Hyperlipidemia in primary gout

Barlow, Keith A.

doi:10.1016/0026-0495(68)90132-7

Cited by 56 publications

(11 citation statements)

References 17 publications

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“…The 29% incidence of hypertriglyceridaemia in these gouty patients is similar to that reported previously (Feldman and Wallace, 1964;Rosselin and others, 1966), and is less than rates up to 75% reported by others (Berkowitz, 1966;Barlow, 1968). The mean triglyceride value in the present study agrees with the mean level of 174 mg/100 ml reported recently (Wiedemann and others, 1972).…”

Section: Discussionsupporting

confidence: 91%

Abnormal regulation of carbohydrate metabolism in primary gout.

Diamond¹,

Carter²,

Feldman³

1974

Annals of the Rheumatic Diseases

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Section: Discussionsupporting

confidence: 91%

Abnormal regulation of carbohydrate metabolism in primary gout.

Diamond¹,

Carter²,

Feldman³

1974

Annals of the Rheumatic Diseases

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“…The plasma level of uric acid may be raised in patients with hyperlipoproteinaemia (Harris-Jones, 1957;Strejcek and Kucerova, 1968) and elevation ofplasma glyceride has been reported previously in patients with primary gout (Berkowitz, 1964;Feldman and Wallace, 1964;Barlow, 1968;Bluestone, Lewis, and Mervant, 1971). The present study confirms this association and shows also in patients with gout an elevation of phospholipids and unesterified fatty acids.…”

Section: Discussionmentioning

confidence: 75%

Plasma lipid levels in gout.

Darlington¹,

Scott²

1972

Annals of the Rheumatic Diseases

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A number of investigations have previously been carried out to examine inter-relationships between hypercuricaemia, gout, and levels of plasma lipids, usually with particular reference to glycerides and cholesterol. The present study was designed to compare the levels not only of glycerides and cholesterol, but also of phospholipids and free fatty acids, in gout patients with those in a group of very closely matched control subjects; and to determine, in the gout patients, whether there was any relationship between levels of these lipid fractions and the endogenous production of uric acid as measured by urinary levels of uric acid on a low-purine diet.Plan of study 27 British patients with primary gout (25 men and 2 women) participated in the study. Some of them were on urate-lowering treatment (allopurinol or uricosuric agents) at the time when blood was taken for lipid estimations, but plasma and urinary levels of uric acid had been estimated on a low-purine diet before treatment was started.A control group of 27 subjects was taken from hospital patients suffering from a wide variety of medical and surgical conditions. None had gout or hyperuricaemia; all were of reasonable social orientation, all were taking normal diets and none was grossly obese. Initial investigations in all subjects, gout and control, excluded predisposing causes for hyperlipidaemia. The control group was matched with gout patients for age, sex, blood pressure, alcohol intake, and the presence of ischaemic vascular disease. The two groups were also matched for ponderal index 13igh (in.) which tends to be lower \VYweight (lb.)

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“…[1][2][3][4] Gout is related to metabolic abnormalities such as diabetes mellitus, hypertriglyceridemia, and obesity as well as hypertension. 5,6 Hyperuricemia, on the other hand, is considered a marker of the X syndrome or metabolic syndrome, which is characterized by hyperglycemia or diabetes mellitus, hypertriglyceridemia, hyperuricemia, obesity, and hypertension. Besides the fact that some of these elements are known to increase the risk for cardiovascular disease, patients with metabolic syndrome have a high prevalence of atherosclerosis and consequently a high risk of IHD.…”

mentioning

confidence: 99%