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PubMed1999

[Spinal cord compression due to tophaceous vertebral gout: a case report and literature review].

INTRODUCTION: Acute gout arthritis and tophaceous gout of the spine is rare. EXEGESIS: We report the case of a 54-year-old man with chronic low back pain. Physical examination and myelography showing neurological compression on L4 laminectomy evidenced tophaceous gout. CONCLUSION: Gout arthritis should always be suspected and investigated in patients with either chronic low back pain or non-specific spinal cord compression.

Arthritis, Gouty↗
PubMed2005

Surgical versus pharmacologic treatment of intraspinal gout.

UNLABELLED: A controversy between pharmacologic and surgical treatment of intraspinal gout exists in the literature. If gout is diagnosed timely, pharmacologic therapy may avert the need of surgery. The lack of readily available synovial fluid makes the diagnosis particularly difficult. The purpose of this study was to evaluate the clinical pictures and magnetic resonance imaging features in rapid differentiations of intraspinal gout. I retrospectively evaluated lumbar intraspinal tophaceous gout without the classic radiographic punched-out lesions. Four patients (average age, 65 years) had a history of hyperuricemia with multiple tophaceous deposits in the joints or visceral organs or both. The common presentations were low back pain with or without inflammatory reaction (fever, elevated C-reactive protein level, and mild leukocytosis). The patients also presented with intermittent claudication or radiculopathy of variable duration or both. The gouty tophi yielded homogeneous and hypointense masses on T1- and T2-weighted images, with multiple hypointense speckles. The masses were located in bilateral lumbar facet joints in all patients, with additional midline extension along the ligamentum flavum in three. All patients had uneventful outcomes after surgical decompression and pharmacologic treatment. Rapid deposition of tophi may aggravate nerve compression. If neurologic deficits are found, surgical decompression can provide a satisfactory outcome. LEVEL OF EVIDENCE: Therapeutic study, Level IV. See the Guidelines for Authors for a complete description of levels of evidence.

Aged↗
PubMed2003

Tophaceous gout in a patient with thalassemia.

We report a 46-year-old Greek female with thalassemia intermedia, who presented to our hospital with end stage renal disease of unknown etiology and tophaceous gout. In addition, skeletal manifestations characteristic of thalassemia were noted with massive extramedullary hematopoiesis presenting as posterior mediastinal masses. We report the first case in English literature of crystal proven gout in thalassemia intermedia and provide a review of the literature that indicates the relative rarity of gout in this clinical setting, despite evidence of urate overproduction in one report. The long survival and renal insufficiency may have contributed to our patients' tophaceous gout.

Journal Article↗
PubMed2004

Spinal gout: case report and review of the literature.

Spinal involvement is considered to be a rare complication of gout. We report a case of a 48-year-old woman with chronic tophaceous gout, recently desensitized to allopurinol, who presented with an L4 radiculopathy. A magnetic resonance image (MRI) of the lumbosacral spine revealed an extradural process at L4 level. Three months before this episode, for unrelated reasons, the patient had an MRI of her entire spine, which was normal. Laminectomy was performed revealing a large gouty tophus. The fact that a large gouty tophus formed over this short a period of time causing neurologic symptoms highlights the importance of aggressive medical management of patients with longstanding tophaceous gout with urate-lowering agents. Spinal extradural gout could lead to neurologic deficits necessitating emergent surgery for decompression, exposing the patient to further risk. Every effort should be made to lower the serum uric acid level by maximizing the pharmacologic regimen and, if necessary, desensitizing the patient, like in our case, if there is a history of allergy to allopurinol.

Journal Article↗
PubMed2004

Metabolic syndrome and ischemic heart disease in gout.

BACKGROUND: For decades, gout has been associated with several metabolic abnormalities and with ischemic heart disease (IHD). OBJECTIVE: Our aim was to determine the prevalence of metabolic syndrome by Adult Treatment Panel III criteria (ATP III) and ischemic heart disease (IHD) by electrocardiogram (EKG) and/or single photon emission computed tomography (SPECT) in patients with gout. METHODS: We included 64 consecutive outpatients with primary gout, but no history of IHD, attending our clinic for the first time. Demographic and clinical data were recorded and resting electrocardiogram, lipid profile, fasting insulin, and SPECT with Tc sestamibi were performed. Metabolic syndrome was defined according to ATP III criteria (> or =3 of the following data: 1) hyperglycemia (fasting glucose > or =110 mg/dL) or previous diagnosis of diabetes mellitus, 2) hypertension (> or =130/85 mm Hg) or previous diagnosis, 3) high-density lipoprotein (HDL) <40 mg/dL (men) or <50 mg/dL (women), 4) triglycerides > or =150 mg/dL, and 5) obesity. RESULTS: IHD was diagnosed in 10 patients (16%); 2 had EKG changes compatible with previous silent myocardial necrosis and the other 8 had abnormal SPECT. The prevalence of metabolic syndrome was 82%, all patients had at least 1 metabolic abnormality, but all the patients with IHD had metabolic syndrome (3 criteria according with ATP III). Patients with IHD differed from those without IHD in the percentage of HDL levels <40 mg/dL (100% vs. 82%; P = 0.05) as well as glucose and insulin levels in the fasting state (129.3 +/- 6.1 mg/dL vs. 92.7 +/- 16.7 mg/dL; P = 0.000; and 21.1 +/- 6.0 vs. 17.5 +/- 8.6 UI/mL; P = 0.03) and low-density lipoproteins (143.9 +/- 21.3 mg/dL vs. 118.2 +/- 47.7 mg/dL; P = 0.014). In contrast, serum creatinine and urea (1.02 +/- 0.13 mg/dL vs. 1.5 +/- 1.5 mg/dL; P = 0.024; and 33.9 +/- 9.3 mg/dL vs. 48.7 +/- 46.1 mg/dL; P = 0.039) and creatinine clearance <50 mL/min (10% vs. 37%; P = 0.06) were higher in patients without IHD. CONCLUSIONS: In this work, metabolic syndrome was very common among patients with gout. Sixteen percent of the patients, although previously asymptomatic, had IHD, they all had metabolic syndrome. Gouty patients frequently first seek medical care from a rheumatologist. The rheumatologist can have an important role in detecting metabolic syndrome and risk factors for cardiovascular disease.

Journal Article↗
PubMed2004

Efficacy and safety profile of treatment with etoricoxib 120 mg once daily compared with indomethacin 50 mg three times daily in acute gout: a randomized controlled trial.

OBJECTIVE: To evaluate the efficacy and safety of etoricoxib and indomethacin in the treatment of patients with acute gout. METHODS: A randomized, double-blind, active-comparator study was conducted at 42 sites. A total of 189 men and women (> or =18 years of age) who were experiencing an acute attack (< or =48 hours) of clinically diagnosed gout were treated for 8 days with etoricoxib, 120 mg/day (n = 103), or indomethacin, 50 mg 3 times a day (n = 86). The primary efficacy end point was the patient's assessment of pain in the study joint (0-4-point Likert scale) over days 2-5. Safety was assessed by adverse experiences (AEs) occurring during the trial. RESULTS: Etoricoxib demonstrated clinical efficacy comparable to that of indomethacin in terms of the patient's assessment of pain in the study joint. The difference in the mean change from baseline over days 2-5 was -0.08 (95% confidence interval -0.29, 0.13) (P = 0.46), which fell within the prespecified comparability bounds of -0.5 to 0.5. Secondary end points over the 8-day study, including the onset of efficacy, reduction in signs of inflammation, and patient's and investigator's global assessments of response to therapy, confirmed the comparable efficacy of the two treatments. The etoricoxib-treated patients had a numerically lower incidence of AEs (43.7%) than did the indomethacin-treated patients (57.0%) and a significantly lower incidence of drug-related AEs (16.5% versus 37.2%; P < 0.05). CONCLUSION: Etoricoxib at a dosage of 120 mg once daily was confirmed to be an effective treatment for acute gout. Etoricoxib was comparable in efficacy to indomethacin at a dosage of 50 mg 3 times daily, and it was generally safe and well tolerated.

Administration, Oral↗
PubMed1998

Decreased serum concentrations of 1,25(OH)2-vitamin D3 in patients with gout.

We measured the serum concentrations of 1,25(OH)2-vitamin D3, 25(OH)-vitamin D3, parathyroid hormone (PTH) in 82 male patients with primary gout whose serum uric acid was significantly higher than that of 41 normal control male subjects (8.8 +/- 0.2 vs 5.6 +/- 0.2 mg/dL, p < 0.001). The serum 1,25(OH)2-vitamin D3 concentration was significantly lower in the patients with gout compared with the control subjects (39.6 +/- 1.4 vs 44.8 +/- 1.7 pg/mL, p < 0.05), while no differences were observed between the two groups in either the serum concentration of 25(OH)-vitamin D3 or PTH. The administration of uric acid lowering agent to the patients for 1 year caused a significant increase in their serum 1,25(OH)2-vitamin D3 concentration which was associated with a significant decrease in their serum uric acid concentration. In contrast, the serum concentrations of 25(OH)-vitamin D3 and PTH were not affected by these drugs. These results suggest that uric acid per se may directly decrease the serum concentration of 1,25(OH)2-vitamin D3 in patients with gout by inhibiting 1-hydroxylase activity.

Allopurinol↗
PubMed1987

Withdrawal of longterm antihyperuricemic therapy in tophaceous gout.

After longterm treatment (mean duration 7.2 years) with antihyperuricemic drugs, ten tophaceous gouty patients requested withdrawal of the medication because they had not felt any arthritic pains for years, the tophi had disappeared, and they disliked the idea of taking the medicine daily for the rest of their lives. Five patients (Group I) had no recurrence of either arthritis or tophi during follow-up for 18 to 52 months (average duration 33 months). Five patients (Group II) had a recurrence of arthritis 5 to 29 months (average 15.8 months) after cessation of therapy and two of them developed tophi again at 29 months and resumed treatment. Group II patients tended toward obesity, more severe hyperuricemia and an earlier age onset of gout, as compared with Group I patients. The creatinine concentration determined before, during, and after treatment showed no change. On the basis of the present findings it seems justified to withdraw medication in cases of tophaceous gout in remission when aggravating factors such as obesity and severe hyperuricemia are absent. Attacks of gout and tophi are likely to recur, but so far in our series the duration of the symptom-free period without medication is almost three years for Group I patients, who are now considered as "asymptomatic hyperuricemics".

Adult↗
PubMed2004

[Gout].

In most cases gout is the clinical manifestation of familial hyperuricemia. Pathogenesis of hyperuricemia, clinical manifestations, diagnosis and differential diagnosis of hyperuricemia and gout are described. Treatment of hyperuricemia consists of dietary measurements and administration of uric acid lowering drugs, such as allopurinol or uricosuric agents. Nonsteroidal antiinflammatory drugs, colchicine and glucocorticosteroids are the treatment of choice for the acute gout attack. Prophylaxis of acute uric acid nephropathy consists of hydration, urine alkalinization and administration of allopurinol or rasburicase. For treatment of acute uric acid nephropathy rasburicase is the drug of choice.

Allopurinol↗
PubMed2006

Excellent response to the clinical treatment of tophaceous gout.

Gout continues to be a health problem around the world, and the treatment may turn into a real challenge when the patient presents a certain degree of chronic renal failure (CRF). We discuss a case of tophaceous gout in a 68-year-old male patient without urolithiasis and with uric acid (UA) underexcretion and CRF (creatinine clearance of 42 ml/min). Uricosuric treatment with benzbromarone and urinary alkalinization was administered, and acute gouty attacks improved substantially. Subsequently, allopurinol was added to the treatment to accelerate tophi reduction in the hands, feet, elbows and knees. After 30 months of treatment, serum UA declined from 10 to 3.2 mg/dl. Urinary UA excretion of 0.44 g/24 h in the baseline rose to 0.85 g/24 h, returning to the baseline value after 30 months. UA clearance tripled, rising from 3.05 ml/min before treatment to 9.48 ml/min, and remained at this level. It is worth stressing that even in cases of severe tophaceous gout, the response to clinical treatment may be satisfactory with substantial reduction of tophi and full acute gouty attack remission even in patients presenting a certain degree of CRF.

Aged↗
PubMed1986

Chronic polyarticular gout in the elderly: a report of six cases.

This report describes six elderly patients with previously undiagnosed and untreated chronic polyarticular gout, five of whom were seen at a Geriatric Rehabilitation and Assessment Unit within a 3-month period. All were on long-term diuretic therapy. Four patients had coexisting osteoarthritis. Three patients were unable to recall any prior history of attacks of acute arthritis and four patients were significantly disabled from gout. Chronic polyarticular gout in these patients was previously misdiagnosed and inadequately treated, resulting in otherwise preventable disability.

Aged↗
PubMed1998

Efficacy of allopurinol and benzbromarone for the control of hyperuricaemia. A pathogenic approach to the treatment of primary chronic gout.

OBJECTIVES: To study the efficacy of allopurinol and benzbromarone to reduce serum urate concentrations in patients with primary chronic gout. METHODS: Prospective, parallel, open study of 86 consecutive male patients with primary chronic gout. Forty nine patients (26 normal excretors and 23 under excretors) were given allopurinol 300 mg/day and 37 under excretors benzbromarone 100 mg/day. After achieving steady plasma urate concentrations with such doses, treatment was then adjusted to obtain optimal plasmatic urate concentrations (under 6 mg/dl). RESULTS: Patients receiving allopurinol 300 mg/day showed a mean reduction of plasmatic urate of 2.75 mg/dl (from 8.60 to 5.85 mg/dl) and 3.34 mg/dl (from 9.10 to 5.76 mg/dl) in normal excretors and under excretors respectively. Patients receiving benzbromarone 100 mg/day achieved a reduction of plasmatic urate of 5.04 mg/dl (from 8.58 to 3.54 mg/dl). Fifty three per cent of patients receiving allopurinol and 100% receiving benzbromarone achieved optimal plasma urate concentrations at such doses. The patients with poor results with allopurinol 300 mg/day achieved a proper plasma urate concentration with allopurinol 450 to 600 mg/day, the mean final dose being 372 mg/day. Renal function improved and no case of renal lithiasis was observed among benzbromarone treated patients, whose mean final dose was 76 mg/day. CONCLUSION: Benzbromarone is very effective to control plasma urate concentrations at doses ranging from 50 to 100 mg/day. Uricosuric treatment is a suitable approach to the treatment of patients with gout who show underexcretion of urate.

Adult↗
PubMed2001

Relation between adverse events associated with allopurinol and renal function in patients with gout.

BACKGROUND: Because serious adverse reactions to allopurinol have been related to a reduce creatinine clearance rate and prolonged half life of oxypurinol, it has been recommended that the dose should be adjusted according to the rate of creatinine clearance. However, in some patients with gout the dose is not sufficient to reduce serum levels of uric acid (< or =390 micromol/l) and to halt disease progression. OBJECTIVE: To determine the prevalence of adverse reactions attributable to allopurinol in patients with primary gout according to dose and creatinine clearance rate. METHODS: Data on 120 patients with gout receiving allopurinol, in whom the starting dose was adjusted according to creatinine clearance rate and later increased in some patients to control the disease, were retrospectively reviewed. Two groups were compared: group A, 52 patients receiving creatinine clearance adjusted maintenance doses of allopurinol and group B, 68 patients receiving non-adjusted higher maintenance doses of allopurinol. RESULTS: During follow up 57% required higher allopurinol doses than those recommended according to their creatinine clearance rate. Only five (4%) of 120 consecutive patients developed allopurinol related adverse reactions: four minor skin reactions and one allopurinol hypersensitivity syndrome (AHS). Three of these (including the case of AHS) occurred in group A and two in group B (p=NS). The duration of allopurinol treatment was the same in both groups (group A: 2.3 (3.3) years; group B: 3.7 (4.8) years). No patient in group A, but 44% in group B had a creatinine clearance rate of <50 ml/min. None of the patients received concomitant diuretics, ampicillin, or azathioprine. CONCLUSIONS: No increase was seen in the prevalence of adverse reactions to allopurinol in patients who received higher allopurinol maintenance doses than those recommended according to creatinine clearance rate.

Adult↗
PubMed1979

Piroxicam in the treatment of acute gout: a multicentre open study in general practice.

Twenty-nine patients with acute gout were treated with piroxicam (40 mg daily for 5 days) in a multicentre general practitioner study. Pain relief was noticeable within 4 hours of the first dose and thereafter proceeded steadily, together with the early relief of other symptoms associated with acute gout. The prompt relief of symptoms was accompanied by a fall in serum uric acid. Piroxicam was well tolerated, eight experiencing side-effects that were mainly mild and gastro-intestinal in nature. The drug seems to be highly effective and safe in the treatment of acute gout.

Acute Disease↗
PubMed1999

Gout: beyond the stereotype.

Not all gout presents with involvement of the big toe, and not all gout patients are middle-aged men. Chronic gout may mimic rheumatoid arthritis; hyperuricemia may develop in postmenopausal women and in organ transplant recipients who are being treated with immunosuppressive agents. Both classic and nonclassic cases may benefit from new therapeutic agents.

Aged↗
PubMed2004

Compliance with allopurinol therapy among managed care enrollees with gout: a retrospective analysis of administrative claims.

OBJECTIVE: Poor compliance with gout medications has been recognized, but seldom studied. We investigated compliance with allopurinol among managed care enrollees suspected to have gout. METHODS: This was a retrospective, administrative claims-based analysis of patients with gout. Compliance with allopurinol was measured using prescription-fill dates and days-supplied amounts. Compliance was defined for each prescription period as the presumed use of allopurinol on at least 80% of the days of that period. RESULTS: Of 9482 patients identified, 65.9% filled at least one prescription for allopurinol during the 24 month followup period; 10.4% of allopurinol users filled one prescription and then discontinued use. Of the remaining patients, 13.7% never achieved compliance with therapy; 18% were compliant throughout the entire followup period. Patients were compliant with therapy for an average of 56% of their treatment periods and noncompliant for an average of 44%. In multivariate analysis, male sex was associated with decreased compliance (p < 0.01), although the effect was mitigated by increasing age. For subjects of both sexes, increasing age was associated with increased compliance (p < 0.05). CONCLUSION: Compliance with allopurinol in this population was low. Because untreated gouty arthritis can lead to serious adverse outcomes (such as recurrent gouty arthritis, chronic gouty arthropathy, tophi, and urolithiasis) that are usually avoidable with antihyperuricemic therapy, efforts to achieve better compliance are warranted.

Adolescent↗
PubMed2004

Crystal arthritis. Gout and pseudogout in the geriatric patient.

Gout and pseudogout are inflammatory arthritides due to monosodium urate and calcium pyrophosphate dihydrate crystal formation. Both are prevalent among geriatric patients, and can present as acute mono- or oligoarticular disease, or as a chronic polyarthropathy resembling osteoarthritis or rheumatoid arthritis. Gout in the geriatric patient is a disease affecting women, commonly associated with diuretic usage, often involves the fingers, may be complicated by the development of masses of uric acid crystals (tophi) in soft tissues, and is frequently polyarticular. Pseudogout in the geriatric patient has a variety of clinical presentations, may be acute or chronic, and should be considered in evaluating any patient with osteoarthritis occurring in an atypical distribution. Treatment includes the use of nonsteroidal anti-inflammatory drugs, colchicine, or corticosteroids. Gout may be impacted by dietary factors, weight reduction, and avoidance of certain forms of alcohol; uric acid-lowering agents are effective for refractory or chronic tophaceous disease.

Adrenal Cortex Hormones↗
PubMed2005

Epidemiology of hyperuricemia and gout.

Gout is an increasingly common medical problem. The traditional risk factors of male sex and high red meat or alcohol consumption have been joined by a wave of newer risk factors, such as increased longevity, the metabolic syndrome (hypertension, diabetes, dyslipidemia, truncal obesity, increased cardiovascular disease risk), use of diuretics, low-dose aspirin, or cyclosporine, and end-stage renal disease. Atypical presentations of gout in the elderly can mimic osteoarthritis and rheumatoid arthritis. There is a resurgence of interest in hyperuricemia as an independent and potentially modifiable cardiovascular risk factor. The pharmacologic management of gout in general practice suffers from a number of quality-control issues. This article reviews these and other new epidemiologic data on this ancient disease.

Adult↗