Adrenocortical Steroid Treatment of Rheumatic Diseases

Stern, Michael P.

doi:10.1001/archinte.1973.03650070083013

Cited by 73 publications

(4 citation statements)

References 23 publications

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“…Some previous studies reported positive associations between corticosteroid use and traditional coronary risk factors, such as total plasma cholesterol (7-9,12,13,17,31), systolic BP (7), triglycerides (12)(13)(14)17,32,33), LDL cholesterol (13,14,31), Apo B (10), and hyperinsulinemia (33). However, most of these studies did not adjust for disease activity, which in our cohort was correlated both with corticosteroid dose (r ϭ 0.32) and with most CHD risk factors, and therefore may act as a confounder.…”

Section: Discussionmentioning

confidence: 99%

Recent corticosteroid use and recent disease activity: Independent determinants of coronary heart disease risk factors in systemic lupus erythematosus?

Karp

Abrahamowicz

Fortin

et al. 2008

Arthritis & Rheumatism

102

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Section: Discussionmentioning

confidence: 99%

Recent corticosteroid use and recent disease activity: Independent determinants of coronary heart disease risk factors in systemic lupus erythematosus?

Karp

Abrahamowicz

Fortin

et al. 2008

Arthritis & Rheumatism

102

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“…Certainly less than 5% of diabetics suffer from gout but, when a group of patients with gout is studied, a large proportion is found to have abnormalities of glucose tolerance [30] and the associated diabetes is mostly insulin-independent, with obesity as a frequent concomitant [121 ]. This could lead to a sequence whereby reduced glucose tolerance resulted in compensatory hyperinsulinaemia lead ing to increased production of lipoproteins with type IV hyperlipoprotein aemia and its associated hyperuricaemia [117]. Thus, apart from those factors which result in hypertriglyceridaemia, there appears to be no definite relation ship between diabetes mellitus and hyperuricaemia [18].…”

Section: Diabetesmentioning

confidence: 99%

Abnormal Renal Urate Homeostasis in Systemic Disorders

Emmerson

Ravenscroft

1975

Nephron

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Abnormalities of renal handling of urate occur in a wide variety of physiological and pathological conditions and are mediated by factors including renal blood flow, glomerular filtration rate, urine flow rate, urinary constituents, metabolites, hormones and drugs. The determination of the aetiological factors in each abnormal situation is complex and the problem is discussed in relation to a variety of conditions including renal tubular disorders and metal intoxications, hypertension, toxaemia of pregnancy, glycogen storage disease, fructose administration, hereditary fructose intolerance, as well as obesity, regular alcohol consumption and hyperlipoproteinaemia. Apart from those diseases, usually genetically determined, which are associated with excessive production of urate, the most common causes of hyperuricaemia act at a renal level and result in a reduction in the net renal excretion of urate.

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“…Myocardial infarction increasingly has become an importent cause of death related to connective tissue diseases, and atherosclerosis is a frequent cause of myocardial infarction (2). In patients receiving steroid therapy, abnormality in serum lipid metabolism (remarkable increases in serum cholesterol and triglycerides) frequently is observed.…”

Section: Discussionmentioning

confidence: 99%

Effect of Bezafibrate on Soluble Adhesion Molecules and Platelet Activation Markers in Patients With Connective Tissue Diseases and Secondary Hyperlipidemia

Kagawa

Nomura

Nagahama

et al. 2001

Clin Appl Thromb Hemost

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We evaluated the plasma concentrations of soluble adhesion molecules, platelet activation markers, and platelet-derived microparticles (PMPs) in patients with connective tissue diseases who had secondary hyperlipidemia caused by long-term steroid administration (n = 22) before and after treatment with bezafibrate. There were differences in levels of platelet activation markers both before and after treatment (platelet CD62p: 15.11+/-2.03 vs 10.38+/-8.53%, P < 0.05; platelet CD63: 12.12+/-9.17 vs 9.90+/-7.20%, P < 0.05). There were also differences in the levels of PMPs and soluble adhesion molecules both before and after treatment (PMP: 514+/-273 vs 401+/-201 /10(4) platelet. P < 0.05; soluble vascular cell adhesion molecule-1: 724+/-191 vs 666+/-157 ng/mL, P < 0.01). After 6 months of treatment, serum lipid concentrations were reduced by 9% for total cholesterol (TC) and 32% for triglyceride (TG). The level of PMPs, activated platelets, and soluble adhesion molecules were all significantly decreased after treatment with bezafibrate. These findings suggest that bezafibrate may be useful for inhibiting both PMP-dependent and -independent vascular damage in patients with connective tissue diseases complaining of secondary hyperlipidemia.

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Adrenocortical Steroid Treatment of Rheumatic Diseases

Cited by 73 publications

References 23 publications

Recent corticosteroid use and recent disease activity: Independent determinants of coronary heart disease risk factors in systemic lupus erythematosus?

Recent corticosteroid use and recent disease activity: Independent determinants of coronary heart disease risk factors in systemic lupus erythematosus?

Abnormal Renal Urate Homeostasis in Systemic Disorders

Effect of Bezafibrate on Soluble Adhesion Molecules and Platelet Activation Markers in Patients With Connective Tissue Diseases and Secondary Hyperlipidemia

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