Gout is a metabolic disorder classically represented as acute inflammatory monarthritis (Rott & Agudelo, 2003); that is known to be initiated by the crystallization of uric acid (UA) within the joints. Uric acid is the end product of metabolism of purine. …
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When urates in the blood reach the physiological saturation levels, they crystallize to form monosodium urate (MSU) and gradually accumulate in tissues. This leads to development of asymptomatic hyperuricemia which results into gout (Luk & Simkin, 2005). The clinical manifestations of gout include acute gouty arthritis, deposition of MSU crystals in soft tissues leading to formation of ‘tophi’, urate urolithiasis along with rare incidences of nephropathy. The disease develops in four stages; an asymptomatic hyperuricemia, acute gout with intermittent flares, the intercritical period, and chronic gout (Sundram, 2010). The prevalence of gout have been on a rise during the last few decades chiefly due to changes in life style patterns and increased longevity. In US prevalence has been estimated to be 5.1 million during the period spanning 1988-1994 by the third national health and nutrition examination survey (NHANES III). 5.2 cases per 1000 have been reported by the US managed care database during the year 1999 compared to 2.9 cases in 1990. The disease prevalence rates reportedly are higher in older men than those of rheumatoid arthritis. Incidences of gout have also escalated during the last two decades with annual levels reported by Rochester Epidemiology Project to be twice as high as those reported two decades earlier for primary gout. Higher incidences of disease are reported in men than in women with increased incidences reported with advancing age in both sexes (Weaver, 2008). Despite high prevalence and severe burden of the disease, frequent mismanagement of the disease leads to avoidable incidences of morbidities and mortality (Luk & Simkin, 2005). The current report aims to present an in depth exploration of the risk factors, pathogenesis and treatment modalities of gout. RISK FACTORS Sex Men have a higher level of serum urate rendering them significantly more vulnerable to gout with higher probability of development of gout in men below the age of 30 compared to women of comparable age. The risk of gout development in men peaks in the age range of 75-84 years, while in women the risks are higher during post menopausal phase. After the age of 60, both men and women are equally vulnerable to the disease (Rott & Agudelo, 2003). Diuretics Diuretic intake is a major cause of hyperuricemia since it causes significant enhancement of reabsorption of uric acid in kidney (Rott & Agudelo, 2003). Several other medications such as low dose aspirin, cyclosporine (increases tubular reabsorption of urate), pyrazinamide, ethambutol, and niacin also lead to hyperuricemia (Weaver, 2008). Comorbidities Individuals with hypertension, insulin resistance, cardiovascular diseases, neuropathy, hyperlipidemia, chronic kidney diseases and metabolic syndrome are highly vulnerable to gout (Rott & Agudelo, 2003). Lead exposure has also been found to be associated with gout (Sundram, 2010). Poor urate clearance may render a hemodialysis patient vulnerable to urate deposition and gout. Obesity Individuals with a body mass index (BMI) in the range of 21-22 have been reported to be at much lower risk of developing gout compared to individuals with higher BMI. Alevel of 35 raise the risk three fold. Obesity has been found to be associated with enhance urate synthesis and lower excretion of urate from the kidneys; thereby leading to raised serum urate levels (Weaver, 2008). Dietary Habits A diet rich in meat such as red meat, organ meat; and sea food has been associated with higher vulnerabilities to gout. The same has also been reported for alcohol consumption; especially beer (Choi et al. 2004). On the contrary, purine rich vegetables exhibit no correlation with gout development and dairy products lower the risk marginally (Weaver,
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The author states that overproduction of uric acid leads to increased phosphoribosyl pyrophosphate (PRPP) synthetase activity and deficiency of hypoxanthine‐guanine phosphoribosyl transferase (HGPRT ), which is responsible for the conversion of hypoxanthine to ionsinic acid and guanine to guanylic acid.
But these metabolic disorders were not related to the abnormalities of the cardiovascular system at that time. Gerald Phillips later on found out that the aspects of ageing, obesity, and diabetes were directly related to heart diseases. It was then in 1988 that Reaven found out a connection between hyperglycemia, insulin resistance, dyslipidemia and the cardiovascular diseases.
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When an individual suffers from bipolar disorder, they experience changes in their mood that can be either short and abrupt, happening without warning, or else can last for weeks at a time. Believed to be caused by chemical imbalances in the brain, bipolar disorder affects the way that an individual feels and acts, often despite the experiences that they are going through in life.
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