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

In our modern society hyperuricemia is one of the most frequent metabolism disturbances. So far, every fourth man and every tenth woman suffer from an asymptomatic or a symptomatic hyperuricemia named gout. Mostly, over nutrition and malnutrition as well as other secondary factors with a genetically determined renal secretion disturbance of uric acid lead to an increase of serum uric acid. By deposition of uric acid crystals in tissues with intermittent immunologic activation of inflammation cells a manifestation of gout can be seen. The clinical image of gout varies widely. It may manifest as acute or chronic arthritis, tophi on the skin, subcutaneous tissue and the skeletal system as well as urate nephropathy. To eliminate the consequences of hyperuricemia in the long term, apart from a thorough anamnesis of nutritional habits a general examination of metabolic parameters is necessary to exclude a metabolic syndrome and other causes for a secondarily caused hyperuricemia. As gout is very often primarily caused by a renal secretion disturbance of uric acid special diagnostics should be done. Basing on literature research and inclusion of experts opinions this article represents the therapeutically options in treatment of hyperuricemia and gout with their resulting side effects and contraindications.
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PMID:[Hyperuricemia and gout: diagnosis and therapy]. 1658 30

After introduction of urate-lowering therapy, asympotomatic hyperuricemia was treated with allopurinol or uricosuric agents in the belief that hyperuricemia and/or gout caused chronic kidney disease. Epidemiologic studies in the 1970s, however, failed to confirm the view that hyperuricemia and gout were independent risk factors for chronic kidney disease. As a result, urate-lowering pharmacotherapy is generally not recommended at the present time in the management of asymptomatic hyperuricemia even though recent epidemiological, experimental, and clinical studies have prompted reexamination of a causal role for hyperuricemia (with or without gout) in chronic kidney disease as well as other important disorders including cardiovascular disease, hypertension, and metabolic syndrome. The issue of such a role remains unresolved and this article reviews the current status of the relationship between hyperuricemia and associated disorders.
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PMID:Hyperuricemia and associated diseases. 1671 80

Gout is the most frequent cause of acute arthritis in men over 40 years of age. In the recent years, gout incidence has been increasing in developed countries probably due to dietary changes, alcohol consumption, ageing of population and also application of high-risk medications. Hyperuricemia is one of the symptoms of hyperinsulinism and metabolic syndrome. The level of uricemia correlates with the degree of insulin resistance. Correlation of uric acid levels and the risk of coronary and cerebral accidents were reported both in diabetic and non-diabetic population. It has not been explained satisfactorily whether this is the direct result of hyperuricemia or concurrently present symptom of metabolic syndrome. The study describes symptomatology of clinical signs of gout and discusses about appropriate therapeutic approach in each stage of the disease. New therapeutic possibilities that are still in the stage of clinical studies are mentioned. Also, we focus on alternative dietary recommendations for hyperuricemia and gout patients. The reason of changes in dietary regime is the effort to alleviate the signs of metabolic syndrome. The study emphasises the practical significance of screening of metabolic syndrome signs during examination of gout patients so that appropriate targeted therapeutic intervention could be performed. On the contrary, increased risk of gout-induced movement disorders should be taken into account in patients with diagnosed insulin resistance.
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PMID:[Gout and diabetes]. 1677 Oct 97

Gout affects more than 1% of adults in the USA, and it is the most common form of inflammatory arthritis among men. Accumulating data support an increase in the prevalence of gout that is potentially attributable to recent shifts in diet and lifestyle, improved medical care, and increased longevity. There are both nonmodifiable and modifiable risk factors for hyperuricemia and gout. Nonmodifiable risk factors include age and sex. Gout prevalence increases in direct association with age; the increased longevity of populations in industrialized nations may contribute to a higher prevalence of gout through the disorder's association with aging-related diseases such as metabolic syndrome and hypertension, and treatments for these diseases such as thiazide diuretics for hypertension. Although gout is considered to be primarily a male disease, there is a more equal sex distribution among elderly patients. Modifiable risk factors for gout include obesity, the use of certain medications, high purine intake, and consumption of purine-rich alcoholic beverages. The increasing prevalence of gout worldwide indicates that there is an urgent need for improved efforts to identify patients with hyperuricemia early in the disease process, before the clinical manifestations of gout become apparent.
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PMID:Epidemiology, risk factors, and lifestyle modifications for gout. 1682 41

An acute attack of gouty arthritis is one of the most painful experiences reported throughout medical history. Therefore it is paramount to initiate appropriate therapy quickly in order to terminate the acute phase. This goal can be achieved with non-steroidal anti-inflammatory agents, colchicine, or corticosteroid-based therapies. Rarely, because of contraindications to these agents, only symptomatic treatment can be given until the attack subsides. The next step is to lower the serum urate level below the limit of solubility (i.e., below 40.8 mmol/L, or 6.8mg/dL) which reduces recurrences and begins to return the total body urate pool to normal. This equally important goal can be achieved by uricosuric agents or xanthine oxidase inhibitors, although the latter is generally favored. Allopurinol is the agent most commonly preferred because of its safety profile and ease of use, but there are known serious allergic reactions and untoward side effects that occasionally require discontinuation. Febuxostat, a xanthine oxidase inhibitor, and pegylated uricase are new agents under development and may be beneficial in these situations or when other comorbid conditions prevent the use of conventional treatments. Alcohol and dietary consumption are also related to hyperuricemia and acute gout. Recently beer, wine, and liquor were studied and the risk of gout varied according to the alcohol ingested. Furthermore, recent data sheds light on important dietary modifications that may help in the treatment of gout, and dispels certain beliefs about protein ingestion and the occurrence of acute gout. As we learn more about the associated conditions of hypertriglyceridemia, hypertension, and the metabolic syndrome, it may allow the tailoring of medical regimens that directly prevent or reduce recurrent attacks of gouty arthritis. There are specific approved treatments for these common comorbidities that have parallel effects of lowering serum urate levels. These recent findings may be especially important for treating refractory cases. While patient education remains a cornerstone to ensure compliance, other quality indicators for the management of this disease have been reported and should guide the clinician in the treatment of gout and result in improved care.
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PMID:Advances in the management of gout and hyperuricaemia. 1688 87

The prevalence of gout appears to be rapidly increasing worldwide and is no longer a disorder suffered primarily by over-fed alcohol consumers. Emerging risk factors include longevity, metabolic syndrome, and new classes of pharmacologic agents. In some ethnic populations, no obvious risk factors can explain the high incidence of hyperuricemia and gout, suggesting a genetic liability. Studies to identify genes associated with gout have included families with defects in purine metabolism, as well as families in whom the occurrence of gout is secondary to renal disorders such as juvenile hyperuricemic nephropathy and medullary cystic kidney disease. Case-control studies of isolated aboriginal cohorts suffering from primary gout have revealed several chromosomal loci that may harbor genes that are important to the development and/or progression of gout.
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PMID:New developments in the epidemiology and genetics of gout. 1690 Oct 80

Studies have shown that hepatitis C (HCV) is associated with type 2 diabetes mellitus (DM2) possibly due to insulin resistance and inflammation. Metabolic syndrome is a risk factor for DM2. Our objectives were to assess the relationship between HCV and metabolic syndrome and inflammatory markers. We used data from The Third National Health Nutrition and Examination Survey (NHANES-III). We excluded pregnant women, subjects with diabetes, those taking non-steroidal anti-inflammatory drugs, and those diagnosed with concomitant infection. We analyzed the data controlling for demographic variables, body mass index, use of contraceptives, had arthritis, and had gout. Among the 10,383 subjects, 2.3% had HCV and 16.7% had metabolic syndrome using the ATP III criteria. After controlling for the confounders, HCV was not associated with metabolic syndrome but associated with HOMA insulin resistance and inflammatory marker ferritin. Among subjects with both HCV and metabolic syndrome, the adjusted HOMA insulin level was higher than those without HCV and metabolic syndrome. In addition, the serum ferritin level was a strong predictor of HOMA insulin resistance. In clinical practice, serum ferritin can be obtained along with routine blood tests in any laboratory, and it has a potential to be a surrogate marker of insulin resistance in people with HCV and metabolic syndrome.
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PMID:Hepatitis C, metabolic syndrome, and inflammatory markers: results from the Third National Health and Nutrition Examination Survey [NHANES III]. 1691 55

Background A 53-year-old man with a history of hypertension and gout was referred to our clinic for severe hypertriglyceridemia, diagnosed 3 years previously. He was asymptomatic and had no history of abdominal pain, pancreatitis or diabetes, but consumed six cans of beer per night. Over the previous 2 years, he had been treated unsuccessfully with multiple medications; during this period his fasting triglycerides ranged from 5.41 mM to 55.04 mM (479 to 4,871 mg/dl). Investigations Physical examination including fundoscopy, medication review, and laboratory tests.Diagnosis Severe hypertriglyceridemia due to a genetic combined hyperlipidemia, exacerbated by persistent excessive alcohol intake and metabolic syndrome. Management Cessation of alcohol intake, initiation of a fat-restricted diet, and fibrate therapy, with close follow-up. Once serum triglycerides were controlled, attention was turned to lowering LDL-cholesterol concentration according to The National Cholesterol Education Program, Adult Treatment Panel III guidelines.
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PMID:Severe hypertriglyceridemia with a history of treatment failure. 1692 66

We examined the components of metabolic syndrome associated with gout in different age strata by a large-scale case-controlled study. Totally, 12,179 gouty subjects were divided into three groups according to their ages at first visit: young- (19-44 years), middle- (45-64 years), and old-aged (>or=65 years) groups. Their clinical and laboratory data, as well as the risk of gout by the metabolic syndrome, were analyzed in three age groups and compared with a control population. The numbers of the cases in the young-, middle-, and old-aged groups in the gout population were 4,698, 4,847, and 2,634, respectively. The serum urate level and the percentage of positive family history of gout were the highest in young-aged group and declined with increasing age. When compared with the data of the control population, the incidence of overweight (body mass index, >or=24.2 kg/m(2)) and hypertriglyceridemia (triglyceride, >or=2.26 mmol/l) were significantly higher in the gout population for all age groups. The incidence of type 2 diabetes was significantly higher in the gout as well for all age groups, and the odds ratio was highest in the young-aged group [odds ratio (95% confidence interval), 5.55 (3.05-10.09)]. In all, except for the old-aged groups, the incidence of hypercholesterolemia was significantly higher in the gout than in the control population, whereas the incidence of hypertension was significantly higher in the gout than in the control population only in the old-aged group. Various clinical and laboratory data were suggested to be the risks of gout in different degrees between age strata.
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PMID:Manifestations of metabolic syndrome associated with male gout in different age strata. 1725 1

Uric acid nephrolithiasis is typically found in individuals with a low urine pH and a normal concentration of urinary uric acid. Patients with a history of gout are at greater risk of forming uric acid stones, as are patients with obesity, diabetes, or the complete metabolic syndrome. The unifying renal tubular abnormality of these disorders appears to be the excretion of abnormally acidic urine. This article focuses on the relationship of these disorders to the development of uric acid stones. The diagnosis of uric acid stones can be elusive, because pure uric acid stones are radiolucent on plain radiographs. Ultrasound, or preferably noncontrast helical CT scanning, is required for their detection. The treatment of uric acid stones should focus on alkalinization of the urine with citrate or bicarbonate salts. Additional interventions such as increase in fluid intake and decrease in animal protein ingestion are often beneficial. Patients with documented hyperuricemia often require specific therapy to lower serum uric acid concentration and subsequent excretion.
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PMID:Uric acid nephrolithiasis. 1753 Nov 80


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