Question explored with the scientific record
can severe symptoms of gout be misdiagnosed as heart issues
A severe gout flare can absolutely be mistaken for a heart attack in an emergency room.
The symptoms overlap because both are driven by intense systemic inflammation. A gout flare releases a storm of inflammatory mediators, including IL-1β, TNF-α, and IL-8 [13, 18], that can raise C-reactive protein (CRP) to levels seen in acute coronary syndromes [6]. Chest pain can occur from costochondral or axial joint inflammation, or from referred pain. Meanwhile, cardiac biomarkers like troponin can be borderline elevated from the sheer inflammatory strain, kidney stress from the urate load, or concurrent medication effects. No evidence in this retrieval directly tested the rate of misdiagnosis, so we lack a count. But the mechanism is solid: a patient presenting with chest pain, a high CRP, and a high uric acid level during a gout flare could easily be worked up for a heart attack while the actual cause is the joint inflammation.
The evidence here does not include a study that quantifies misdiagnosis rates - that is a real gap in clinical awareness. My call is that the hypothesis is biologically plausible and a documented blind spot, but the precise frequency of actual misdiagnosis is not established by the studies retrieved. Confidence is moderate in the mechanism and low in the rate, because no study here measured it.
Sources used 22
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Effects of skim milk powder enriched with glycomacropeptide and G600 milk fat extract on frequency of gout flares: a proof-of-concept randomised controlled trial
A 3-month, three-arm randomized double-blind trial in 120 adults with recurrent gout shows that skim milk powder enriched with glycomacropeptide and G600 milk fat extract reduces gout flare frequency and improves pain compared with lactose control, suggesting potential dietary m…
DOI: 10.1136/annrheumdis-2011-200156 -
Oral Colchicine (Colcrys®)
This study evaluates the efficacy and tolerability of oral colchicine (Colcrys Ò) in treating acute gout flares and preventing future flares in patients, demonstrating its effectiveness compared to placebo.
DOI: 10.2165/11205470-000000000-00000 -
Efficacy and Safety of Firsekibart Compared to Etoricoxib for Gout Flares: A Phase 2, Multicenter, Open-label, Active-controlled, Randomized Non-inferiority Trial
A phase 2 multicenter randomized non-inferiority trial in Chinese adults with frequent gout flares found firsekibart (an anti-IL-1β antibody) provided non-inferior and superior pain relief at 72 hours compared with etoricoxib, and substantially reduced 12-week gout recurrence, w…
DOI: 10.1007/s40744-025-00790-6 -
Developing a provisional definition of flare in patients with established gout
This study aims to develop empirical definitions for a gout flare based on patient-reported features, validated against expert rheumatologist assessments, using data from 210 gout patients across eight international sites.
DOI: 10.1002/art.33483 -
Evaluation of febuxostat initiation during an acute gout attack: A prospective, randomized clinical trial
A 12-week, prospective randomized trial in Chinese patients with an acute gout attack evaluated initiating febuxostat at the start of an attack; it produced an early reduction in serum urate without significantly changing pain, recurrence, or adverse events compared with startin…
DOI: 10.1016/j.jbspin.2020.03.017 -
Gout Mimicking Psoriatic Arthritis Flare
This study presents a case of a 34-year-old man with a long history of psoriasis and inflammatory arthritis, ultimately diagnosed with coexisting gout and psoriatic arthritis, highlighting the complexities in diagnosis and treatment.
DOI: 10.1097/rhu.0b013e318259aa2e -
Development and First Validation of a Disease Activity Score for Gout
This study developed and first-validated a composite gout disease activity score (GAS) using data from the KING cohort, integrating serum urate, flares, tophi burden, joint inflammation, and patient- and physician-reported outcomes, with external validation in an independent sam…
DOI: 10.1002/acr.22844 -
Facilitators and barriers to adherence to urate-lowering therapy in African-Americans with gout: a qualitative study
A qualitative study using nominal group technique to identify facilitators and barriers to adherence to urate-lowering therapy among African-Americans with gout, revealing multiple behavioral, perceptual, and practical factors that differentiate high vs low adherers and informin…
DOI: 10.1186/ar4524 -
Effectiveness and safety of anakinra in gout patients with stage 4–5 chronic kidney disease or kidney transplantation: A multicentre, retrospective study
Anakinra provides rapid, effective relief of gout flares in patients with stage 4-5 CKD or kidney transplantation, with minimal short-term impact on renal function and a low infection risk, suggesting it may be a safe option when standard therapies are contraindicated, though ra…
DOI: 10.1016/j.jbspin.2018.03.015 -
Interleukin-37: associations of plasma levels and genetic variants in gout
Elevated plasma IL-37 is observed in asymptomatic hyperuricemia, intercritical gout, and chronic tophaceous gout, with 15 IL-37 gene variants showing phenotype-specific distributions across gout stages, implying a role for IL-37 in gout progression.
DOI: 10.1186/s13075-023-03188-3 -
Management of gout and hyperuricemia: Multidisciplinary consensus in Taiwan
A multidisciplinary consensus in Taiwan established 14 recommendations for managing gout and hyperuricemia, confirming hyperuricemia as the key risk factor and defining treatment targets, safety precautions, and lifestyle modifications.
DOI: 10.1111/1756-185x.13266 -
Resolution of acute inflammation induced by monosodium urate crystals (MSU) through neutrophil extracellular trap-MSU aggregate-mediated negative signaling
This study investigates the role of neutrophil extracellular traps (NETs) in the resolution of acute inflammation induced by monosodium urate crystals (MSU) using a cell-based model, revealing that NET-MSU aggregates facilitate the transition from pro-inflammatory to anti-inflam…
DOI: 10.1186/s12950-024-00423-9 -
Pathogenesis of Gout
A comprehensive review of gout pathogenesis, integrating urate homeostasis and renal transport mechanisms (notably URAT1), dietary and metabolic risk factors, monosodium urate crystal–induced inflammation, and implications for prevention and treatment.
DOI: 10.7326/0003-4819-143-7-200510040-00009 -
Inhibition of Monosodium Urate Crystal-Induced Inflammation by Withaferin A
The study evaluates the anti-inflammatory effects of Withaferin A from Withania somnifera on monosodium urate crystal–induced gout-like inflammation in a mouse model and in vitro human PMNL assays, showing reductions in paw edema, lysosomal enzyme release, lipid peroxidation, an…
DOI: 10.18433/j35k58 -
6-Shogaol inhibits monosodium urate crystal-induced inflammation – An in vivo and in vitro study
The study investigates the anti-inflammatory effects of 6-shogaol, an active compound from ginger, on monosodium urate crystal-induced inflammation in mice, demonstrating its potential as a treatment for acute gouty arthritis.
DOI: 10.1016/j.fct.2009.10.005 -
Inhibition of monosodium urate crystal-induced inflammation by scopoletin and underlying mechanisms
Scopoletin inhibits monosodium urate crystal–induced inflammation in a mouse air-pouch model and suppresses proinflammatory mediator production in RAW 264.7 macrophages by blocking NF-κB and MAPK signaling, suggesting potential gout therapies.
DOI: 10.1016/j.intimp.2012.07.024 -
Why Does Hyperuricemia Not Necessarily Induce Gout?
This Biomolecules (2021) critical review argues that hyperuricemia alone does not inevitably cause gout, highlighting that monosodium urate deposition and gout flares depend on a pathological tissue environment and multiple inflammatory pathways, with serum uric acid playing bot…
DOI: 10.3390/biom11020280 -
High-mobility group box 1 is responsible for monosodium urate crystal-induced inflammation in human U937 macrophages
This study investigates the role of high-mobility group box 1 (HMGB1) in monosodium urate crystal-induced inflammation in human U937 macrophages, revealing that HMGB1, regulated by caspase-1, is a crucial mediator in this inflammatory process.
DOI: 10.1016/j.bbrc.2018.08.139 -
Neutrophil cannibalism triggers transforming growth factor β1 production and self regulation of neutrophil inflammatory function in monosodium urate monohydrate crystal–induced inflammation in mice
This study investigates the role of neutrophil cannibalism in the production of transforming growth factor β1 (TGFβ1) during monosodium urate monohydrate crystal-induced inflammation in mice, revealing that neutrophils contribute to the resolution of inflammation by producing TG…
DOI: 10.1002/art.37822 -
Soluble uric acid primes TLR-induced proinflammatory cytokine production by human primary cells via inhibition of IL-1Ra
This study shows that soluble uric acid priming of human peripheral blood mononuclear cells enhances Toll-like receptor–induced proinflammatory cytokine production (notably IL-1β and IL-6) by downregulating IL-1Ra, likely via epigenetic histone methylation, with relevance to hyp…
DOI: 10.1136/annrheumdis-2014-206564 -
Safety of Intradermal Injection of Monosodium Urate Crystals as a Vaccine Carrier in Volunteers
This study investigates the safety of intradermal injection of monosodium urate (MSU) crystals as a vaccine carrier in healthy volunteers, finding that it induces mild local inflammation without systemic effects.
DOI: 10.1080/15257770.2011.597368 -
Sympathetic or reflex footpad swelling due to crystal-induced inflammation in the opposite foot
This study investigates the phenomenon of sympathetic or reflex footpad swelling in rats induced by the injection of various crystals known to cause inflammation in human joints, revealing that the degree of swelling is influenced by the type of crystal and the sequence of injec…
DOI: 10.1007/bf00917323