Hyperuricemia literally means a raised uric acid level in the body. This occurs due to a variety of factors ranging from genetic to dietary ones. It may be symptomatic or asymptomatic. The treatment involves modifying the metabolism of uric acid to either decrease production or increase excretion of uric acid from the body.
Some cases of hyperuricemia are asymptomatic while others manifest particular symptoms. The typical presentation is gout, usually of a single joint, seen most often in the big toe. Other joints affected include the ankle and knee. High serum uric acid levels also result in nephrolithiasis. This presents with flank and groin pain, hematuria, nausea, and vomiting.
Entire Body System
- Hodgkin Lymphoma
We report the first clinical use of PEG-modified Arthrobacter protoformiae uricase (PEG-uricase) to treat hyperuricemia in a patient with non-Hodgkin lymphoma and renal insufficiency who was allergic to allopurinol. [ncbi.nlm.nih.gov]
Hyperuricemia and tumor lysis syndrome in children with non-Hodgkin’s lymphoma and acute lymphoblastic leukemia. [tjh.com.tr]
"Hyperuricemia and tumor lysis syndrome in children with non-Hodgkin's lymphoma and acute lymphoblastic leukemia / Non-Hodgkin lenfoma ve akut lenfoblastik losemili cocuklarda hiperurisemi ve tumor lizis sendromu." [go.gale.com]
Patients with acute lymphoblastic leukemia and non-Hodgkin’s lymphoma, particularly Burkitt’s lymphoma, are at greatest risk because of the high sensitivity of the cells to chemotherapy. [link.springer.com]
Liver, Gall & Pancreas
The initial investigations carried out to confirm the diagnosis should include a complete blood count, urinalysis, blood urea, serum uric acid, as well 24-hour urine sample collection for determining uric acid levels. The next step of investigation involves assessing the type of hyperuricemia. For identifying primary hyperuricemia, various enzyme assays are conducted which include hypoxanthine-guanine phosphoribosyltransferase levels as well as glucose-6 phosphate dehydrogenase levels among others. Secondary hyperuricemia may be due to decreased excretion or excessive production. These two can be differentiated by assessing a 24-hour urine sample for uric acid without dietary restriction.
Treatment for hyperuricemia involves the use of drugs which either inhibit xanthine oxidase and hence synthesis of uric acid, or drugs which accelerate uric acid excretion from the body . Xanthine oxidase inhibitors include allopurinol as a first choice in the USA  and febuxostat; Uricosuric drugs include drugs like probenecid and benzbromarone  . Another upcoming class of drugs includes those which degrade uricase and include rasburicase and pegloticase  .
Treatment for hyperuricemia is not advised when it is asymptomatic as it is likely to remain asymptomatic for years . However, uric acid lowering treatment with allopurinol, an effective and economical option  , is indicated in patients who have had more than one episode of acute gout, all patients with chronic gout and tophi as well as patients with uric acid nephrolithiasis . Other cases where allopurinol is indicated include the inherited enzyme deficiency disorders, such as Lesch-Nyhan Syndrome and Kelley-Seegmiller syndromes, as well as the uses for prophylaxis before chemotherapy for cancer .
FDA approved dose of allopurinol in patients with preserved renal function have been reinforced by EULAR guidelines  . The starting dose is 100 mg daily which may be increased by another 100 mg over one to four weeks, in order to achieve a serum urate level of >6mg/dL  . Uricosuric agents like probenecid are used as a last resort, despite their rapid mode of action , because of the need for frequent dosing, the 24-hour urine analysis prior to beginning therapy  and the increased likelihood of causing urolithiasis in people with acidic urine .
Patients should also be educated to modify their diet and lifestyle as adjunctive therapy; this includes avoiding red meat, shellfish and alcohol as well as incorporating exercise in one’s daily routine . Uric acid levels must be maintained at 5-6 md/dL, as above this level uric acid solubility decreases and starts to deposit in the body .
Hyperuricemia occurs due to overproduction, underexcretion or a combination of these two mechanisms . Overproduction or ‘renal overload type’  of uric acid occurs only in a minority of patients and may be due enzyme defects resulting in either increased de novo synthesis of purines or their increased breakdown . According to a study, hyperuricemia in children was most often due to an attack of gastroenteritis, with upper respiratory tract infections and cardiac problems being the next most common causes . Underexcretion of uric acid occurs in the majority of patients suffering from hyperuricemia and is involved in diabetic ketoacidosis, excessive intake of aspirin, diuretics (such as thiazides and loop-diuretics), antituberculous drugs (such as pyrazinamide and ethambutol) and cyclosporine A . It is also the leading cause for hyperuricemia leading to gout .
Hyperuricemia occurring due to a combination of both overproduction and underexcretion of uric acid is seen mostly after alcohol consumption . According to studies conducted in the United States, the progressive increase in obesity, hypertension, diabetes and kidney problems is associated with a concomitant increase in serum uric acid levels .
Although the upper limit of uric acid in children is 5mg/dL, the likelihood of developing hyperuricemia increases with age especially over 65 years. This is due to an increased prevalence of conditions associated with hyperuricemia such as hypertension, chronic kidney disease, metabolic syndrome, diabetes and cardiac diseases and increased intake of diuretics and aspirin in this age range   . It has also been noted that hyperuricemia occurs more often in men than in women, and according to a survey the men to women ratio is between 7:1 and 9:1 . However, the incidence is higher is post-menopausal women .
According to research, the levels of serum uric acid depend on many genes. It is seen more often in African Americans, due to a higher rate of obesity, renal disease and hypertension , in Maoris, Samoans and Filipinos, due to their genetic makeup and dietary factors such as increased intake of seafood , and in certain native races of the Pacific, due to a lower rate of uric acid excretion .
Hyperuricemia is classified into three types: overproduction, underexcretion and mixed type. The overproduction type of hyperuricemia is seen in conditions like Lesch-Nyhan Syndrome, where there is deficiency of the hypoxanthine guanine phosphoribosyl transferase enzyme because of a deficiency of the HPRT gene, intake of purine rich foods, and after cytolysis occurring due to chemotherapy in leukemias . It also occurs after ingestion of purine rich foods such as red meat and seafood  . Research has shown that fructose particularly increases serum uric acid levels by accelerating the metabolism of nucleotides containing adenine. This has been further proved by a study showing that serum uric acid levels were found to be 35% higher six hours after ingestion of five apples .
The underexcretion type of hyperuricemia occurs in familial juvenile hyperuricemic nephropathy due to abnormality of the uromodulin gene sudden weight loss; with the mixed type is seen in cases of deficiency of glucose 6-phosphatase enzyme as a result of a defective glucose 6-phosphatase gene and increased intake of alcohol . Hyperuricemia is usually seen in patients suffering from the metabolic syndrome. In fact, studies are now showing that hyperuricemia itself may be a risk factor for cardiovascular disease . The transporters found to be associated with urate transport include URAT1, a urate/anion exchanger, hOAT1, a human organic anion transporter and UAT, another urate transporter. Studies have found that variants of the gene SLC2A9 are strongly associated with uric acid transport . Humans and other primates excrete uric acid as the end product of purine metabolism because they lack the enzyme uricase, which in other animals breaks down uric acid to a more soluble product: allantoin .
The best method to prevent hyperuricemia is to modify the diet so that it includes less quantities of foods contributing to a high serum uric acid level like red meat, seafood, beans and peas, and more quantities of foods which tend to lower uric acid levels. The latter includes eggs, cheese and starches, to name a few. Regular exercise, weight reduction, keeping blood pressure under control and drinking plenty of water daily also help prevent the development of hyperuricemia.
Hyperuricemia is the presence of excessive uric acid in the body. The normal level of uric acid in adult females is 360 µmol/L or 6 mg/dL and in adult males it is 400 µmol/L or 6.8 mg/dL. Uric acid is the byproduct of protein metabolism and is also produced as a result of cell turnover. Most of the uric acid is eliminated from the body via the urine and the rest via the gastrointestinal system. Excessive production or defective excretion may result in high serum uric acid levels.
Hyperuricemia is a condition in which the levels of uric acid in the blood rise above the normal limit. This increase may be silent or may start causing problems like gout or renal stones. There are many etiological factors that can be responsible for the development of hyperuricemia, such as genetic, dietary, renal diseases or simply the taking certain drugs. The treatment depends upon whether the hyperuricemia is silent or manifested. In case there are signs and symptoms of high serum uric acid such as tophaceous gout or kidney stones, then appropriate treatment should be sought so as to keep the uric acid within normal limits. The long term outcome depends on the reason behind the raised uric acid levels and how well it is treated and followed-up.
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