Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018099 (gout)
 5,192 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The characteristic phenomena of acute gouty arthritis are acute arthritis in a middle-aged male, associated with serum uric acid above 6 mg. per 100 cc. and a satisfactory response to colchicine. Roentgenographically observable changes do not occur early. In recent years uric acid metabolism has been studied by means of isotope techniques utilizing labeled substances. Uric acid is excreted in relatively constant amounts by humans and is little affected by variations in dietary intake, except for purine or nucleic acid substances. Persons with gout have a greater total amount of uric acid and a lower turnover than normal persons. In the treatment of acute attacks of gout colchicine is still the most practical single drug, even though its pharmacologic action remains unknown. Benemid (probenecid) is a powerful uricosuric agent of low toxicity which has been subjected to extensive clinical trial for three years. It causes inhibition of the resorption of urate from the glomerular filtrate; the site of action is believed to be the tubular cells. The author's usual dose is 2 gm. a day. This has caused a lowering of the uric acid in the serum and an increase in the urinary output.
Calif Med 1953 Sep
PMID:Diagnosis and treatment of gouty arthritis. 1308 23

Advantages and risks related to the use of selective COX-2 inhibitors when treating arthritis are currently being scrutinized by authorities and public. The discussion tends towards exaggerated claims for or against their usefulness. The issue of cardiovascular safety is still not finally settled. In an experimental study using patients with severe coronary disease, administration of celecoxib resulted in improved endothelial function together with reduced CRP levels. Gastrointestinal tolerance was studied in patients who had recently recovered from peptic ulcer bleeding. In this group of high risk patients, celecoxib was as safe as combined therapy using omeprazol and diclofenac when given for 6 months. However, both COX inhibitors caused hypertension and adverse renal effects. The second generation of selective inhibitors is being launched. Etoricoxib--related to rofecoxib--was shown to be as potent as indomethacin in the treatment of acute gout, but it caused fewer adverse reactions. In general, however, any advantage of second generation as compared to first generation COX-2 inhibitors remains to be proven. The Swedish Council on Technology Assessment in Health Care, in its "SBU Alert", has published an appraisal of celecoxib and rofecoxib, in which the need for further long-term safety studies is emphasized.
Lakartidningen 2003 Sep 18
PMID:[New studies of COX-inhibitors, yet issues remain]. 1455 11

Urate, a purine metabolite, is a cause of gout(hyperuricemia), which is an independent risk factor for cardiovascular disease. Urate is a scavenger of reactive oxygen radicals that are involved in numerous diseases. Because humans have a renal urate reabsorption system and have lost hepatic uricase by mutational silencing in evolution, urate is present in human blood at high levels. We identified the long-hypothesized urate transporter in the human kidney (URAT1, encoded by SLC22A12), a urate anion exchanger regulating blood urate levels and targeted it with uricosuric and antiuricosuric agents. Moreover, we demonstrated that patients with renal hypouricemia have mutational defects in SLC22A12.
Rinsho Byori 2003 Sep
PMID:[Urate transporter and renal hypouricemia]. 1456 Jun 59

In this follow-up study, 526 persons were followed for almost 5 years to assess the reversibility and predictive value of four kidney biomarkers in a field epidemiology setting. This study examined (a) whether elevations in urinary albumin, N-acetyl-beta-D-glucosaminidase, retinol-binding protein, and alanine aminopeptidase remained elevated at follow-up and (b) whether these initial elevations were predictive of kidney disease (as measured by markers of kidney dysfunction: serum creatinine, serum cystatin C, creatinine clearance, and urine osmolality) at follow-up. Study participants were 8-76 years of age at baseline and were followed for an average of 4.5 years. Approximately 50% of adults who had an elevated biomarker did not have an elevation at followup. Youths with elevated biomarkers at baseline, but who completed adolescence by the time of the follow-up, no longer had any elevations in biomarkers at follow-up. Adult participants who had elevated biomarkers and selected health conditions at baseline (diabetes and, to a lesser extent, heart disease, hypertension, gout, and urinary tract disease) were more likely to show early indicators of kidney impairment at follow-up. Participants with these health conditions and normal kidney biomarker values at baseline had kidney test results at follow-up that were similar to results of study participants who did not have these health conditions at baseline. The presence or absence of elevated biomarkers at baseline among generally healthy participants was not associated with the development of early indicators of kidney impairment at follow-up. This longitudinal study confirmed the utility of these four kidney biomarker tests as markers of preclinical organ dysfunction among adults with certain preexisting medical conditions.
Ren Fail 2003 Sep
PMID:Confirming the utility of four kidney biomarker tests in a longitudinal follow-up study. 1457 88

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.
Semin Musculoskelet Radiol 2003 Sep
PMID:Advanced imaging of gout. 1459 58

Calcium pyrophosphate dihydrate (CPPD) crystal deposition disease is characterized by the accumulation of pyrophosphate dihydrate crystals in articular and periarticular tissues. Various terms have been utilized to describe this arthropathy, which has led to some confusion. CPPD crystal deposition disease is among many conditions that may result in crystal deposition within cartilage. Chondrocalcinosis is a pathologic and radiographic term denoting calcification of cartilage within joints including both hyaline articular cartilage and fibrocartilage. Pseudogout is a clinical term applied to an acute inflammatory process in a joint(s) mimicking a gout attack. Pseudogout is just one of the multiple clinical presentations for CPPD crystal deposition disease. Pyrophosphate arthropathy is a term that has been used to describe the peculiar pattern of joint destruction associated with CPPD crystal deposition disease. This article reviews the protean manifestations of CPPD crystal deposition disease with emphasis on diagnostic imaging.
Semin Musculoskelet Radiol 2003 Sep
PMID:Calcium pyrophosphate dihydrate crystal deposition disease. 1459 59

The clinical features of 567 patients with crystal proven gout (489 males, 78 females) seen in a University Hospital in northern Thailand was reviewed. The mean age at onset and mean duration of disease was 60.0 +/- 11.7 years and 5.2 + 4.8 years, respectively. Recurrent attacks accounted for 94 per cent. The knee and ankle were the 2 most common joints affected during the first attack and each one was seen in 55.6 per cent of cases. During a recurrent attack, the ankle, knee and first metatarsophalangeal joint were the 3 most common joints affected and were seen in 94.5 per cent, 81.2 per cent and 80.2 per cent of cases, respectively. Thirty-six per cent of the patients had tophi. Hypertension, hyperlipidemia, diabetes mellitus and ischemic heart disease were commonly associated diseases. Thirty-five per cent had renal calculi, and fifty-four per cent had renal insufficiency. Of 59 patients who tested with normal renal function, twelve per cent were hyperexcretor. The clinical features of gout seen in the university hospital in northern Thailand were similar to those reported in Bangkok, but with a higher incidence of tophaceous gout, renal failure and renal calculi.
J Med Assoc Thai 2003 Sep
PMID:A clinical study of crystal-proven gouty arthritis in a university hospital. 1464 72

MR imaging is not routinely used for the evaluation of tophaceous gout. However, gout may have atypical clinical and radiologic findings. It should be considered in the differential diagnosis when a mass reveals heterogeneous and low signal intensity on T2 weighted images. We present MR imaging characteristics of gout tophi and arthritis in two patients.
Tani Girisim Radyol 2003 Sep
PMID:[Case report: MRI findings in gout]. 1466 5

Gout is a disorder of uric-acid metabolism. The Pacific Austronesian population, including Taiwanese aborigines, has a remarkably high prevalence of hyperuricemia and gout, which suggests a founder effect across the Pacific region. We report here a genomewide linkage study of 21 multiplex pedigrees with gout from an aboriginal tribe in Taiwan. From observations of familial clustering, early onset of gout, and clinically severe manifestations, we hypothesized that a major gene plays a role in this trait. Using 382 random polymorphic markers spread across 22 autosomes, we demonstrated a highly significant linkage for gout at marker D4S2623 on chromosome 4q25 (P=.0002 by nonparametric linkage [the NPL(all) statistic]; empirical P=.0006; LOD=4.3, P=4.4x10-6 by logistic regression). When alcohol consumption was included as a covariate in the model, the LOD score increased to 5.66 (P=1.3x10-6). Quantitative traits, including serum uric acid and creatinine, also showed a moderate linkage to this region. To our knowledge, this is the first genome-scan report to identify a genetic locus harboring a gout-susceptibility gene.
Am J Hum Genet 2004 Sep
PMID:Genomewide scan for gout in taiwanese aborigines reveals linkage to chromosome 4q25. 1525 57

The aim of this study was to assess the synovial fluid (SF) neurotransmitter excitatory amino acid (EAA) levels, including glutamate (Glu) and aspartate (Asp), in the context of SF levels of other amino acids, TNF-alpha and chemokines from patients with active arthropathies. The SF was collected from patients with active rheumatoid arthritis (RA), gout, or osteoarthritis (OA). The SF samples were analysed for levels of neurotransmitters glutamate and aspartate, tumour necrosis factor-alpha (TNF-alpha), Regulated upon Activation Normally T-cell Expressed and Secreted (RANTES), macrophage inhibitory factor-1 alpha (MIP-1alpha) and interleukin 8 (IL-8). SF WBC counts were also determined. Correlations between SF EAA, TNF-alpha and chemokines were determined by the Pearson product-moment correlation. Primary cultures derived from SF from active RA and gout patients were incubated with added l-glutamate, to assess if exposure to Glu could increase TNF-alpha levels. There were significant elevations in SF EAA, SF TNF-alpha and SF RANTES in RA patients compared to gout or OA patients. Significant correlations between SF EAA and SF RANTES, MIP-1alpha and IL-8 levels were seen, and SF EAA and SF TNF-alpha or SF WBC levels approached significance. Addition of exogenous neurotransmitter glutamate significantly increased TNF-alpha levels in primary cell cultures derived from RA and gout patients. The SF neurotransmitter EAA levels significantly correlated to selected SF chemokine levels, in clinically active RA, gout and OA patients, independent of disease. Added Glu resulted in significantly increased TNF-alpha levels in primary synovial cell cultures. These data expand the relationship of SF neurotransmitter EAA levels to SF cytokines and chemokines in patients with clinically active arthritis, and suggest that neurotransmitters Glu and Asp contribute to peripheral inflammatory processes.
Clin Exp Immunol 2004 Sep
PMID:Excitatory amino acids, TNF-alpha, and chemokine levels in synovial fluids of patients with active arthropathies. 1532 Sep 17


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