An elevated serum uric acid level, typically more than 6 mg/dL in women and 7 mg/dL in men, is referred to as hyperuricemia. An estimated 38 million Americans have elevated serum uric acid, and the number of cases is rising globally as more developing nations embrace Western diets and lifestyles. The majority of those who have this condition won’t show any overt symptoms, but it’s unknown how long-term hyperuricemia will affect renal function, general morbidity, and cardiovascular health in general. Increased uric acid production, decreased excretion, or a combination of the two can lead to hyperuricemia.

About one-third of the body’s daily production of serum uric acid comes from endogenous sources; the remainder is attributed to dietary purines. Additionally, accelerated purine degradation in high cell turnover states (such as hemolysis, rhabdomyolysis, and tumor lysis) and decreased excretion (such as in genetic disorders, renal insufficiency, and metabolic syndrome) have been linked to elevated uric acid levels. The kidneys excrete about two thirds of uric acid, while the gastrointestinal (GI) tract excretes the remaining one third. These ratios, however, may vary based on medication interactions or problems with the GI or renal systems.

Overproduction of Uric Acid

.Alcohol (especially beer), bacon, beef, lamb, turkey, veal, venison, organ meats, and some fish and shellfish (such as anchovies, cod, tuna, sardines, herring, mussels, shrimp, lobster, codfish, scallops, trout, and haddock) are examples of foods high in purines.

.Because fructose is metabolized by the liver via the aldolase reductase pathway, it results in hyperuricemia. Full-sugar sodas and high-fructose corn syrup are particularly detrimental and linked to childhood and teenage obesity.

.Purine metabolism errors include phosphoribosylpyrophosphate (PRPP) synthetase overactivity and hypoxanthine-guanine phosphoribosyltransferase (HPRT or HGPRT) deficiency.

.High rates of cell lysis or turnover include those caused by chemotherapy, intense exercise, lymphoproliferative disorders, myeloproliferative disorders, polycythemia vera, Paget disease, psoriasis, tumor lysis, hemolysis, and rhabdomyolysis.

Mechanism of Hyperuricemia

Purine breaks down into uric acid (2,6,8 thiopurine-C5H4N4O3). Ionized urate, or uric acid, circulates at the normal physiological pH of 7.4. Purine metabolism can happen in any tissue that contains xanthine oxidase, including cardiac and pulmonary tissue, but it mostly happens in the liver. Roughly two-thirds of the uric acid that the body produces is eliminated through the kidneys, with the remaining third entering the intestine. Ninety percent of the ureate that is filtered and secreted by the kidneys is reabsorbed in the proximal tubule. Because of the activity of uricase, which changes urate into the more water-soluble allantoin, other mammals have much lower levels of uric acid. This enzyme is inactive in humans and higher primates, though.

Uric acid production is accelerated by purine-rich diets, endogenous purine production, and high cell breakdown. Particularly high in purines, beer raises blood levels of uric acid. Phosphoribosylpyrophosphate (PRPP) synthetase activity and a malfunction in the regulatory enzyme hypoxanthine-guanine phosphoribosyltransferase (HPRT) can both speed up the body’s natural production of purines. Conditions such as rhabdomyolysis, hemolysis, psoriasis, myeloproliferative disorders, and tumor lysis are examples of accelerated cell turnover or breakdown.

Symptoms of of hyperuricemia may include:

 

TREATMENT :

Certain dietary changes may help decrease the level of uric acid in your blood. If your hyperuricemia is tied to gout, dietary changes may lower your risk of gout attack and slow the progression of any joint damage.

Remember that uric acid is formed when purines break down in your body. Although purine occurs naturally, it’s also present in certain foods. Avoiding these foods may be beneficial.

WHAT TO AVOID :

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