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PubMed2000

Continuous veno-venous hemodiafiltration for the treatment of spontaneous tumor lysis syndrome complicated by acute renal failure and severe hyperuricemia.

We describe a case of Burkitt's lymphoma presenting as spontaneous tumor lysis syndrome (TLS) complicated by severe hyperuricemia and anuric acute renal failure presumed to be secondary to uric acid nephropathy. The patient was treated with continuous veno-venous hemodiafiltration (CVVHDF) using a dialysate flow rate of 2.5 l/h, and a replacement fluid rate of 1.5 l/h (administered in pre-dilution). Mean clearances during CVVHDF for urea, creatinine, uric acid, and phosphorus were, respectively, 55.8 +/- 3.8, 48.9 +/- 2.6, 45.1 +/- 2.6 and 47.0 +/- 3.3 ml/min (or 80, 70, 65 and 68 l/day, respectively). Serum urea, creatinine, uric acid, and phosphorus decreased from 42 to 9 mmol/l, 533 to 189 micromol/l, 1980 to 372 micromol/l, and 2.0 to 1.4 mmol/l, respectively, after 48 hours of CVVHDF. Previously, we reported the use of continuous arteriovenous hemodialysis (CAVHD) at a high dialysate flow rate of 4 l/h for the treatment of acute renal failure and TLS, which provided excellent continuous clearances of small molecular weight solutes. This last modality was very efficient and prevented deleterious rebound in serum solute concentrations frequently observed in TLS after intermittent hemodialysis (IHD). It was concluded that high-dialysate flow rate CAVHD was a more potent form of treatment than conventional IHD. With recent advances in technology, veno-venous continuous renal replacement therapies are becoming more popular than arterio-venous modalities since they are safer and less cumbersome. Furthermore, flow rates being precisely regulated, solute clearances can be steadily maintained. With CVVHDF flow rates as used in this report, we achieved excellent solute clearances and metabolic control. We propose CVVHDF as an ideal treatment for acute renal failure in TLS. In our opinion, CVVHDF is an advantageous alternative to treat TLS complicated by acute renal failure.

Acute Kidney Injury↗

PubMed1992

Gout and hyperuricemia.

A number of investigators have applied the tools of molecular biology to characterize genes responsible for the control of urate homeostasis and clarify the roles of uric acid precursors in inflammation. Some, using the tools of clinical medicine, continue to provide novel descriptions of gout and to explore better ways for evaluating hyperuricemia and for understanding the pathophysiology of disorders such as familial urate nephropathy. Others link the disciplines of basic research and clinical medicine in approaching the perplexing questions of crystal-induced inflammation.

Crystallization↗

PubMed2004

The efficacy of combined low dose of Allopurinol and benzbromarone compared to standard dose of Allopurinol in hyperuricemia.

OBJECTIVE: To compare the efficacy of combined low dose of hypouricemic drugs (Allopurinol 100 mg and benzbromarone 20 mg; Allomaron) and standard dose 300 mg of allopurinol in hyperuricemia. MATERIAL AND METHOD: A prospective, open study of 94 hyperuricemic patients was done at King Chulalongkorn Memorial Hospital. Each group of 47 patients was given a combined low dose of hypouricemic drugs (Allopurinol 100 mg and benzbromarone 20 mg; Allomaron) and a standard dose 300 mg of allopurinol. Serum uric acid was measured before and 4 weeks after receiving the drugs. The efficacy was measured from the difference of the level of serum uric acid before and after receiving the drugs. RESULTS: The patients receiving the combined low dose of hypouricemic drugs and standard dose of allopurinol showed a mean reduction of serum uric acid of 2.5+/-3.4 mg/dl and 4.1+/-2.7 mg/dl consecutively. There was a statistically significant difference between the 2 groups (P = 0.010). CONCLUSION: This study demonstrates that the efficacy of standard dose 300 mg of allopurinol is superior to a combined low dose of allopurinol and benzbromarone in lowering the level of serum uric acid level.

Allopurinol↗

PubMed1975

[Diet in hyperuricemia (author's transl)].

The idea that, in view of potent drugs, the dietary treatment of a metabolic disease must be reserved for a small group of particularly susceptible patients or even for a minority of neurotically structured patients who would alone be capable of bearing the hardship of a consequent change of accustomed feeding habits needs correction. Considerably greater importance must be attached to dietetics in disorders of uric acid metabolism than formerly, particularly with a view to the status already gained by the dietary treatment of diabetes mellitus a long time ago. Dietetic therapy of familial hyperuricemia and its later clinical manifestation, gout, is a basic therapy of a preventive character. Because today, superiority is increasingly conceded to prophylaxis rather than to the treatment of late sequelae.

Adenosine Monophosphate↗

PubMed1991

Transient renal insufficiency in the neonate related to hyperuricemia and hyperuricosuria.

Transient renal insufficiency in the neonate is frequently the result of hypoperfusion of the kidneys due to circulatory compromise and is associated with a normal renal ultrasound scan. We describe an infant with transient renal insufficiency associated with hyperuricemia, hyperuricosuria and increased echogenicity of the renal medullary pyramids. Transient uric acid nephropathy may be a more common occurrence in the neonate than previously recognized.

Acute Kidney Injury↗

PubMed1991

[Postoperative hyperuricemia of cyanotic and acyanotic congenital cardiopathies].

In a prospective study, 10 children with congenital heart disease were studied before and after surgery (24-48 h). Mean age and weight, type of disease and surgery performed are described in Table 1. Six patients had acyanotic disease and 4 were cyanotic. Before surgery, the acyanotic group (AG) showed hyperuricemia compared to normal children of the same chronological age (mean +/- SE: 5.53 +/- 0.42 vs 4.27 +/- 0.22, p less than 0.02). Initial seric creatinine (sCr), increased in 3 patients of the AC and in the 4 patients of the cyanotic group (CG) compared to normal values of sCr for height (AG: 0.47 +/- 0.05 vs 0.34 +/- 0.03, p less than 0.05; CG: 0.63 +/- 0.05 vs 0.38 +/- 0.05, p less than 0.01). Post-surgery, sCr and serum uric acid (sUA) increased significantly at 24 and 48 h in both groups (Fig 1); at 24 h the increment in sUA in the AG was higher than that in the CG (p less than 0.05). There was a direct and significant correlation between the increment in sUA and sCr in the AG (Fig. 2). The urine excretion of uric acid paralleled the increment of sUA in the CG (Table 2). Fractional excretion of, sodium (FENa) was less than 1% and greater than 1% in the AG and the CG, respectively, being the basal FENa of the AG significantly lower (Table 3).(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiopulmonary Bypass↗

PubMed1991

Gout and hyperuricemia.

Accurate diagnosis is essential since gout is overdiagnosed by a factor of three. Asymptomatic hyperuricemia is not associated with adverse consequences and should not ordinarily be treated. The acute attack of gout responds to any nonsteroidal anti-inflammatory drug, and antihyperuricemic therapy with allopurinol, probenecid or sulfinpyrazone is effective in lowering uric acid and preventing further attacks. Except for prophylaxis, colchicine is not recommended for the treatment of gout because of unacceptable levels of toxicity. Diet therapy, once a mainstay of treatment, is usually not indicated since drug therapy alone is far more efficacious.

Chronic Disease↗

PubMedDate not supplied

[Effect of allopurinol on the indicators of immunity in podagra and experimental hyperuricemia].

The authors studied the immunity indices in patients with gout against the background of a long-term (one year) therapy with allopurinol, and in animals with experimental hyperuricemia. During treatment the authors observed normalization of blood immunoglobulin M level, a considerable decrease in circulating immune complexes and anti-renal antibodies, a tendency to a rise in the function of T-lymphocytes, great enhancement of the activity of polymorphonuclear phagocytes in tests with Staphylococci and nitro-blue tetrazolium. Mechanisms of action of the given drug are discussed.

Adult↗

PubMedDate not supplied

[Does hyperuricemia involve a specific cardiac or renal risk? (author's transl)].

Hyperuricemia, commonly found in hypertensive patients, is a daily problem for the practitioner, especially those induced by diuretic therapies. The most divergent opinions are being given about the cardiovascular potential risk of hyper-uricemia. This article raises the problem of the use of those substances which change the metabolism of uric acid, whether they are hyper- or hypo-uricemic. It serves to remind that one must not prescribe hypo-uricemic diuretics to patients whose uricemia is increased, because they may involve serious risks, especially renal ones.

Heart Diseases↗

PubMed1989

[Cancer and hyperuricemia--an analysis of 316 cancer patients].

Blood uric acid level in patients with solid tumor was seldom reported. Blood uric acid was measured in 316 cancer patients, 173 men and 143 women and was found higher in all patients than in normal subjects. The positive rate for cancer of kidney and urinary bladder was 93.30% and 90.90%, respectively. For other types of cancer, it was 51.27-69.23%. The level of urea was elevated in 75% of the hyperuricemic patients. The mechanisms of hyperuricemia in cancer patients were briefly discussed.

Adult↗

PubMed1977

[The treatment of hyperuricemia after kidney transplantation].

In this study of 17 renal transplant recipients with hyperuricemia the effects of allopurinol vs. benzbromarone were compared. Both drugs effectively lowered serum uric acid concentrations by 19 vs. 35% of pretreatment values. Adverse reaction to allopurinol consisted in augmenting of azathioprin toxicity for bone marrow, with occurrence of an isolated fall in the hematocrit in several patients. With benzbromarone no drug interactions were observed. However, one patient exhibited uric acid stone formation in the damaged kidney.

Allopurinol↗

PubMed1987

Vasopressin-resistant diabetes insipidus, liver dysfunction, hyperuricemia and decreased renal function. A case report.

A case of transient nephrogenic diabetes insipidus occurred in late pregnancy, the first associated with biopsy-proven hepatitis. Five previously reported cases occurred in pregnancy. All six patients demonstrated similar but transient signs, symptoms and laboratory abnormalities suggesting a syndrome peculiar to pregnancy. The characteristics of this syndrome are elevated liver function studies, decreased renal function, hyperuricemia and transient vasopressin-resistant diabetes insipidus.

Adult↗

PubMed1979

[Effect of uric acid lowering drugs in low dosage in patients with hyperuricemia and hypertriglyceridemia in a randomized group study].

The serum uric acid lowering effects of 100 mg Allopurinol (A), 20 mg Benzbromarone (B) and the combination of both were tested in a randomized block-trial in 12 male patients suffering from hyperuricemia and hyperlipoproteinemia type IIb/IV. Therapy periods lasted 4 weeks each. Allopurinol lowered the uric acid concentrations from 7,54 mg/100 ml to 5,95 mg/100 ml, Benzbromarone from 7,54 mg/100 ml to 6,11 mg/100 ml and the combination from 7,54 mg/100 ml to 4,90 mg/100 ml, all three significantly. The difference between the effect of the combination drug and Allopurinol and Benzbromarone respectively was also significant. An additive effect of both components is evident. Serum creatinin concentration remained constant. Uric acid and creatinin excretion could not be evaluated because of failure of patient compliance in the collecting of urine.

Adult↗

PubMed1969

Current concepts of hyperuricemia and gout.

Recent studies have confirmed that gout is an inborn error of metabolism. It has now become evident that the hyperuricemia associated with gout might occur either due to overproduction of uric acid, underexcretion of uric acid or a combination of these processes. Furthermore, patients with excessive purine synthesis may have a specific enzyme defect resulting in altered feedback inhibition of purine synthesis. A neurological disease manifest by mental retardation, choreo-athetosis, aggressive behavior, lip-biting and self-mutilation and associated with decidedly increased purine biosynthesis serves as a prototype of this kind of disorder. Other defects in regulation of purine biosynthesis have been postulated but their existence not yet confirmed. It has been demonstrated that urate crystals which are deposited from hyperuricemic body fluids set up an acute inflammatory reaction by means of a variety of chemical mediators. Thus, acute gouty arthritis is now recognized as an example of "crystal induced" synovitis. The treatment of gout consists of (1) the control of acute gouty attacks, and (2) the maintenance of normal serum uric acid concentrations. This latter may be achieved either with uricosuric drugs or with xanthine oxidase inhibition. With these principles in mind, it is now possible to avoid many of the severe crippling effects of gout and to restore the vast majority of gouty patients to useful and productive lives.

Chemical Phenomena↗

PubMed1984

Management of gout and hyperuricemia.

The medical management of gout follows a logical course in eventually controlling the underlying hyperuricemia. Approached properly, it is one of the most gratifying rheumatic diseases for a physician to treat.

Allopurinol↗

PubMed1978

[The effect of benzbromarone on fasting-hyperuricemia as a model (author's transl)].

The effect of daily therapeutic doses of 100 mg benzbromarone (Normurat) and 2.0 g probenecid on the purine metabolism of 40 test subjects was investigated. Fasting-hyperuricemia was used as the model and particular attention paid to the mechanisms of renal elimination. Urate concentration remains under the solubility threshold when benzbromarone is administered, in contrast to medication with probenecid. The significantly greater hypouricemic effect of benzbromarone correlates with a significant rise in the excretion and clearance of uric acid in comparison to probenecid, accompanied by a stronger depression of tubular reabsorption. Serum levels, clearances and reabsorption rates demonstrate the prolonged effect of the benzofurane derivative Normurat even during strict fasting. Supplementary allantoin and urea determinations gave no indication of increased enterobacterial uricolysis. Normurat was well tolerated, side effects were not noted.

Adolescent↗

PubMed1983

[The spine and polytopic hyperostoses in gout and hyperuricemia].

Investigations were made on a total of 92 patients with gout and hyperuricemia. 30% had no clinical signs of spinal involvement. The remaining 70% were examined radiologically and by xero-radiography. Examination revealed signs of erosion of vertebral bodies, spondylodiscitis, osteopenia, manifestations of Forestier's disease and changes on sacroiliac joints. In 35% of subjects there were polytopic hyperostoses including an increased incidence of calcifications around the large joints and periosteal appositions at the periphery, particularly on the finger and toe tips. The hypothesis was raised that massive calcifications and manifestations of hyperostosis and ossification of the ligaments and tendons (osteodesmosis) in gout may correlate with a latent glycide metabolism disorder like in Forestier's disease.

Female↗

PubMedDate not supplied

Fructose-induced hyperuricemia in psoriasis and psoriatic arthritis.

Acute intravenous infusion of fructose was given to 30 normal subjects and 27 normo-uricemic patients affected by psoriasis, 12 with cutaneous involvement only and 15 with psoriatic arthritis. Serum uric acid was measured before and after infusion. A significantly lower increase in serum uric acid levels was found in psoriatic patients in comparison to controls, and the increase rate appeared to be significant only in controls. Moreover, the overall fructose-induced hyperuricemia was significantly lower in the group of patients with psoriatic arthritis than in normal subjects. Since the fructose-induced increase of serum uric acid is most probably achieved by an augmented turnover of preformed purine nucleotides, it is suggested that in normouricemic patients with psoriasis the "pool" of purine nucleotides is lower than normal. Such a condition seems to be more evident in psoriatic arthritis.

Adolescent↗