Identification of the causes of persistent hyperuricaemia

doi:10.1016/0140-6736(91)93141-U

The Lancet

Volume 337, Issue 8755, 15 June 1991, Pages 1461-1463

https://doi.org/10.1016/0140-6736(91)93141-U Get rights and content

Abstract

Accurate identification of the factors that contribute to hyperuricaemia in an individual may enable some of these factors to be modified, and lead to permanent correction of the hyperuricaemia. A protocol is described which can supplement clinical assessment. Measurement of the effects on serum urate and urinary urate excretion of a low-purine diet for 7 days facilitates the identification of the contributions made by urate production (either endogenous or from purine consumption) and renal underexcretion of urate (either as a low urate clearance in the absence of renal disease or due to renal glomerular insufficiency).

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Cited by (35)

Formate metabolism in health and disease
2020, Molecular Metabolism
Citation Excerpt :
Some of these factors have been studied in the context of gout, a type of arthritis caused by the accumulation of urate crystals in the joints [118]. A low purine diet causes about a 25% reduction of serum urate levels in humans [119]. In contrast, drinking beer increases mean urate excretion by 15% in gout patients and by 20% in healthy controls [120].
Formate is a one-carbon molecule at the crossroad between cellular and whole body metabolism, between host and microbiome metabolism, and between nutrition and toxicology. This centrality confers formate with a key role in human physiology and disease that is currently unappreciated.
Here we review the scientific literature on formate metabolism, highlighting cellular pathways, whole body metabolism, and interactions with the diet and the gut microbiome. We will discuss the relevance of formate metabolism in the context of embryonic development, cancer, obesity, immunometabolism, and neurodegeneration.
We will conclude with an outlook of some open questions bringing formate metabolism into the spotlight.
Uric acid excretion in healthy subjects: A nomogram to assess the mechanisms underlying purine metabolic disorders
2012, Metabolism: Clinical and Experimental
Citation Excerpt :
This study aimed to assess the normal limits for uric acid excretion in control subjects over a wide range of serum urate concentrations. The results show that among the 5 urinary variables proposed to determine uric acid excretion in adult healthy subjects [2-7], the best bilateral correlation coefficient over a wide range of serum urate concentrations was obtained for the 24-hour urinary uric acid excretion. The nomogram drawn, with its 95% confidence limits (Fig. 1), relating serum urate levels to 24-hour urinary uric acid excretion, proved to be very useful to differentiate the mechanisms underlying a myriad of diseases manifested by an increased or decreased serum urate concentration or 24-hour uric acid excretion (Fig. 2).
The reference range for urinary uric acid excretion has not been precisely defined. Different urinary variables have been proposed to determine the renal contribution to increased or decreased serum urate concentrations. We examined which urinary variable best indicates uric acid excretion over a wide range of serum urate concentrations. Purine metabolism was studied in 10 healthy male subjects (aged 26-58 years) both at their endogenous normal serum urate levels (normouricemic state) and after the oral administration of allopurinol (300 mg/24 h for 5 days) and ribonucleic acid (4 g/8 h for 4 days) to decrease (hypouricemic state) and increase (hyperuricemic state) serum urate concentrations, respectively. The results from patients with several conditions known to affect uric acid synthesis and/or the renal excretion of uric acid were used to validate a constructed nomogram. Over a wide range of mean serum urate levels (from 2.7 to 9.5 mg/dL) and mean 24-hour urinary uric acid excretion (171 to 1368 mg/[24 h 1.73 m²]), the highest correlation coefficient between serum urate and uric acid excretion was obtained for the 24-hour uric acid determination (r = 0.928; P < .001). The constructed nomogram allowed the definition of the mechanism underlying hyperuricemia and hypouricemia in patients with a myriad of diseases known to affect purine metabolism. The urinary variable that best correlates with a wide range of serum urate concentrations is 24-hour urinary uric acid excretion. The constructed nomogram allows the identification of the kidney contribution to a given purine metabolic abnormality.
Capillary electrophoresis with contactless conductivity detection for uric acid determination in biological fluids
2009, Analytica Chimica Acta
Citation Excerpt :
Above serum concentrations of 400 μM, the risk for developing gouty arthritis rises sharply [16]. Urinary excretion of urate is in the range of 2–4 mmol/24 h, resulting in a renal clearance of 6–11 mL min−1[15]. Many different methods for the determination of uric acid in biological samples have been reported.
The suitability of capillary electrophoresis (CE) with capacitively coupled contactless conductivity detection (C⁴D) for the direct determination of uric acid in human plasma and urine was investigated. It was found that a careful optimization of the buffer composition and pH was necessary to achieve selective determination in the complex sample matrices. An electrolyte solution consisting of 10 mM 2-morpholinoethanesulfonic acid (MES), 10 mM histidine and 0.1 mM hexadecyltrimethylammonium bromide (CTAB), pH 6.0, was finally found suitable for use as running buffer for both sample matrices. The limit of detection (3 S/N) was determined as 3.3 μM. The linearity of the response was tested for the range between 10 and 500 μM and a correlation coefficient of 0.9996 was obtained. Intra- and inter-day variabilities were <10%. Quantitative analysis of urine and plasma samples showed a good correlation with the routine enzymatic method currently used at the University Hospital of Basel.
Dietary Factors Associated with Hyperuricemia in Adults
2008, Seminars in Arthritis and Rheumatism
Although diet has long been assumed to be associated with hyperuricemia, the association between diet and hyperuricemia remains to be verified.
The Nutrition and Health Survey in Taiwan (NAHSIT) implemented between 1993 and 1996 was a nationwide survey using a stratified multistage sampling design. A food frequency questionnaire (FFQ), 24-hour diet recall, and blood samples were utilized. Hyperuricemia was defined as serum urate >7.7 mg/dL for men and >6.6 mg/dL for women.
In total, 2176 adults, 987 (45%) men and 1189 (55%) women, were recruited. Mean serum urate was 6.81 ± 1.66 mg/dL (range, 2.5-16.8 mg/dL) and 5.47 ± 1.55 mg/dL (range, 1.4-11.5 mg/dL) for men and women, respectively. Multiple logistic regression analysis indicated that beer consumption in both the FFQ and the 24-hour diet recall were significantly associated with hyperuricemia in men after adjusting for age, total caloric intake, body mass index, and geographic area. In FFQ, the adjusted odds ratio was 1.49 for men who imbibed 0.1 to 11.6 g ethanol (<1 standard drink) daily and 1.56 for men who imbibed ≥11.7 g ethanol (≥1 standard drink) daily, when compared with that for men who did not drink beer (P = 0.035). In the 24-hour diet recall, the adjusted odds ratio for men who drank <5 cans of beer daily was 1.13, and for men who drank ≥5 cans daily was 1.28 when compared with that for men who did not drink beer (P = 0.003).
This cross-sectional survey demonstrated that beer intake is independently associated with increased risk of hyperuricemia in men. Restricted beer intake may help prevent hyperuricemia in the population. The finding of elevated mean serum urate levels over recent decades warrants further study.
Primary prevention in rheumatology: The importance of hyperuricemia
2004, Best Practice and Research: Clinical Rheumatology
Hyperuricemia (HU) is present in 5–30% of the general population, although the prevalence is higher among some ethnic groups and seems to be increasing worldwide. Classically, chronic HU has been considered a risk factor for gout or lithiasis and is associated with alcoholism, obesity, hypertension, dyslipidemia, hyperglicemia/diabetes mellitus, renal failure and intake of certain drugs.
HU is also associated with cardiovascular diseases such as hypertension, vascular disease, pre-eclampsia, pulmonary arterial hypertension, stroke, heart failure, ischemic heart disease and also metabolic syndrome, renal disease and increased mortality. It is uncertain if these associations are dependent or not, especially cardiovascular and renal diseases. Patients with chronic HU and also those with gout require both medical investigation for associated diseases or drugs as well as nutritional counseling and life-style changes. HU should alert physicians to possible complications.
The role of the laboratory in the investigation and management of hyperuricemia
1998, Pathology

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CLINICAL PRACTICEIdentification of the causes of persistent hyperuricaemia

Abstract

Metabolism

Effect of purine restriction on serum and urine urate in normal subjects

Adv Exp Med Biol

Uric acid production in gout

J Clin Invest

Hyperuricaemia and gout in clinical practice

CLINICAL PRACTICE
Identification of the causes of persistent hyperuricaemia