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Query: UMLS:C0018099 (gout)
 5,192 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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PMID:Excellent response to the clinical treatment of tophaceous gout. 1704 91

The aim of this study was to investigate the clinical characteristics of patients with coexisting ankylosing spondylitis (AS) and gout. Between July 1987, and October 2004, sixty-five patients with coexisting AS and gout were enrolled. The clinical manifestations of both AS and gout in these patients were studied. Of the 65 patients included in the study, 61 were men and four were women (men-to-women ratio, 15.3:1). Sixty-three subjects were Han Chinese, and two were Atayal Aborigines. Mean ages at onset of AS and gout were 29.3 +/- 15.6 years (range 7-63) and 42.2 +/- 13.2 years (range 20-74), respectively. Fifty-six patients developed gout after (15.5 +/- 11.2 years; range, 1-51 years) onset of AS; nine patients developed gout before (average, 3.4 +/- 2.2 years; range. 1-7 years) onset of AS. Forty-four (67.7%) patients had chronic peripheral arthritis and all 65 (100%) patients had acute peripheral arthritis. Thirty-three (50.8%) cases had heel pain (enthesopathy), including 22 (33.9%) with chronic heel pain, seven (10.8%) with acute heel pain, and four (6.2%) with concurrent acute and chronic heel pain. Sixty-one (93.9%) subjects were HLA-B27 antigen positive. Medical conditions potentially associated with hyperuricemia or gout were urolithiasis (n = 17), hypertension (n = 21), diabetes mellitus (n = 8), hyperlipidemia (n = 34), congestive heart failure (n = 6), coronary heart disease (n = 5), and stroke (n = 3). The following drugs were prescribed: diuretics (n = 7), low-dose aspirin (n = 4), antituberculous drugs (n = 1), and sulphasalazine (n = 34). Six (6.2%) patients had iatrogenic Cushing syndrome with adrenal insufficiency. Patients with coexisting AS and gout are not rare. Distinguishing between peripheral arthritis or enthesopathies of AS and gout is essential, especially when the course of AS arthritis becomes acute or the course of gout becomes chronic.
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PMID:Coexisting ankylosing spondylitis and gouty arthritis. 1735 31

Uric acid urolithiasis develops from various causes. To investigate the clinical and biochemical presentation of patients with uric acid urolithiasis, a retrospective study was designed. A total of 46 cases were enrolled between January 2004 and December 2005. The compositions of the stones were analyzed by infrared spectrophotometry. There were 39 males (84.8%) and seven females (15.2%), with a mean age of 61.5 +/- 10.6 years and mean body mass index (BMI) of 26.7 +/- 3.1 kg/m2. The stone location was kidney in 10 (21.7%), ureter in 22 (41.8%), and bladder in 14 (30.5%). Multiple stones were diagnosed in 36 patients (78.3%). Pre-existing comorbidities included diabetes mellitus in 11 patients (23.9%), hypertension in 23 (50%), gout in 13 (28.2%), and benign prostatic hyperplasia in 14 (30.4%). Mean serum creatinine and uric acid was 1.6 +/- 0.6 mg/dL and 7.6 +/- 1.8 mg/dL, respectively. There were 27 patients (58%) with creatinine > 1.4 mg/dL. The mean urinary pH was 5.42 +/- 0.46. Patients with uric acid urolithiasis were predominantly male, older, with higher BMI, multiple stone presentation, with lower urinary pH, and hyperuricemia. Exacerbation of the renal function should also be of concern because of the high proportion of patients with renal insufficiency diagnosed in this study.
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PMID:Clinical study of uric acid urolithiasis. 1752 14

Uric acid is the end-product of purine catabolism. Hyperuricaemia is implicated in disorders such as gout and urolithiasis and recent epidemiological evidence suggests an association between increasing uric acid levels and increased cardiovascular morbidity and mortality. A direct causal role remains to be established but recent studies of losartan, atorvastatin and fenofibrate suggest that uric acid reduction contributes to attenuation of cardiovascular risk. Furthermore, several small studies of xanthine oxidase inhibition (the most common method of uric acid reduction) have shown improvements in measures of cardiovascular and endothelial function of a similar magnitude to those of other proven preventative strategies. This review introduces the epidemiological data, discusses strategies to lower uric acid and outlines the available clinical trial data supporting uric acid reduction as a potential and novel method of reducing the burden of cardiovascular disease.
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PMID:Uric acid reduction: a new paradigm in the management of cardiovascular risk? 1762 23

Hypoxanthine-guanine phosphoribosyltransferase (HPRT) deficiency is a genetic disease of purine metabolism resulting in uric acid overproduction. Allopurinol, which inhibits the enzyme xanthine oxidase and reduces uric acid synthesis, is widely used for the treatment of gout and uric acid overproduction. The aim of the study was to analyze the long-term efficacy and safety of allopurinol in patients with HPRT deficiency. Nineteen patients (13 with Lesch-Nyhan syndrome and 6 with partial HPRT deficiency) were treated with allopurinol (mean dose, 6.4 mg/kg body weight per day; range, 3.7-9.7 mg/kg body weight per day) and followed up for at least 12 months (mean follow-up, 7.6 years). The efficacy of allopurinol was evaluated by serial measurement of purine metabolic parameters and renal function as well as by clinical manifestations. Safety was assessed by recording adverse events. Treatment with allopurinol normalized serum urate level in all patients and resulted in a mean reduction in serum urate of 47%. Allopurinol treatment was associated with a mean 74% reduction in urinary uric acid-to-creatinine ratio. In contrast, allopurinol treatment increased mean hypoxanthine and xanthine urinary excretion rates 5.4- and 9.5-fold, respectively, compared with baseline levels. The decrease in uric acid excretion in complete and partial HPRT-deficient patients was not accompanied by a stoichiometric substitution of hypoxanthine and xanthine excretion rates. Allopurinol-related biochemical changes were similar in patients with either complete or partial HPRT deficiency. Renal function remained stable or improved with treatment. Three patients had urolithiasis during allopurinol treatment. In 2 patients, xanthine stones were documented and they required allopurinol dose adjustments aimed at reducing excessive oxypurine excretion rates. No allopurinol hypersensitivity reactions occurred. Neurologic manifestations were not influenced by allopurinol therapy. In conclusion, allopurinol is efficacious and generally safe for the treatment of uric acid overproduction in patients with HPRT deficiencies. Xanthine lithiasis, developing as a consequence of allopurinol therapy, should be preventable by adjustment of allopurinol dose.
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PMID:Efficacy and safety of allopurinol in patients with hypoxanthine-guanine phosphoribosyltransferase deficiency. 1769 59

The introduction of extracorporeal shockwave lithotripsy (ESWL), with its noninvasive removal of stones and considerable reduction in the morbidity of stone disease, has revolutionized the therapy of urolithiasis. Unfortunately the propensity for stone recurrence is not altered by removal of stones with ESWL and stone recurrence is still about 50%. Progress in medical treatment has shown how different therapies can prevent the stone recurrence, even though it is often difficult to predict which patient will go on to become a recurrent stone former. With the right evaluation, however, the cause of calculi formation can be treated in 97% of the patients. Primary prevention of urolithiasis includes general prophylaxis in a no-risk population that has never been affected by urinary tract stones, is without familial predisposition, metabolic or genetic alterations, or urinary tract abnormalities or infections and who live in a geographical area that is at risk. Secondary prevention or metaphylaxis of stone disease is aimed at the population at risk, that is patients already affected by the stone disease, with familial predisposition, with urinary tract alterations, with metabolic or genetic alterations (gout, bone or bowel diseases) and urinary infection.
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PMID:Metaphylaxis of nephrolithiasis. 1772 53

We examined the incidence of renal function deterioration (RFD) in a population of male gout patients and to identify associated risk factors. Subjects who had been regularly followed up for more than 2 years and had visited Chang Gung Memorial Hospital-Kaohsiung Medical Center Rheumatology Clinic between June 1, 2006 and January 31, 2007 were enrolled. Four subjects were excluded as secondary gout was suspected. Group I (Gr I) comprised subjects without RFD and group II (Gr II) comprised subjects with RFD during the follow-up period. RFD was defined as absolute increment in creatinine (Cr) levels over 0.4 mg/dl for subjects with baseline Cr levels <or=1.4 mg/dl or as more than 50% increment of baseline Cr level per 12-month interval in average for subjects with baseline Cr levels >1.4 mg/dl. Clinical parameters were analyzed to study the potential risk factors of RFD. Of 318 male gout patients, 296 (93.1%) were categorized as Gr I, and 22 (6.9%) were categorized as Gr II. The observation periods for Gr I and Gr II were 81.20+/-53.29 and 92.41+/-46.72 months, respectively (p=0.338). Initial Cr levels are similar between the two groups (1.25+/-0.51 vs 1.25+/-0.61, p=0.963). Multiple logistic regression analysis revealed that current age, age at disease onset, disease duration, treatment duration, body weight, height, family history of gout, tophi, urolithiasis, tobacco use, alcohol consumption, history of cerebral vascular accident, hypertension, diabetes mellitus, dyslipidemia, base-line and final Cr, blood urea nitrogen level, serum uric acid level, and body-mass index were not independent risk factors. However, history of ischemic heart disease [IHD; odds ratio (OR) 7.68, 95% confidence interval (CI) 1.99-29.70] and greater waist circumference (WC; OR 1.06, 95% CI 1.01-1.11) were two independent risk factors of RFD. Additionally, the Cox multivariable analysis disclosed that IHD (p<0.001) and greater WC (p=0.011) deteriorated kidney function in these patients. The incidence of RFD in male gout patients is 6.9%. History of IHD and greater WC are two independent risk factors for developing RFD.
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PMID:Ischemia heart disease and greater waist circumference are risk factors of renal function deterioration in male gout patients. 1803 May 16

Urolithiasis is a clinically important complication of gout. For effective prevention of this complication, it is necessary to comprehend the factors known to be important in its development. Our analysis of stones in gout patients revealed that the incidence of common calcium salt stones was over 60%, while that of uric acid stones was only about 30%. This implies that the disruption of uric acid metabolism promotes not only uric acid stones but also calcium salt stones. Twenty-four per cent of gout patients showed acidic urine throughout the day. Urinary management, which consists of hydration and alkalization of urine, is indispensable along with control of the serum urate level in the treatment of gout.
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PMID:[Urolithiasis and nephropathy complicated with gout]. 1840 21

Urate lowering treatment is indicated in patients with recurrent acute attacks, tophi, gouty arthropathy, radiographic changes of gout, multiple joint involvement, or associated uric acid nephrolithiasis. Uricosuric agents like benzbromarone and probenecid are very useful to treat hyperuricemia as well as allopurinol (xanthine oxidase inhibitor). Uricosuric agents act the urate lowering effect through blocking the URAT1, an urate transporter, in brush border of renal proximal tubular cells. In order to avoid the nephrotoxicity and urolithiasis due to increasing of urinary urate excretion by using uricosuric agents, the proper urinary tract management (enough urine volume and correction of aciduria) should be performed.
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PMID:[Uricosuric agent]. 1840 25

Two cases are reported in which it is suggested that water deprivation in laying hens resulted in urolithiasis as well as acute renal disease. With either condition birds appeared to have died terminally from renal failure with lesions of visceral gout.
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PMID:Water deprivation as a cause of renal disease in chickens. 1877 Feb 28


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