Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011860 (type 2 diabetes)
 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The incidence of fasting HLP in 326 diabetics was 68.4 percent. The common types of HLP were type IV, IIb, IIa and III respectively. There was one case of type V. HDLC was decreased in all three groups of diabetics together with elevated ratio of TC to HDLC comparing with the controls of similar age and sex VLDL and TG were significantly elevated in NIDDM aged 60 and over comparing with IDDM but not significantly different from NIDDM aged below 60. The early detection and treatment of HLP along with optimum control of blood glucose are of utmost importance to prevent further complications caused by atherosclerosis.
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PMID:Lipid disorders in Thai diabetics. 668 May 38

Fatty acid (FA) profiles of total serum lipids were determined by capillary gas chromatography in Type 2 diabetic patients (NIDDM) with diverse types of hyperlipidemia. In patients with hypertriglyceridemia (DM-HTG) and combined hypertriglyceridemia and hypercholesterolemia (DM-HLP), a significantly different total FA composition was found compared with healthy controls or diabetics with normal serum lipids. In particular, the proportions of saturated and monounsaturated FA were increased and the proportions of n-6 polyunsaturated FA were decreased. In DM-HLP patients, PUFA n-6 metabolites and C20-C22 PUFA were also decreased. Thus, hyperlipidemia shifts significantly the serum FA composition in NIDDM patients into an atherogenic profile. More study is needed, however, to understand if serum FA changes may contribute to the increased atherogenesis commonly found in these patients.
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PMID:The effect of hyperlipidemia on serum fatty acid composition in type 2 diabetics. 932 91

We performed a cost-effectiveness simulation of acipimox, bezafibrate, fenofibrate and gemfibrozil in patients with hyperlipoproteinaemia type IIb and IV (Frederickson). A distinction was made between patients with HLP type IIb and IV and HLP associated with diabetes mellitus type II (NIDDM). Direct costs were assessed as those incurred by social security for the treatment, and indirect costs were not taken into account. In appropriate dosages, all 4 substances can be considered equally efficacious in lowering lipid levels, although gallstones occur 3 times more frequently in patients treated with fibrates than in those treated with acipimox. Acquisition costs of the 4 drugs under consideration are comparable. Thus, when hospitalisation costs for treatment of gallstones are taken into account, therapy with acipimox is more cost effective than fibrate therapy.
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PMID:Cost-effectiveness study of a lipid-lowering therapy in hyperlipoproteinaemia type IIb and type IV (Frederickson). 1014 61

Four apolipoprotein (apo) E variants have been reported to be associated with lipoprotein glomerulopathy (LPG), which is characterized by type III hyperlipoproteinemia (type III HLP) and proteinuria and frequently leads to nephrotic syndrome. We report the histologic findings in the kidneys of a type III HLP patient with an apo E variant, apo E Toranomon, in which the glutamine at residue 187 in apo E is substituted by glutamic acid (Q187E). The patient also had type 2 diabetes mellitus. No evidence of lipoprotein thrombi suggestive of LPG was detected, however, and the histologic diagnosis was diabetic nephrosclerosis. This unique case illustrates that not all apo E variants result in LPG, and the location of mutations in the apo E protein is one of the important determinants for the development of LPG.
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PMID:A patient with apolipoprotein E2 variant (Q187E) without lipoprotein glomerulopathy. 1187 95

At present, literally no one disputes hyperlipoproteinaemia and dyslipidemia (HLP and DLP) treatment as a rational therapeutic approach in the prevention of cardiovascular diseases (CVD). This approach is in line with the current principles of evidence-based medicine (EBM) and is sufficiently evidenced particularly by the results of large intervention studies. Nevertheless! When the results of the recent studies are critically appraised, these by no means are (mostly, there, obviously, are exceptions) as conclusive as the studies conducted in 1980s and 1990s. Consequently, positive results are being sought in subanalyses, subgroup evaluations and multiple-study metaanalyses. This paper is not intended as a critique of new drugs. These certainly are developed to be safe, effective and well-tolerated. However, the newer studies suffer from a range of issues: the populations studied are already very well managed, it is not possible to compare against placebo and sometimes, let us be honest, the trial design itself is problematic (often it is an uncritical effort to treat as wide as possible range of patients as well as new groups of patients who might not be suitable for the given treatment). Certainly, we should not start disputing the well-evidenced hypotheses and seek alternatives to the long-established arguments and approaches as a consequence to some less convincing studies. We must not overlook the most robust results of statin studies as well as 'positive' studies with other hypolipidemics. There is no doubt that the effect ofstatins on LDL-cholesterol represents a significant move towards cardiovascular disease prevention. Despite this, we currently recognise with increased intensity that this very effective and well-evidenced treatment has its limits and that a high proportion of patients dies or are faced with cardiovascular diseases even though they are treated with a correct dose ofa statin and a target LDL-C level is achieved. This remaining risk (represents more than 50% ofevents) has been termed 'RESIDUAL RISK'. The issue of residual risk is crucial in patients with type 2 diabetes mellitus (DM2T) or in all patients with HDL-C-low DLP. As was repeatedly emphasised, a statin will be a cornerstone of pharmacological treatment of a DLP. However, a question arises what to combine it with. The most convincing data exist for niacin (combination of niacin with laropiprant minimising the incidence of unwanted flushes). We surely should not marginalize other hypolipidemics used mainly in combinations: resin and ezetimibe to treat LDL-C, niacin, fibrates and possibly omega-3-fatty acids to manage the residual risk (HDL and TG). Last but not least we should not forget non-pharmacological treatment as the pivotal treatment approach in all patients.
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PMID:[Hyperlipoproteinaemia and dyslipoproteinaemia II. Therapy: non-pharmacological and pharmacological approaches]. 2084 7

Cardiovascular diseases (CVD) represent a significant health problem in all countries world-wide and in the developed world, including the Czech Republic, in particular. The underlying cause in the majority of CVD patients is atherosclerosis and its complications, respectively. The present paper focuses on prevention and timely treatment of atherosclerosis. Management should be comprehensive and should target the risk factors (RF). Hypertension, hyperlipoproteinaemia and dyslipidemia (HLP and DLP), type 2 diabetes mellitus (T2DM), visceral fat obesity and cigarette smoking are the dominating RFs. Even though all RFs have to be managed simultaneously and it is not possible to focus on just one of them, for the sake of clarity, this paper discusses hypertension and the use of telmisartan, a representative of one the most up-to-date group of antihypertensives. There is a growing evidence that it is not always just a reduction of a specific risk that is important but also the mode of treatment. For example, to reduce a CV risk in a patient with hypertension but also, for example, with metabolic syndrome, it is more beneficial to treat the patient with rennin-angiotensin system (RAS) blocking agents, possibly in a combination with calcium channels antagonists, than to use "traditional" (older) treatment approach with a combination of a beta/blocker and diuretic. Among the RAS-modifying agents, ACE inhibitors and sartans are the most widely used. Among sartans, telmisartan is very well-tolerated and has evidence from a large interventional study for its effect on reducing the CV risk.
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PMID:[Comprehensive management of cardiovascular risk. Focusing on telmisartan]. 2084 16

LDLP and VLDLP have different biological functions: phylogenetically older LDLP transfer FA that serve as substrates for intracellular production of energy and ATP while VLDLP transfer FA--precursors of cell membranes and eicosanoids. The cells absorb LDLP via apoB-100 endocytosis and VLDLP through apoE/B-100 receptors. VLDLP consist of palmitic and oleic VLDLP and LDLP of linoleic and linolenic LDLP. The contribution of LDLP to the development of HLP atherosclerosis and atheromatosis is negligible. LDLP form palmitic and oleic VLDLP with hydrated LDLP density. Blockade of LDLP absorption by apoB endocytosis and deficit of poly-FA constitute the etiological basis of atherosclerosis. Its pathogenetic basis is the excess of palmitic VLDLP with LDPL density in the intercellular space that block absorption of linoleic LDLP with all transferred SC poly-FA. Atheromatosis is clinically and prognostically most significant symptom of atherosclerosis associated with accumulation of ligand-free VLDLP and LDLP in arterial intima of the elastic type as the local pool of interstitial tissue for intravascular pool of intercellular medium. Type 2 diabetes mellitus in aged patients is a symptom of atherosclerosis resulting from SC poly-FA deficit and GLUT4 incompetence. Insulin-dependent cells differ in the degree of insulin resistance. Non-alcoholic fatty liver disease, synthesis of a physiological palmitic TG by hepatocytes and excessive formation of palmitic VLDLP in liver integrate pathogenesis of atherosclerosis and hepatic steatosis. The main pathogenetic factor is the excess of palmitic s-FA and palmitic TG.
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PMID:[Low and very low density lipoproteins: pathogenetic and clinical significance]. 2365 66