Adult cardiologists or hyperlipidemia experts have advocated no screening and no treatment for children with familial hyperlipidemia.
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[Comparative pharmacokinetics of theophylline in hyperlipidemia in animals and humans].
The incidence of hereditary hyperlipidemia amounts to about 8% and rises when secondary causes of lipid metabolism disturbances are taken into consideration. In contemporary literature there is paucity of data on the influence of hyperlipidemia on pharmacokinetics of drugs. That is especially important in the case of drugs characterized by a narrow therapeutic index, such as theophylline, which can be administered to patients affected by an altered lipid status. The investigation was aimed at evaluating the feasibility of an animal model of hyperlipidemia for pharmacokinetic studies of theophylline in humans suffering from lipid metabolism disturbances. The study was carried out on male rabbits divided into two groups: a control and an experimental one, fed on a high-fat diet. Humans were also ascribed to two groups: controls and those affected by primary, mixed-form of hyperlipidemia. The animals were given theophylline intravenously in a single dose of 12 mg/kg, whereas humans received intravenously injected theophylline in a single dose of 3.5 mg/kg. Blood was sampled after 5, 10, 15, 30, 45 minutes and 1, 2, 4, 6, 8, 12, 24 hours following theophylline administration. FPIA method was used to determine blood serum concentrations of theophylline (Tab. 1,3). The two-compartment open model for intravenous administration was applied for calculations. Considerable alterations of theophylline pharmacokinetics in humans suffering from mixed form of hyperlipidemia were observed (Tab. 4), whereas no marked changes were noted in animals with alimentary-induced hyperlipidemia (Tab. 2). In hyperlipidemic rabbits theophylline behaves as lipophilic agent, despite its poor penetration into the adipose tissue. A considerable decrease in area under the concentration-time curve of theophylline, increase in transfer constants as well as accelerated elimination of the drug were observed in humans with mixed form of hyperlipidemia. The behaviour of theophylline in hyperlipidemic rabbits was different from that in patients with mixed form of hyperlipidemia. Comparison of theophylline pharmacokinetics in hyperlipidemic animals and in human subjects revealed that an animal model of hyperlipidemia was inappropriate for studying the effect of lipid metabolism disturbances on pharmacokinetics of drugs as it is shown in the study on theophylline. This can be explained, to some extent, by different mechanisms of hyperlipidemia in rabbits and in humans. Hyperlipidemia in rabbits was induced by alimentary factors, while in humans lipid metabolism disturbances were of primary origin. Basing on the results of the present study it may be suggested that there are no general rules for anticipating the influence of hyperlipidemia on the pharmacokinetics of drugs in various organisms. Therefore, it is most likely that studies on the influence of hyperlipidemia on the pharmacokinetics of drugs should be performed for every particular drug separately.
Adult↗
Enhanced in vivo platelet release reaction and malondialdehyde formation in patients with hyperlipidemia.
Plasma level of beta-thromboglobulin (beta TG), a useful marker of in vivo platelet "release reaction,"was determined by radioimmunoassay in 69 patients, with three types of primary hyperlipidemia (IIa, IIb, IV) and compared with the findings in age- and sex-matched healthy controls and 57 patients with established atherosclerosis and peripheral vascular disease. Malondialdehyde (MDA) formation, used for assessment of prostaglandin synthesis, was determined in 51 and plasma platelet factor 4 (PF4), measured by radioimmunoassay, in 48 of the patients with hyperlipidemia. Results were correlated to five serum lipids and lipoprotein levels in the patients with hyperlipidemia. beta TG was significantly increased in the patients with hyperlipidemia and peripheral vascular disease, compared to those in the controls (p < 0.001); it was significantly higher in the patients with hyperlipidemia than in those with peripheral vascular disease. PF4 and MDA formation were also increased in the patients with hyperlipidemia, and significantly higher levels of MDA were obtained in patients with type IIb and type IV hyperlipidemia than in those with type IIa hyperlipidemia (p < 0.02). beta TG and MDA correlated weakly with total serum cholesterol triglycerides and very low density lipoprotein-triglyceride. There was also a significant correlation between beta TG and PF4, and MDA production. These results indicate that in vivo platelet "release reaction" and MDA formation are increased in hyperlipidemic patients. The release reaction is more enhanced in those with hyperlipidemia than in the patients with peripheral vascular disease. They suggest that the abnormal platelet function is related to the elevated levels of serum lipids and lipoproteins in the hyperlipidemic patients and not only to the atherosclerotic changes associated with hyperlipidemia.
Aged↗
Oxidant stress in hyperlipidemia-induced renal damage.
Hyperlipoproteinemia can aggravate glomerulosclerosis and chronic tubulointerstitial (ti) damage in kidneys without primary immunologic disease. We evaluated whether the effect of hyperlipidemia on progression of renal damage differed between kidneys without preexisting glomerular disease and kidneys with mesangioproliferative glomerulonephritis and whether the renal actions of hyperlipidemia were dependent on oxidant-antioxidant balance. Hyperlipidemia was induced by high-fat and high-cholesterol diet in uninephrectomized rats. In rats without glomerulonephritis, hyperlipidemia led to a rise in glomerular and ti generation of reactive oxygen species (ROS). Oxygen radicals were mainly generated by enhanced xanthine oxidoreductase (XO), which rose with protein concentration and activity during hyperlipidemia; concurrently, glomerulosclerosis and chronic ti injury were noticed during hyperlipidemia [ti damage (% of total tubulointerstitium (TI) after 150 days): normolipidemia 0.1 +/- 0% vs. hyperlipidemia 3.4 +/- 0. 9%; P < 0.05]. In mesangioproliferative Thy-1 nephritis, ti injury was significantly accelerated by hyperlipidemia (ti damage after 150 days: normolipidemic Thy-1 nephritis 2.5 +/- 0.6% vs. hyperlipidemic Thy-1 nephritis 12.5 +/- 3.1%; P < 0.05). Antioxidant enzyme activities decreased and XO activity rose markedly in the TI (XO activity in TI after 150 days: normolipidemic Thy-1 nephritis 2.2 +/- 0.5 vs. hyperlipidemic Thy-1 nephritis 4.5 +/- 0.7 cpm/microg protein; P < 0.05). In hyperlipidemic Thy-1 nephritis rats, which had a higher urinary protein excretion than normolipidemic rats, hypochlorite-modified proteins, an indirect measure for enhanced myeloperoxidase activity, were detected in renal tissue and in urine, respectively. During hyperlipidemia, chronic damage increased in renal TI. Enhanced generation of ROS, rise in oxidant enzyme activity, and generation of hypochlorite-modified proteins in renal tissue and urine were noticed. These data suggest that oxidant stress contributed to the deleterious effects of hyperlipidemia on the renal TI.
Animals↗
When and how to treat hyperlipidemia.
The recently completed NHLBI sponsored multicenter double-blind Coronary Heart Disease Prevention Trial has provided the long sought-after proof that hyperlipidemia is a major CAD risk factor and that the incidence of CHD and its complications can be favorable modified by control of hyperlipidemia with appropriate diet-drug therapy. This nationwide study confirms and validates the earlier reports on the feasibility to stabilize or to promote regression of atherosclerotic arterial lesions through hyperlipidemia control. Current investigations suggest that in most instances, simple differentiation of hyperlipidemias into hypercholesterolemia and hypertriglyceridemia (major components of low-density and very low-density lipoprotein) can supply adequate information for clinical practice. In difficult-to-control hyperlipidemias, the application of lipoprotein analysis may provide insight of the underlying genetic-metabolic abnormality for selection of more specific therapeutic modality. Before considering hypolipemic therapy, secondary hyperlipidemias should be excluded. In those cases, treatment should be directed to the primary disease(s) for the solution of the hyperlipemic problem. Life-long dietary modification is the key step to treatment of all types of hyperlipidemias, and especially the primary hyperlipidemias. In this latter group, both the patient and the family should be educated on the principles and the importance of dietary modification to boost compliance. In familial hyperlipidemias, a specifically effective hypolipemic drug, or a combination of drugs with minimal or no long-term toxic and side effects, should be prescribed to augment the therapeutic diet to lower the elevated plasma lipid levels and stabilize them at normal range. Early detection and control of atherosclerosis-prone hyperlipidemias in children and young adults should be vigorously promoted to improve cardiovascular health of the population and to reduce the escalation of health care expenses.
Adult↗
Plasma lipoproteins in familial combined hyperlipidemia and monogenic familial hypertriglyceridemia.
Plasma lipoprotein concentration, composition, and size were evaluated in two common familial forms of hypertriglyceridemia and compared with those in normal subjects. The very low density lipoproteins (VLDL) were triglyceride-enriched in familial hypertriglyceridemia (triglyceride/apoprotein B ratio: 25.7 +/- 8.9) as compared to normal (9.6 +/- 12.2, P < 0.001) or familial combined hyperlipidemia (9.7 +/- 3.3, P < 0.001). The diameter of VLDL was larger in familial hypertriglyceridemia (3.27 +/- 0.28 pm) than in familial combined hyperlipidemia (2.87 +/- 0.16 pm, P < 0.02). Although in familial hypertriglyceridemia VLDL tended to be larger, and in familial combined hyperlipidemia VLDL tended to be smaller than normal (3.08 +/- 0.48 pm), neither of these differences were significant. While VLDL was normally distributed in the control population, the size was skewed to larger particles in familial hypertriglyceridemia with fewer small particles (P < 0.05) and skewed to smaller particles in familial combined hyperlipidemia with fewer large particles (P < 0.05). VLDL was reciprocally related to low density lipoproteins (LDL) in familial combined hyperlipidemia (r = -0.80 to -0.87) suggesting that the concentrations of these individual lipoprotein groups were somehow interrelated. There was no significant relationship between these two lipoprotein classes in familial hypertriglyceridemia or in normals. In familial combined hyperlipidemia, the apoprotein A-I/A-II ratio was below normal (P < 0.01) suggestive of low HDL(2) levels. This change in apoprotein composition was independent of VLDL or LDL concentration. In familial hypertriglyceridemia, high density lipoprotein (HDL) cholesterol was reduced (33% below mean normal) and HDL triglyceride was increased (by 46%), while the concentration of apoA-I and apoA-II was normal. VLDL triglyceride was inversely related to HDL cholesterol in familial hypertriglyceridemia (r = -0.74, P < 0.005), but not in familial combined hyperlipidemia. The large, triglyceride-enriched VLDL observed in familial hypertriglyceridemia is compatible with the reported increase in VLDL triglyceride synthesis seen in this disorder. The increase in VLDL apoprotein B synthesis previously reported in familial combined hyperlipidemia was associated with VLDL of normal composition. The changes in HDL cholesterol in these two disorders might reflect exchange of triglyceride between VLDL and HDL or could be related to transfer of surface components during the catabolism of VLDL. The reciprocal relationship between various components of VLDL and LDL seen in familial combined hyperlipidemia, but not in familial hypertriglyceridemia or in normal subjects, might provide some insight into the pathological abnormalities in these disorders. The differences between these two common familial forms of hypertriglyceridemia provide further support that they are distinct entities.-Brunzell, J. D., J. J. Albers, A. Chait, S. M. Grundy, E. Groszek, and G. B. McDonald. Plasma lipoproteins in familial combined hyperlipidemia and monogenic familial hypertriglyceridemia.
Adult↗
Drug treatment of combined hyperlipidemia.
Combined hyperlipidemia is increasing in frequency and is the most common lipid disorder associated with obesity, insulin resistance and diabetes mellitus. It is associated with other features of the metabolic syndrome including hypertension, hyperuricemia, hyperinsulinemia and highly atherogenic subfractions of lipoprotein remnant particles including small dense low density lipoprotein-cholesterol. This review examines the mechanisms by which combined hyperlipidemia arises and the various drugs including fibric acid derivatives, hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, and nicotinic acid which can be used either as monotherapy or in combination to manage it and to improve prognosis from atherosclerotic disease in diabetes mellitus, insulin resistant states and primary combined hyperlipidemia. The therapeutic approach to combined hyperlipidemia involves determination of whether the cause is hepatocyte damage or metabolic derangements. Combined hyperlipidemia due to hepatocyte damage should be treated by attention to the primary cause. In the case of metabolic dysfunction because of imbalance in glucose and fat metabolism, therapy of diabetes mellitus and obesity should be optimised prior to commencement of lipid lowering drugs. Both fibric acid derivatives and HMG-CoA reductase inhibitors can be used in the treatment of combined hyperlipidemia with fibric acid derivatives having greater effects on triglycerides and HMG-CoA reductase inhibitors on LDL-C though both have effects on the other cardiovascular risk factors. There is some evidence of benefit with both interventions in mild combined hyperlipidemias and large scale trials are underway. Fibric acid derivatives and HMG-CoA reductase inhibitor therapy can be combined with care, provided that gemfibrozil is avoided, fibric acid derivatives are given in the mornings and shorter half -life HMG-CoA reductase inhibitors are used at night. Combined hyperlipidemia emergencies occur with predominant hypertriglyceridemia in pregnancy or as a cause of pancreatitis. Therapy in the former should aim to reduce chylomicron production by a low fat diet and intervention to suppress VLDL-C secretion using omega-3 fatty acids. In the latter case, fluid therapy alone and medium chain plasma triglyceride infusions usually reduce levels satisfactorily though apheresis may be required. Blood glucose levels also need aggressive management in these conditions. Combined hyperlipidemia is likely to become an increasing problem with the increase in the prevalence of obesity and diabetes mellitus and needs aggressive management to reduce cardiovascular risk.
Acute Disease↗
Hyperlipidemia intensifies cerulein-induced acute pancreatitis associated with activation of protein kinase C in rats.
AIM: To investigate the effects of hyperlipidemia on acute pancreatitis (AP) and the possible mechanisms. METHODS: Rat models of hyperlipidemia and AP were established by Triton WR1339 and cerulein respectively. Human albumin was used to treat AP complicated by hyperlipidemia. In each group, we compared the histological score, volume of ascites, ratio of pancreatic wet/dry weight, serum amylase (AMY) and pancreatic acinar cell apoptosis. The level of protein kinase C (PKC) membrane translocation in pancreatic tissue was detected by Western blot. RESULTS: In the hyperlipidemia model established by Triton WR1339, triglyceride (TG) increased remarkably and reached its peak 6 h after injection, and most rats developed mild acute pancreatitis. Histological score, volume of ascites, ratio of wet/dry weight and serum AMY in AP animals with hyperlipidemia were obviously higher than those in AP animals (P < 0.05) and decreased after albumin therapy but not significantly (P > 0.05). Apoptotic cells detected by terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) increased in AP animals with hyperlipidemia and did not change distinctly after albumin therapy. PKC membrane translocation level increased in AP animals with hyperlipidemia and decreased remarkably after albumin therapy (P < 0.05). CONCLUSION: Hyperlipidemia may induce AP or intensify pancreatic injury. Albumin therapy can not alleviate pancreatic lesion effectively. PKC activation may be one mechanism by which AP is intensified by hyperlipidemia.
Acute Disease↗
Effects of hyperlipidemia on the pharmacokinetics of nifedipine in the rat.
PURPOSE: The effect of hyperlipidemia on nifedipine pharmacokinetics was studied. The mechanisms by which hyperlipidemia affects pharmacokinetics of drugs are mainly undetermined. Hyperlipidemia may decrease the fraction of unbound drug in plasma and/or decrease intrinsic ability of the cytochrome P-450 systems due to excess membrane cholesterol. Hyperlipidemia is a primary risk factor for coronary artery disease leading to hypertension and ischemic heart disease, for which nifedipine, a calcium channel blocker, is used. METHODS: Poloxamer 407 (P407)-induced hyperlipidemic rat model was used to study the effects of hyperlipidemia on the pharmacokinetics of nifedipine (6 mg kg-1 given i.v., i.p. and p.o.). Total plasma cholesterol levels increased from 0.82-2.02 to 5.27-11.05 mmol L-1 48 h post P407 administration (1 g kg-1, i.p.). Protein binding studies were conducted by an ultrafiltration method. RESULTS: Hyperlipidemia significantly decreased CLTB by 38% and CLTB/F by 45 and 42% following po and i.p. doses, respectively, thereby increasing AUC0-infinity, Cmax and half-life. Absolute bioavailability and Vdss remained unchanged. AUC0-infinity was affected to the same extent in each route of administration, therefore, the effect was mainly systemic rather than presystemic. Hyperlipidemia significantly lowered the fraction unbound in plasma by approximately 31%. CONCLUSIONS: The altered pharmacokinetics of nifedipine by P407-induced HYPERLIPIDEMIA may be, at least in part, due to the decrease in fraction unbound in plasma. A decrease in intrinsic clearance, however, cannot be ruled out.
Animals↗
Treatment of hyperlipidemia in HIV-infected patients.
The treatment of hyperlipidemia in patients infected with HIV is discussed. Hyperlipidemia is common in HIV-infected patients receiving antiretroviral therapy, especially protease inhibitors and stavudine. The recommendations of the National Cholesterol Education Program (NCEP) may not entirely apply to HIV-infected patients. The pathogenesis of hyperlipidemia in these patients may make them refractory to traditional pharmacotherapy, and NCEP's emphasis on diet and exercise may be unrealistic. Other factors that may complicate treatment of hyperlipidemia include metabolism of many antiretroviral drugs by the cytochrome P-450 isoenzyme system, polypharmacy, and drug-food interactions. A patient's cardiac risk should first be assessed. Nonpharmacologic measures, such as a low-fat diet, weight reduction, and exercise, should be considered. Drug therapy is indicated for patients with familial combined hyperlipidemia that is associated with atherogenesis and for patients with triglyceride concentrations exceeding 1000 mg/dL. Drug therapy for hyperlipidemia involves niacin and statins, in addition to fibric acid derivatives and probucol. Switching among antiretroviral agents when one is found to cause hyperlipidemia should be done cautiously because of the risk for viral rebound and disease progression. NCEP guidelines recommend monitoring low-density-lipoprotein cholesterol levels four to six weeks after the start of lipid-lowering therapy and then at three months; more frequent monitoring may be necessary in HIV-infected patients. The treatment of hyperlipidemia in HIV-infected patients is complicated by their need for antiretroviral drugs, which can themselves contribute to lipid disorders.
Anti-HIV Agents↗
Association between antipsychotic treatment and hyperlipidemia among California Medicaid patients with schizophrenia.
OBJECTIVE: To examine the risk of hyperlipidemia among people with schizophrenia exposed to new antipsychotics (clozapine, olanzapine, quetiapine, risperidone) compared with those exposed to older generation antipsychotics. METHODS: A case-control study of Medi-Cal claims. Cases developed hyperlipidemia after being diagnosed with schizophrenia (ICD-9: 295) and were exposed to only one antipsychotic drug at some point within 12 weeks prior to the hyperlipidemia diagnosis. Hyperlipidemia was defined by diagnostic claim (ICD-9: 272.1-272.4) or prescription claim for antilipemic agents. Cases were matched on gender and age +/- 3 years to patients with schizophrenia who did not develop hyperlipidemia. Conditional logistic regression assessed the risk of antipsychotic exposure, controlling for age, ethnicity, prior type 2 diabetes or hypothyroidism, and exposure to other medications that may cause hyperlipidemia. Analyses were repeated using a 24- and 52-week retrospective exposure windows. RESULTS: For the 12-week exposure window, olanzapine (OR = 1.20, 95% CI 1.08-1.33) was associated with increased risk of developing hyperlipidemia compared with older antipsychotic medications. Exposure to clozapine (OR = 1.16, 95% CI 0.99-1.37), risperidone (OR = 1.00, 95% CI 0.90-1.12), and quetiapine (OR = 1.01, 95% CI 0.78-1.32) was not. Hypothesis tests comparing the 4 atypicals to one another revealed that the odds ratio for olanzapine was greater than that for risperidone (P = 0.002). Other than clozapine's odds ratio being significant at 24 weeks (OR = 1.22, 95% CI 1.03-1.45), increasing the exposure window to 24 or 52 weeks did not substantially alter the results. CONCLUSIONS: Compared with older generation antipsychotics, exposure to olanzapine and, somewhat less consistently, to clozapine is associated with an increased risk of hyperlipidemia among people with schizophrenia.
Adolescent↗
The prevalence of hypertension, hyperlipidemia, diabetes mellitus and depression in men with erectile dysfunction.
PURPOSE: We quantified the prevalence of diagnosed hypertension, hyperlipidemia, diabetes mellitus and depression in male health plan members with erectile dysfunction (ED). MATERIALS AND METHODS: We used a nationally representative managed care claims database that covered 51 health plans with 28 million lives for 1995 through 2002. Based on 272325 identified patients with ED population and age specific prevalence rates were calculated for the same period. RESULTS: The crude population prevalence rates were 41.6% for hypertension, 42.4% for hyperlipidemia, 20.2% for diabetes mellitus, 11.1% for depression, 23.9% for hypertension and hyperlipidemia, 12.8% for hypertension and diabetes mellitus, and 11.5% for hyperlipidemia and depression. The crude age specific prevalence rates varied across age groups significantly for hypertension (4.5% to 68.4%), hyperlipidemia (3.9% to 52.3%), and diabetes mellitus (2.8% to 28.7%), and significantly less for depression (5.8% to 15.0%). Region adjusted population prevalence rates were 41.2% for hypertension, 41.8% for hyperlipidemia, 19.7% for diabetes mellitus and 11.9% for depression. Only 87163 patients with ED (32%) had no comorbid diagnosis of hypertension, hyperlipidemia, diabetes mellitus or depression. CONCLUSION: Hypertension, hyperlipidemia, diabetes mellitus and depression were prevalent in patients with ED. This evidence supported the proposition that ED shares common risk factors with these 4 concurrent conditions. Therefore, as a pathophysiological event, ED could be viewed as a potential observable marker for these concurrent diseases. This finding suggests that clinicians could include ED in the assessment profile of these concurrent conditions for earlier detection and treatment.
Adolescent↗
Retrospective analysis of hyperlipidemia management in a transplant population.
STUDY OBJECTIVES: To determine the prevalence of hyperlipidemia and the effectiveness of hyperlipidemia management in a large population of transplant recipients. A secondary objective was to assess the effect of the National Cholesterol Education Program (NCEP) Adult Treatment Panel III guidelines on hyperlipidemia management compared with the effect from earlier guidelines. DESIGN: Retrospective review of computerized records. SETTING: University-affiliated transplantation center. PATIENTS: Three thousand four hundred fourteen patients with liver, kidney, or pancreas transplants. MEASUREMENTS AND MAIN RESULTS: To determine a diagnosis of hyperlipidemia and the effectiveness of treatment, we assessed the patients's lipid levels. Hyperlipidemia was defined as a total cholesterol level above 200 mg/dl and/or the use of antihyperlipidemic drugs. Of the 3414 patients in the study, 1638 (48%) had hyperlipidemia. Of these, 711 (43%) were receiving antihyperlipidemic drugs; 227 (32%) of the 711 patients had achieved the total cholesterol goal of 200 mg/dl or below. Low-density lipoprotein cholesterol (LDL) levels were available for 1953 (57%) patients. Of these, 537 patients were receiving cholesterol-lowering drugs, and 384 (72%) of the 537 patients achieved the LDL goal of less than 130 mg/dl. CONCLUSION: Although NCEP guidelines recommend monitoring LDL, only slightly more than half of these transplant recipients were monitored. In addition, the patients identified as having hyperlipidemia were not effectively treated to lower their cholesterol levels. Clinicians must be aggressive in diagnosing, monitoring, and treating hyperlipidemia to decrease the rate of cardiovascular disease and to prolong patient survival after transplantation.
Adult↗
[The effects of non-pharmacotherapy in decreasing the levels of serum lipid in patients with hyperlipidemia].
OBJECTIVE: To develop a non-pharmacotherapy program for patients with hyperlipidemia and assess its effectiveness. METHODS: A cluster control trial was used. The experimental group was given non-pharmacotherapy for hyperlipidemia once a week for 6 weeks; the content of non-pharmacotherapy included the basic knowledge about hyperlipidemia, a guide of changing unhealthy diet and life-style. Patients were followed for once every two weeks in the department of out-patient. The control group received general care conducted by university clinicians, without the non-pharmacotherapy program. A self-completion questionnaire on hyperlipidemia-related knowledge level, questionnaires on diet and exercise, body weight, body height and the serum TG, TC were measured at entry point and at the end of 6 month. RESULTS: One hundred and fifty-four patients in experimental group and 150 patients in control group completed the study. The non-pharmacotherapy group showed a significant increase of knowledge on hyperlipidemia in the experimental group comparing with the control group: the mean (sd) score of hyperlipidemia-related knowledge were 22.5 (4.8), 17.4 (4.2) (95% CI: 4.1, 6.1). The diet score and the proportion of regular physical activity had increased 27.20%, 21.78% respectively in experimental group. The mean (sd) of serum TG, TC and body mass index (BMI) for experimental group [2.0 (0.9) mmol/L, 5.4 (0.9) mmol/L, 23.4 (1.9)] lowered significantly comparing to those for control group [2.4 (0.9) mmol/L, 5.9 (1.0) mmol/L, 24.2 (3.0)]. CONCLUSION: Non-pharmacotherapy seemed to be an important intervention for the patients with hyperlipidemia. If same patients with hyperlipidemia failed to respond to non-pharmacotherapy, it is necessary to use pharmacotherapy. However, non-pharmacotherapy should be viewed as basic therapy.
Adult↗
[Subclasses of serum HDL in hyperlipidemia].
OBJECTIVE: To detect the change of composition and ratio of serum HDL subclasses and explore the relationship between these changes and the plasma lipid level in patients with hyperlipidemia. METHODS: The subclasses of serum HDL in 168 patients with hyperlipidemia were determined by two-dimensional gel electrophoresis in conjunction with immunodetection method. RESULTS: Compared to the healthy controls, the pre-beta 1 HDL, pre-beta 2 HDL, HDL3c, HDL3b, and HDL3a increased significantly (P < 0.01, P < 0.01, P < 0.05, P < 0.01 and P < 0.01), while the HDL2a and HDL2b decreased significantly (P < 0.01) in the patients with hyperlipidemia. The pre-beta 1 HDL and HDL3b were significantly higher (P < 0.01) while the HDL2a and HDL2b were significantly lower (P < 0.01) in men than in women with hyperlipidemia. The pre-beta 1 HDL was significantly higher (P < 0.05) while the HDL2b was significantly lower (P < 0.05) in the male control group than in the female control group. In the patients with hyperlipidemia, the serum TG was positively correlated with pre-beta 1 HDL, pre-beta 2 HDL, HDL3b, and HDL3a (r = 0.583, 0.196, 0.130, and 0.370 respectively) and negatively correlated with HDL2a and HDL2b (r = -0.293 and -0.456 respectively); The serum TC was positively correlated with pre-beta 1 HDL and HDL3b (r = 0.348 and 0.219); The serum LDL-C was positively correlated with HDL3b (r = 0.187); The serum HDL-C was negatively correlated with pre-beta 1 HDL and HDL3a (r = -0.354 and -0.292 respectively) and positively correlated with HDL2a and HDL2b (r = 0.254 and 0.256); The TG/HDL-C ratio was positively correlated with pre-beta 1 HDL, pre-beta 2 HDL, HDL3b, and HDL3a (r = 0.593, 0.225, 0.123, and 0.394) and negatively correlated with HDL2a and HDL2b (r = -0.317 and -0.459). CONCLUSION: The particle of HDL in the patients with hyperlipidemia shows a general shift towards smaller size, which indicates that the maturation of HDL could be abnormal in patients with hyperlipidemia. The change of subclasses of HDL in the patients with hyperlipidemia might be associated with coronary artery diseases.
Adult↗
Mutations in Japanese subjects with primary hyperlipidemia--results from the Research Committee of the Ministry of Health and Welfare of Japan since 1996--.
Primary hyperlipidemia is caused by various molecular defects in lipid metabolism. The Research Committee on Primary Hyperlipidemia organized by the Ministry of Health and Welfare of Japan (present: the Ministry of Health, Labour and Welfare) has investigated reported mutations in Japanese patients with primary hyperlipidemia and related disorders (including hypolipidemia), and has created a database based on the questionnaire sent to the members of council board of the Japan Atherosclerosis Society. Mutations in the following genes were investigated: low density lipoprotein receptor, lecithin: cholesteryl acyltransferase, lipoprotein lipase (LPL), hepatic lipase, apolipoproteins A-I, A-II, A-IV, B, C-II, C-III and E, microsomal triglyceride transfer protein, and cholesterol ester transfer protein (CETP). Until 1998, 922 patients with primary hyperlipidemia and related disorders has been registered with the Research Committee, and 190 mutations in 15 genes had been reported, showing a marked variation in Japanese patients with primary hyperlipidemia and related disorders. So-called "common mutations" have been described in Japanese patients with familial hypercholesterolemia, LPL deficiency and CETP deficiency. The genetic defect of familial combined hyperlipidemia (FCHL) is still unknown although FCHL is speculated to be the most prevalent genetic hyperlipidemia, and further investigations should be performed to elucidate the molecular mechanisms of FCHL
Asian People↗
Transient, severe hyperlipidemia in patients with acute lymphoblastic leukemia treated with prednisone and asparaginase.
BACKGROUND: Corticosteroids and asparaginase inhibit protein synthesis. Many of their side effects are familiar to oncologists. Conversely, the possibility of therapy-induced hyperlipidemia generally is not appreciated. The incidence of severe hyperlipidemia during therapy of patients with acute lymphoblastic leukemia (ALL) who received prednisone and asparaginase was evaluated. METHODS: During therapy with prednisone and asparaginase, a 10-year-old girl with precursor B ALL was identified with a peak plasma triglyceride and cholesterol level of 20,600 mg/dl and 1640 mg/dl, respectively. The lipid profile of the 60 patients in the protocol with this patient, the lipid profile of 64 patients on the previous high-risk ALL therapy program, and the literature were reviewed. RESULTS: Five of 60 patients on the New York-II protocol experienced transient, marked (triglyceride level > or = 1000 mg/dl), benign hyperlipidemia. No such problem was observed in the 64 patients on the New York-I protocol. Five similar cases were found in the literature during therapy with steroids (2), asparaginase (2), or both (1). There were no characteristics that distinguished these 10 patients from the vast majority of patients on similar therapy without severe hyperlipidemia. Prolonged therapy with either agent seemed to increase the possibility of hyperlipidemia. CONCLUSION: Severe hyperlipidemia during induction therapy for ALL is random, transient, and benign. Given the serious nature of the underlying disorder and the value of asparaginase and prednisone in its treatment, antileukemic therapy should not be modified when severe hyperlipidemia is observed.
Adolescent↗
A moderate-fat diet for combined hyperlipidemia and metabolic syndrome.
A low-fat diet is recommended for hyperlipidemia. However, low-density lipoprotein (LDL) responses depend on the type of hyperlipidemia (ie, simple hypercholesterolemia or combined hyperlipidemia). In combined hyperlipidemia, which is typical of patients with metabolic syndrome, LDL levels are only one third as responsive to fat and cholesterol as simple hypercholesterolemia. The diminished dietary sensitivity of combined hyperlipidemia is explained by diminished intestinal absorption of cholesterol, a feature of metabolic syndrome. In turn, combined hyperlipidemia is caused by heightened lipid secretion by the liver. A moderate-fat, moderate-carbohydrate diet employing allowable fats has the promise of reducing endogenous lipoprotein production in combined hyperlipidemia. Triglyceride, LDL, and small-dense LDL should be lower, and high-density lipoprotein, apoprotein A-I, and buoyant LDL should be higher. A test of this dietary strategy on lipoproteins and downstream benefits on inflammatory mediators, oxidative stress, and vascular reactivity is now underway.
Diet, Fat-Restricted↗