Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Lp(a), an independent risk factor of thrombotic and arteriosclerotic diseases, was determined in subjects undergoing health examinations, and the significance of the determination of Lp(a) in such examinations was investigated by studying its relation wih other risk factors for arteriosclerosis, etc. The subjects were 838 individuals. Lp(a) was determined by latex immunoassay (LIA). The mean Lp(a) value for all of the subjects was 10.9 +/- 7.2 mg/dl. Both gender groups were compared by age, but no significant changes were observed. In a study of Lp(a) in accordance with complications, there was no significant difference between the DM group and the non-DM group. There was also no significant difference between the IHD group and the non-IHD group. In the hyperlipemia group, the value of Lp(a) tender to be higher than in the non-hyperlipemia group. In the abnormal ECG group, the Lp(a) value was significantly higher than in the normal ECG group. When the relation between Lp(a) and other factors was studied, there was positive correlation with TC, beta Lp and LDLC, and a significant negative correlation with TRG. There was significant negative correlation with GOT, GPT and TTT. When the incidence of disease was compared by cut-off value, the incidence of abnormal ECGs was significantly higher at Lp(a) values of 25 mgdl or higher. In this study, Lp(a) showed positive correlations with TC, beta Lp and LDLC, the atherogenic risk of Lp(a) was evident. Because of the significant incidence of abnormal ECGs at the Lp(a) cut-off value of 25 mg/dl or higher, the risk range for Lp(a) should probably be considered as 25 mg/dl or higher.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The significance of determination of Lp(a) in health examinations]. 793 55

Diabetes mellitus is a systemic disease with several major complications affecting both the quality and length of life. One of these complications is periodontal disease (periodontitis). Periodontitis is much more than a localized oral infection. Recent data indicate that periodontitis may cause changes in systemic physiology. The interrelationships between periodontitis and diabetes provide an example of systemic disease predisposing to oral infection, and once that infection is established, the oral infection exacerbates systemic disease. In this case, it may also be possible for the oral infection to predispose to systemic disease. In order to understand the cellular/molecular mechanisms responsible for such a cyclical association, one must identify common physiological changes associated with diabetes and periodontitis that produce a synergy when the conditions coexist. A potential mechanistic link involves the broad axis of inflammation, specifically immune cell phenotype, serum lipid levels, and tissue homeostasis. Diabetes-induced changes in immune cell function produce an inflammatory immune cell phenotype (upregulation of proinflammatory cytokines from monocytes/polymorphonuclear leukocytes and downregulation of growth factors from macrophages). This predisposes to chronic inflammation, progressive tissue breakdown, and diminished tissue repair capacity. Periodontal tissues frequently manifest these changes because they are constantly wounded by substances emanating from bacterial biofilms. Diabetic patients are prone to elevated low density lipoprotein cholesterol and triglycerides (LDL/TRG) even when blood glucose levels are well controlled. This is significant, as recent studies demonstrate that hyperlipidemia may be one of the factors associated with diabetes-induced immune cell alterations. Recent human studies have established a relationship between high serum lipid levels and periodontitis. Some evidence now suggests that periodontitis itself may lead to elevated LDL/TRG. Periodontitis-induced bacteremia/endotoxemia has been shown to cause elevations of serum proinflammatory cytokines such as interleukin-1 beta (IL-1 beta) and tumor necrosis factor-alpha (TNF-alpha), which have been demonstrated to produce alterations in lipid metabolism leading to hyperlipidemia. Within this context, periodontitis may contribute to elevated proinflammatory cytokines/serum lipids and potentially to systemic disease arising from chronic hyperlipidemia and/or increased inflammatory mediators. These cytokines can produce an insulin resistance syndrome similar to that observed in diabetes and initiate destruction of pancreatic beta cells leading to development of diabetes. Thus, there is potential for periodontitis to exacerbate diabetes-induced hyperlipidemia, immune cell alterations, and diminished tissue repair capacity. It may also be possible for chronic periodontitis to induce diabetes.
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PMID:Periodontitis and diabetes interrelationships: role of inflammation. 1188 55

Antiretroviral protease inhibitors have been shown to cause hyperlipidemia, raising concerns for the possibility of cardiovascular complications among HIV-infected patients. Statins have been successfully used in the management of hypercholesterolemia and were shown to exert antitumor effects. We report here that lovastatin and saquinavir exert cytostatic/cytotoxic effects against Daudi and Raji human lymphoma cells. Importantly, lovastatin potentiates the antitumor effects of saquinavir against these lymphomas in an additive manner. Addition of statins to antiretroviral treatment might therefore decrease some of its side effects while potentiating the antitumor effectiveness.
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PMID:Lovastatin potentiates antitumor effects of saquinavir against human lymphoma cells. 1554 65