Uric acid elevated serum levels

Etiology - In the study of the causes of atherosclerosis. the factors found most likely to be present in the living system prior to death, in relation to the proven presence of coronary atherosclerosis at autopsy, are advanced age, elevated serum cholesterol, and elevated blood pressure, with elevated blood lipids and the presence of diabetes appearing influential. Other measurable metabolic parameters found to correlate as coronary heart disease risk factors are elevated serum uric acid, , lowered serum albumin levels, lowered lipoprotein lipase and lowered endogenous heparin. Of these factors, "cholesterol" continues as a favorite research topic. 

In those with gout, the serum uric acid level is usually elevated. Sulfinpyrazone increases the excretion of uric acid by the kidneys, which lowers serum uric acid levels and consequently retards the deposit of urate crystals in the joints. Probenecid (Benemid) works in the same manner and may be given alone or with colchicine as combination therapy when there are frequent, recurrent attacks of gout. Probenecid also has been used to prolong the plasma levels of the penicillins and cephalosporins. 

The serum uric acid level often is elevated but may be normal during an acute attack. 

Hyperuricemia Elevated serum uric acid concentration, defined as a level greater than 7.0 mg/dL. 

Workers at a molybdenum-roasting plant with time-weighted average (TWA) exposures of approximately 9.5mgMo/m to soluble dusts had increased plasma and urine levels of molybdenum the only adverse biochemical findings were large elevations in serum ceruloplasmin levels and some increase in serum uric acid levels. ... 

Diarrhea nausea vomiting jaundice liver enzyme abnormalities. Azotemia elevated BUN/creatinine increased serum uric acid levels (in patients predisposed to gouty arthritis) thrombocytopenia megaloblastic anemia weakness dizziness Hypokalemia headache dry mouth anaphylaxis. ... 

Serum uric acid - Serum uric acid levels are elevated by salicylate levels less than 10 mg/dL and decreased by levels more than 10 mg/dL. 

Adverse reactions may include anaphylactoid reactions, dermatitis, pruritus, decreases in visual acuity, anorexia, nausea, vomiting, Gl upset, abdominal pain, fever, malaise, headache, dizziness, mental confusion, disorientation, possible hallucinations, peripheral neuritis, elevated serum uric acid levels, precipitation of acute gout, transient impairment of liver function, and joint pain. 

The thiazides have a variable effect on elimination of uric acid, which also is secreted by the renal acid secretory mechanism. Administration of thiazide diuretics, especially at low doses, may elevate serum uric acid levels and cause goutlike symptoms. Following large doses, thiazides may compete with uric acid for active reabsorption and thereby may promote uric acid elimination rather than impair it (see Chapter 37). 

The addition of a phenylsulfoxide moiety to the end of the side chain markedly changes the activity of this class of compounds. This product, sulfinpyrazone (97-11), stimulates uric acid excretion, making it a valuable dmg for dealing with the elevated serum uric acid levels associated with gout. The compound is stiU one of the more important uricosuric agents available today. The starting ester (96-9) is available by alkylation of the dianion from ethyl malonate with 2-chloroethylphenyl thioether. Condensation with diphenylhydrazine (97-3) in the presence of a base then affords the pyrrazolodione (97-10). Oxidation of sulfur with a controlled amount of hydrogen peroxide leads to the sulfoxide and thus sulfinpyrazone (97-11) [107]. 

All thiazides are secreted by the organic acid secretory system in the proximal tubule and compete with the secretion of uric acid by that system. As a result, thiazide use may blunt uric acid secretion and elevate serum uric acid level. 

A 42-year-old male cancer patient undergoing radiation therapy develops severe pain in his right big toe. Laboratory analyses indicate an elevated serum uric acid level and urate crystals in his urine. This patient s pain is caused by the overproduction of the end product of which of the following metabolic pathways ... 

Uric acid, an end product of protein catabolism, was identified as the cause of gout in the middle of the 19th century. Patients with primary hyperuricemia have elevated serum uric acid levels because of increased production of uric acid or impaired renal excretion of uric acid. 

Monitor for hyperuricemia (elevated serum uric acid level). 

There have been reports of young children with elevated serum uric acid levels, some of whom appeared to have concurrent mental aberrations (C2, R7). In at least one case there were no symptoms other than those normally associated with gout (R13). 

Elevated serum uric acid levels leukocytosis... 

On the other hand, if the patient had a severe attack of gouty arthritis, a complicated course of uric acid lithiasis, a substantially elevated serum uric acid level (> 10 mg/dL), or a 24-hour urinary excretion of uric acid of more than 1000 mg, then prophylactic treatment should be instimted immediately after resolution of the acute episode. Prophylactic therapy is also appropriate for patients with frequent attacks (more than two or three per year) of gouty arthritis. 

Allopurinol is used not only in treating the hyperuricemia associated with gout but also in the secondary hyperuricemia associated with the use of antineoplastic agents. Therefore, allopurinol may be used in the management of patients with leukemia, lymphoma, and solid tumor malignancies who are receiving cancer therapy that causes elevations of serum and urinary uric acid levels. Allopurinol may interfere with the metabolism of antineoplastic agents such as azathioprine and 6-mercaptopurine. 

Candidates for teriparatide treatment include women who have a history of osteoporotic fracture, who have multiple risk factors for fracture, or who failed or are intolerant of previous osteoporosis therapy. Teriparatide should not be used in patients who are at increased baseline risk for osteosarcoma (including those with Paget s disease of bone, unexplained elevations of alkaline phosphatase, open epiphyses, or prior radiation therapy involving the skeleton). Full-length PTH(l-84), which is in clinical trials, has not been associated with osteosarcomas. Other adverse effects have included exacerbation of nephrolithiasis and elevation of serum uric acid levels. 

Mechanism Uricosuric agents (probenecid, sulfinpyrazone) are weak acids that compete with uric acid for reabsorption by the weak acid transport mechanism in the S2 segment of the proximal renal tubule. At low doses, these agents may also compete with uric acid for secretion by the tubule and (occasionally) can even elevate serum uric acid concentration. Elevation of uric acid levels by this mechanism occurs with aspirin (another weak acid) over much of its dose range. 

Side effects and adverse reactions of thiazides are electrolyte imbalances, hyperglycemia, hypemricemia (elevated serum uric acid level), and hyperUpi-demia (elevated blood lipid levels). They affect the metaboUsm of carbohydrates. 

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