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Intravenous intralipid 10% vs. 20%, hyperlipidemia, and increase in lipoprotein X in humans.

To clarify the mechanisms of hyperlipidemia caused by infusion of Intralipid 10%, we compared lipoprotein metabolism during intravenous Intralipid 10% and Intralipid 20%, which contains only half the amount of egg yolk lecithin for the same content of triglyceride as Intralipid 10%. Ten patients receiving 20 ml.kg-1.day-1 of Intralipid 10% and 10 receiving 10 ml.kg-1.day-1 of Intralipid 20% were fed exclusively by total parenteral nutrition (TPN) providing 1.1 g amino acid and 30 kcal.kg-1.day-1 for 4-6 wk. Intravenous Intralipid 10% caused a marked increase in low-density lipoprotein (LDL), together with increases in phospholipid and cholesterol, especially free cholesterol. The progressive increase in lipoprotein X was in proportion with that of LDL or total lipid, whereas no increase in lipids, LDL, or lipoprotein X was observed during intravenous Intralipid 20%. A significant increase in apolipoproteins CIII and E with Intralipid 10% also caused a rise in lipoprotein X. With Intralipid 20%, however, the alterations in apolipoproteins were not observed. Lecithin:cholesterol acyltransferase (LCAT) activity was significantly elevated with Intralipid 10 but not 20%. Disappearance of lipoprotein X after cessation of Intralipid 10% was relatively rapid, and the half-life was 24-60 h. From these findings, the hyperlipidemia with Intralipid 10% was caused almost exclusively by the increase in lipoprotein X. The excess lecithin may be responsible for the formation of and increase in lipoprotein X. Furthermore, it was revealed that Intralipid 20% could be safely used without inducing hyperlipidemia.

Adult↗

Comparison of combined statin-fibrate treatment to monotherapy in patients with mixed hyperlipidemia.

BACKGROUND: Statins are the preferred drugs for the treatment of hypercholesterolemia, and fibrates for hypertriglyceridemia. In patients with mixed hyperlipidemia, monotherapy with one of these agents may not be effective and combined treatment may be preferable. AIM: To compare retrospectively the efficacy and safety of combined statin-fibrate treatment in patients with mixed hyperlipidemia in whom previous monotherapy with one of these agents occurred ineffective. METHODS AND RESULTS: The initial study group consisted of 327 patients who received micronised fenofibrate and 93 patients who received simvastatin for 12 months. Both agents caused significant changes in lipid profile. Following fibrate therapy, total cholesterol (TC), LDL-cholesterol (LDL-C) and triglyceride (TG) levels decreased by 27.9%, 28.2% and 58%, respectively, and following simvastatin therapy by 33.6%, 42.8% and 37.5%, respectively. The HDL-cholesterol (HDL-C) level increased after fenofibrate by 14.8% and remained unchanged following simvastatin therapy. The TC/HDL-C ratio decreased following fenofibrate by 35.6%, and following simvastatin by 35.3%. In some patients the required reduction in lipid parameters was not achieved fenofibrate or simvastatin. Subsequently, 93 patients underwent combined therapy by adding a second agent (simvastatin in a dose of 20 mg/day or fenofibrate in a dose of 200 mg per day) which was continued for another 12 months. The addition of simvastatin to fenofibrate decreased TC, LDL-C and TG levels by 35.5%, 42.1% and 59.6%, respectively in comparison to before treatment volumes. HDL-C level was increased by 11.1%, and TC/HDL-C ratio decreased by 45.3%. The addition of fenofibrate to simvastatin decreased TC, LDL-C and TG levels by 39.3%, 48.9% and 51,6%, respectively. HDL-C level was increased by 13.4%, and TC/HDL-C ratio decreased by 49.3%. No clinical side effects nor an increase in the transaminase levels, requiring termination of the treatment, were observed. CONCLUSIONS: Combined therapy with 20 mg of simvastatin and 200 mg of micronised fenofibrate is highly effective and safe in patients with mixed hyperlipidemia.

Adult↗

[Effects of ginsenoside-Rb on blood lipid metabolism and anti-oxidation in hyperlipidemia rats].

OBJECTIVE: To observe effects of ginsenoside-Rb (G-Rb) on total cholesterol, lipoprotein cholesterol metabolism and anti-oxidation in experimental hyperlipidemia rats. METHOD: Hyperlipidemia rats were respectively given G-Rb 50, 100, 200 mg x kg(-1) x d(-1) ig for twelve days. Total cholesterol, lipoprotein cholesterol and lipid peroxidation (LPO) contents, prostacycline (PGI2), thromboxane (TXA2), superoxide dismutase (SOD) and blood viscosity were measured. Fat accumulation in liver was also observed. RESULT: Triglyceride (TG), total cholesterol (TC), low density lipoprotein cholesterol (LDL-c) in serum, TXA2 in plasma, LPO in serum and liver, and blood viscosity were decreased significantly. High density lipoprotein cholesterol (HDLc) in serum, PGI2 in plasma and SOD in serum and liver were significantly increased by G-Rb (100, 200 mg x kg(-1)) in experimental hyperlipidemia rats. In addition, G-Rb could decrease TC/HDL-c, LDLc/HDL-c ratio, increase PGI2/TXA2 ratio and inhibit fat accumulation in liver. CONCLUSION: G-Rb could have anti-arteriosclerosis effect by improving cholesterol and lipoprotein-cholesterol metabolism, suppressing lipid peroxidation, increasing anti-oxidase activity and PGI2/TXA2 ratio.

Animals↗

Atypical antipsychotic therapy and hyperlipidemia: a review.

Ziprasidone (Geodon), risperidone (Risperdal), and aripiprazole (Abilify) appear to be associated with a relatively low risk for hyperlipidemia, whereas quetiapine (Seroquel), olanzapine (Zyprexa), and clozapine (Clozaril) are associated with a relatively high risk for hyperlipidemia. Possible underlying causes of lipid dysregulation include weight gain, dietary changes, and glucose intolerance. Given the multiple cardiovascular risk factors reported for patients with schizophrenia, great care must be exercised to minimize the additional risk for hyperlipidemia when choosing antipsychotic therapy. It is recommended that a lipid panel be obtained at baseline for all patients with schizophrenia and annually thereafter for patients taking relatively low-risk agents or quarterly thereafter for patients taking relatively high-risk agents. Patients with persistent dyslipidemia should be referred for lipid-lowering therapy or switched to a less lipid-enhancing antipsychotic agent.

Antipsychotic Agents↗

Switching to atazanavir improves metabolic disorders in antiretroviral-experienced patients with severe hyperlipidemia.

OBJECTIVE: To describe the efficacy and change in lipid profile in patients with severe hyperlipidemia after switch to an atazanavir-containing highly active antiretroviral therapy regimen. DESIGN AND METHODS: Open-field, 24-week, prospective observational cohort study including 33 HIV-infected, antiretroviral-experienced patients with hyperlipidemia. Changes in lipid profiles were evaluated by analyses of triglycerides, total cholesterol, high- and low-density lipoprotein (HDL and LDL) cholesterol, and efficacy by HIV RNA and CD4 cell changes, both from baseline to week 24. RESULTS: A rapid and significant decrease of 46% (5.81 +/- 4 mmol/L vs. 3.16 +/- 2.6 mmol/L, P = 0.002) in triglyceride levels was shown. Similarly, a sustained improvement of 18% was observed in total cholesterol levels during the first 24 weeks after switching to atazanavir (6.45 +/- 1.9 mmol/L vs. 5.3 +/- 1.3 mmol/L, P = 0.001). After 24 weeks of treatment there was a significant decrease of 22% in non-HDL cholesterol (5.76 +/- 1.9 mmol/L at baseline vs. 4.5 +/- 1.3 mmol/L at 24 weeks; P = 0.003). HDL and LDL cholesterol profiles did not change significantly as did the viral load or CD4 cell count. CONCLUSIONS: Switching to atazanavir results in a significant improvement in HIV therapy-induced hyperlipidemia. A switch to atazanavir is proposed as a valuable option to improve atherogenic lipid profiles while maintaining virologic control.

Adolescent↗

The effect of fenofibrate on serum paraoxonase activity and inflammatory markers in patients with combined hyperlipidemia.

BACKGROUND: Lipid lowering therapy with statins is beneficial because of improvement in lipoprotein concentrations and additional pleiotropic effects. However, less is known about the pleotropic effect of fibrates. AIM: To investigate the effects of fenofibrate therapy on inflammatory markers and serum paraoxonase activity in patients with combined hyperlipidemia in addition to their lipid lowering effects. METHODS: Fifty patients (18 women, 32 men, mean age 50+/-8.7 years) with a history of combined hyperlipidemia and coronary artery disease were enrolled into the study. Serum lipids, inflammatory markers (high sensitivity C-reactive protein (hs-CRP) and fibrinogen levels) and paraoxonase levels were determined before and after two months of 250 mg per day of fenofibrate treatment. RESULTS: Fenofibrate decreased plasma fibrinogen level by 41% (from 3.9+/-0.9 mg/dl to 2.3+/-0.48 mg/dl, p<0.0001) and hs-CRP level by 71% (from 1.28 mg/dl to 0.36 mg/dl; p<0.0001). Changes in hs-CRP levels were not correlated with the changes in lipid levels. Compared with baseline, serum paraoxonase level was significantly increased after fenofibrate treatment (from 200+/-77U/L to 232+/-82U/L; p<0.001). We found a significant correlation between changes in HDL cholesterol and paraoxonase activity after two months of treatment (r=0.46, p=0.018). CONCLUSION: This study demonstrates that beyond improving lipids and lipoprotein levels, fenofibrate treatment increases paraoxonase activity and decreases inflammatory markers in patients with combined hyperlipidemia.

Adult↗

Hyperlipidemia in patients with periodontitis.

BACKGROUND: Periodontitis is a bacterial infection, which has been classified as a local chronic inflammation. This, as well as cardiovascular disease, may share common risk factors such as smoking, diabetes, behavioral factors, aging, and male gender. The aim of this study was to evaluate the association between hyperlipidemia and periodontitis. MATERIALS AND METHODS: The levels of plasma lipids in 40 subjects with periodontitis (CPITN score III or IV, pocket depth 4 mm) with mean age 32.3 +/-1.2 years were measured and compared with those obtained from 40 age and sex matched controls. Both groups were systemically healthy according to their medical history. RESULTS: Total cholesterol (CHL) and triglycerides (TG) were significantly higher in the case group (P=0.045 and P=0.016, respectively). HDL and LDL cholesterols were higher in patients but did not have any significant differences with controls. The frequency of persons with pathologic values of TG and CHL were significantly higher in cases compared with controls. CONCLUSIONS: These results showed hyperlipidemia may be associated with periodontitis in healthy people. However, it is unclear whether periodontitis causes an increase in levels of serum lipids or hyperlipidemia is a risk factor for both periodontitis and cardiovascular disease.

Adult↗

Effects of pravastatin on serum lipids and apolipoproteins in hyperlipidemia of the nephrotic syndrome.

The nephrotic syndrome is often accompanied by hyperlipidemia associated with an increased risk of accelerated atherosclerosis. The present study was undertaken to evaluate the effects of pravastatin, a novel competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase, on the serum lipids and apolipoproteins in patients with this syndrome and marked hyperlipidemia. Eleven adult patients received 10 mg of pravastatin twice daily for 4 to 8 weeks. The total serum cholesterol decreased from 426 +/- 44 to 309 +/- 18 mg/dl (-27.4%, mean +/- S.E.; p less than 0.01) following administration of pravastatin. The serum triglyceride decreased from 332 +/- 122 to 229 +/- 50 mg/dl (-30.9%), although this change was not significant. Despite the fact that the HDL cholesterol level was barely changed (51 +/- 7 to 51 +/- 6 mg/dl), the LDL cholesterol fell from 313 +/- 30 to 211 +/- 16 mg/dl (-32.5%; p less than 0.005), and the LDL to HDL cholesterol ratio fell from 7.57 +/- 1.59 to 4.94 +/- 0.88 (-34.8%; p less than 0.05). These changes caused the atherogenic index to decline from 9.6 +/- 2.4 to 6.1 +/- 1.2 (-36.5%; p less than 0.05). No significant alterations could be found among apolipoproteins A-1, A-2, B, C-2, C-3, and E. During the present study period, pravastatin was well tolerated and did not affect the serum protein, albumin, serum urea nitrogen, creatinine levels, or urine protein excretion. Also, there were no serious adverse effects. Pravastatin appears to be effective for treating patients with hyperlipidemia of the nephrotic syndrome.

Adult↗

[The effects of dietetic hyperlipidemia on the development of testes and penises in male New Zealand rabbits].

OBJECTIVE: To study the effects of dietetic hyperlipidemia on the development of testes and penises in male New Zealand rabbits. METHODS: The animal model of dietetic hyperlipidemia was established by feeding 36 male New Zealand rabbits which were divided into the test group (n = 20) and the control group (n = 16) at random with rich fat. The concentration of TC, TG, HDL-C as well as LDL-C was determined by using automatic biochemistry analyzer. Radioimmunoassay methods were used to measure the level of T, LH and FSH as well. Alterations of testicular and penial development in morphology were observed by HE staining. RESULTS: Compared with the control group, concentrations of TC, TG and LDL-C increased dramatically as well as the levels of T, LH and FSH decreased obviously. There are significant differences between the two groups (P <0.01). Compared with the control group, the penial length was short (P < 0.05) and testicular coefficient declined (P < 0.01) in the test group. With light microscope, the following phenomenon was manifestly detected: the sabotage of spermatogenic epithelium and the adipocyte sedimentation of the penial tissue. CONCLUSION: It is obvious that intaking a large quantity of food with rich fat from juvenile would induce dietetic hyperlipidemia, result in the functional disorder of hypothalamo-pituitary-gonadal axis, and leads to short penis in development and the damage of spermatogenesis function as well.

Animal Feed↗

Management of hyperlipidemia: new LDL-C targets for persons at high-risk for cardiovascular events.

Coronary heart disease (CHD) remains the leading cause of mortality in the United States, and is associated with significant health care costs. Current evidence overwhelmingly confirms the role of low-density lipoprotein cholesterol (LDL-C) in the pathogenesis of atherosclerosis and the risk of CHD events. The approach to the management of hyperlipidemia has evolved dramatically over the past decade. Randomized clinical trails have provided strong evidence that lowering plasma cholesterol with statins reduces the risk of cardiovascular events, particularly in high-risk patients, irrespective of baseline cholesterol levels. The National Cholesterol Education Program (NCEP) report was released in July 2004. The report examined the results of recently concluded clinical trials and provided consensus recommendations on the management of hyperlipidemia. The report expands on the core content of the previously published guidelines. However, it is by far the most aggressive approach to date for reducing CHD risk. A focal element of the report is the modification of LDL-C goal in high-risk patients to <70 mg/dL. This goal is provided as a therapeutic option and is based on findings of recently concluded clinical trials. The more aggressive recommendations add challenges to the health care system, as the number of patients requiring drug therapy is likely to increase. In spite of the challenges, there are ample opportunities for improving the management of hyperlipidemia. Adherence to the recommendations will vastly reduce morbidity and mortality associated with CHD.

Azetidines↗

Missed opportunity in the treatment of hyperlipidemia in patients with coronary heart disease: the primary care setting.

BACKGROUND: Multiple clinical trials have established the benefits of controlling hyperlipidemia in patients with coronary heart disease (CHD). Nonetheless, many patients still remain untreated or not at goal low-density lipoprotein (LDL). There is limited data concerning the control of this risk factor in CHD patients in the primary care outpatient setting. METHODS: We evaluated the treatment of hyperlipidemia in the main primary care clinics of an academic, urban hospital. We identified 147 patients in a one-month period with a diagnosis of CHD and assessed the frequency of lipid-lowering therapy as well as the number of patients with LDL values that were at goal according to the National Cholesterol Education Program (NCEP) guidelines. RESULTS: A large proportion of patients were minorities and of low income, with 91.8% being African-American and 54.4% female. Although the frequency of statin therapy was relatively high (74.8%), only 55 patients (45.8%) were at goal LDL: < 100 mg/dl. The mean dose of statin prescribed (primarily simvastatin) was 33.3 +/- 17.1 mg. Only seven patients (6.5%) were on the maximum statin dose of 80 mg. CONCLUSIONS: These data show that while the frequency of lipid-lowering therapy in CHD patients in the primary care outpatient setting is relatively high, there remains a treatment gap. Specific areas for improvement are the initiation of higher doses of statins and more aggressive statin titration. The primary care outpatient setting may represent an ideal opportunity to improve control of hyperlipidemia in CHD patients.

Chi-Square Distribution↗

[Effects of Yifuning capsule on blood lipids of ovariectomized hyperlipidemia rats].

OBJECTIVE: To observe the effects of Yifuning (YEN) capsule on blood lipids of ovariectomized hyperlipidemia rats. METHOD: Fifty-six female mature Sprague-Dawley rats were randomized into 7 groups: normal control group, model control group, diethylstilbestrol tablets (DT) group, Xuezhikang group, YFN high, middle and low dose groups. The ovariectomized rats were fed on high fat diet and administrated with the drugs for 3 weeks, then were killed and estimated body weight, liver index and five items of blood lipid (TC, TG, HDL-C, LDL-C, VLDL) by test kit. Enzyme (such as HP, LDL, and whole lipase) was detected too. RESULT: The weight and liver index of model control group increased obviously as compared with normal group. YFN could reduce TG, TC, and LDL-C (P < 0.05) of ovariectomized hyperlipidemia rats obviously and increase HP, LDL and whole lipase (P < 0.05) on the other hand. CONCLUSION: YFN can ameliorate blood lipids of ovariectomized hyperlipidemia rats.

Animals↗

[Effects of acupuncture on blood-lipid levels in the patient of cerebral infarction with hyperlipidemia].

OBJECTIVE: To observe therapeutic effect of acupuncture method for consciousness-restoring resuscitation on cerebral infarction with hyperlipidemia. METHODS: Sixty cases of apoplexy with hyperlipidemia were randomly divided into a consciousness-restoring resuscitation acupuncture group (treatment group) and a Chinese medicine control group (control group), 30 cases in each group. TCM symptomatic scores and indexes of blood lipids were detected before and after treatment in the two groups. RESULTS: The total effective rate for improvement of blood lipids was 72.4% in the treatment group, which was not different from that (65.5%) in the control group (P> 0.05); the total effective rate for clinical symptoms was 89.7% in the treatment group, which was better than that (62.1%) in the control group (P < 0.05). The treatment group was superior to the control group in improvement of numbness and twinge in extremities, dizziness, distention and oppressed feeling in chest and hypochondrium, anorexia, sleepy and weakness (P < 0.05). CONCLUSION: Acupuncture method for consciousness-restoring resuscitation can regulate metabolic disorder of lipids and improve main clinical symptoms in the patient of cerebral infarction with hyperlipidemia.

Acupuncture Therapy↗

Reduction in proteinuria attenuates hyperlipidemia in the nephrotic syndrome.

Hyperlipidemia in the nephrotic syndrome is characterized by increased synthesis of lipids as well as reduced removal of lipids from the blood. When rats with nephrotic syndrome are fed a 40% protein diet, urinary albumin excretion and rate of albumin synthesis increase. Serum cholesterol and triglyceride concentration increase as well. If the increase in albuminuria, but not the increase in the rate of albumin synthesis resulting from dietary protein augmentation, is prevented by the administration of enalapril, serum triglyceride and cholesterol concentration are not increased but are reduced nearly to within the normal range. Proteinuria, and not an increased rate of albumin synthesis, thus plays a causal role in nephrotic hyperlipidemia. Therapy directed at correcting altered glomerular permselectivity, while perserving an increased rate of albumin synthesis, may be effective in managing nephrotic hyperlipidemia.

Angiotensin-Converting Enzyme Inhibitors↗

Physician management of hyperlipidemia in Saskatchewan: temporal trends and the effect of a CME program.

OBJECTIVE: To assess current trends in the management of hyperlipidemia by Saskatchewan physicians, and to evaluate the effect of a specific continuing medical education (CME) program. DESIGN: Using a quasi-experimental design, physicians in an intervention area received the CME program while those in a comparison area did not. Management of hyperlipidemia was assessed before and after the program via a self-administered questionnaire. SETTING: All family physicians, general internists and cardiologists practising in the two areas were eligible. SUBJECTS: Of 439 eligible physicians, 308 (70%) completed the first survey, while 268 of 447 (60%) completed the second survey. Analysis was conducted on the 221 physicians who completed both surveys. INTERVENTION: Physicians in the intervention area received printed materials and attended a series of seminars between November 1988 and February 1989. Program content was based upon the recommendations of the Canadian Consensus Conference on Cholesterol (1988). MAIN RESULTS: Over the study period the mean level of serum cholesterol considered 'ideal' for a 40- to 60-year-old male decreased significantly from 5.43 to 5.03 mmol/L (P less than 0.001). The mean level at which diet therapy was begun decreased from 6.60 to 5.78 mmol/L (P less than 0.001) with a significantly greater proportion of physicians in the intervention area (58.0%) than in the comparison area (43.2%) initiating therapy in the 5.2 to 5.6 mmol/L range (P = 0.03). The mean level of serum cholesterol at which drug therapy is begun also decreased from 7.59 to 6.82 mmol/L (P less than 0.001), with a significantly greater proportion of physicians in the intervention (41.6%) than in the comparison area (25.0%) starting therapy in the 6.2 to 6.6 mmol/L range (P = 0.03). CONCLUSIONS: The management of hyperlipidemia reported by physicians in Saskatchewan changed dramatically between July 1988 and March 1989. The effect of the CME program is modest in comparison with this large temporal trend. The study provides further evidence that significant changes in the practice patterns of groups of physicians will only occur when the educational process is highly focused and personalized.

Adult↗

Hyperlipidemia in acute pancreatitis. Relationship with etiology, onset, and severity of the disease.

Serum lipid (triglycerides and cholesterol) concentrations were studied in 49 patients with acute pancreatitis (AP). The aims of the study were to investigate the prevalence of hyperlipidemia (HL) in patients with AP according to etiology and to evaluate whether HL precedes or is a consequence of AP. Moreover, we analyzed the relationship between HL and the development of pancreatic necrosis. At admission, 23 patients (47%) had HL: 9 of 19 patients with alcoholic pancreatitis, 5 of 18 patients with biliary pancreatitis, and 9 of 12 patients with AP of miscellaneous etiologies (p less than 0.05). Severe HL (serum triglycerides greater than 20 mmol/L) was observed in five patients. Serum lipid levels in patients with AP and HL decreased markedly during the first 72 h of evolution, but remained slightly above the upper normal limit in most of them after 15 d. The prevalence of HL was similar in edematous and necrotizing pancreatitis. Necrotizing pancreatitis was significantly associated with the presence of hypertriglyceridemia in conjunction with hypercholesterolemia (p less than 0.05). The observations that a) hyperlipidemia is an early event in acute pancreatitis, (b) serum lipid values decrease during the acute phase of the disease, (c) hyperlipidemia has a different prevalence in different etiologies, and (d) high serum lipid levels are not always associated to pancreatic necrosis suggest that HL is a preexistent metabolic abnormality with respect to AP. On the other hand, HL may play a role in aggravating AP.

Acute Disease↗

[Detection and distriburion of slow pre-betalipoprotein in agar gel electrophoresis of total serum in 204 cases of mixed hyperlipidemia].

The demonstration in certain sera by electrophoresis an Agar gel, according to Noble's technique, of a further band of intermediate pre-betalipoprotein, between the betalipoproteins and the usual rapid pre-betalipoproteins, led to the designation of this fraction under the name of slow pre-betalipoprotein or pre-beta-lipoprotein. To the rare studies so far published on this subject, we bring here our contribution in the form of a routine analysis of the variations, and not only the presence, but also the relative concentration of the slow pre-beta-lipoproteins with regard to the rapid prebetalipoproteins. On the fasting serum, after 12 hours fasting, comparative studies of normal control subjects (104 cases) of essential hypercholesterolemia, with or without tendinous xanthomas, corresponding to type IIa (110 cases), mixed hyperlipidemia of type II + IV or III, on paper electrophoresis, corresponds usually to type IIb (204 cases) and, finally, massive endogenous hypertriglyceridemia, corresponding to type IV (95 cases). These indicate clearly the elective concentration of the band of slow pre-betalipoproteins persisting after 12 hours fasting in cases of mixed hyperlipidemia (73% of cases), whilst it is rare in the other groups (no more than 5% of cases). A more complete study of 204 cases of mixed hyperlipidemia showed that the high frequency of slow pre-betalipoproteins is situated in a fairly narrow range of relatively moderate hypertriglyceridemia, between the lower limit of 1.50 and the upper limit of 6 to 7 g/l: the maximum frequency and intensity is situated within the area of 2.50 to 4 g/l. The cases who have already had cardiovascular accidents are more often found to have this band than the cases without complications in a fairly similar age group. However, longitudinal studies, both midterm in relation to therapeutic correction, and short term throughout the day or between the 8th and 12th hour of fasting, have clearly revealed the potential labile nature of this fraction, and show the pathological nature of its sometimes massive persistence beyond the 8th hour and even beyond the 12th hour of fasting. This is a sign of pathological blocking of its transformation rather than of a constitutional lipoprotein abnormality.

Adult↗

Hyperlipidemia, dyslipoproteinemia and apolipoproteinopathia--classification and risk of atheroslcerosis. Part I: Principles of classification and methods of dyslipoproteinemia determination.

This paper sums up new findings in the field of pathogenetic relations between lipid and lipoprotein metabolical disorders on the one hand and the risk of early forms of atherosclerosis on the other hand. Detail classification of disorders proceeds from precise clinical and biochemical criteria, genetic considerations and therapeutical aspects. It provides definitions of hyperlipidemia, hyperlipoproteinemia, normolipidemic (latent) dyslipoproteinemia, secondary hyperlipidemia, apolipoproteinopathia and relatively harmless (benign) hyperlipidemia. The paper provides detail tables and systematic graphs.

Adult↗