Transient changes of serum lipoprotein(a) as an acute phase protein

Maeda, Shin; Abe, Akira; Seishima, Mitsuru; Makino, Kazuhiko; Noma, Akio; Kawade, Masato

doi:10.1016/0021-9150(89)90218-9

Cited by 322 publications

(153 citation statements)

References 19 publications

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“…It has been previously reported that the thrombotic tendency and the abnormal fibrinolysis is related to the disease activity (6). Also, Lp(a) is known as an acute phase protein and is significantly correlated with acute phase reactants (13,14). The change of plasma Lp(a) concentration was confirmed by the present study in patients with Behgefs disease.…”

Section: Discussionsupporting

confidence: 84%

Plasma Lipoprotein(a) and Its Relationship with Disease Activity in Patients with Behçet’s Disease

Örem

Çimşit²,

Karahan³

et al. 1995

CCLM

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Summary:Behufs disease is characterized by orogenital ulccrations and ocular lesions, Other features include arthritis, thrombophlebitis, neurological abnormalities and skin lesions. The disease is characterized by a relapsing inflammatory process of unknown aetiology. Lipoprolcin(a) is an LDL-likc particle with a large glycoprotein called apolipoprotein(a) attached to its npolipoprotcin B moiety through one or more clisulphidc bonds. Apolipoprotein(a) is related to plasminogcn from which the cn/yme plasmin, that hydrolyscs fibrin blood clots, is released by tissue plasininogcn activators. The unique structural features of Lp(a) give it the potential for atherogenie and thrombogenic activities. In the present study 35% of patients with /ic j //(.'t'/\s disease were shown to have higher Lp(a) concentrations than the cut-off point (0.30 g/l) for atherosclerosis. Plasma Lp(a) concentrations in the remission period were also found 1ο be lower than during the active period in the same patients (23% decreased). Lp(a) showed significant correlations with acute phase rcaclanls such as crythrocyte sedimentation rate, polymorphonuclcar leukocytes and polymoφhonuclear leukocyte elastase activity. Therefore, it was concluded that the fluclations of plasma Lp(a) levels with the activity of disease may be a contributing risk factor in the development of (hrombogcnic complications in patients with Belief $ disease.In conclusion, we suggest that plasma Lp(a) concentrations be determined for patients with Belter* disease, and that patients with high Lp(a) levels be kept under close controls especially during the active period of the disease, and taken into remission as soon as possible.

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Section: Discussionsupporting

confidence: 84%

Plasma Lipoprotein(a) and Its Relationship with Disease Activity in Patients with Behçet’s Disease

Örem

Çimşit²,

Karahan³

et al. 1995

CCLM

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“…There is also evidence that Lp(a) lipoprotein, which is associated with coronary heart disease in Type II diabetes [26,27], is an acutephase protein [9,28]. 2 A model for the role of cytokines and the innate immune system in the aetiology of Type II diabetes.…”

Section: Evidence For An Acute-phase Response In Type II Diabetesmentioning

confidence: 99%

Is Type II diabetes mellitus a disease of the innate immune system?

1998

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The cause of the common type of Type II (non-insulin-dependent) diabetes mellitus, which affects at least 100 million people throughout the world, is not known. One of the foremost challenges we face is to account mechanistically for not only the defining hyperglycaemia but also for the myriad of other biochemical and physiological abnormalities which are characteristic of this disease. For example, it is now clear that Type II diabetes and lesser degrees of glucose intolerance commonly occur together with a collection of clinical and biochemical features which have been called metabolic syndrome X [1, 2].These features include central obesity, hypertension, accelerated atherosclerosis, hypertriglyceridaemia and low serum concentrations of high-density lipoprotein (HDL) cholesterol. Though insulin resistance seems to be a central abnormality, the origin of the impaired insulin action and how it explains the many other abnormalities of Type II diabetes is not known.In recent years, we have been gathering evidence that in Type II diabetes there is a cytokine-associated acute-phase reaction, part of the innate immune response. As an alternative direction for research into the aetiology of Type II diabetes, we propose that it may be helpful to consider whether the mechanisms involved in the acute-phase response can be major contributors to the pathophysiology of many of the features of Type II diabetes and syndrome X, including glucose intolerance, insulin resistance, impair- Diabetologia (1998) Summary Type II (non-insulin-dependent) diabetes mellitus is associated with increased blood concentrations of markers of the acute-phase response, including sialic acid, a-1 acid glycoprotein, serum amyloid A, C-reactive protein and cortisol, and the main cytokine mediator of the response, interleukin-6. The dyslipidaemia common in Type II diabetes (hypertriglyceridaemia and low serum levels of HDL cholesterol) is also a feature of natural and experimental acutephase reactions. We review evidence that a long-term cytokine-mediated acute-phase reaction occurs in Type II diabetes and is part of a wide-ranging innate immune response. Through the action of cytokines on the brain, liver, endothelium, adipose tissue and elsewhere, this process could be a major contributor to the biochemical and clinical features of metabolic syndrome X (glucose intolerance, dyslipidaemia, insulin resistance, hypertension, central obesity, accelerated atherosclerosis) but also provides a mechanism for many other abnormalities seen in Type II diabetes, including those in blood clotting, the reproductive system, metal ion metabolism, psychological behaviour and capillary permeability. In the short-term, the innate immune system restores homeostasis after environmental threats; we suggest that in Type II diabetes and impaired glucose tolerance long-term lifestyle and environmental stimulants, probably in those with an innately hypersensitive acute-phase response, produce disease instead of repair. [Diabetologia (1998

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“…Percent change was positively related to the concentration of globulin, which did not correlate with basal Lp(a) concentration in all subjects. Because none of the subjects had diseases that can raise the concentration of globulin, and because some authors insist that Lp(a) is an acute-phase protein, 37 one possible explanation is stress due to postmenopausal symptoms, which can be improved markedly after therapy. Nevertheless, the significance is obscure and further evaluation is needed.…”

Section: Discussionmentioning

confidence: 99%

Effect of Hormone Replacement Therapy on Lipoprotein(a) and Lipid Levels in Postmenopausal Women

Kim¹

1996

Arch Intern Med

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High concentrations of lipoprotein(a) [Lp(a)], an independent risk factor for atherosclerosis, cannot be managed by the usual lipid-lowering agents. It has been suggested that Lp(a) levels are related to female sex hormones. Estrogen replacement therapy makes the lipid profiles favorable for delaying atherosclerosis in postmenopausal women. The effects of the combination therapy of estrogen and progesterone on lipids are controversial. This study was designed to evaluate the effect of female sex hormones on the concentration of Lp(a) and to clarify the influence of progesterone on the effect of estrogen in postmenopausal women. Postmenopausal women (n=184) were divided into four groups: control; 0.625 mg conjugated equine estrogen (CEE) plus 10 mg medroxyprogesterone acetate (MPA); 0.625 mg CEE plus 5 mg MPA; and 0.625 mg CEE only. Medication for 2 months lowered the concentrations of Lp(a) by 20% in all treated groups. The decrease was more pronounced in subjects with a relatively higher basal Lp(a) concentration. Estrogen replacement therapy raised the concentration of high-density lipoprotein cholesterol and decreased low-density lipoprotein cholesterol without changing total cholesterol. The combination therapy of estrogen and progesterone abolished the effect of estrogen on highdensity lipoprotein cholesterol. Hormone replacement therapy lowered Lp(a) levels in postmenopausal women. The effect was prominent in subjects with high basal Lp(a) levels. This decrease may be one of the mechanisms of the cardioprotective effects of estrogen. The cardioprotective effect of estrogen cannot be applied to the combination therapy due to the adverse effect of progesterone on high-density lipoprotein cholesterol. It cannot be lowered by the usual treatments for hyperlipidemia, 912 and only a few drugs reduce Lp(a) concentrations. 1318 Recently, epidemiological investigations have reported that concentrations of Lp(a) are higher in postmenopausal women than in premenopausal women 19 and that postmenopausal women taking female sex hormones have lower Lp(a) levels than those not taking such medication. 20 Small-sized studies 21 -22 also show that hormone replacement therapy (HRT) in postmenopausal women lowers the concentration of Lp(a) markedly.Premenopausal women have lower cardiovascular morbidity and mortality than men of a similar age. After menopause, the incidence of cardiovascular diseases increases and no difference is noticed during the eighth decade between men and women. 23 Female sex hormones have been used for the alleviation of postmenopausal symptoms and the treatment of osteoporosis. Most but not all reports have shown that estrogen replacement therapy in postmenopausal women re-

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Transient changes of serum lipoprotein(a) as an acute phase protein

Cited by 322 publications

References 19 publications

Plasma Lipoprotein(a) and Its Relationship with Disease Activity in Patients with Behçet’s Disease

Plasma Lipoprotein(a) and Its Relationship with Disease Activity in Patients with Behçet’s Disease

Is Type II diabetes mellitus a disease of the innate immune system?

Effect of Hormone Replacement Therapy on Lipoprotein(a) and Lipid Levels in Postmenopausal Women

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