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PubMed2001

Gout: can management be improved?

Ongoing reviews of Cochrane collaboration show that there is still very little reliable information based on randomized controlled trials on which to base treatment decisions in acute and chronic gout. Recent studies have stressed that avoidance of factors contributing to development of gouty attacks such as diuretic therapy, weight gain, and alcohol consumption may lead to a decrease in gouty arthritis. Attention to minidose aspirin and its effect on serum uric acid levels was addressed. A low carbohydrate, high protein and unsaturated fat diet was recommended for gouty patients since they all enhance insulin sensitivity and therefore may promote a reduction in serum uric acid levels. Treatment of gout in transplant recipients brings into focus some of the issues regarding management of gout, because gout is a common problem among transplant patients.

Acute Disease↗
PubMed2004

[Gout].

In the presence of a clinical acute monoarthritis, a differential diagnosis has to be made between septic arthritis, gout and diffuse chondrocalcinosis. Gout comes from a purine nucleotide metabolism disorder leading to serum urate level elevation. This hyperuricemia can lead to the deposition of monosodium urate crystals in the joints, causing acute attacks. After long-term evolution, others tissues as the kidneys can be involved: it is chronic gout. The definite diagnosis is based on the presence of monosodium urate crystals in the joint fluid. The diagnosis of gout should prompt a search for associated medical conditions that may affect both urate levels and longevity. These include alcoholism, various nephropathies, myeloproliferative disorders, and hypertension.

Arthritis, Infectious↗
PubMed1982

Hyperuricemia and gout.

Although chronic tophaceous gout has become increasingly uncommon, hyperuricemia and acute gout are still common clinical entities. Most patients with hyperuricemia are under-excreters, and many of these cases are drug induced. Since longstanding asymptomatic hyperuricemia does not appear to cause progressive renal insufficiency, and uric acid renal stones are uncommon in underexcreters, these patients generally require no treatment. The minority of patients who overproduce uric acid are at increased risk for urolithiasis, and therapy should be decided on an individual basis. Acute gout is best treated with colchicine or indomethacin. The newer non-steroidal anti-inflammatory drugs (ie, ibuprofen, sulindac) may prove to be equally effective and are associated with fewer gastrointestinal side effects. Prophylaxis should be undertaken in patients with recurrent gout or documented uric acid urolithiasis. Although uricosuric drugs appear to be less toxic than allopurinol, they should not be used in patients who overproduce uric acid or in patients who have a history of urolithiasis or renal insufficiency. The allopurinol hypersensitivity syndrome is being reported with increased frequency and may be fatal.

Allopurinol↗
PubMed1977

Secondary gout in hemoglobinopathies: report of two cases and review of the literature.

Although patients with hemolytic hemoglobinopathies characteristically are over-producers of urate, and hyperuricemia is frequently recognized, clinical gout has rarely been reported in such patients. Our evaluation of 2 premenopausal women with gout led to the diagnosis of previously unrecognized hemoglobinopathies (SC disease and CC disease). Investigation of these 2 patients and review of the reported cases of gout in patients with hemoglobin S or C disorders suggest that relatively minor abnormalities of renal function in these patients may lead to early development of significant hyperuricemia. With increasing lifespan of patients with hemolytic hemoglobinopathies and the likelihood of increased occurrence of renal function abnormalities, it is anticipated that gout will more frequently be responsible for joint symptoms in such patients.

Adolescent↗
PubMed1988

Comparison of parenteral adrenocorticotropic hormone with oral indomethacin in the treatment of acute gout.

One hundred male patients who presented with acute gouty arthritis were alternately assigned to 2 treatment groups. Seventy-six patients completed the study protocol, in which each gout attack during a 1-year period was treated. For each gout episode, 36 patients received a single intramuscular injection of 40 IU of adrenocorticotropic hormone (ACTH), and 40 patients received oral indomethacin, 50 mg 4 times daily with meals, until the pain abated. The time interval until the pain was relieved, as well as any untoward effects, were recorded for each gout attack treated. Both groups were of similar age, and had similar values for intercritical serum uric acid, 24-hour urinary uric acid, and creatinine clearance (1 month after entry into the study). The mean interval (+/- SD) to relief of pain was significantly shorter for the ACTH group (3 +/- 1 hours) than for the indomethacin group (24 +/- 10 hours). No side effects were noted in the ACTH group. However, of the 40 patients receiving indomethacin, 22 had abdominal discomfort of dyspepsia, 15 had headaches, and 12 had difficulty with mentation. Single-dose parenteral ACTH appeared to be effective more rapidly and was associated with fewer side effects than oral indomethacin in the treatment of acute gout.

Acute Disease↗
PubMed1980

The natural history of hyperuricemia among asymptomatic relatives of patients with gout.

1. Hyperuricemia is common among the gouty relatives as reported by others (8-11). It is of interest to note that serum urate fluctuates periodically. Hyperuricemia is not necessarily maintained in a steady state throughout the years. Thus a single determination of serum uric acid can be misleading. 2. Development of gout from asymptomatic hyperuricemia is often correlated with the degree of hyperuricemia as observed from population or family studies (12-14). The data presented indicate that unequivocal hyperuricemia is more often accompanied by excessive excretion of uric acid, diminished excretion of ammonia and abnormally high plasma glutamic acid. All are undoubtedly important risk factors for gout. 3. The elevated glutamate could be due to a deficiency of glutamic dehydrogenase, as postulated by Pagliara and Goodman (15). In presence of intracellular accumulation of glutamate in glutamic dehydrogenase deficiency, renal production of ammonium may be reduced due to its inhibitory action on glutaminase 1. As a result of a renal block of ammonia formation, the glutamine in surplus may be diverted for uric acid synthesis. 4. Long-term studies indicate serum urate in most hyperuricemia relatives of gout can be modified by environmental factors, such as diet, weight and changes of life style. When hyperuricemia is under better control, the potential hazard of developing symptomatic gout may be circumvented.

Amino Acids↗
PubMed1991

A biochemical investigation on chicken gout observed in the Marmara region in Turkey.

Poultry breeding has economical importance for the people living in Bursa and surrounding villages. Similar to some sporadic disease, gout can also be reason for production loses and death in laying and broiler chickens. Gout cases have been observed in some pens of a big poultry company. In this study 20 healthy control and 40 sick Studler Iso-Brown chickens were used as research materials. Blood were taken from heart by syringe to plastic tubes with EDTA. Plasma were collected and analyzed for total protein, uric acid, bicarbonate, vitamin A, calcium and orotic acid. The blood levels of healthy and sick groups were; total protein % 4.60-5.98 gr, uric acid % 10.19-38.09 mg, bicarbonate 27.37-35.73 mEq/l, vitamin A % 42.20-35.55 mcg, calcium % 8.38-8.25 mg and orotic acid % 1.42-1.97 mg, respectively. Statistical analysis was done by t test. There were statistical importance for total protein, bicarbonate (p less than 0.01) and for uric acid (p less than 0.001) differences. Feeding program analysis was done and a feeding disturbance was determined. Chicken in gout observed pens have fed with chicken developing feed for two weeks earlier. For this case diet was the reason of gout.

Animals↗
PubMed1988

A DNA polymorphism of an apoprotein gene associates with the hypertriglyceridaemia of primary gout.

Genomic hybridization analysis has been used to investigate allelic frequencies of the genes coding for the four major apoproteins of high density lipoprotein (HDL); apoproteins AI, AII, CII and CIII, in a group of Caucasian subjects with primary gout. An uncommon allelic variant of the apoprotein CIII gene (the S2 allele) was significantly more common among the patients with gout (9/48, 19%) than among normouricaemic controls who were either randomly selected (1/41, 2%, P = 0.03) or normotriglyceidaemic (0/33, 0%, P = 0.013). Approximately 46% (22/48) of the subjects with gout were hypertriglyceridaemic (with a serum triglyceride greater than 2.1 mmol/l). Of the 22 patients in this subgroup, 5 (23%) had the uncommon S1S2 genotype, which was also a significantly greater proportion than among the normotriglyceridaemic controls (P = 0.015). These data suggest that the hypertriglyceridaemia associated with primary gout may have a genetic basis. In contrast, we found no differences in the frequencies of restriction fragment length polymorphisms of the genes for apoproteins AI, AII and CII.

Apoproteins↗
PubMed1996

Unusual localisation of tophaceous gout. A report of four cases and review of the literature.

We report four cases with very unusual manifestations of tophaceous gout. All patients were male, aged between 29 and 67 years. Only one patient had an acute gouty arthritis in his medical history, whereas the other three had never developed clinical symptoms from their hyperuricemia. Two patients had gout tophi in the patella, while the others showed gout tophi in the space of bipartite bones, one in a bipartite patella and one in a tripartite sesamoid bone of the first toe. To our knowledge, gout tophi in the space of bi- or tripartite bones has never been described before.

Adult↗
PubMed1994

[Gout tophi and Heberden nodules in hyperuricemia].

The tophus is a characteristic and pathognomonic sign of chronic gout. Before effective drugs were available for the treatment of hyperuricaemia about 50-60% of patients with gout developed clinically and radiologically apparent urate crystal deposits. Clinical cutaneous manifestations of chronic gout are now rarely observed. However, the presence of degenerative tissues, as in idiopathic osteoarthritis of the fingers, may predispose to the deposition of urate crystals. We report on a patient with secondary--probably diuretic-induced--hyperuricaemia and gout tophiin Heberden's nodes.

Aged↗
PubMed2004

Determination of uric acid in human saliva by capillary electrophoresis with electrochemical detection: potential application in fast diagnosis of gout.

The clinical manifestations of gout result from the formation and deposition of uric acid (UA) crystals. The monitoring of UA level in less invasive biological samples such as saliva is suggested for diagnosis and therapy of gout, hyperuricemia and the Lesch-Nyhan syndrome. In order to investigate the correlation between trace amounts of UA in human saliva and urine and explore the potential application in fast diagnosis of gout, capillary electrophoresis with electrochemical detection (CE-ED) was applied for the determination of UA in human saliva and urine in this work. Under the optimum conditions, UA and three coexisting analytes could be well separated within 14 min at the separation voltage of 14 kV in 80 mmol L(-1) borax running buffer (pH 7.8). A good linear relationship was established between peak current and concentration of analytes over two orders of magnitude with detection limits (S/N = 3) ranging from 1.09 x 10(-7) to 5.0 x 10(-7) mol L(-1) for all analytes. This proposed method has been successfully applied for study of the correlation between the UA content of human saliva and urine, providing an alternative and convenient method for rapid diagnosis of gout.

Electrochemistry↗
PubMed2001

Gout: radiographic findings mimicking infection.

OBJECTIVE: To describe radiographic features of gout that may mimic infection. DESIGN AND PATIENTS: We report five patients with acute bacterial gout who presented with clinical as well as radiological findings mimicking acute bacterial septic arthritis or osteomyelitis. Three patients had delay in the appropriate treatment with the final diagnosis being established after needle aspiration and identification of urate crystals under polarized light microscopy. Two patients underwent digit amputation for not responding to antibiotic treatment and had histological findings confirming the diagnosis of gout. CONCLUSION: It is important for the radiologist to be aware of the radiological manifestations of acute gout that can resemble infection in order to avoid inappropriate diagnosis and delay in adequate treatment. The definitive diagnosis should rely on needle aspiration and a specific search for urate crystals.

Acute Disease↗
PubMed2004

Spontaneous rupture of extensor pollicis longus tendon with tophaceous gout infiltration.

INTRODUCTION: Spontaneous rupture of the extensor pollicis longus (EPL) tendon has been reported in the literature. Various mechanisms have been proposed to account for this problem, but gouty infiltration is a rare mechanism. Here we report a patient with a long-standing history of gout who presented with sudden loss of interphalangeal extension of the left thumb. Spontaneous rupture of the EPL tendon caused by gout was discovered. MATERIALS AND METHODS: The successful treatment done involved surgical exploration and extensor indicis proprius tendon transfer. Postoperative thumb spica immobilization for 6 weeks was applied. RESULTS: Pathology disclosed urate crystals deposited within the ruptured EPL tendon. The functional recovery is satisfactory at the 1-year follow-up. CONCLUSION: Spontaneous rupture of the EPL tendon caused by gout is rare. Successful treatment was done with surgical management. Life-long medical follow-up to prevent a repeated acute attack can lower the risk of a large amount of tophaceous gout infiltration in tendons and may possibly prevent acute spontaneous tendon rupture.

Aged↗
PubMed2000

Continuous recruitment, co-expression of tumour necrosis factor-alpha and matrix metalloproteinases, and apoptosis of macrophages in gout tophi.

Gout tophi are characterised by foreign body granulomas consisting of mono- and multinucleated macrophages surrounding deposits of monosodium urate microcrystals. After primary formation, granulomas grow associated with degradation of the extracellular matrix. Based on this background, we have sought (1) to investigate whether during granuloma's growth new macrophages are recruited into the tophi, (2) to find in situ evidence for macrophages' active role in matrix degradation and (3) to examine whether shrunk cells seen within gout tophi are apoptotic. Immunohistochemistry showed that perivascular localised mononuclear cells are CD68+, S100A8+, S100A9+, 25F9-, representing freshly migrated monocytes/macrophages. In contrast, almost all CD68+ mono- and multinucleated cells arranged within granulomas were S100A8-, S100A9-, 25F9+, representing mature (non-migrating) macrophages. Serial sections revealed that macrophages co-express tumour necrosis factor (TNF)-alpha and matrix metalloproteinases (MMPs) 2 and 9. In situ end-labelling of fragmented DNA demonstrated that CD68+ macrophages undergo apoptosis within gout tophi. Our data show that macrophages are continuously recruited into the gout tophi. These macrophages co-produce the proinflammatory cytokine TNF-alpha and two TNF-alpha inducible lytic enzymes, MMP-2 and MMP-9, suggesting that TNF-alpha may induce MMP production followed by matrix degradation within foreign body granulomas. In parallel, macrophages undergo apoptosis, a phenomenon that may restrict the destructive potential of inflammatory macrophages.

Apoptosis↗
PubMed2003

Hyperuricemia and gout.

Gout is not a new disease for clinicians; nevertheless, there are still many secrets awaiting discovery for improving knowledge with respect to uric acid metabolism and monosodium urate crystal-induced inflammation. This review of the literature will focus on new insights on the pathogenesis of idiopathic hyperuricemia, and on secondary hyperuricemia and gout. There are also important advances on the pathophysiology of acute gout, especially as a self-limited process (switch from monocyte to macrophage, peroxisome proliferator activated receptor-gamma, and nitric oxide), but also of chronic gouty arthropathy. Armaments for treating hyperuricemia and gout may be already improved by losartan or fenofibrate and, in the future, by urate oxydase-polyethylene glycol 20 and renal handling regulatory molecules. Finally, control of hyperuricemia may also be considered in the prevention and treatment of cardiovascular disease.

Gout↗
PubMed1982

Phosphoribosyl pyrophosphate synthetase and glutathione reductase in erythrocytes from hyperuricaemic and gout patients.

The enzymic activities of erythrocyte phosphoribosyl pyrophosphate synthetase (EC 2.7.6.1) and glutathione reductase (EC 1.6.4.2) have been measured in 54 primary gout patients, 35 individuals having hyperuricaemia and 51 healthy controls. Statistical analyses have shown a significant increase (p less than 0.01) in the enzymic activity of erythrocyte PRPP synthetase in both the hyperuricaemic and gout groups compared with the controls. No correlation between activity and age was found in any of the three clinical groups. A significant decrease (p congruent to 0.01) was found in the enzymic activity of red cell glutathione reductase in the gout group compared with the other two groups. The biochemical significance of the changes in enzymic activities of the two enzymes in primary gout is discussed.

Erythrocytes↗
PubMed1986

Renal handling of uric acid in gout: impaired tubular transport of urate not dependent on serum urate levels.

Metabolic studies were conducted in 56 patients with primary gout and in ten normal subjects to assess differences in the tubular transport mechanisms of urate. Renal handling of uric acid was examined by means of pyrazinamide and probenecid tests at increased and pharmacologically reduced serum urate concentrations in both groups. Patients with gout showed similar serum urate levels and glomerular filtration rates than controls at both serum urate levels. Pyrazinamide decreased urinary uric acid excretion to less than 1.0% of the urate filtered load in both groups at increased and diminished serum urate concentrations. The maximum uricosuric response promoted by probenecid at high serum urate levels was (mean +/- SD) 3,707 +/- 443 micrograms/min/1.73 m2 in controls and 2,215 +/- 738 micrograms/min/1.73 m2 in patients with gout (P less than 0.01). Forty-four patients had a daily uric acid excretion rate below 700 mg/1.73 m2, and all of them showed a diminished uricosuric response to probenecid. When serum urate was reduced in normal subjects and 30 patients to a mean of 2.1 and 2.3 mg/dL, respectively, probenecid elicited a significantly lower urate excretion rate in gout (532 +/- 202 micrograms/min/1.73 m2) than in controls (922 +/- 136 micrograms/min/1.73 m2; P less than 0.01). Among these 30 patients examined in their basal state and at decreased serum urate levels, uric acid excretion following probenecid was normal in six and diminished in 24 in both situations. The difference between maximum uricosuria and basal urate excretion was not increased in gouty patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1983

Gout and hyperuricemia associated with sickle-cell anemia.

Since the initial description, in 1958, of gouty arthritis occurring in association with SCA, more than 12 cases have been reported. The high proportion of women and the relatively young ages are noteworthy. Since 1968, studies of patients with SCA have shown a high prevalence of hyperuricemia, beginning during childhood. The initial event in the development of hyperuricemia presumably is increased synthesis of nucleic acids occurring as part of the erythropoietic response to hemolysis. Catabolism of the nucleic acids generates urate. Increased production of UA normally is compensated for by increased urinary excretion of UA. This response occurs in patients with SCA, but during the third decade of life hyperuricosuria can be reduced, probably by damage to the renal tubules caused by infarction and hypoxia resulting from sickling. Impairment of the compensatory renal response leads to more severe and sustained hyperuricemia, and gouty arthritis may then develop. A number of questions about hyperuricemia and gout in SCA remain unanswered. The prevalence of gout among patients with SCA, both in general and in relation to age and sex, has not been determined. The relationships between specific aspects of SCA and of hyperuricemia and gout need to be determined. These include any effect of sickle cell crises on SUA and attacks of gout, and correlation of abnormalities in renal handling of urate with other indices of tubular function and with the pathologic anatomy of the kidney. Finally, it is important to learn whether hyperuricemia and hyperuricosuria contribute to the renal manifestations of SCA; if so, allopurinol might be useful in the prevention and treatment of the renal disease.

Adolescent↗