms — critical drug interactions in transplant recipients: colchicine + cyclosporine/tacrolimus → P-gp inhibition → severe colchicine toxicity (myopathy + pancytopenia — reported deaths) → use with extreme caution at reduced doses (maximum 0.3 mg/day) or avoid + allopurinol + azathioprine (common immunosuppressant) → XO inhibition → accumulation of 6-mercaptopurine → severe hematologic toxicity (leukopenia) → absolute CONTRAINDICATION — if allopurinol is essential: switch to mycophenolate mofetil (MMF) + febuxostat: preferred over allopurinol in transplant recipients on azathioprine (no interaction) — possible interaction with tacrolimus (monitor levels); Gout and pregnancy: physiological hyperuricemia during pregnancy (increased GFR → increased filtration + urate excretion) → gout attacks during pregnancy are rare — treatment of an attack during pregnancy: corticosteroids (prednisone 20–40 mg/day × 5–7 days): safest option (avoid in the 1st trimester if possible) + acetaminophen + NSAIDs: avoid in the 3rd trimester (premature closure of the ductus arteriosus) + colchicine: contraindicated during pregnancy (experimental teratogen — insufficient human data — avoid) + urate-lowering therapy: allopurinol and febuxostat are CONTRAINDICATED during pregnancy → discontinue before conception if possible; gout and uric acid-modifying drugs — monitor and optimize: replace thiazide diuretics with alternatives if possible (amlodipine + ACEI/ARB — losartan has a modest uricosuric effect — useful in hypertensive gout) + replace low-dose aspirin with clopidogrel if possible in patients with coronary artery disease and gout (controversial — CV risk vs. uric acid-lowering benefit) — cyclosporine: switch to tacrolimus or MMF if possible (rheumatology and transplant teams in consultation) |
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Never stop allopurinol during a gout flare: One of the most frequent errors in gout management is stopping urate-lowering therapy during an acute flare. This practice is counterproductive: variations in uricemia resulting from stopping and restarting treatment can prolong and worsen the flare. The rule is to maintain the urate-lowering therapy unchanged and add anti-inflammatory treatment (colchicine + NSAIDs + corticosteroids) to control the flare. Systematically inform the patient of this principle at each consultation.
Situations requiring urgent medical assessment
Feverish, hyperalgesic acute monoarthritis (Temp > 101.3°F) + chills + general malaise → rule out septic arthritis urgently → arthrocentesis + Gram stain + culture + polarized light analysis → do not inject intra-articular corticosteroids before ruling out infection.
Ulcerated tophus + fever + peripheral cellulitis + signs of sepsis → superimposed tophaceous infection → hospitalization + IV antibiotic therapy (staphylococcus coverage: IV cefazolin or IV cloxacillin) + drainage if fluctuant abscess.
Gout + allopurinol initiation + generalized rash + fever + eosinophilia within 8 weeks of initiation → DRESS syndrome → immediate discontinuation of allopurinol + hospitalization + dermatology consultation + IV corticosteroids depending on severity.
Transplanted patient + gout attack + cyclosporine treatment + colchicine prescribed → Risk of severe colchicine toxicity (P-gp + CYP3A4 interaction) → drastic dose reduction + hematological monitoring + favor inhaled or oral corticosteroids as an alternative.
Consult at Clinique Omicron
Clinique Omicron physicians manage gout at all its stages—treatment of acute attacks, initiation and monitoring of hypouricemic treatment, dose adjustments according to target uricemia, and screening for associated comorbidities (hypertension, metabolic syndrome, kidney failure). Referral to rheumatology is organized for severe or treatment-resistant tophaceous forms. These services are available at several service points in Quebec as well as through telemedicine. To make an appointment, visit cliniqueomicron.ca.
The content of this page is for informational purposes only and does not replace the advice of a physician or rheumatologist. Any febrile monoarthritis should be rapidly evaluated to rule out septic arthritis, which is a medical emergency.
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