Acute monoarticular crystal arthritis from monosodium urate deposition; classically the first MTP joint.
Also known as: gout, podagra, urate arthropathy, hyperuricemia
Overview
Crystal-induced arthropathy caused by deposition of monosodium urate (MSU) crystals in joints, tendons, and soft tissues, triggered by sustained hyperuricemia. Manifests as recurrent acute monoarticular flares progressing in some patients to chronic tophaceous disease.
Epidemiology
Most common inflammatory arthritis in men. Prevalence ~4% of US adults; rises with age, obesity, metabolic syndrome, and CKD. Premenopausal women relatively protected (estrogen is uricosuric).
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Question 1MusculoskeletalMedium
A 65-year-old man with a 3-year history of gout has had three acute flares in the past 12 months despite dietary modification. He has stage 3 chronic kidney disease (eGFR 45 mL/min/1.73 m2). He is currently between flares with no active joint inflammation. Serum uric acid is 8.9 mg/dL. He takes no urate-lowering medication. Which of the following is the most appropriate initial urate-lowering therapy?
AAllopurinol 50 mg once daily
BPegloticase 8 mg every 2 weeks
CFebuxostat 80 mg once daily
DProbenecid 500 mg twice daily
Reveal answer & full explanation
Correct answer: A — Allopurinol 50 mg once daily
AAllopurinol 50 mg once daily✓
BPegloticase 8 mg every 2 weeks
CFebuxostat 80 mg once daily
DProbenecid 500 mg twice daily
Why Allopurinol 50 mg once daily is correct
Per current ACR gout guidance, urate-lowering therapy is indicated for two or more flares per year, tophi, radiographic joint damage, or gout with stage 3 or higher chronic kidney disease — this patient qualifies on flare frequency and CKD
Allopurinol is the preferred first-line urate-lowering agent, including in CKD; it is started low (50–100 mg/day) and titrated slowly to a serum urate target below 6 mg/dL
A low starting dose with slow titration reduces the risk of allopurinol hypersensitivity and of mobilization flares
Prophylactic low-dose colchicine or an NSAID is co-prescribed during the first 3–6 months of titration
Why the others are wrong
Pegloticase 8 mg every 2 weeks — a pegylated uricase that does lower urate, but it is reserved for refractory tophaceous gout after xanthine oxidase inhibitors have failed, and its anaphylaxis and infusion-reaction risk make it indefensible in a urate-lowering-naive patient (right-goal-wrong-line)
Febuxostat 80 mg once daily — an effective xanthine oxidase inhibitor but reserved as second-line after allopurinol failure or intolerance given its boxed cardiovascular-mortality warning, and 80 mg is a high starting dose; this is the right-class-wrong-first-choice trap
Probenecid 500 mg twice daily — a uricosuric whose efficacy falls with reduced renal function and is generally avoided in stage 3 CKD; it sets the trap of ignoring the renal limitation
Question 2MusculoskeletalMedium
A 55-year-old man with a history of gout presents with 1 day of severe pain, swelling, warmth, and erythema of the right first metatarsophalangeal joint. He has stage 3 chronic kidney disease (eGFR 38 mL/min/1.73 m²) and a prior hospitalization for NSAID-induced upper gastrointestinal bleeding. Arthrocentesis yields fluid with negatively birefringent, needle-shaped crystals. Which of the following is the most appropriate treatment for this acute flare?
AOrally administered indomethacin
BOrally administered oxycodone
COrally administered colchicine
DIntra-articular triamcinolone
Reveal answer & full explanation
Correct answer: D — Intra-articular triamcinolone
AOrally administered indomethacin
BOrally administered oxycodone
COrally administered colchicine
DIntra-articular triamcinolone✓
Why intra-articular triamcinolone is correct
The negatively birefringent, needle-shaped crystals confirm an acute monosodium-urate (gout) flare in a single accessible joint.
Two comorbidities block the usual systemic options: stage 3 chronic kidney disease (eGFR 38) and a prior NSAID-induced upper GI bleed.
An intra-articular corticosteroid delivers targeted anti-inflammatory effect with minimal systemic absorption and no renal or GI toxicity — ideal for a single joint when NSAIDs and colchicine are limited. Per current ACR gout guidance, glucocorticoids (intra-articular for a single joint) are a first-line flare option.
Why the others are wrong
Orally administered indomethacin — an NSAID, contraindicated by both the reduced eGFR and the prior GI bleed; right-disease-wrong-drug trap.
Orally administered oxycodone — provides analgesia only and does nothing to suppress the crystal-induced synovitis, so the flare runs its full course; opioids are at most an adjunct, and they add sedation, constipation, and fall risk without treating the disease.
Orally administered colchicine — effective for acute gout but requires major dose reduction in CKD and risks neuromyotoxicity at eGFR 30 to 50, so it is not the safest choice here; a near-miss for a learner who forgets the renal caveat.
Additional high-yield points
Oral prednisone is a reasonable systemic alternative when several joints are involved or injection is not feasible.
Start or resume urate-lowering therapy only after the flare settles, paired with anti-inflammatory prophylaxis.
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Sustained serum urate above the saturation threshold (~6.8 mg/dL at 37 °C) leads to MSU crystal formation in cooler peripheral tissues. Crystals are phagocytosed by macrophages, activating the NLRP3 inflammasome and releasing IL-1β, which drives neutrophil influx and acute inflammation. Chronic deposition produces tophi and erosive arthropathy.
Clinical presentation
Symptoms
Sudden onset (often nocturnal) severe monoarticular pain peaking within 12-24 hours
Classic site: first metatarsophalangeal joint (podagra) in ~50% of first attacks
Other sites: midfoot, ankle, knee, wrist, elbow, fingers
Self-limited untreated attacks resolve in 7-14 days
Recurrent flares with eventual chronic polyarticular involvement
Tophi — firm, painless subcutaneous nodules on extensor surfaces, helix of ear, Achilles tendon, finger pulps (chronic disease)
Classic findings
Podagra: red, hot, exquisitely tender first MTP joint.
Differential diagnosis
Septic arthritis — Fever, prior bacteremia, prosthetic joint; can coexist with gout — must perform arthrocentesis with Gram stain and culture in every suspected first gout attack
Pseudogout (CPPD) — Knee or wrist most common; rhomboid positively birefringent crystals; chondrocalcinosis on radiograph
Cellulitis — Diffuse erythema without joint capsule signs; no crystals; arthrocentesis distinguishes
Rheumatoid arthritis flare — Polyarticular, symmetric; tophi may be confused with rheumatoid nodules
Trauma / fracture — Mechanism and radiographs distinguish
Diagnostic workup
Diagnostic criteria
Definitive: identification of MSU crystals in joint fluid or tophus. 2015 ACR/EULAR classification criteria available for cases where aspiration is not feasible.
Gram stain and culture on every arthrocentesis to exclude concurrent septic arthritis
Serum urate (may be NORMAL during acute attack; recheck 2-4 weeks later)
CBC, ESR/CRP often elevated
BMP, urate excretion (24-h urine urate) to classify under- vs over-excretors if planning therapy
Lipid panel and A1c — frequent comorbidities
Imaging
Plain radiographs — early attacks usually normal; chronic disease shows 'rat-bite' periarticular erosions with overhanging edges, sparing of joint space until late
No urate-lowering; treat underlying metabolic disease
Gout vs pseudogout — polarized microscopy is the definitive distinction.
Treatment
First-line
Acute flare (treat ASAP, ideally within 24 h of onset):
• NSAIDs — indomethacin, naproxen, ibuprofen at full anti-inflammatory dose × 5-7 days (avoid in CKD, HF, GI bleed)
• Colchicine 1.2 mg PO, then 0.6 mg one hour later, then 0.6 mg daily-BID (renal dose adjustment; avoid in severe CKD or with strong CYP3A4/P-gp inhibitors)
• Glucocorticoids — prednisone 30-40 mg/day × 5 days with taper, or intra-articular triamcinolone (preferred if monoarticular and septic excluded)
• IL-1 inhibitor — anakinra or canakinumab for refractory or contraindication to others
Do NOT start urate-lowering therapy during an attack, but do NOT stop it if already on it
Complications
Chronic tophaceous gout with joint destruction and disability
Urate nephrolithiasis
Chronic urate nephropathy
Coexistent metabolic syndrome and cardiovascular disease
Drug reactions: allopurinol hypersensitivity (SJS/TEN), febuxostat CV events
Septic arthritis can coexist with gout — never assume monomicrobial
PANCE pearls
Serum urate may be normal during an acute attack — do not use it to rule out gout.
First arthrocentesis MUST include Gram stain and culture; septic arthritis and gout coexist.
Negatively birefringent (yellow when parallel to red compensator) needle-shaped crystals = gout. Positively birefringent rhomboid crystals = pseudogout (mnemonic: 'PPP' — Positive Pseudogout, Parallel).
Initiating allopurinol during a flare can prolong it — but if a patient is already on it, continue without interruption.
Always co-prescribe anti-inflammatory prophylaxis (colchicine or low-dose NSAID) for 3-6 months when starting urate-lowering therapy to prevent mobilization flares.
References
ACR 2020 — 2020 American College of Rheumatology Guideline for the Management of Gout (FitzGerald et al., Arthritis Care Res 2020)
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