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PubMed2005

Gout induced by intoxication of sodium bicarbonate in Korean native broilers.

Gout is a metabolic disorder that results in hyperuricemia and the deposition of positively birefringent monosodium urate crystals in various parts of the body. Intoxication of sodium bicarbonate (SBC) for 35 days in Korean native broilers was investigated. Sixty birds, aged 2 weeks, divided into 5 groups were exposed to excess SBC: 2 g/L (group A), 7.5 g/L (group B), 20 g/L (group C), 40 g/L (group D). Toxicopathological examination of all exposed birds revealed the manifestation of visceral and articular gout in group C, while birds of group D showed acute kidney damage with manifestation of excessive visceral gout. Interestingly, few birds in group D also showed signs of rare condition of acute articular gout. Dose-dependent increments in erythrocytic count, hematocrit values, and hemoglobin levels of the exposed birds were observed. Hypernatremia, hyperuricemia, hypokalemia, and hypochloremia were common findings among exposed birds. Microscopic examination of birds that manifested visceral gout revealed significant urate deposit, tubular necrosis, and tophi formation in renal interstitium. These findings provide a pathophysiological link that SBC intoxication may support hyperuricemia, which is an independent risk factor for gout and other renal dysfunctions. Further study is required to delineate the effect of lowering uric acid on progression of gout and other renal diseases.

Animals↗
PubMed2003

Trends in the manifestations of gout in Taiwan.

OBJECTIVE: To elucidate the recent changes in the clinical manifestations, risk factors and disorders associated with gout. METHODS: All gouty cases in Ho-Ping Gout Database were divided into two groups according to the date of first visit to our clinic: 1983-1991 (earlier group) and 1992-1999 (later group). Study variables were compared between these two groups. RESULTS: In the later group, the age at onset of gout was lower by 2.7 yr (P < 0.0001) and the percentages of female gout and familial gout were higher (P = 0.0046 and P < 0.0001, respectively). Joint counts and the percentage of frequency of attacks > or =6 times/yr were lower in the later group (P < 0.0001), while the percentage of tophaceous gout was higher by 0.8% in the later group (P = 0.0004). The percentage of first attack at ankle was higher (P < 0.0001), while those at Achilles tendon, knee and upper extremity were lower in the later group (P < 0.0001). The percentages of diuretic use and alcohol consumption were lower in the later group (P < 0.0001). The percentages of obesity, hypertriglyceridaemia and nephrolithiasis were higher (P < 0.0001), while the percentages of hypertension and hypercholesterolaemia were lower in the later group (P < 0.0001 and P = 0.0003, respectively). The percentages of type 2 diabetes mellitus and renal insufficiency were not significantly different in multivariate analyses. CONCLUSION: The age of onset, clinical manifestations, risk factors and disorders associated with gout have recently changed in Taiwan.

Adolescent↗
PubMed1989

Hyperuricemia, gout, and autosomal dominant polycystic kidney disease.

The relationship between hyperuricemia, gout, and autosomal dominant polycystic kidney disease (ADPKD) is not widely recognized. In an attempt to further clarify this relationship, the authors have studied 17 patients with ADPKD, 9 controls, 9 patients with proven gout and chronic renal failure, 11 patients with gout and normal renal function, and 11 patients with chronic renal failure. The mean serum uric acid concentration was higher in patients with ADPKD as a group than in controls (8.0 +/- 1.7 mg/dl vs. 6.4 +/- 1.6 mg/dl, p less than .02). Clinical gout was identified in 24% of patients with ADPKD; none of the patients with chronic renal failure of other etiologies had gout. Fractional excretion of uric acid and the activity of the enzyme hypoxanthine guanine phosphoribosyl transferase (HGPRT) were not different among the groups studied. From this study the authors conclude that ADPKD should be included among those diseases associated with hyperuricemia and gout. A partial deficiency in HGPRT or abnormal renal handling of uric acid do not appear to be responsible for the increased incidence of gout in patients with ADPKD.

Aged↗
PubMed1991

Calcium pyrophosphate dihydrate gout and other crystal deposition diseases.

The number of crystal or birefringent particles associated with arthritis is increasing, and a uniform taxonomy is needed. The term gout has been proposed as a generic term for these diseases based on historical, clinical, and crystallographic reasons. Calcium pyrophosphate dihydrate gout follows monosodium urate gout in frequency, and its spectrum of clinical manifestations continues to grow. Familial calcium pyrophosphate dihydrate gout was described for the first time in kindreds studied in England and Tunisia; new Jewish and Spanish kindreds were also reported. Type I collagen was shown to nucleate nativelike calcium pyrophosphate dihydrate crystals, and pyrophosphate elaboration was explored in cartilage explants in an attempt to reproduce the in vivo metabolic or endocrine disorders associated with calcium pyrophosphate dihydrate gout. The effect of pyrophosphatase and different cofactors such as magnesium in dissolving calcium pyrophosphate dihydrate crystals was investigated. High-resolution electron microscopy was used to study the interrelation between apatite and other basic calcium phosphate crystals in apatite gout. Raman microscopy was applied for the first time to identify crystals in biologic specimens. A simple and specific technique for basic calcium phosphate crystal identification is necessary to understand the relationship between different calcium phosphate crystals and osteoarthritis. Several reports about children and young patients with primary oxalate gout described the effect of oxalate on eyes, periodontal tissues, and bone. Multicenter studies showed poor results of renal transplantation, but favored combined liver and renal transplantation.(ABSTRACT TRUNCATED AT 250 WORDS)

Calcinosis↗
PubMed2001

Tophaceous gout of the spine mimicking epidural infection: case report and review of the literature.

OBJECTIVE AND IMPORTANCE: Tophaceous gout uncommonly affects the axial skeleton. The clinical presentations of gout of the spine range from back pain to quadriplegia. Gout that presents as back pain and fever may be difficult to distinguish from spinal infection. We present a case of a patient with tophaceous gout of the lumbar spine who was initially diagnosed with and treated for an epidural infection. The clinical and diagnostic features of tophaceous gout of the spine are reviewed. CLINICAL PRESENTATION: A 70-year-old man presented with a 2-day history of fever and back pain. A physical examination revealed that he had flank tenderness and evidence of polyarthritis affecting the elbows, knees, and right first metatarsophalangeal joint. A magnetic resonance imaging scan of the patient's lumbar spine showed an extensive area of abnormal gadolinium enhancement of the paramedian posterior soft tissues from L3 to S1 with an area of focal enhancement extending into the right L4-L5 facet joint. INTERVENTION: A laminectomy was performed at L4-L5, and a chalky white material in the facet joint was found eroding into the adjacent pars intra-articularis. Light and polarizing microscopy confirmed the presence of gouty tophus. No evidence of infection was found. CONCLUSION: Gouty arthritis of the spine is rare. Thirty-seven previous cases have been reported. When the clinical presentation includes acute back pain and fever, differentiation of spinal gout from spinal infection may be difficult. The clinical suspicion of spinal gout may lead to the correct diagnosis by a less invasive approach than exploration and laminectomy.

Aged↗
PubMed2004

Reduced incidence of hyperuricemia, gout, and renal failure following liver transplantation in comparison to heart transplantation: a long-term follow-up study.

BACKGROUND: Hyperuricemia and gout are common complications of heart transplantation, reaching a prevalence of 84% and 30%, respectively, in heart transplant recipients. In contrast, they are seldom reported following orthotopic liver transplantation (OLT). METHODS: We retrospectively evaluated 75 consecutive liver transplant recipients and 47 consecutive heart transplant recipients, followed for at least 3 years after transplantation in a single transplantation center in Jerusalem, Israel. Data was collected on demographic and clinical variables, levels of uric acid, the occurrence of gout, renal function, and variables effecting hyperuricemia, such as weight and medications. RESULTS: Clinical gout was significantly more prevalent in heart recipients than in liver recipients (25.5% and 2.6%, respectively). Hyperuricemia was present in 100% of heart recipients, with an average uric acid level of 451 micromol/l, as compared with 85.7% and 403 micromol/l for liver recipients (P < 0.001 for both variables). Univariate analysis identified several parameters which significantly influenced the difference in hyperuricemia and gout among the two groups including age, gender, rejection episodes, hypertension, diabetes mellitus, the level of uric acid prior to transplantation, and the use of cyclosporine A, diuretics, steroids, and aspirin. Use of tacrolimus and azathioprine were associated with decreased incidence of hyperuricemia and gout. Multivariate analysis identified the type of transplantation as the only independent risk factor predicting the development of hyperuricemia and gout. CONCLUSION: Clinical gout and hyperuricemia were significantly more prevalent in heart recipients than in liver recipients. The disparity can be explained by differences in age, gender and renal function among the groups, as well as by the use of different medication regimens.

Adult↗
PubMed1978

A prospective study of gout in New Zealand Maoris.

Results are reported from the first prospective study of gout in New Zealand Maoris based on a sample of 388 males and 378 females. At baseline, high mean levels of serum uric acid (SUA) were found, 0.422 +/- 0.092 mmol/1 (7.05 +/- 1.54 mg/100 ml) in males and 0.350 +/- 0.091 mmol/1 (5.85 +/- 1.52 mg/100 ml) in females. On the basis of traditional criteria (SUA above 0.42 mmol/1 (7.0 mg/100 ml) in males and above 0.36 mmol/1 (6.0 mg/100 ml) in females) the prevalence of hyperuricaemia was 49% in males and 42% in females. The baseline prevalence of gout (8.8% for males and 0.8% for females) and the subsequent 11-year incidence rates (10.3% for males and 4.3% for females) are discussed in relation to specified SUA classes. When traditional, sex-specific criteria for hyperuricaemia were used, no relationship was found between the prevalence of hyperuricaemia and the incidence of gout. There was, however, a sharp increase in the incidence rate of gout in both sexes when SUA levels were above 0.48 mmol/1 (8.0 mg/100 ml). In subjects with a baseline SUA above this level, the age-standardised 11-year incidence rate of gout was 29.1% for males and 37.2% for females. A previously unreported relationship linking muscle size to the incidence of gout in males is presented as a major finding of the study. Other risk factors associated with gout were body mass and blood pressure.

Adolescent↗
PubMed1975

[Gout, hyperuricemia and femur head osteonecrosis (FHON)].

The authors report on 14 cases of osteonecrosis of the femoral head (ONFH) in patients suffering from gout. The cases of association were discovered over a period of 10 years among 232 patients with ONFH and 651 with gout. The necrosis had no particular characteristics except that there was a clear preponderence in males and a slight tendency to be bilateral; it occurred, perhaps, at a slightly earlier age. The patients with gout did not show any special clinical features ; the gout always preceded the necrosis, on average by 7 1/2 years. There was no obvious history of painful crises in the hip that could be attributed to the acute gout, except in one case. The excess of urate was detected by the baseline level of uricaemia (91 mg/litre on average), by the frequency of tophus (4 out of 14), and by the frequency of urinary lithiasis (2 out of 14), and did not appear to be any greater in the patients with gout and ONFH than it was in the whole of the population of gout patients. In those patients in whom it was estimated, the lipid analysis showed most frequently an increase in total lipids, in triglyceridaemia, and in cholesterolaemia. In the 5 patients in whom the investigations were sufficiently detailed, the dyslipidaemia was of Frederickson type II + IV (mixed hyperlipidaemia according to de Gennes' classification). Different physiopathological hypotheses are discussed by the authors, notably those concerned with micro-particulate fatty emboli (lipomicrons), which may obstruct, among others, the terminal arteries of the femoral head. Of the 6 patients for whom it was possible to obtain information, for an average period of 10 years since the onset of the necrosis, 2 had presented with untreated hyperlipidaemia and a severe general vascular illness (myocardial infarction in one case and regressive hemiplegia in the other). These findings lead to the conclusion that correction of the hyperlipidaemia by diet is indispensable to ensure the long-term survival of these patients.

Adrenal Cortex Hormones↗
PubMed2005

Prevalence and risk factors for urolithiasis in primary gout: is a reappraisal needed?

OBJECTIVE: To assess the prevalence and risk factors for urolithiasis in primary gout. METHODS: One hundred forty patients with primary gout were studied. Urolithiasis was defined as a history of urolithiasis, or nephrolithiasis detected via ultrasonography in patients with no previous record of urolithiasis. Patient age, duration of gout, presence of tophi, obesity, alcoholism, high blood pressure, diabetes, hyperlipidemia, family history of urolithiasis, daily urine output, uricemia, urine pH, FeNa, FeUrate, urine pH/FeUrate index, and daily urine excretion of urate, sodium, calcium and potassium were compared between lithiasic and non-lithiasic subjects. RESULTS: Fifty-five (39%; 95% CI 31-47) patients had urolithiasis, of which 37 (26%) were diagnosed by clinical history and 18 (13%) by ultrasonography. Patients with a silent kidney stone diagnosed by ultrasound tended to have shorter evolution of gout. Aside from urinary H+ ion concentration (lithiasic subjects 5.17 +/- 3.9 microM/l; non-lithiasic subjects 3.80 +/- 3.01 microM/l; p = 0.02), no difference was found between lithiasic and non-lithiasic subjects for the other variables studied. CONCLUSION: Ultrasonography increased the probability of diagnosing urolithiasis by 50%, meaning the prevalence of urolithiasis in gout is likely higher than previously reported. A higher urinary H+ ion concentration was the only variable associated with urolithiasis. Due to advances in diagnosis of gout and urolithiasis, as well as biochemical assays, the prevalence and risk factors for urolithiasis in gout require reassessment.

Adult↗
PubMed1989

Predicting acute gout in diuretic-treated hypertensive patients.

Factors predisposing to diuretic-induced acute gout were investigated in a case-control study. Seventy hypertensive patients with acute gout occurring during diuretic treatment were identified and matched for age and sex to 140 hypertensive controls who took diuretics but did not develop gout. Gout was related more strongly to the use of loop diuretics than thiazides, with 30% of cases taking a loop diuretic compared to 14% of controls (P less than 0.01). In a sub-group of men who took a thiazide and no other diuretic, gout was significantly associated with obesity (odds ratio 3.7, 95% confidence interval 1.4, 9.1) and high alcohol intake (odds ratio 3.3, 95% confidence interval 1.1, 9.8). In these patients, 23% of gout was attributable to obesity and 16% to high alcohol consumption. Approximately 40% of acute gout might have been prevented by avoiding thiazides in those 20% of men who weighed more than 90 kg and/or consumed more than 56 units of alcohol per week.

Acute Disease↗
PubMed1977

Gout and hyperlipidaemia. Effect of overweight on the levels of circulating lipids.

A study of the serum lipids in 90 patients with gout and 90 controls matched for age and weight index demonstrated that in gout there was a significant elevation of the mean serum levels of cholesterol (282 +/- 55 mg/100 ml), triglycerides (183 +/- 161 mg/100 ml) and phospholipids (270 +/- 61 mg/100 ml) compared with the controls whose mean values were respectively 243 +/- 41 mg, 95 +/- 53 mg and 245 +/- 36 mg. Hyperlipidaemia of mixed type was the most common lipid defect in the patients with gout; there was no difference in the frequency of pure hypercholesterolaemia (without hypertriglyceridaemia) between gout and the controls. The frequency of anomalies of blood lipid levels in gout does not result from (or not solely from) obesity since patients with gout and controls were matched for their weight and height. There was a correlation between the serum lipid levels and obesity in the controls but this was not demonstrable in the patients with gout.

Adult↗
PubMed1995

Runner with gout and an aortic valve nodule.

A 33-yr-old male ran 10 miles, drank some beer, and developed pain in his left knee and ankle. He took some leftover antibiotics but was no better after 6 d, when a heart murmur and an aortic valve nodule were discovered. He was presumed to have endocarditis with septic arthritis and was started on intravenous antibiotics. On the second hospital day, synovial fluid analysis revealed acute gout, and the patient improved very rapidly on anti-gout therapy. The valvular nodule remained unexplained, but one very rare cause of valvular heart nodules is visceral gout. An unsuccessful attempt to resorb the nodule was made by using allopurinol. This patient demonstrates several points about gout in endurance athletes: 1) acute gout can mimic infectious endocarditis, 2) misdiagnosed or undertreated gout often leads to multiple joint involvement and sometimes to visceral tophi, and 3) athletes who exercise in warm weather and quench their thirst with cold beer are at risk for acute gout.

Acute Disease↗
PubMed1995

Does renal impairment protect from gout?

OBJECTIVE: To test whether renal impairment protects from the development of gout. METHODS: We conducted a retrospective cohort study in which 40 hyperuricemic patients (serum uric acid > 0.54 mM/l) with renal impairment (serum creatinine > 200 microM/l) and 40 equally hyperuricemic patients with normal renal function (serum creatinine < 120 microM/l) were given a telephone questionnaire eliciting a history of gout, its pattern and severity, and other features of medical and family history. RESULTS: There was no significant difference among the prevalence of gout (relative risk 1.1, confidence interval 0.73-1.67), the pattern and severity of gout, and the presence of tophi between the 2 groups. A positive family history of gout was significantly increased in the patients with gouty arthritis (p < 0.05). CONCLUSION: Renal impairment does not protect from gout. There may be a familial factor in the development of gout that is independent from the familial tendency for hyperuricemia.

Adult↗
PubMed1993

Hereditary nephropathy associated with hyperuricemia and gout.

BACKGROUND: The clinical characteristics of hereditary nephropathy associated with hyperuricemia or gout have not been fully described, and the pathogenetic role of increased serum urate concentration is controversial. METHODS: We examined the clinical characteristics of 14 patients and purine metabolism of seven patients, while they were on a purine-restricted diet, in two families with hereditary nephropathy associated with asymptomatic hyperuricemia or gout. Results of plasma and urinary purine measurements were compared with those obtained in 25 patients with gout and renal insufficiency and in 25 normal subjects. Eight subjects in both families were followed up for a mean of 44 months. Allopurinol was given to all patients and enalapril maleate to hypertensive subjects. RESULTS: All patients had some combination of hyperuricemia, gout, renal insufficiency, arterial hypertension, and reduced kidney size. Decreased glomerular filtration rate was proportional to the decreased renal plasma flow. Renal vascular resistance was markedly increased in the patients with diminished renal plasma flow. All patients with familial nephropathy showed diminished urinary uric acid, hypoxanthine, and xanthine excretion rates. Purine under-excretion was more severe in affected patients with familial nephropathy than in patients with gout and renal insufficiency. Kidney biopsy specimens from three patients with familial nephropathy showed tubulointerstitial lesions and ischemic changes in glomeruli but no uric acid crystals. The kidney uric acid content was normal. Allopurinol treatment normalized serum urate levels, but serum creatinine concentrations increased and creatinine clearance decreased in all patients with familial nephropathy. One patient with gout only at initial evaluation developed renal failure during the follow-up period. CONCLUSIONS: Increased serum urate concentrations in hereditary nephropathy associated with hyperuricemia and gout are due to severe impairment of uric acid excretion. Hyperuricemia does not appear, however, to be of pathogenetic relevance and may be a consequence of a primary disruption of renal hemodynamics.

Adolescent↗
PubMed1989

Saturnine gout.

The history of saturnine gout is almost as old as civilization itself. Studies carried out in recent decades explain the development of hyperuricaemia and gout, with the inhibiting effect of lead on the tubular urate transport causing decreased urate excretion. In the case of lead intoxication these effects are often associated with renal failure but may occur without clinical features of lead toxicity and renal damage. The clinical features of saturnine gout are essentially similar to those of primary gout; however, acute attacks tend to occur in the knee more frequently than the first metatarsophalangeal joint. Acute attacks in saturnine gout are frequently polyarticular and tophi rarely develop. The diagnosis of saturnine gout rests on the history of exposure to lead, clinical features of lead toxicity, biochemical confirmation of high serum lead levels and other biochemical abnormalities, and the exclusion of other forms of gout. Treatment consists of excluding the patient from further exposure to lead, the use of chelating agents to remove lead, and control of acute gouty arthritis and hyperuricaemia.

Arthritis, Gouty↗
PubMedDate not supplied

[Tophaceous gout in plurimetabolic syndrome].

Aim of this paper is to describe and discuss, on the basis of the available current literature, the case of a female patient affected by a tophaceous gout associated with plurimetabolic syndrome. Hyperuricemia and gout may be seen today in all the populations of developed countries, with increasing frequency on the last fifty years. Increased production or reduced urinary excretion of uric acid (and hypoxanthine and xanthine) are the most important pathogenetic mechanisms of primary or secondary hyperuricemia. Gout is an acute rheumatic disorder (characterized by a limited range of manifestations) which occurs in humans in connection with deposition of crystals of monosodium urate (the final product of purine metabolism) in the articular and soft periarticular tissues. Hyperuricemia and/or gout are often associated with hyperinsulinemia, obesity, diabetes mellitus, hyperlipemia, hypertension and atherosclerosis to form the syndrome called "Plurimetabolic syndrome" or "Syndrome X". Here we report the clinical case of a 64-year-old female patient who had android obesity, type 2 diabetes mellitus, hypertension, dyslipidemia and hyperuricemia and had been suffering (over many years) from intermittent episodes of severe pain and inflammatory joint swelling (first metacarpo- and metatarso-phalangeal joints) with development of pronounced multiple tophi in bone articular and soft periarticular tissues. Hyperuricemia and acute episodes had never been treated with anti-hyperuricemic drugs because gouty arthritis had never been diagnosed. This severe tophaceous gout associated to multiple metabolic disorders prompted us to present knowledge on gout and to focus on the interrelationships between hyperuricemia and/or gout and plurimetabolic syndrome, important risk factors for coronary heart disease.

Arteriosclerosis↗
PubMed2006

Colchicine for acute gout.

BACKGROUND: Gout is one of the most common rheumatic diseases worldwide. Colchicine is regarded as beneficial in the treatment of acute gout, but has a high frequency of gastrointestinal adverse events. OBJECTIVES: To evaluate the efficacy and safety of colchicine for relief of the signs and symptoms of acute gouty arthritis, compared to placebo and other treatment interventions. SEARCH STRATEGY: We searched the following electronic databases to March 2006: Cochrane Central Register of Controlled Trials (CENTRAL, Issue 1, 2006), MEDLINE (from 1966), EMBASE (from 1980), CINAHL (from 1982), AMED (from 1985), Web of Science (from 1945) and Current Controlled Trials. SELECTION CRITERIA: Published randomised controlled trials (RCTs) and controlled clinical trials evaluating symptom relief and adverse outcomes of colchicine therapy in acute gout were considered for this review. DATA COLLECTION AND ANALYSIS: Two reviewers independently screened search results for inclusion, collected the data in a standardized form and assessed the methodological quality of the trial using validated criteria. Results for continuous outcome measures were expressed as weighted mean differences. Dichotomous outcome measures were pooled using relative risk. The number needed to treat was calculated for significant outcomes. MAIN RESULTS: One RCT (N=43) comparing colchicine to placebo for the treatment of acute gout was included in this review. The results favour the use of colchicine over placebo with an absolute reduction of 34% for pain and a 30% reduction in clinical symptoms such as tenderness on palpation, swelling, redness, and pain. The number needed to treat (NNT) with colchicine versus placebo to reduce pain was 3 and the NNT to reduce clinical symptoms was 2. All participants treated with colchicine experienced gastrointestinal side effects (diarrhea and/or vomiting) and the number needed to harm (NNH) with colchicine versus placebo was 1. No studies comparing colchicine to NSAIDs or other treatments such as corticosteroids or ACTH were identified. AUTHORS' CONCLUSIONS: Colchicine is an effective treatment for the reduction of pain and clinical symptoms in patients experiencing acute attacks of gout, although in the regimen studied its low benefit to toxicity ratio limits its usefulness. It should be used as a second line therapy when NSAIDs or corticosteroids are contraindicated or ineffective. More evidence is needed to compare the efficacy of colchicine to that of NSAIDs or corticosteroids, the current first line therapy for acute gout.

Colchicine↗
PubMed2026

Postoperative complications and outcomes after surgical treatment for tophaceous gout: A systematic review and meta-analysis.

BACKGROUND: Surgical treatment remains necessary for selected patients with tophaceous gout, particularly when mechanical limitation, nerve compression, ulceration, infection, deformity, or failure of conservative treatment is present. However, postoperative outcomes after surgery for tophaceous gout have not been comprehensively quantified. This systematic review and meta-analysis evaluated postoperative complication profiles and recurrence burden after surgical treatment for tophaceous gout. METHODS: A systematic search of PubMed, Embase, Web of Science, and the Cochrane Library was conducted from database inception to March 25, 2026. Original studies reporting postoperative outcomes after surgical treatment for tophaceous gout were included. Pooled event rates with 95% confidence intervals (CIs) were calculated using a random-effects single-arm meta-analytic approach. Primary outcomes were postoperative infection, delayed wound healing, and recurrence. Secondary outcomes were reoperation, amputation, and overall complications. Functional outcomes were summarized descriptively. RESULTS: 18 retrospective studies were included. The pooled postoperative infection rate was 11.3% (95% CI 8.0%-15.7%), delayed wound healing 9.9% (95% CI 5.1%-18.2%), and recurrence 8.5% (95% CI 4.7%-14.9%). Secondary pooled rates were 9.7% (95% CI 5.5%-16.7%) for reoperation, 3.7% (95% CI 2.0%-6.8%) for amputation, and 24.0% (95% CI 14.0%-38.1%) for overall complications. Significant subgroup differences were identified only for infection according to anatomic site and intervention type. Sensitivity analyses showed that pooled estimates were robust. The certainty of evidence was very low for all outcomes. CONCLUSIONS: Surgical treatment for tophaceous gout is associated with measurable postoperative risks, particularly infection and overall complications. These findings support careful perioperative counseling, structured postoperative surveillance, integrated long-term urate-lowering management, and more standardized reporting of perioperative risk factors and postoperative outcomes in future surgical studies of tophaceous gout.

Humans↗