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PubMed2004

Hyperlipidemia aggravates renal disease in B6.ROP Os/+ mice.

INTRODUCTION: Reduction of renal mass is frequently associated with progressive loss of kidney function. We examined the effects of hyperlipidemia on renal pathology and mediators of tissue damage in B6.ROP Os/+ mice, a model of reduced renal mass. METHODS: C57BL/6 control mice and B6.ROP Os/+ mice were fed normal rodent chow or a high fat, high cholesterol (HFHC) diet for 12 weeks. Kidney function and renal pathology were assessed. RESULTS: Hyperlipidemia led to a decline in kidney function in C57BL/6 mice. Renal pathology was characterized by an increase in glomerular matrix and cellularity, glomerular and tubulointerstitial macrophage influx, and increased tubular epithelial cell turnover. Chow-fed B6.ROP Os/+ animals demonstrated glomerular hypertrophy with an increase in mesangial matrix and cellularity that was characterized by macrophage influx and increased proliferation. The tubulointerstitium showed increased macrophages as well as tubular atrophy and dilation. Renal pathology was accompanied by an increase in blood urea nitrogen (BUN) and proteinuria. Hyperlipidemia in B6.ROP Os/+ mice resulted in increased plasma BUN compared to chow-fed B6.ROP Os/+ animals and aggravated renal pathology by further increasing glomerular matrix and glomerular hypercellularity. Glomerular hypercellularity was associated with increased expression of platelet-derived growth factor-B (PDGF B) and its receptor beta. Glomerular transforming growth factor-beta (TGF-beta) mRNA expression was increased in B6.ROP Os/+ mice, hyperlipidemic C57BL/6 mice and hyperlipidemic B6.ROP Os/+ animals compared to controls and correlated with the amount of mesangial matrix. CONCLUSION: This study demonstrates that hyperlipidemia worsens renal pathology in B6.ROP Os/+ mice with a decline in renal function mediated at least in part through increased renal expression of the cytokines PDGF B and TGF-beta.

Animals↗
PubMed2005

Hyperlipidemia attenuates the infarct size-limiting effect of ischemic preconditioning: role of matrix metalloproteinase-2 inhibition.

Hyperlipidemia attenuates the cardioprotective effect of preconditioning via unknown mechanisms. We have reported previously that in normolipidemic rats, preconditioning decreased ischemia-induced activation and release of myocardial matrix metalloproteinase (MMP)-2 into the coronary perfusate. Here, we investigated whether hyperlipidemia interferes with the cardioprotective effect of preconditioning through modulation of MMP-2. Hearts isolated from male Wistar rats fed 2% cholesterol-enriched or control chow for 9 weeks were subjected to a preconditioning protocol (three intermittent periods of ischemia/reperfusion of 5-min duration each) or a time-matched nonpreconditioning protocol. This was followed by a test ischemia/reperfusion (30-min ischemia and 120-min reperfusion) in both groups. Preconditioning decreased infarct size in the control but not the cholesterol-fed group. Cardioprotection in the preconditioned control group but not in the cholesterol-fed group was associated with an 18 +/- 3% (p < 0.05) inhibition of test ischemia/reperfusion-induced activation and release of myocardial MMP-2 into the perfusate. Myocardial protein levels of tissue inhibitors of MMPs [tissue inhibitor of metalloproteinases (TIMP)-2 and TIMP-4] were not changed in either group. A reduction of infarct size in nonpreconditioned hearts from both control and cholesterol-fed group was produced by the MMP inhibitor ilomastat at 0.25 microM, a concentration producing MMP-2 inhibition comparable with that of preconditioning in the control group. We conclude that hyperlipidemia blocks preconditioning-induced cardioprotection, hyperlipidemia abolishes preconditioning-induced inhibition of myocardial MMP-2 activation and release, preconditioning-induced inhibition of MMP-2 activation and release is not mediated by TIMPs, and pharmacological inhibition of MMPs produces cardioprotection in both normal and hyperlipidemic rats.

Animals↗
PubMed1992

Treatment of hyperlipidemia with probucol suppresses the development of focal and segmental glomerulosclerosis in chronic aminonucleoside nephrosis.

We have recently reported that a lipid-lowering agent, probucol, reduces proteinuria in puromycin aminonucleoside (PA)-induced nephrotic rats (PAN). In this study, we examined whether a long-term treatment of hyperlipidemia with probucol can suppress the development of focal and segmental glomerulosclerosis (FSGS) in chronic PAN. A chronic PAN model was made with repeated intraperitoneal injections of PA (initially 100 mg/kg body weight followed by 25 mg/kg 5 times at 2-week intervals). Two weeks after the first injection of PA, either normal rat chow with or without 1% probucol was given to the nephrotic rats for 10 weeks. Chronic PAN exhibited remarkable proteinuria, hypoalbuminemia and severe hyperlipidemia with all lipoprotein fractions increased. Probucol treatment significantly reduced the lipid concentration in all major lipoproteins, significantly reduced proteinuria and increased plasma albumin concentration. Plasma albumin inversely correlated with cholesterol or phospholipid in low-density and high-density lipoproteins, suggesting that the lipid-lowering effect of probucol may ameliorate the hypoalbuminemia associated with nephrosis. In light microscopic examination, various degrees of FSGS with tubulointerstitial lesions were observed in the renal cortex from chronic PAN. The degree of FSGS was scored from grades 1 to 4 according to severity. One half of the untreated PAN (4/8) was classified into grade 4 and the other into grades 2 or 3, whilst one half of treated PAN (4/8) was classified either into grade 1 or 2. The grading of FSGS correlated negatively with plasma albumin concentration. These results demonstrate that probucol is highly effective upon nephrotic hyperlipidemia and suggest that a long-term treatment of secondary hyperlipidemia can suppress progressive renal injury associated with chronic nephrosis.

Animals↗
PubMed1995

Relation between cholesterol ester transfer protein activities and lipoprotein cholesterol in patients with hypercholesterolemia and combined hyperlipidemia.

Cholesterol ester transfer protein (CETP) promotes the transfer of cholesterol esters among different lipoprotein classes-high-density lipoproteins (HDL), very-low-density lipoproteins, intermediate-density lipoproteins, and low-density lipoproteins (LDL). The current study was carried out to determine whether CETP activities are correlated with lipoprotein cholesterol levels in a large number of patients having elevated LDL cholesterol and normal triglycerides (hypercholesterolemia) and elevated LDL cholesterol and high triglycerides (combined hyperlipidemia). Compared with 50 normolipidemic male patients, 113 hypercholesterolemic patients had a 42% higher mean activity of CETP, and approximately 60% of these patients had CETP activities outside the normal range. A similar elevation of CETP was observed in 47 patients with combined hyperlipidemia. Furthermore, in those with combined hyperlipidemia, CETP activities were highly correlated with LDL cholesterol, non-HDL cholesterol, and non-HDL/HDL ratios. Similar high correlations were obtained by combining normotriglyceridemic patients with and without elevated LDL cholesterol. Since patients with elevated LDL cholesterol had a significantly lower mean level of HDL cholesterol, a high CETP activity also was related to a reduced HDL cholesterol level. Our results are consistent with this concept, although they do not constitute final proof that high CETP activities contribute to elevated cholesterol concentrations and reduced HDL cholesterol levels in patients with hypercholesterolemia and in those with combined hyperlipidemia.

Aged↗
PubMed2002

How well are hypertension, hyperlipidemia, diabetes, and smoking managed after a stroke or transient ischemic attack?

BACKGROUND AND PURPOSE: Stroke prevention clinics (SPCs) are not usually involved with the active management of hypertension, hyperlipidemia, diabetes, and smoking. The effect of consultations generated at SPCs on the adequacy of the management of these risk factors for stroke has not been well described, and few studies have long-term follow-up. METHODS: We performed a prospective study of 119 consecutive patients referred to an SPC for secondary prevention. One year after their baseline visit, patients were re-evaluated for the adequacy of the management of the above risk factors, and the proportion of improvement was assessed. RESULTS: One-hundred twelve patients returned for their 1-year follow-up visit. Sixty-six were male, and the average age was 65 years. Hypertension was present in 83 patients, hyperlipidemia in 92, diabetes in 26, and smoking in 38, and 80 had multiple risk factors. At baseline, 66% of patients with hypertension, 17% of patients with hyperlipidemia, and 23% of diabetics had adequate management of their respective risk factors. During 1 year of follow-up, hypertension management improved 20% (P<0.001) and lipid management improved 32% (P<0.001). There was no significant improvement in diabetes management or smoking cessation. CONCLUSIONS: Although our understanding of the benefit of addressing hypertension, hyperlipidemia, diabetes, and smoking for secondary prevention of stroke is evolving, we found marked room for improvement in the management of these four risk factors. SPCs may need to be more actively involved in the management of these modifiable risk factors, if we are to significantly impact the risk of recurrent stroke.

Adult↗
PubMed1988

Hyperlipidemia in association with childhood sensorineural hearing loss.

In adults there has been an association noted between hyperlipidemia and sensorineural hearing loss. Etiologic considerations include hyperviscosity of the serum, vascular occlusion and an increased susceptibility to noise. Until now this correlation, to our knowledge, has not been made in the pediatric population. Several children with bilateral fluctuating sensorineural hearing losses have been identified with hyperlipidemia. The fluctuations in hearing varied with lipid levels. With dietary controls, the cholesterol levels returned to what would be near the norm for the pediatric population and hearing returned to near baseline. Unexplained fluctuating sensorineural hearing losses in children warrant the consideration of hyperlipidemia. Discovering a potentially reversible etiology for hearing loss is significant but more importantly, may lead to the early detection of hyperlipidemia in the young patient.

Auditory Threshold↗
PubMed1992

Effect of hyperlipidemia on cardiovascular responses to adrenergic stimulation in piglets.

This study was designed to assess the effect of hyperlipidemia on cardiovascular responses to adrenergic stimulation in a porcine model. Four-week-old piglets (n = 10) were divided into two groups; one fed a control diet and the other was fed an atherogenic diet for 8 weeks. Cardiovascular responses were evaluated to both norepinephrine (NE; 0.5 and 2.5 micrograms/kg) and isoproterenol (ISO; 0.1 and 0.5 microgram/kg) from simultaneous recordings of femoral arterial pressure, heart rate, left intraventricular pressure and left intraventricular dP/dt. It was found that no significant difference in the baseline values of cardiovascular function was observed between the control and hyperlipidemic groups. However, in the hyperlipidemic group as compared with the control group: 1) arterial blood pressure responses to NE were significantly increased (P less than 0.05), 2) cardiac contractile responses to NE and ISO were significantly potentiated (P less than 0.05), and 3) reflex bradycardia in response to increasing arterial blood pressure did not occur. These findings indicate that hyperlipidemia can potentiate the cardiovascular responses to adrenergic stimulation, whereas reflex cardiovascular regulation is somewhat altered by hyperlipidemia. Conceivably, these observations may have relevance to the possible role of the mechanism of the interaction of hyperlipidemia and hypertension in atherogenesis.

Analysis of Variance↗
PubMedDate not supplied

Hyperlipidemia associated with protease inhibitor therapy.

OBJECTIVE: To report a case of extreme hyperlipidemia associated with protease inhibitor-based antiretroviral therapy and review the relevant literature concerning lipid abnormalities with HIV infection and antiretroviral therapy. CASE SUMMARY: A 35-year-old HIV-infected man developed a serum cholesterol of 1472 mg/dL and fasting serum triglycerides of 8660 mg/dL after initiation of antiretroviral therapy consisting of ritonavir, saquinavir, nevirapine, and didanosine. All other medications had been stable during this time period and the abnormality resolved after discontinuation of antiretroviral therapy and initiation of lipid-lowering therapy. The elevated cholesterol and triglyceride concentrations did not recur when therapy was reinstituted with nelfinavir, saquinavir, nevirapine, and didanosine. The hyperlipidemia then was attributed to ritonavir. DISCUSSION: Lipid abnormalities are common in patients with HIV infection and usually consist of hypocholesterolemia and moderate hypertriglyceridemia. Hypercholesterolemia and hypertriglyceridemia have been reported with ritonavir and, less commonly, with other currently available protease inhibitors. Some cases of ritonavir-associated hyperlipidemia have been extreme. Although an association between hyperlipidemia and clinical consequences such as pancreatitis and atherosclerotic disease has not been well described with protease inhibitor therapy, pancreatitis is common in HIV-infected patients. It is possible that in some cases, protease inhibitor-induced hypertriglyceridemia may contribute to the development of pancreatitis. CONCLUSIONS: Optimal management of lipid abnormalities in HIV-infected patients is controversial. The potential benefit of reducing the incidence of pancreatitis and atherosclerotic events must be weighed against the risk of intolerance, toxicity, and drug interactions.

Adult↗
PubMed1998

Hyperlipidemia and kidney disease: concepts derived from histopathology and cell biology of the glomerulus.

The association between hyperlipidemia and renal disease was noted by Virchow as early as the 19th century. Subsequently, similar histopathological lipid depositions were confirmed-in diverse human and experimental renal disease. Although, no studies have been established in man to suggest a causal relationship between lipids and the pathogenesis of renal disease, compelling evidence accumulated in experimental animals suggests a direct role of lipids in the initiation and progression of glomerular disease. These studies showed that cholesterol-feeding to various experimental animals induced the development of glomerular injury. Furthermore, the treatment of hyperlipidemic animals with lipid lowering drugs prevented the development of glomerulosclerosis. In this article, we will review recent advances made in understanding various aspects of lipid-mediated renal injury including biochemical mechanisms of hyperlipidemia, a possible direct role of hyperlipidemia in the pathogenesis of renal disease, pathobiological accumulation of lipids and lipoproteins, biochemical and histological similarities between systemic atherosclerosis and glomerulosclerosis, and cellular processes involved in the development of glomerular disease. Furthermore, we will define cellular and molecular hypotheses that provide putative mechanisms by which hyperlipidemia and atherogenic lipoproteins induce series of cytoregulatory peptide-mediated events involved in the development of glomerular disease.

Animals↗
PubMed1995

Atypical hyperlipidemia and nephropathy associated with apolipoprotein E homozygosity.

Hyperlipidemia has been implicated in the pathogenesis of experimental progressive glomerulosclerosis, but its role in human renal injury is controversial. This report describes a 12-yr-old boy presenting with massive proteinuria, hepatomegaly, anemia, severe mixed hyperlipidemia, and progressive renal failure. The initial renal biopsy disclosed large numbers of foam cells that were shown to be monocytes. Evidence is presented suggesting that apoprotein-E2 homozygosity in our patient, together with an 88% reduction in plasma lipoprotein lipase activity associated with severe nephrotic syndrome, is responsible for the atypical clinical features, lipoprotein phenotype III with chylomicronemia, and renal lipidosis. A regimen of dietary lipid restriction, gemfibrozil, and niacin resulted in significant but partial improvement of the dyslipidemia and resolution of the hepatomegaly and ascites. This report stresses the importance of characterizing unique lipid disorders in patients with nephrotic syndrome in order to prescribe effective lipid-lowering strategies. Moreover, the striking resemblance of the clinical and nephrohistologic features of this patient to those occurring in experimental models of coexisting glomerular injury and hyperlipidemia led to the speculation that, in this setting, the hyperlipidemia may contribute to the development of progressive glomerulosclerosis.

Apolipoproteins E↗
PubMed2000

Treatment of hyperlipidemia.

In the treatment of hyperlipidemia, when to begin and end therapy is important. In recent years, potent anti-hyperlipidemia drugs have been widely used, and the results of many intervention trials have shown that combinations of diet, exercise and drug therapies are effective for the primary and secondary prevention of coronary heart disease. The present paper summarizes these trials; introduces the therapy guidelines for adult hyperlipidemia established by Japan Atherosclerosis Society in 1997; and discusses the drugs for hyperlipidemia.

Clinical Trials as Topic↗
PubMed1994

Remission of proteinuria following correction of hyperlipidemia in NIDDM patients with nondiabetic glomerulopathy.

OBJECTIVE: Animal studies suggest that hyperlipidemia may play a direct role in glomerular damage. In patients with non-insulin-dependent diabetes mellitus (NIDDM), dyslipidemia occurs early in the course of nephropathy and may be involved in the progression of renal disease. CASES: We report on two young NIDDM patients with marked hyperlipidemia and proteinuria, in whom renal biopsy demonstrated nondiabetic glomerulopathy. In both cases, the decrease in blood lipid levels was associated with a major decrease in proteinuria. Episodes of hyperlipidemia were associated with a resumption of heavy proteinuria in one patient with serum triglyceride levels and proteinuria being closely correlated. CONCLUSIONS: These two cases suggest that hyperlipidemia has an important role in the pathogenesis of glomerular disease.

Adult↗
PubMed1995

Effects of gemfibrozil (Lopid) on hyperlipidemia in acitretin-treated patients. Results of a double-blind cross-over study.

Hyperlipidemia is a common side-effect of oral retinoid treatment, which sometimes interferes with long-term therapy. To evaluate the safety and efficacy of the lipid-lowering drug gemfibrozil on retinoid-associated hyperlipidemia, we studied the clinical response and the plasma lipoprotein levels in 22 acitretin-treated (0.25-0.75 mg/kg) patients mainly suffering from psoriasis. Gemfibrozil or placebo was given in a double-blind cross-over fashion to 14 patients, who after 8 weeks of acitretin therapy and dietary advice exhibited hyperlipidemia (triglyceride levels > or = 50% above baseline and/or > or = 2.0 mmol/l). Serum triglycerides remained high (3.7 +/- 2.4 mmol/l) during placebo treatment but were reduced after 8 weeks of gemfibrozil treatment (p < 0.01). The total cholesterol level decreased slightly (p < 0.05) during gemfibrozil treatment, but the LDL/HDL ratio did not change significantly. No untoward effects of gemfibrozil on acitretin dose-response and clinical side-effects were noted. Gemfibrozil thus appears useful in patients prone to retinoid-induced hyperlipidemia unresponsive to dietary treatment and acitretin dose reductions.

Acitretin↗
PubMed1994

Correlation between plasma fibrinogen and serum lipids in rats with hyperlipidemia induced by cholesterol free-high fructose or high cholesterol diet.

We studied the coagulative and fibrinolytic activity in intrinsic or extrinsic hyperlipidemia using 4-week-old male Wistar rats. Intrinsic hyperlipidemia was induced by a cholesterol-free high-fructose diet (HFD) and extrinsic hyperlipidemia, by a high-cholesterol diet (HCD) for 14 days. In intrinsic hyperlipidemic rats fed on the HFD, serum lipids were significantly increased as compared with the levels in control rats fed on a standard diet. An apparent increase in plasma fibrinogen level and coagulant factor XIII activity was also observed in HFD rats. In extrinsic hyperlipidemic rats fed on the HCD, significant increases in plasma fibrinogen level compared with that of control rats were found with the increases in serum lipids. Activities of antithrombin III and alpha 2-plasmin inhibitor in HFD-fed rats significantly increased compared with those of control and HFD rats. There was a significant positive correlation between plasma fibrinogen and serum total cholesterol, free cholesterol, or phospholipid in diet-induced hyperlipidemia (p < 0.01). Because of the increase in coagulant XIII activity in HFD-fed rats and the increase in alpha 2-plasmin inhibitor activity in HCD-fed rats, both diet-induced hyperlipidemic rats were shown to have enhanced coagulative activity compared with the control rats. These results suggest that the HFD as well as the HCD causes a pre-hypercoagulative state due to the increase in plasma fibrinogen level and activities in other coagulative and fibrinolytic factors.

Animals↗
PubMedDate not supplied

Combination of gemfibrozil and orlistat for treatment of combined hyperlipidemia with predominant hypertriglyceridemia.

OBJECTIVE: To present a case of combined hyperlipidemia with predominant hypertriglyceridemia unresponsive to conventional diet and single-agent drug therapy but successfully treated with a combination of gemfibrozil and orlistat. METHODS: We describe a nonobese Asian Indian man with combined hyperlipidemia. Predominant hypertriglyceridemia was unresponsive to conventional therapy. Orlistat was added to the maximal dose of gemfibrozil, and baseline lipid profiles were compared with posttreatment values after repeated challenges with each drug individually and in combination. The relevant literature was also reviewed. RESULTS: At baseline, the patient's serum triglyceride level was 766 mg/dL and total cholesterol level was 241 mg/dL. On repeated measurements 4 months later, these values were 959 mg/dL and 309 mg/dL, respectively. With use of a reduced-fat diet and gemfibrozil (600 mg orally twice a day), serum triglyceride levels were 830 mg/dL and 909 mg/dL on two different occasions. Combination treatment with the same dosage of gemfibrozil and orlistat at 120 mg orally three times a day reduced triglyceride levels to 279 mg/dL and 244 mg/dL on two separate occasions. Rechallenges with drug monotherapy yielded triglyceride levels of up to 1,159 mg/dL with gemfibrozil alone and of up to 896 mg/dL with orlistat alone. A reduction of serum triglyceride levels to 269 mg/dL and 224 mg/dL occurred when combined treatment with both gemfibrozil and orlistat was reinstituted on two additional occasions. CONCLUSION: The combination of gemfibrozil and orlistat was extremely effective in reducing serum triglyceride levels in this patient with combined hyperlipidemia and predominant hypertriglyceridemia, whereas either one of these agents, when used alone, was ineffective. Determining the mechanisms of this synergy will necessitate further investigation. Additional studies of the use of the gemfibrozil-orlistat combination in patients who have combined hyperlipidemia with predominant hypertriglyceridemia are needed.

Adult↗
PubMed1997

Identifying and managing patients with hyperlipidemia.

Cardiovascular disease related to hyperlipidemia is a significant cause of morbidity and mortality in the United States. The benefit of lowering lipid levels in patients with and without cardiovascular disease has been demonstrated in numerous clinical trials. The results of these trials prompted the National Heart, Blood, and Lung Institute to form the Nation Cholesterol Education Panel (NCEP). This panel developed guidelines for identifying and treating lipid disorders. Before starting antilipemic therapy, patients should be evaluated for secondary causes of hyperlipidemia, including disease states and medications. Risk factors for cardiovascular disease should be identified and used to determine the patient's goal low-density lipoprotein level. Regardless of the drug therapy used, the cornerstone treatment for hyperlipidemia is dietary changes. The NCEP recommendation for dietary modification follows a two-step plan to reduce intake of cholesterol and dietary fats. Other nonpharmacologic treatments for hyperlipidemia include exercise, weight reduction for obese patients, reduction of excessive alcohol use, and smoking cessation . Drug therapy should be considered in patients who do not respond to an adequate trial of dietary modifications and lifestyle changes. The principal lipid-lowering agents currently used are the bile acid sequestrants, nicotinic acid, 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase inhibitors, and fibric acid derivatives. Estrogen, fish oil, and alcohol also can decrease the risk of developing heart disease. In pharmacoeconomic studies, lipid-lowering drug therapy has been shown to decrease the number of procedures, hospitalizations, and other medical interventions required by patients with cardiovascular disease.

Cardiovascular Diseases↗
PubMed1997

[Effect of tongxinluo capsule on experimental myocardial ischemia, arrhythmia and hyperlipidemia].

OBJECTIVE: To study the effects of Tongxinluo capsule (TXLC) on experimental myocardial ischemia and infarction, arrhythmia and hyperlipidemia. METHODS: Using the methods of epicardial mapping and NBT-ink double staining and the ratio of tissue in myocardial infarction in which the anterior coronary artery was ligated in anesthetized dogs, acute myocardial ischemia was induced with pituitrin and hyperlipidemia was induced with feeding high lipid diet in rats, arrhythmia was induced with chloroform in mice. RESULTS: The TXLC reduced significantly the myocardial ischemic limits, degree and the myocardial infarction area, inhibited obviously the ocurrence of arrhythmia and reduced the level of hyperlipidemia. CONCLUSION: The TXLC could improve significantly the myocardial ischemia mycardial infarction and prevent obviously the ocurrence of arrhythmia and hyperlipidemia.

Animals↗
PubMed1999

[Effect of hydroxylation polymorphism on the concentration of propranolol in the blood of humans with hyperlipidemia].

An influence of hydroxylation phenotype on the concentration of propranolol [corrected] was examined in 52 subjects with hyperlipidemia divided into 4 groups: 1--control, normolipemic, 2--hypercholesterolemic, 3--hypertriglyceridemic, and 4--mixed-form hyperlipidemic. Each study group included extensive metabolizers and one subject characterized by a poor hydroxylation phenotype. Propranolol was given intragastrically at a single dose of 80 mg [corrected]. Blood was sampled within 24 hours following the drug administration. HPLC method was used for determining blood serum concentrations of propranolol. In each study group mean blood serum concentrations of propranolol in poor metabolizers were at maximum in subject with hypertriglyceridemia, at minimum in the normolipemic one, and intermediate in hypercholesterolemic (upper) and mixed-form hyperlipidemic ones. Lipid metabolic disturbances also affected blood serum concentrations. They were the highest in hypertriglyceridemic patients, whereas in hypercholesterolemic were, in early stage of observation, even lower then in normolipemic subjects. Blood serum concentrations of propranolol [corrected] attained minimal values in patients with mixed form of hyperlipidemia. In the light of the present study we can state that hyperlipidemia modifies the blood serum concentrations of propranolol [corrected]. Although, the type of hyperlipidemia and lipophilic propranolol are not the only determinants affecting blood serum concentrations of propranolol, but also a genetic factor, i.e. hydroxylation phenotype may play an important role.

Adolescent↗