Clinical and epidemiological aspects of gout, a dysmetabolic disabling disorder (original) (raw)
Related papers
New insights into the epidemiology of gout
Gout is a true crystal deposition disease caused by formation of monosodium urate crystals in joints and other tissues. It is a common inflammatory arthritis that has increased in prevalence in recent decades. Gout normally results from the interaction of genetic, constitutional and environmental risk factors. It is more common in men and strongly age related. A major determinant is the degree of elevation of uric acid levels above the saturation point for urate crystal formation, principally caused by inefficient renal urate excretion. Local joint tissue factors may influence the topography and extent of crystal deposition. Recent studies have provided information on dietary risk factors for gout: higher intakes of red meat, fructose and beer are independently associated with increased risk, whereas higher intakes of coffee, low-fat dairy products and vitamin C are associated with lower risk. Several renal urate transporters have been identified including URAT1 and SLC2A9 (GLUT9) and polymorphisms in these genes are associated with an increased risk of hyperuricaemia and gout. Many drugs influence serum uric acid levels through an effect on renal urate transport. Comorbidities, including the metabolic syndrome and impaired renal function are common in gout patients. The usual initial presentation of gout is with rapidly developing acute inflammatory monoarthritis, typically affecting the first MTP joint. If left untreated it may progress with recurrent acute attacks and eventual development of chronic symptoms and joint damage. New knowledge of the modifiable risk factors for gout can be integrated into the management strategy to optimize long-term patient outcomes.
Gout--current diagnosis and treatment
2009
G out, a result of hyperuricemia above 390 µmol/L (6.5 mg/dL), is often associated with other metabolic disorders such as obesity, diabetes mellitus, and hypertonia, and carries an increased risk of cardiovascular problems (1-3, e1). Because of changing dietary and other lifestyle habits, at least 1% to 2% of all adults in the industrialized nations are now affected by gout. In the Framingham Study, 9.2% of men and 0.4% of women had hyperuricemia, and 19% of these suffered from gout (e2).
Diagnostic and therapeutic procedures in gout
Medical Research Journal
Gout, a rheumatic disease caused by crystals (crystal arthropathy), is a form of inflammatory arthritis caused by monosodium urate depositing in the synovial fluid and as time goes by outside the joints as well (in other tissues and organs).Gout attacks are sudden and often result from a dietary mistake. In 2015 the European and American Rheumatological Associations (EULAR and ACR) published joint classification criteria for gout. The criteria involve gout-specific clinical symptoms, irregular results of laboratory tests and lesions visible in imaging tests. The "golden standard" of diagnostics still remains the presence of uric acid crystals in a sample of synovial fluid, the contents of the bursa and of the gouty tophus. The course of treatment for patients with gout depends on the stage of the disease, but it comes down to implementing various forms of preventing hyperuricemia by modifying the patient's lifestyle and diet, reducing risk factors (such as overweight and obesity) and pharmacological treatment, both in-between and during attacks.
Gout: Joints and beyond, epidemiology, clinical features, treatment and co-morbidities
Maturitas, 2014
Gout is a common inflammatory arthritis precipitated by an inflammatory reaction to urate crystals in the joint. Gout is increasingly being recognised as a disease primarily of urate overload with arthritis being a consequence of this pathological accumulation. It is associated with a number of important co-morbidities including chronic kidney disease, obesity, diabetes and cardiovascular disease.
GSC Biological and Pharmaceutical Sciences, 2018
Gout is a type of inflammatory arthritis with drastically increasing incidence since last twenty years. Increased serum uric acid levels and deposition of urate crystals in joints and soft tissues are known to stir-up the symptoms of gout. Patient's quality of life (Qol) suffers markedly due to inflammation, pain, restricted mobility, health economic burden and suboptimal therapeutics associated with gout. Related articles published between 2007 and 2018 were reviewed with the help of different databases including PubMed, Springer link, Medline, Google scholar and Science direct. To ensure the accuracy and credibility of data, articles published only in indexed journals were considered. Gout is a common metabolic disorder that is provoked by increased level of serum uric acid. Presence of other comorbidities i.e. hypertension, diabetes and cardiac diseases precipitate the rate of mortality. Number of gout patients is shown to increase in developed countries whereas developing countries remain at high risk category. The enormous increase in gout is due to chronicity, lack of awareness among patients, poor diagnosis, suboptimal treatment and economic burden. Risk factors associated with gout are well identified and pathophysiology is well-established hence, measures can be taken to improve diagnosis and to ensure cost effective options for the treatment. To curtail the global health burden and to improve patient quality of life there is need: to reduce exposure to risk factors, to promote awareness, to institute robust prophylactic measures, to modify lifestyle, to establish signs for early diagnosis and to develop optimized treatment strategies and policies.
The Biochemical & Physiological Implication of Gout
The article focuses on several underlying biochemical features regarding the manifestation of Gout. The high level Uric Acid (UA) built up in circulation is a major indication of the disease which is found only within human and higher apes. In moderate briefing it describes the nature, causes, sexual biasness and de-novo synthesis of UA and its excretion from the body under physiologic condition at the onset of this metabolic disorder. Categorically, the information offered is classified as follows: A. General knowledge about the disease caused due to higher UA / Urate level inside circulating plasma normally termed Hyperuricemia viewed commonly among the Gout sufferers including the role of purine enriched food and excessive alcohol consumption associated with its higher incidence. B. The physico-chemical mechanism of crystal formation and the cause of its deposition in faraway joints. C. The faulty Purine synthesis / metabolism or malfunctioning of Urate excretion through the kidney by various transporters leading to the manifestation of Hyperuricemia or Gout and simultaneously including its versatility, nature, ability and genetic identity. D. The discussion involving enzymatic pathway behind Hyperuricemia viewed within the Gout sufferers in the light of Purine synthesis and metabolism along with the genetic abnormality. E. The non-expression of Uricase gene in human due to nonsense mutation helps exacerbate the accumulation of UA when other enzymatic problem came into effect. AJBBL http://www.ajbbl.com/ Volume 01 Issue 01 2012 F. The immunological problem created by the deposition of Urate crystal due to Hyperuricemia initiating the Gout attack causing pain, swelling and flare ups are elaborated along with their remedies. G. The pharmacological mechanism and the adverse roles of any drugs commonly used during treatment either for the short term or long term purposes in controlling or preventing its future recurrence is also included in this review.