Serum urate concentrations in the Australian aboriginal.

Emmerson, B. T.; Douglas, William; Doherty, R. L.; Feigl, Polly

doi:10.1136/ard.28.2.150

Cited by 28 publications

(12 citation statements)

References 20 publications

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“…In 1969 Emmerson and colleagues measured the serum uric acid concentration in 382 Gulf of Carpentaria Aborigines and significantly higher serum urate concentrations were noted 15. The men compared with the women had consistently higher concentrations in keeping with reports in all racial groups studied throughout the world and concentrations tended to increase with age in both sexes.…”

Section: Rheumatic Diseasesmentioning

confidence: 78%

Rheumatic disease and the Australian Aborigine

Roberts‐Thomson

1999

Annals of the Rheumatic Diseases

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Objective-To document the frequency and disease phenotype of various rheumatic diseases in the Australian Aborigine. Methods-A comprehensive review was performed of the archaeological, ethnohistorical, and contemporary literature relating to rheumatic diseases in these indigenous people. Results-No evidence was found to suggest that rheumatoid arthritis (RA), ankylosing spondylitis (AS), or gout occurred in Aborigines before or during the early stages of white settlement of Australia. Part of the explanation for the absence of these disorders in this indigenous group may relate to the scarcity of predisposing genetic elements, for example, shared rheumatoid epitope for RA, B27 antigen for AS. In contrast, osteoarthritis appeared to be common particularly involving the temporomandibular joint, right elbow and knees and, most probably, was related to excessive joint loading in their hunter gatherer lifestyle. Since white settlement, high frequency rates for rheumatic fever, systemic lupus erythematosus, and pyogenic arthritis have been observed and there are now scanty reports of the emergence of RA and gout in these original Australians. Conclusion-The occurrence and phenotype of various rheumatic disorders in Australian Aborigines is distinctive but with recent changes in diet, lifestyle, and continuing genetic admixture may be undergoing change. An examination of rheumatic diseases in Australian Aborigines and its changing phenotype may lead to a greater understanding of the aetiopathogenesis of these disorders.

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Section: Rheumatic Diseasesmentioning

confidence: 78%

Rheumatic disease and the Australian Aborigine

Roberts‐Thomson

1999

Annals of the Rheumatic Diseases

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“…Similarly, Emmerson et al (1969) in a study of 80 male and 133 female subjects found no correlation between serum uric acid and height, weight, or surface area in the male population. A slight significant correlation was noted between serum uric acid and weight in the females (r = 0.17); no significance was noted between serum uric acid and height or surface area.…”

Section: Discussionmentioning

confidence: 89%

The relationship between uric acid and potassium in normal subjects.

Kennedy¹,

Boddy²,

King³

et al. 1978

Annals of the Rheumatic Diseases

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SUMMARYThe serum uric acid concentration in normal healthy subjects has been studied in relation to sex, height, weight, lean body mass measured from total body potassium and predicted from the Hume-Weyers formula (1971), total body potassium, plasma potassium and urea, and packed cell volume. The strongest correlation was found with sex, but height, weight, total body potassium, lean body mass (measured and predicted) also correlated significantly with serum uric acid concentration. However, when the sex variable was removed, the other factors lost their significant correlation. Finally, total red blood cell and plasma volumes were predicted (Hume and Goldberg, 1964) and from these an estimate of total plasma uric acid, total plasma potassium, and total red blood cell potassium obtained. Measured total body potassium was found to correlate well with total plasma potassium and total red blood cell potassium independent of sex. Total plasma uric acid correlated well with measured total body potassium when both sexes were considered and when separated into male and female groups the males retained a significant correlation as did the female group.

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“…Detailed genetic studies on the Ayatal tribe of Taiwanese Aborigines have recently been performed and are described below. Other Aboriginal populations that have been studied include Australian Aborigines, in whom the occurrence of gouty arthritis was originally reported to be rare [26,27], although the prevalence of hyperuricemia was reported to be higher in Aboriginals compared with non-Aboriginals [28]. A recent report by Chan and Segasothy [29], however, suggests that gout may be more common than previously thought in this native population.…”

Section: Epidemiology Of Hyperuricemia and Gout In Genetically Isolatmentioning

confidence: 95%

New developments in the epidemiology and genetics of gout

Zaka¹,

Williams

2006

Curr Rheumatol Rep

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The prevalence of gout appears to be rapidly increasing worldwide and is no longer a disorder suffered primarily by over-fed alcohol consumers. Emerging risk factors include longevity, metabolic syndrome, and new classes of pharmacologic agents. In some ethnic populations, no obvious risk factors can explain the high incidence of hyperuricemia and gout, suggesting a genetic liability. Studies to identify genes associated with gout have included families with defects in purine metabolism, as well as families in whom the occurrence of gout is secondary to renal disorders such as juvenile hyperuricemic nephropathy and medullary cystic kidney disease. Case-control studies of isolated aboriginal cohorts suffering from primary gout have revealed several chromosomal loci that may harbor genes that are important to the development and/or progression of gout.

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Serum urate concentrations in the Australian aboriginal.

Cited by 28 publications

References 20 publications

Rheumatic disease and the Australian Aborigine

Rheumatic disease and the Australian Aborigine

The relationship between uric acid and potassium in normal subjects.

New developments in the epidemiology and genetics of gout

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