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Page: Pathogenesis
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Gout arises directly from elevated levels of uric acid within the blood. The amount of uric acid within the body is determined by the balance between the amount being produced and the amount being excreted. Uric acid is produced when purines are broken down by enzymes in the liver. Purines can be generated by the body itself (via the breakdown of cells in normal cellular turnover) or can be ingested in purine-rich foods (e.g. seafood, beer). Most people with gout, however, do not produce more than the normal amount of uric acid. Instead, most people with gout tend to be underexcretors. The kidney is responsible for about one third of uric acid excretion, with the gut responsible for the rest. It may be possible that defects in the kidney that may be genetically determined are responsible for the predisposition of individuals for developing gout.
There are also different racial propensities to develop gout. The prevalence of gout is high among the peoples of the Pacific Islands, and the Ma-ori of New Zealand, but rare in the Australian aborigine despite the latter's higher mean concentration of serum uric acid. In the United States, gout is twice as prevalent in African American males as it is in Caucasians.
Hyperuricemia is considered an aspect of metabolic syndrome, although its prominence has been reduced in recent classifications. This explains the increased prevalence of gout among obese individuals.
Many still believe that gout is caused by a combination of dietary factors and "laziness". In particular, many believe that gout develops following several years of excessive alcohol consumption combined with an ongoing lack of physical activity and a diet completely lacking in purine-neutralising foods, such as berries, as well as other specific fruit and vegetables (see below). Others have refined this theory, saying that some are genetically predisposed to gout and some are not. As a result, people who are not predisposed can live over-indulgent lifestyles and not develop gout, while others who are predisposed can develop gout, despite being physically active and having a well-rounded diet. However, most in the "genetic predisposition" school of thought nonetheless believe that the condition is much more likely to develop in the predisposed if the other factors are present over several years (excess alcohol, inactivity and failure to eat purine-neutralising foods). It is known that lead sugar was used to sweeten wine, and that chronic lead poisoning is a cause of gout, which condition is then known as saturnine gout, because of its association with alcohol and excess.
Gout can also develop as co-morbidity of other diseases, including polycythaemia, leukaemia, intake of cytotoxics, obesity, diabetes, hypertension, renal disorders, and hemolytic anemia. This form of gout is often called secondary gout. Diuretics (particularly thiazide diuretics) have traditionally been blamed for precipitating attacks of gout, but a Dutch case-control study from 2006 appears to cast doubt on this.
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Important notice:
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