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PubMed1994

Familial interstitial nephropathy without hyperuricemia.

Progressive hereditary nephropathy is described in 6 members of a single family. Renal biopsies, performed in 3 patients, revealed tubular atrophy, interstitial fibrosis, and lymphomonocytic infiltration associated with severe vascular lesions. These features were disproportionately serious when related to age, arterial pressure, and renal function. Similar familial nephropathy has been reported in the literature, generally in association with gout or asymptomatic hyperuricemia. The patients described here had normal blood concentrations of uric acid. It is proposed that the members of the present group of patients are suffering from the same interstitial nephropathy as that described in the literature and that the hyperuricemia found by other investigators is coincidental and does not play a pathogenetic role.

Adult↗
PubMedDate not supplied

Rasburicase: an innovative new treatment for hyperuricemia associated with tumor lysis syndrome.

Rasburicase is a new treatment for hyperuricemia, a metabolic manifestation of tumor lysis syndrome (TLS). Rasburicase has a unique mechanism of action that allows uric acid byproducts to be easily excreted in the urine. Clinical trials have shown that rasburicase has a rapid onset of action that allows chemotherapy to be delivered on time and prevents hyperuricemia-related complications, including renal compromise. The drug has been used successfully in adults and children. The main side effect of rasburicase is the potential for a hypersensitivity reaction. The drug is contraindicated in patients with glucose 6-phosphate dehydrogenase (G6PD) deficiency because this can precipitate hemolytic anemia. The drug has not been studied in patients with a history of allergies or asthma. Oncology nurses play a major role in the assessment and management of TLS-related complications. They must assess patients for G6PD deficiency and signs and symptoms of hypersensitivity reaction before and during chemotherapy or other therapeutic interventions. Nurses play a direct role in preventing complications related to TLS and contributing to the quality of life in this patient population.

Child↗
PubMed1994

Hyperuricemia and insulin resistance.

The associates of gout-obesity, hypertriglyceridemia, glucose intolerance, and hypertension, strikingly resemble those of insulin resistance. In the present study we determined whether hyperuricemia is associated with insulin resistance and, if so, whether this association can be explained by other components of the syndrome. For this purpose we quantitated insulin sensitivity (euglycemic clamp) in 37 nondiabetic subjects (aged 30-68 yr) exhibiting varying degrees of the metabolic syndrome (body mass index, 21.5-35.7 kg/m2; serum triglycerides, 0.4-22.0 mmol/L; high density lipoprotein cholesterol 0.38-1.86 mmol/L; blood pressure, 190-100/116-60 mm Hg). In simple linear regression analysis, the serum uric acid concentration (range, 182-568 mumol/L) was inversely correlated with insulin sensitivity (rate of glucose utilization; r = -0.61; P < 0.001) and positively with serum triglycerides (r = 0.68; P < 0.001), but not with body mass index, age, or the plasma glucose concentration. In multiple linear regression analysis, both insulin sensitivity (P < 0.05) and serum triglycerides (P < 0.005) were independently associated with the serum uric acid concentration, and together explained 50% of its variation. Addition of body mass index or age to the model did not improve the degree of explanation. Acute elevation of serum triglycerides about 3-fold, of plasma FFA about 9-fold, or of serum insulin about 28-fold had no effect on the serum uric acid concentration in healthy volunteers. The data indicate that hyperuricemia is indeed an inherent component of the metabolic syndrome and could also be used as a simple marker of insulin resistance.

Adult↗
PubMed1998

Determination of uric acid in scalp hair for non-invasive evaluation of uricemic controls in hyperuricemia.

The uric acid concentration in blood has been widely accepted as a diagnostic indicator of hyperuricemia and gout, and its assay method is well established. In the present study, we developed a simple and rapid method for the determination of uric acid in hair, which can be obtained non-invasively. The concentration (nmol/mg hair) of uric acid extracted from 10-20 mg hair with 0.1 M potassium hydroxide was determined by an enzymatic method using uricase. The concentration of uric acid (nmol/mg hair, mean+/-S.D.: 0.49+/-0.157, n=16) in hair from hyperuricemic patients was significantly higher than that (0.26+/-0.107, n=8) in healthy volunteers (p<0.01). The within-run and between-day precision (CVs) of the assay was 9.6-10.3% (n=10 each) and 11.6-16.3% (n=7 each), respectively. The concentration (nmol/mg hair, y) of uric acid in hair correlated well with that in serum (mg/l, x): y=0.09x-0.12 (r=0.75, Syx=0.122, n=23). Changes in the concentration of uric acid in the hair of antihyperuricemic drug-treated patient paralleled that in serum, suggesting that the concentration of uric acid in hair is a reliable indicator of the metabolic control in hyperuricemia.

Adult↗
PubMed1978

Hyperuricemia associated with hypertension. A 4-year follow-up study of hyperuricemic hypertensives.

We investigated the prognosis of 153 hypertensive patients, whose initial concentration of serum uric acid had been evaluated. One hundred and seventeen subjects could be followed up after 4 years and 16 of them died during the follow-up period. Cerebrovascular disease was seen in 6 subjects, 4 of whom died from the disease. Myocardial infarction and heart failure occurred in 9 and 7 of them died as a result. The frequency of these diseases was greater among the hyperuricemic group and 8 of the 11 who died belonged to this group. Four men were struck by gouty attacks. They were all hyperuricemic and had been proven to have at least one family member with asymptomatic hyperuricemia and/or gout. It is reasonable to regard the presence of hyperuricemia as one of the poor risk factors for vascular diseases. I addition, we must investigate more closely personal and family histories of gout when we see hyperuricemic subjects, regardless of absence of gouty symptoms.

Adolescent↗
PubMed1992

Circadian rhythm of plasma uric acid and handling stress-induced hyperuricemia in conscious cebus monkeys.

An apparent circadian rhythm of plasma uric acid and the effect of handling stress on plasma uric acid level in conscious cebus monkeys were demonstrated. The lowest level of plasma uric acid in the circadian rhythm occurred early in the morning and the highest, before bedtime at night. With experimental handling stress, the plasma uric acid level rose to much more than the maximum level of the circadian rhythm. Stress-induced hyperuricemia could be inhibited without an increase of urinary uric acid excretion by the minor tranquilizer diazepam at doses of more than 1 mg/kg, p.o. On the other hand, benzbromarone at 20 mg/kg, p.o. significantly inhibited the hyperuricemia with a hyperuricosuric effect, while probenecid at 50 mg/kg, p.o. had no effect on either the increased plasma uric acid or urinary uric acid excretion. Accordingly, it is concluded that the plasma uric acid level in conscious cebus monkeys easily fluctuates with experimental conditions and that the animals can be utilized to evaluate the hypouricemic and hyperuricosuric property of benzbromarone-like agents.

Animals↗
PubMed2000

Hyperuricemia in severe pulmonary hypertension.

STUDY OBJECTIVE: Hyperuricemia occurs frequently in patients with myeloproliferative and lymphoproliferative disorders and in patients with congenital heart disease associated with polycythemia. Whether hyperuricemia is common in patients with severe pulmonary hypertension is not known. DESIGN, PATIENTS, MEASUREMENTS: In the Pulmonary Hypertension Center at the University of Colorado Health Sciences Center between September 1991 and August 1997, 442 consecutive patients were evaluated with right heart catheterization; 191 patients also had a measurement of the serum uric acid (UA) in close temporal proximity to the hemodynamic evaluation. RESULTS: Of the 191 patients with a complete data set, 99 patients had primary pulmonary hypertension (PPH) and 92 had secondary pulmonary hypertension. For the entire cohort with severe pulmonary hypertension (n = 191), there was a positive correlation between the natural logarithm of the serum UA (lnUA) and the mean right atrial pressure (RAP; r = 0.47; p < 0.001). When analyzed separately, the correlation between lnUA and RAP was stronger in the patients with PPH (r = 0.642; p < 0.001). This correlation cannot be explained by diuretic use or impaired hepatocellular function. Neither mean pulmonary artery pressure nor cardiac output was as well correlated with the RAP when compared with the lnUA. Some patients with PPH had serum UA measurements repeated during treatment with chronic IV prostacyclin infusion. Eleven of these 18 patients (61%) demonstrated a decrease in serum UA during prostacyclin treatment. CONCLUSION: There is a positive correlation between the RAP elevation and the serum UA levels in patients with PPH. Serum UA levels drop in some, but not all PPH patients during chronic prostacyclin infusion therapy.

Adult↗
PubMed1988

Diuretics and hyperuricemia in the elderly.

Serum uric acid (SUA) was studied in a rural population of 420 males and 592 females aged 65 years or more. The mean SUA concentration was 0.313 mmol/l in males and 0.316 mmol/l in females. In males, 47 (11.2%) and in females 60 (10.1%) had a SUA level of 0.42 mmol/l or more. Both the mean serum values and the frequency of hyperuricemia were higher than 11 years earlier in another, similar study. The SUA concentration was 0.361 mmol/l in the 435 individuals using diuretics and 0.281 mmol/l in the remaining 578. Of the 107 hyperuricemic individuals, 82% used diuretics, and only 2 out of those 20 where the SUA level was 0.50 mmol/l or more did not use diuretics. Apart from diuretics, only the serum creatinine concentration, the Body Mass Index, body weight and the hematocrit level were significantly associated with hyperuricemia in both sexes.

Aged↗
PubMed1988

Use of polyethylene glycol-modified uricase (PEG-uricase) to treat hyperuricemia in a patient with non-Hodgkin lymphoma.

Modification by covalent attachment of monomethoxypolyethylene glycol (PEG) can reduce the immunogenicity and prolong the circulating life of injected enzymes, making their use as therapeutic agents feasible. 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. Two intramuscular injections totaling 3 U/kg body weight during the first 30 hours of treatment lowered the plasma urate level from 910 to 190 mumol/L (15.3 to 3.2 mg/dL), after which a dose of 2 U/kg every 5 to 6 days maintained the plasma urate level at 540 mumol/L (9 mg/dL) or lower. After the injection of PEG-uricase, uricase activity appeared in plasma rapidly, peaking within 24 hours and persisting for approximately 5 days; an inverse relation between plasma uricase activity and plasma urate concentration was noted. The agent was nontoxic and well tolerated. No antibody to either PEG-uricase or unmodified uricase developed over a 3-week period, during which four doses of PEG-uricase were administered. Because of its long circulating life, PEG-uricase is probably a more effective hypouricemic agent than unmodified uricase, which has previously had limited use. As an adjunct to cytolytic therapy for hematologic malignancies when protection from hyperuricemia is needed rapidly, PEG-uricase deserves further study.

Drug Administration Schedule↗
PubMed1999

Gout and hyperuricemia.

Gout is a condition characterized by the deposition of monosodium urate crystals in the joints or soft tissue. The four phases of gout include asymptomatic hyperuricemia, acute gouty arthritis, intercritical gout and chronic tophaceous gout. The peak incidence occurs in patients 30 to 50 years old, and the condition is much more common in men than in women. Patients with asymptomatic hyperuricemia do not require treatment, but efforts should be made to lower their urate levels by encouraging them to make changes in diet or lifestyle. Acute gout most commonly affects the first metatarsal joint of the foot, but other joints are also commonly involved. Definitive diagnosis requires joint aspiration with demonstration of birefringent crystals in the synovial fluid under a polarized light microscope. Treatment includes nonsteroidal anti-inflammatory drugs (NSAIDs), colchicine, corticosteroids and analgesics. In patients without complications, NSAID therapy is preferred.

Acute Disease↗
PubMed1999

[The central mechanisms regulating the blood circulation in hyperuricemia].

In experiments conducted on male Wistar rats for elucidation the role of central mechanisms in development alterations of heart electric stability was studied activity of 5(1)-nucleotidase and adenosine desaminase in sensomotor cortex, hypothalamus and hippocamp. Were shown that changes of heart function were in case increased adenosine content in neurons of sensomotor cortex, hypothalamus and hippocamp. Introduction to animals with hyperuricemia DOCA, with activate 5(1)-nucleotidase and adenosine desaminase, was accompanied by changes of cAMP and cGMP content in neurons. Developing alterations of heart electric stability suggest the responsibility of injury adenosine metabolism in different brain structures of animals with hyperuricemia in alterations of central regulatory mechanisms of systemic blood flow.

Adenosine↗
PubMed1999

[Hyperuricemia and arthralgia during pyrazinamide treatment].

We studied 51 pulmonary tuberculosis patients who were initially treated with pyrazinamide (PZA) at our hospital between April 1996 and December 1997. PZA dosage was less than 1.5 g per day, and the chemotherapy course lasted 2 months. Uric acid levels of higher than 8 mg/dl were observed in 44 patients (86%). Arthralgia was observed in 9 patients. Acute gout was observed in only 1 patient who had hyperuricemia prior to PZA treatment and a predisposition for gout. The other 8 patients with arthralgia had symptoms in the shoulders and knees, but no gouty pain. Arthralgia was not related to serum uric acid level and disappeared after PZA treatment was stopped. We concluded that PZA can be used for up to 2 months without the combined administration of allopurinol or benzbromarone even if hyperuricemia or arthralgia develops.

Antitubercular Agents↗
PubMed1975

[Reversible hyperuricemia in case of ureteral colics (author's transl)].

On about one fourth of the patients ureteral colics caused by oxalate and phosphate calculi lead to a reversible hyperuricemia. This result seems to be important, because we might wrongly diagnose a uric acid calculus. The reason for hyperuricemia is a temporary diuretic disturbance of the uric acid. It cannot be explained by the functional loss of the obstructed kidney, because a nephrectomy does not change the uric acid level. As a possible reason we suppose a ketose by food deficiency and vomiting caused by renal colic.

Blood Urea Nitrogen↗
PubMed1975

Allopurinol and gouty hyperuricemia. Efficacy of a single daily dose.

The effect of daily administration of a single 300-mg tablet of allopurinol on serum urate levels was compared with the effect of divided doses of the drug (100 mg three times a day) in an open-labeled crossover trial of 20 patients with hyperuricemia and gout. Under both regimens of treatment there was a prompt fall in serum urate levels, and analysis of variance indicated no significant difference between the two modes of administration of allopurinol. Nor was there any significant difference in the minimum serum levels of oxypurinol. On the basis of this short-term study, the use of a single 300-mg tablet of allopurinol per day appears to be an effective means of lowering the elevated serum urate levels of individuals with gouty hyperuricemia and compares favorably with the results obtained by allopurinol in divided doses.

Acute Disease↗
PubMed2001

[A case of familial hypokalemic periodic paralysis with hyperuricemia during paralytic attack and genetic analysis of the pedigree].

We reported a 13-year-old boy and his family with hypokalemic periodic paralysis. He showed marked hyperuricemia during his paralytic attack, although neither ischemic forearm exercise test nor bicycle-ergometer exercise test revealed myogenic hyperuricemia when he was free from paralysis. Genetic analysis was performed to the proband and his affected elder brother, mother, and, maternal grand mother. We found the Arg528His mutation of CACNL1A3 gene in all the patients examined. The severity of the attacks and the age of onset did not vary in the different generations, and male predominancy was not evident in this family.

Adolescent↗
PubMed1992

[Treatment of arthritis urica and hyperuricemia].

The diagnosis of gout is confirmed by detection of monosodium urate crystals in the fluid of the joint or from tophi. This article discusses treatment of acute gout, prevention of acute attacks and treatment of hyperuricemia. Non-steroidal anti-inflammatory drugs are recommended as drugs of choice in treatment of acute gout. Self-administration of non-steroidal anti-inflammatory drugs is recommended for prevention of gout. Drugs to counteract hyperuricemia should be used only on specific indications. Measurement of the "24-hour" urinary uric acid content is important when deciding treatment.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMedDate not supplied

Etiology of hyperuricemia.

Hyperuricemia is a common laboratory finding with significant clinical implications. It is easily detected, but its mechanisms may not be clearly elucidated. A scheme of pathogenesis has been outlined and diagrammed but much is conjectural; therefore, the classification is merely tentative. About 45 diseases or categories of conditions, 20 drugs, and nine states of intoxication have been surveyed. Hyperuricemia can be a multifactorial genetic disorder or a discrete response to a specific stimulus. It may be governed by a complex interplay of biochemical disorders for a lifetime duration, or it may be determined by environmental forces for a very transient course. Some conditions have both increased production of uric acid as well as decreased renal outflow. For many patients, the underlying mechanisms have not yet been elucidated.

Anemia↗
PubMed1976

[Plasma fibrinogen activity in diabetes mellitus, hyperlipoproteinemia and hyperuricemia (author's transl)].

Plasma fibrinogen content was measured in 20 normal subjects, 20 patients with diabetes mellitus, 20 patients with hyperlipoproteinemia type II or IV (Fredrickson) and 10 patients with hyperuricemia. These vascular risks were accompanied by significant increase of plasma fibrinogen in comparison with the normal collective. The highest fibrinogen concentrations were found in diabetics, followed by hyperuricemias and hyperlipoproteinemias. The importance of coagulation disturbances is discussed in regard of angiopathogenesis.

Adult↗