Review on Treatment of Gout & Hyperuricemia (original) (raw)

Therapeutic approaches to chronic hyperuricemia and gout

High blood pressure & cardiovascular prevention : the official journal of the Italian Society of Hypertension, 2014

Gout is currently one of the most common causes of inflammatory arthritis in most industrialised countries. Apart from its high frequency, gout is associated with disability, poor quality of life and increased mortality and therefore represents an ever increasing public health concern. Substantial experimental and epidemiological evidence exists supporting the link between elevated levels of serum uric acid and several comorbidities including cardiovascular and kidney diseases. The cornerstone of effective gout management is long-term serum urate lowering below saturation concentrations (<6 mg/dL or <360 μmol/L) in order to promote crystal dissolution and prevent monosodium urate crystals formation. The management of gout includes not only pharmacological approaches, but also a number of nonpharmacologic interventions aiming at lessening attack risk, lowering uric acid levels and promoting general health while preventing the development of comorbidities. It is of great address...

Sherman et al., PEG-Uricase in Gout Management ADDR 60 59-68, 2008

2013

Hyperuricemia results from an imbalance between the rates of production and excretion of uric acid. Longstanding hyperuricemia can lead to gout, which is characterized by the deposition of monosodium urate monohydrate crystals in the joints and periarticular structures. Because such deposits are resolved very slowly by lowering plasma urate with available drugs or other measures, the symptoms of gout may become chronic. Persistent hyperuricemia may also increase the risk of renal and cardiovascular diseases. Unlike most mammals, humans lack the enzyme uricase (urate oxidase) that catalyzes the oxidation of uric acid to a more soluble product. This review describes the development of a poly(ethylene glycol) (PEG) conjugate of recombinant porcine-like uricase with which a substantial and persistent reduction of plasma urate concentrations has been demonstrated in a Phase 2 clinical trial. Two ongoing Phase 3 clinical trials include systematic assessments of gout symptoms, tophus resolution and quality of life, in addition to the primary endpoint of reduced plasma urate concentration.

PEG-uricase in the management of treatment-resistant gout and hyperuricemia

Advanced Drug Delivery Reviews, 2008

Treating to target: a strategy to cure gout

2009

Acute gout attacks and the long-term complications of gout are associated with the deposition of monosodium urate (MSU) monohydrate crystals in the joints and soft tissues, causing acute and chronic inflammation. The aim of long-term treatment is to reduce the serum urate (sUA) level to 6 mg/dl (4360 mol/l), below the saturation point of MSU, so that new crystals cannot form and existing crystals are dissolved. Serial joint aspiration studies confirmed the disappearance of crystals with effective urate-lowering therapy. There is good evidence that achieving sUA <6 mg/dl (360 mol/l) results in freedom from acute gout attacks, and shrinkage and eventual disappearance of tophi. Gout patients must be informed about their diagnosis and educated about gout management including the importance of compliance with long-term treatment. Patients starting urate-lowering therapy need to understand the importance of prophylactic therapy with colchicine or NSAIDs to reduce the risk of 'mobilization flares' in the first few months. In the long term, reduction in the sUA below the target level will result in gout being effectively cured.

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.

Chronic Gout and Hyperuricemia

The Professional Medical Journal

Objective: To assess the urate-lowering efficacy and safety of Febuxostat versusAllopurinol in subjects with hyperuricemia and gout. Study design: Randomized controlled trial.Place and duration of study: Department of Orthopaedic and Trauma Surgery Mardan MedicalComplex Teaching Hospital Bacha khan Medical College Mardan from February 2012 to March2013. Material and Methods: Fifty patients of chronic gout and hyperuricemia fulfilling theinclusion criteria were divided into two equal groups by random method having 25 patients eachand received either a fixed dose(80 mg) of Febuxostat (Group A) or Allopurinol (Group B) 300mgonce daily for 16 weeks. The primary end point was the percentage of patients reaching serumurate level <6.0 mg/dl (360 μ mol per liter) at final visit. The secondary end points includereduction in the incidence of gout flares and adverse drug reactions. Results: There were16(64%) males and 9(36%) females with mean age 44.92 years in group A while group B had15(6...

Pharmacological overview for therapy of gout and hyperuricemia

International journal of health sciences

Hyperuricemia & gout are disease conditions marked by over production and reduced excretion of uric acid. These conditions are linked with unhealthy lifestyle, Hypertension, Diabetes Mellitus, Metabolic syndrome, Cardiovascular & Chronic renal disease. Thus controlling & monitoring uric acid level becomes important. Development in the technology have led to greater insights into the pathophysiology of gout & hyperuricemia. Now we have a better understanding of involvement of interleukin 1β in inflammatory process of gout. Thus with better understanding newer therapeutic targets are being explored for treatment of gout & hyperuricemia. The armamentarium of drugs being used in therapy of acute gout here been expanded with recent addition by interleukin-1 inhibitors especially for refractory patients and patients with comorbidities. As these new therapies are evolving we need to focus on improving the use of Allopurinol through patient education and training of physicians in order to ...

Review on Treatment of Gout & Hyperuricemia (original) (raw)

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