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PubMed1998

Analysis of abnormalities in purine metabolism leading to gout and to neurological dysfunctions in man.

A modelling approach is used to analyse diseases associated with purine metabolism in man. The specific focus is on deficiencies in two enzymes, hypoxanthine:guanine phosphoribosyltransferase and adenylosuccinate lyase. These deficiencies can lead to a number of symptoms, including neurological dysfunctions and mental retardation. Although the biochemical mechanisms of dysfunctions associated with adenylosuccinate lyase deficiency are not completely understood, there is at least general agreement in the literature about possible causes. Simulations with our model confirm that accumulation of the two substrates of the enzyme can lead to significant biochemical imbalance. In hypoxanthine:guanine phosphoribosyltransferase deficiency the biochemical mechanisms associated with neurological dysfunctions are less clear. Model analyses support some old hypotheses but also suggest new indicators for possible causes of neurological dysfunctions associated with this deficiency. Hypoxanthine:guanine phosphoribosyltransferase deficiency is known to cause hyperuricaemia and gout. We compare the relative importance of this deficiency with other known causes of gout in humans. The analysis suggests that defects in the excretion of uric acid are more consequential than defects in uric acid synthesis such as hypoxanthine:guanine phosphoribosyltransferase deficiency.

AMP Deaminase↗
PubMed2000

Gout and other crystal-associated arthropathies.

Intra-articular crystals (monosodium urate monohydrate, calcium pyrophosphate dihydrate, basic calcium phosphates) can cause acute and chronic inflammation and joint damage. Identification of the crystals by polarized microscopy is the key step in diagnosis but improved reliability of synovial examination is required. Treatment of disorders associated with gout or calcium pyrophosphate deposition may reduce non-joint morbidity and assist treatment of the arthritis. Various forms of anti-inflammatory therapy work for acute crystal-induced arthritis; prompt commencement is usually more important than which option is used. In gout, recurrent attacks are usual, but hypouricaemic therapy is almost never urgent, is life-long, and is too often negated by poor compliance. In most patients, allopurinol or any of the potent uricosuric drugs will allow maintenance of normouricaemia but renal failure, renal calculi, transplantation, and allopurinol allergy narrow the options and complicate management.

Calcium↗
PubMed2006

Genetic factors associated with gout and hyperuricemia.

Hyperuricemia and gout are common conditions that have long been known to have a heritable component. Obesity, diabetes, and chronic kidney failure are conditions with multifactorial inheritance that are associated with gout. In addition, social factors such as protein and alcohol intake affect serum uric acid levels. The current review discusses basic uric acid metabolism and the multigenetic inheritance of hyperuricemia. Several monogenic disorders affecting uric acid metabolism are reviewed. The genetics, pathophysiology, diagnosis, and treatment of familial juvenile hyperuricemic nephropathy/medullary cystic kidney disease, autosomal dominant disorders associated with hyperuricemia and progressive kidney failure, are described.

Blood Group Antigens↗
PubMed1999

Case report. Initial manifestation of gout after carpal tunnel release.

A carpal tunnel release was performed on a patient with recurrent carpal tunnel syndrome and asymptomatic hyperuricaemia with no prior history of gouty arthritis. Intraoperatively, the patient was found to have tenosynovitis without crystals or tophaceous deposits in the carpal tunnel. Postoperatively, the patient developed an acutely inflamed hand, which responded dramatically to anti-gout medications. We report this patient as an initial attack of gout after a carpal tunnel release.

Acute Disease↗
PubMed1999

Kienböck's disease and gout.

A relationship between gout and Kienbock's disease has been proposed on the basis of a previously published case report. A review of patients at our institution identified a single case with the combination of both Kienbock's disease and gout. We believe that the association is coincidental.

Arthroscopy↗
PubMed2000

Gout attacks and lunar cycle.

The aim was to search for periodical fluctuations in daily occurrence of gout attacks during the synodic lunar cycle. 126 gout attacks were recorded between 1972 and 1994 at known calendar dates. The synodic plexogram, displaying the number of attacks for each day of the cycle, was processed by cosinor regression. A pronounced cycling was found, with highest peaks under the new and full moon (syzygigies). Thus, the maximal occurrence of attacks coincides with the peaking lunisolar tidal effect. Similar relation of attacks to synodic moon was seen in bronchial asthma of children, and a reciprocal one in paroxysmal tachyarrhythmia. Differing pathogenetic backgrounds of these diseases substantiate the observed differences in their putative reactions on the changing cosmogeophysical environment.

Female↗
PubMed2003

Advanced imaging of gout.

Gout is a metabolic disorder in which there is either an increase in production or a decrease in excretion of uric acid leading to hyperuricemia. Long-lasting hyperuricemia causes the deposition of monosodium urate crystals in the joints and soft tissues triggering gouty arthritis and, if not properly treated, the formation of gouty tophi. Characteristic of gout are well-defined, punched-out erosion with overhanging edges, with preservation of the joint space, lack of periarticular osteopenia, asymmetrical involvement, soft tissue nodules, and intraosseous calcifications. On magnetic resonance imaging, tophi usually have low signal intensity on both TI- and T2-weighted images and a variable enhancement pattern.

Gout↗
PubMed1989

Cyclosporine-induced hyperuricemia and gout.

To evaluate the frequency and the pathogenesis of hyperuricemia and gout during cyclosporine therapy, we studied renal-transplant recipients who were treated with either cyclosporine and prednisone (n = 129) or azathioprine and prednisone (n = 168). Among the patients with stable allograft function and serum creatinine concentrations below 265 mumol per liter, hyperuricemia was more common in the cyclosporine group than in the azathioprine group (84 percent vs. 30 percent; P = 0.0001). Gout developed in nine patients (7 percent) in the cyclosporine group, but no episodes occurred in the azathioprine group. Serum urate levels became elevated in 90 percent of the patients in the cyclosporine group who were treated with diuretics, as compared with 60 percent of those not treated with diuretics (P = 0.001); in the azathioprine group, the corresponding values were 47 percent and 15 percent (P = 0.0001). Serum urate levels did not correlate with trough blood cyclosporine levels in a selected subgroup (n = 40) of patients from the cyclosporine group, who were studied from 4 to 96 weeks after transplantation. Detailed studies of urate metabolism in six cyclosporine-treated patients revealed normal turnover rates for urate and decreases in creatinine and urate clearance, as compared with seven control subjects. We conclude that hyperuricemia is a common complication of cyclosporine therapy and is caused by decreased renal urate clearance. Gouty arthritis is the cause of considerable morbidity among renal-transplant recipients who receive cyclosporine.

Adult↗
PubMed1973

Human phosphoribosylpyrophosphate synthetase: increased enzyme specific activity in a family with gout and excessive purine synthesis.

Among affected members of a family (B. family) with excessive purine production and gout, activity of phosphoribosylpyrophosphate synthetase (EC 2.7.6.1) is 2.5- to 3.0-fold higher than among normal people. The molecular basis for this increased enzyme activity was studied. Antibody to purified human phosphoribosylpyrophosphate synthetase of erythrocytes was obtained from immunized rabbits. Studies with the IgG fraction of this antiserum show the presence of normal quantities of immunoreactive enzyme, but 2.5- to 3.0-fold higher activity per molecule in affected members of the B. family. In addition, by use of a stain for phosphoribosylpyrophosphate synthetase activity, a difference in electrophoretic mobility was demonstrated on cellulose acetate gel between the partially purified enzyme from normal people and an affected member of the B. family. These studies suggest that the enzyme aberration responsible for purine overproduction and gout in the B. family results from a structurally altered enzyme with increased activity per molecule.

Animals↗
PubMed1982

Purine oversecretion in cultured murine lymphoma cells deficient in adenylosuccinate synthetase: genetic model for inherited hyperuricemia and gout.

Alterations in several specific enzymes have been associated with increased rates of purine synthesis de novo in human and other mammalian cells. However, these recognized abnormalities in humans account for only a few percent of the clinical cases of hyperuricemia and gout. We have examined in detail the rates of purine production de novo and purine excretion by normal and by mutant (AU-100) murine lymphoma T cells (S49) 80% deficient in adenylosuccinate synthetase [IMP:L-aspartate ligase (GDP-forming), EC 6.3.4.4]. The intracellular ATP concentration of the mutant cells is slightly diminished, but their GTP is increased 50% and their IMP, four-fold. Compared to wild-type cells, the AU-100 cells excrete into the culture medium 30- to 50-fold greater amounts of purine metabolites consisting mainly of inosine. Moreover, the AU-100 cell line overproduces total purines. In an AU-100-derived cell line, AU-TG50B, deficient in adenylosuccinate synthetase and hypoxanthine/guanine phosphoribosyltransferase (IMP:pyrophosphate phosphoribosyltransferase, EC 2.4.2.8), purine nucleoside excretion is increased 50- to 100-fold, and de novo synthesis is even greater than that for AU-100 cells. The overexcretion of purine metabolites by the AU-100 cells seems to be due to the primary genetic deficiency of adenylosuccinate synthetase, a deficiency that requires the cell to increase intracellular IMP in an attempt to maintain ATP levels. As a consequence of elevated IMP pools, large amounts of inosine are secreted into the culture medium. We propose that a similar primary genetic defect may account for the excessive purine excretion in some patients with dominantly inherited hyperuricemia and gout.

Adenylosuccinate Synthase↗
PubMed2005

Clinicopathology of gout in growing layers induced by high calcium and high protein diets.

1. An experiment was conducted to test the independent and combined effects of high dietary calcium and protein concentrations on the induction of visceral gout in growing birds of a layer strain. 2. One hundred and sixty healthy birds were randomly divided into 4 groups at 35 d of age. The different groups were given 4 diets containing normal or high concentrations of dietary calcium or crude protein in a 2 x 2 factorial experiment for 30 d. The diets contained normal calcium (Ca) and crude protein (CP) (NCNP, 8.5 g Ca/kg and 175g CP/kg), high calcium and normal protein (HC, 36.3 g Ca/kg and 175 g CP/kg), normal calcium and high protein (HP, 8.8 g Ca/kg and 245 g CP/kg) or high calcium and high protein (HCHP, 36.8 g Ca/kg and 242 g CP/kg), respectively. 3. Typical visceral gout was induced by the HCHP diet. The HCHP and HC diet caused severe kidney damage. The HP diet did not cause kidney damage, but significantly increased plasma uric acid and inorganic phosphorus concentrations. 4. The HC diet significantly increased plasma uric acid, calcium and sodium, but significantly decreased plasma inorganic phosphorus, potassium and magnesium concentrations. The HCHP diet significantly increased plasma uric acid, calcium and sodium. 5. Urine volumes were significantly higher on the HCHP and HC diets than on the control. The growers raised on HC and HCHP diets had significantly higher total quantity of 24 h urinary excretion of uric acid, calcium, magnesium, inorganic phosphorus and potassium and a significantly lower 24 h urinary excretion of sodium. The growers fed on the HP diet had a higher 24 h urinary excretion of uric acid and inorganic phosphorus than the control. 6. It is concluded that growing layer birds should not be fed on layer rations.

Animal Feed↗
PubMed1979

Hyperuricemia and gout. A modern approach to diagnosis and treatment.

Diagnosis of gout by crystal identification in synovial fluid is simple and definitive. To treat gout effectively, the physician must determine whether overproduction or underexcretion of uric acid is the underlying mechanism. The acute attack is treated initially with antiinflammatory agents. After the acute phase is controlled, lifelong definitive therapy for hyperuricemia is begun.

Allopurinol↗
PubMed1987

Gout presenting as a popliteal cyst. A case of pseudothrombophlebitis.

A 64-year-old man with progressive swelling and erythema of his right calf preceded by dull aching in the right popliteal fossa was presumed to have deep vein thrombophlebitis. A venogram revealed normal circulation in the right lower leg, and an ultrasound examination of the right popliteal fossa revealed a 2 X 5-cm popliteal cyst. Fluid aspirated from the cyst confirmed the diagnosis of gout. Popliteal cysts associated with gout are rare, and those that rupture, leak, dissect, or enlarge can mimic thrombophlebitis (a phenomenon known as pseudothrombophlebitis). Thus, the primary care physician should consider the diagnosis of popliteal cyst in patients who appear to have deep vein thrombophlebitis.

Diagnosis, Differential↗
PubMed1998

Coexisting psoriatic arthritis, gout, and chondrocalcinosis.

The authors describe the case of a 63-year-old Caucasian man with a history of psoriatic arthritis who subsequently developed gout and chondrocalcinosis. This is the first report documenting the simultaneous occurrence of psoriatic arthritis, gout, and chondrocalcinosis in a single patient. The relations of these rheumatic diseases are discussed.

Arthritis, Psoriatic↗
PubMed2006

An unusual cause of renal amyloidosis secondary to gout: the first description of familial occurrence.

BACKGROUND: AA amyloidosis caused by the chronic inflammation accompanying gouty arthritis is extremely rare and familial occurrence has not been described so far. CASE REPORT: We present the case of two brothers (47 and 44 years old) with 7- and 10-year history of hyperuricaemia and chronic tophaceous gout with polyarticular involvement. The enzymatic assay performed in their erythrocytes proved the partial hypoxanthine-guanine phosphoribosyl transferase deficiency (Kelley-Seegmiller syndrome), the genetic defect of purine metabolism. Later on they developed proteinuria and chronic renal insufficiency /CRI/. Renal biopsy disclosed the combination of AA amyloidosis and gouty nephropathy in both the cases. Despite the standard treatment the older brother progressed to chronic renal failure. On the contrary, the younger one being longterm treated with oral colchicin have stabilized CRI. CONCLUSIONS: Only several cases of AA renal amyloidosis until recently, secondary to gout have been reported. Our case represents the first report of familial occurrence of this extremely rare disease.

Adult↗
PubMed2002

Hyperuricemia and gout in renal transplant recipients.

Hyperuricemia, unlike clinical gout, is extremely common in renal transplant patients. The high prevalence of hyperuricemia is related to prolonged exposure to cyclosporine rather than to its dose or serum concentration. Serum creatinine levels do not show significant correlation with hyperuricemia, behaving more like a surrogate marker for cyclosporine dose and trough level. The low incidence of gout in renal transplant patients, despite the hyperuricemia, may be related to the prolonged immunosuppression effect.

Adult↗
PubMed2004

Pharmacokinetics and pharmacodynamics of febuxostat (TMX-67), a non-purine selective inhibitor of xanthine oxidase/xanthine dehydrogenase (NPSIXO) in patients with gout and/or hyperuricemia.

The diurnal change of sUA and the effect of febuxostat on this change were investigated in 10 patients with gout and/or hyperuricemia. The diurnal sUA change after the last dose during the 4-week treatment phase (20 mg, QD) was almost the same as the pre-treatment value. Considering the dose, the AUC(obs) and Cmax of unchanged drug in patients with gout and/or hyperuricemia were estimated to be similar to those of healthy male adults. The results show that a 6-week treatment with febuxostat is safe and well-tolerated in the target patient population for this drug.

Area Under Curve↗
PubMed1987

Gout and hyperuricaemia in systemic lupus erythematosus.

Coexistent gout and systemic lupus erythematosus (SLE) have received increasing attention. An additional case is reported and published cases reviewed. Common clinical features of this group include nephritis, diuretic and corticosteroid therapy and a tendency to be older and more frequently male. Prevalence of hyperuricaemia (HU) was assessed in 38 patients with SLE. HU was found in 29% and was closely associated with renal involvement particularly proteinuria and diuretic therapy. The presentation of gout in SLE may be modified or suppressed by anti-inflammatory therapy and may be misinterpreted as SLE arthritis.

Adolescent↗