Lipoprotein(a) in diabetes mellitus

Ritter, Michael M.; Loscar, M.; Richter, Werner; Schwandt, P.

doi:10.1016/0009-8981(93)90301-j

Cited by 25 publications

(8 citation statements)

References 22 publications

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“…[42] In this study, patients with normal serum levels of TC control studies [49] (table III). Similarly, a positive association in and TG had a significantly better visual outcome after laser patients with type 2 DM has been reported in some studies [50][51][52][53][54] photocoagulation. [42] but not in others [46] (table III).…”

Section: Mechanisms Of Retinal Damage Due To Hyperlipidemiamentioning

confidence: 76%

“…[95] Higher serum levels of apolipoprotein(a) [Apo(a)] and Lp(a) A proatherogenic dyslipidemic profile is present in patients are present in patients with renal failure of any etiology. [98] Earlier with diabetic nephropathy, including high serum levels of smallstudies involving patients with type 1 [44,50,[99][100][101] and type 2 DM [50] dense LDL-C, intermediate density lipoprotein-cholesterol, and did not find any association between serum Lp(a) levels and post oral fat load hyperlipidemia associated with lower activities diabetic nephropathy (table VI). However, recent literature sugof hepatic triglyceride lipase and lipoprotein lipase enzymes.…”

Section: Mechanisms Of Renal Damage Due To Lipidsmentioning

confidence: 96%

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The Role of Lipids in the Development of Diabetic Microvascular Complications

Misra

Kumar

Vikram

et al. 2003

American Journal of Cardiovascular Drugs

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Dyslipidemia is a major factor responsible for coronary heart disease and its reduction decreases coronary risk in patients with diabetes mellitus. However, the association of dyslipidemia with microvascular complications and the effect of intervention with lipid-lowering therapy in diabetes have been less investigated. We present the systematic review of association and intervention studies pertaining to dyslipidemia and microvascular disease in diabetes and also review possible mechanisms. Dyslipidemia may cause or exacerbate diabetic retinopathy and nephropathy by alterations in the coagulation-fibrinolytic system, changes in membrane permeability, damage to endothelial cells and increased atherosclerosis. Hyperlipidemia is associated with faster decline in glomerular filtration rate and progression of albuminuria and nephropathy. Recent evidence also suggests a role of lipoprotein(a) in progression of retinopathy and nephropathy in patients with diabetes mellitus. Lipid-lowering therapy, using single agents or a combination of drugs may significantly benefit diabetic retinopathy and diabetic nephropathy. In particular, hydroxymethyl glutaryl coenzyme A reductase inhibitors may be effective in preventing or retarding the progression of microvascular complications because of their powerful lipid-lowering effects and other additional mechanisms. However, most of the data are based on short-term studies, and need to be ascertained in long-term studies. Until more specific guidelines are available, aggressive management of diabetic dyslipidemia, according to currently accepted guidelines, should be continued for the prevention of macrovascular disease which would also benefit microvascular complications.

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Section: Mechanisms Of Retinal Damage Due To Hyperlipidemiamentioning

confidence: 76%

Section: Mechanisms Of Renal Damage Due To Lipidsmentioning

confidence: 96%

The Role of Lipids in the Development of Diabetic Microvascular Complications

Misra

Kumar

Vikram

et al. 2003

American Journal of Cardiovascular Drugs

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“…In subjects with IDDM and proteinuria, Lp(a) levels have been reported to be either increased or unchanged [31,[42][43][44][45][46][47]. Several studies of patients with nephrotic syndrome and/or renal failure from various causes have failed to demonstrate a difference in Lp(a) levels in subjects with IDDM compared with in subjects with other causes of renal dysfunction [20,29,65].…”

Section: Discussionmentioning

confidence: 99%

“…Several studies of IDDM subjects have shown that Lp(a) levels increase with worsening glycemic control [35][36][37][38][39][40], although other studies have not [29,33,41,42]. Finally, earlier studies showed a direct correlation between the degree of proteinuria and increasing Lp(a) levels in subjects with IDDM [43][44][45][46], but more recent studies have not [31,42,47]. Many of the above studies were performed on small numbers of patients and had brief follow-up periods.…”

Section: Introductionmentioning

confidence: 99%

Levels of lipoprotein(a), apolipoprotein B, and lipoprotein cholesterol distribution in IDDM. Results from follow-up in the Diabetes Control and Complications Trial

Purnell¹,

Marcovina²,

Hokanson³

et al. 1995

Diabetes

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Levels of lipoprotein (a) [Lp(a)], apolipoprotein (apo) B, and lipoprotein cholesterol distribution using density-gradient ultracentrifugation were measured as part of a cross-sectional study at the final follow-up examination (mean 6.2 years) in the Diabetes Control and Complications Trial. Compared with the subjects in the conventionally treated group (n = 680), those subjects receiving intensive diabetes therapy (n = 667) had a lower level of Lp(a) (Caucasian subjects only, median 10.7 vs. 12.5 mg/dl, respectively; P = 0.03), lower apo B (mean 83 vs. 86 mg/dl, respectively; P = 0.01), and a more favorable distribution of cholesterol in the lipoprotein fractions as measured by density-gradient ultracentrifugation with less cholesterol in the very-low-density lipoprotein and the dense low-density lipoprotein fractions and greater cholesterol content of the more buoyant lowdensity lipoprotein. Compared with a nondiabetic Caucasian control group (n = 2,158), Lp(a) levels were not different in the intensive treatment group (median 9.6 vs. 10.7 mg/dl, respectively; NS) and higher in the conventional treatment group (9.6 vs. 12.5 mg/dl, respectively; P less than 0.01). No effect of renal dysfunction as measured by increasing albuminuria or reduced creatinine clearance on Lp(a) levels could be demonstrated in the diabetic subjects. Prospective follow-up of these subjects will determine whether these favorable lipoprotein differences in the intensive treatment group persist and whether they influence the onset of atherosclerosis in insulin-dependent diabetes. Lp(a) is formed by a molecule of a carbohydrate-rich protein named apo(a) linked by a single disulfide bond to the apo B of an LDL-like lipoprotein. Like LDL, Lp(a) is thought to be atherogeic. Because of the structural homology of apo(a) to plasminogen, it is also thought to have thrombogenic properties. This potential combination of proatherogenic and prothrombotic properties has led to a surge of research into the role of Lp(a) in atherosclerosis. KeywordsIn several case-controlled and prospective studies consisting primarily of white men with at least one preexisting cardiac risk factor, such as a family history of heart disease or an elevated LDL cholesterol level, an increased Lp(a) level has been shown to be an independent risk factor for CAD [5,10,11].Because up to 91 percent of the variability in plasma Lp(a) levels between individuals has been attributed to the apo(a) isoform [5,12], the contribution of age, sex, diet, and exercise to Lp(a) levels is thought to be small. Lp(a) levels have been shown to be higher in familial hypercholesterolemia [13], chronic renal failure [14][15][16][17][18][19], and nephrotic syndrome [20][21][22][23][24][25], and lower levels have been reported in cirrhosis [26]. How Lp(a) levels might be affected by IDDM and its complications and whether Lp(a) contributes to CAD [27,28] in this population remain controversial. Some investigators found elevated Lp(a) levels in subjects with IDDM compared with normoglycemic co...

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“…Other studies that included type 1 and type 2 diabetic patients reported inconsistent results (20,21). The study by James et al (20) reported an association of Lp(a) with ischemic heart disease or macroangiopathy.…”

Section: Research Design and Methods -mentioning

confidence: 99%