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PubMed2006

Simvastatin down regulates mRNA expression of RANTES and CCR5 in posttransplant renal recipients with hyperlipidemia.

Chemokines and hyperlipidemia are involved in the mechanism of chronic allograft nephropathy (CAN). In this study, the mRNA expression of RANTES and its receptor CCR5 on peripheral blood mononuclear cells were measured in renal transplant recipients with hyperlipidemia, and the effect of simvastatin treatment observed to investigate the mechanism and prevention of CAN. Sixty recipients selected from 167 renal transplant recipients were divided into two groups: group A without hyperlipidemia (n = 30) and group B with hyperlipidemia (n = 30). The control group consisted of 30 healthy volunteers. The recipients in group B were treated with simvastatin for 3 months. We estimated serum lipid levels and mRNA expressions of RANTES and CCR5. The mRNA expressions of RANTES and CCR5 were significantly higher in renal transplant recipients compared with controls. The expressions were much higher in group B than in group A patients. In group B patients, serum lipid levels decreased dramatically after simvastatin treatment. Meanwhile, the mRNA expressions of RANTES and CCR5 were reduced significantly after 1.5 months of simvastatin treatment to a level significantly lower than that in group A after 3 months of treatment. The increased expressions of RANTES and CCR5 mRNAs in renal transplant recipients with hyperlipidemia might be involved in CAN due to hyperlipidemia. Simvastatin seemed to reduce the chemokine transcripts in renal recipients with hyperlipidemia.

Adult↗
PubMed2001

Plasma vascular endothelial growth factor and its receptor Flt-1 in patients with hyperlipidemia and atherosclerosis and the effects of fluvastatin or fenofibrate.

Increased vascular endothelial cell growth factor (VEGF) may be important in cardiovascular pathophysiology (perhaps relating to angiogenesis and collateral vessel development) and binds target endothelium via receptors such as Flt-1. We hypothesized that there would be increased levels of plasma VEGF and Flt-1 in patients with atherosclerosis and others with hyperlipidemia compared with controls, and a reduction in these factors with 3 months of lipid-lowering therapy. Twenty patients with uncomplicated hyperlipidemia but no atherosclerosis, 20 patients with hyperlipidemia plus clear atherosclerosis, and 40 matched controls were studied. Plasma VEGF was higher in patient groups than in healthy controls (p <0.01), but Flt-1 was not significantly altered. After lipid-lowering therapy, patients with uncomplicated hyperlipidemia had significantly reduced total cholesterol and VEGF (all p <0.05) but no significant change in Flt-1. Lack of a significant correlation between the von Willebrand factor and VEGF suggests the latter is unrelated to endothelial damage. Plasma VEGF that increases in patients with uncomplicated hyperlipidemia free of major underlying atherosclerosis and in patients with hyperlipidemia plus established atherosclerosis is reduced by successful lipid-lowering treatment. These findings may have implications for the pathophysiology and treatment of hyperlipidemia and atherosclerosis, and suggest an alternative mechanism (i.e., modulation of angiogenesis) by which lipid-lowering therapy may reduce cardiovascular events beyond lipid reduction alone.

Anticholesteremic Agents↗
PubMed2001

Lipoprotein and apolipoprotein abnormalities in familial combined hyperlipidemia: a 20-year prospective study.

In order to characterize the lipoprotein abnormalities in familial combined hyperlipidemia (FCHL) and to describe factors associated with the stability of the FCHL phenotype during 20-year follow-up, 287 individuals from 48 families with FCHL originally identified in the early 1970s (baseline) were studied. Hyperlipidemia was defined as lipid-lowering medication use, or > or =age- and sex-specific 90th percentile for triglycerides or cholesterol. Triglyceride, cholesterol and medical history data were obtained at baseline and 20-year follow-up. Additional follow-up measures included HDL-C, LDL-C, LDL particle size, lipoprotein(a), apolipoprotein (apo) A-I, apoB, and apoE polymorphism. Longitudinally, two-thirds of relatives were consistently normolipidemic or hyperlipidemic, and one third were discordant for hyperlipidemic status at baseline and 20-year follow-up. Individuals with hyperlipidemia at baseline and/or follow-up had higher apoB levels than those with consistently normal lipids (P<0.05), whereas small LDL size was associated with concurrent hyperlipidemia. Among individuals who were normolipidemic at baseline, the following variables were independently associated with development of hyperlipidemia over 20 years: older age at baseline, male sex, greater increase in BMI during follow-up, and apoE alleles epsilon 2 or epsilon 4. In conclusion, apoB is associated with hyperlipidemia and apoE polymorphism is associated with later onset of hyperlipidemia in FCHL.

Adult↗
PubMed1990

Prevalence and expression of familial combined hyperlipidemia in childhood.

The objectives of this study were (1) to determine the incidence of dominantly inherited hyperlipoproteinemia in children referred to our medical center because of hyperlipidemia associated with a family history of premature coronary artery disease and (2) to assess the degree of expression in childhood of the most common inherited hyperlipoproteinemia, familial combined hyperlipidemia. Among 129 families referred to us by area pediatricians, we identified a dominantly inherited hyperlipoproteinemia in 97 of them. Twenty had familial hypercholesterolemia, 65 familial combined hyperlipidemia, 11 hyperapobetalipoproteinemia, and one familial hypertriglyceridemia. As expected, almost half (9/20) of the siblings of probands with familial hypercholesterolemia were affected. Although we expected incomplete gene penetrance in the siblings of the probands with familial combined hyperlipidemia, we found 43 affected and 40 unaffected among the 83 siblings of the 65 probands. Our findings suggest that hyperlipidemia in children, caused by familial combined hyperlipidemia, occurs more than three times as frequently as familial hypercholesterolemia and that in families identified by a child proband, the penetrance is complete. Pediatricians should identify this primary hyperlipidemia in childhood and attempt to prevent the associated risk of premature coronary artery disease by prescribing appropriate diet and life-style modifications.

Adult↗
PubMed1999

Combined hyperlipidemia is associated with increased exercise-induced muscle protein release which is improved by triglyceride-lowering intervention.

Although myopathy is considered an adverse effect of treatment with 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors and fibrates in combined hyperlipidemia, the present study was performed to investigate whether combined hyperlipidemia itself is associated with skeletal muscle pathology and whether lipid-lowering intervention has beneficial effects. To investigate whether combined hyperlipidemia is associated with skeletal muscle pathology, 10 male patients and 15 normolipidemic controls underwent a 45-minute standardized bicycle ergometer test at a load of 2 W/kg lean body mass (parallel study). One- and 8-hour postexercise increments in the plasma level of the muscle proteins creatine kinase (CK), myoglobin (Mb), and fatty acid-binding protein (FABP) were assessed as parameters for (subclinical) skeletal muscle pathology. The 8-hour postexercise increments in CK and Mb and 1-hour postexercise increment in Mb were significantly higher in patients than in controls, thus indicating increased exercise-induced muscle membrane permeability in combined hyperlipidemia. To investigate the effects of lipid-lowering intervention on skeletal muscle in combined hyperlipidemia, 21 subjects with combined hyperlipidemia were randomized double-blindly to receive 6 weeks of treatment with fluvastatin 40 mg/d, gemfibrozil 600 mg twice daily, or combination therapy. All subjects underwent an ergometer test before and after treatment. Gemfibrozil treatment alone reduced the CK increments 8 hours postexercise by 47% and the FABP increments 1 and 8 hours postexercise by 83% and 101%, respectively (all P < .05). Combined treatment reduced Mb increments 1 hour postexercise by 54% and FABP increments 8 hours postexercise by 44% (all P < .05). A highly significant correlation existed between therapy-induced changes in plasma triglycerides and changes in postexercise increments of FABP and Mb. In conclusion, combined hyperlipidemia is associated with an increased exercise-induced release of muscle proteins, which is ameliorated by triglyceride-lowering intervention. As FABP is an indicator for ischemia-induced skeletal muscle pathology, a possible explanation is the impaired muscle blood flow during hypertriglyceridemia, which may be reversed by triglyceride-lowering intervention. The mechanism and clinical relevance of these findings remain to be investigated.

Double-Blind Method↗
PubMed2006

Familial combined hyperlipidemia: upstream transcription factor 1 and beyond.

PURPOSE OF REVIEW: Familial combined hyperlipidemia is a common complex disease that accounts for up to 20% of premature coronary heart disease. The upstream transcription factor 1, located on 1q21, was recently shown to be linked and associated with familial combined hyperlipidemia in Finnish families. Upstream transcription factor 1 is the first gene identified by positional cloning for familial combined hyperlipidemia. Replication studies are critical to investigation of complex diseases because only they can verify the importance of the original findings. We review recent studies that examine the genetic contribution and functional consequence of upstream transcription factor 1 variants to familial combined hyperlipidemia and type 2 diabetes mellitus. Aiming beyond upstream transcription factor 1, we also evaluate novel strategies that have made it possible to globally examine the genome and the transcriptome. RECENT FINDINGS: Three independent studies support the role of upstream transcription factor 1 in familial combined hyperlipidemia. The results for type 2 diabetes mellitus and the metabolic syndrome have been less conclusive highlight novel strategies for gene identification in familial combined hyperlipidemia. SUMMARY: Currently, genetic and functional evidence is supportive of a role for upstream transcription factor 1 in the etiology of familial combined hyperlipidemia and its component traits, although the mechanism of causality still remains largely unknown.

Animals↗
PubMed2005

Apolipoprotein E genotypes as predictors of high-risk groups for developing hyperlipidemia in kidney transplant recipients undergoing sirolimus treatment.

BACKGROUND: Hypercholesterolemia (HCHL) and hypertriglyceridemia (HTRG) have emerged as the most significant metabolic consequences of therapy with sirolimus. Lipid status can be exacerbated by a variety of factors in the posttransplant setting, including genetic factors. Apoliprotein E (Apo E) polymorphism is an established genetic risk factor for hyperlipidemia. We studied the association between Apo E gene polymorphisms and lipids after kidney transplantation in patients undergoing sirolimus treatment. METHODS: We studied 98 kidney transplant patients (KTP) with stable renal allograft undergoing sirolimus treatment: 39 with HCHL and HTRG within 90 days postsirolimus treatment (PST) and 59 without hyperlipidemia PST. Apo E genotyping was performed using INNO-LiPA-ApoE. RESULTS: The cholesterol and the triglyceride values between the groups were 323.3+/-71.6 vs. 180.9+/-31.2 mg/dL (P<0.001) and 318.9+/-97.2 vs. 159.7+/-38.7 mg/dL (P<0.001). There was a significant difference in the genotype distribution of the hyperlipidemia and normal groups (P=0.009) with the percentages in each group as follows: E2/2 and E3/2: 12.8 vs. 5.1%; E3/3: 69.2% vs. 86.4%; and E4/3 and E4/4: 18.0% vs. 8.5%. We observed a higher number of patients with the genotype E3/3 in the group without hyperlipidemia PST (P=0.039). E3/2 and E4/4 genotype frequencies were higher in patients with hyperlipidemia PST. LDL levels in the hyperlipidemia PST group was statistical significant higher (P<0.001) and we observed an association between Apo E allelic distribution and LDL (P=0.005). CONCLUSIONS: Genetic factors, as Apo E genotypes, could allow the early identification of patients who are at a high risk for developing hyperlipidemia PST.

Adult↗
PubMed2006

Hyperlipidemia following treatment with antipsychotic medications.

OBJECTIVE: This study attempted to estimate the relative risk of developing hyperlipidemia after treatment with antipsychotics in relation to no antipsychotic treatment. METHOD: A matched case-control analysis was performed with pharmacy and claims data from California Medicaid (Medi-Cal). Patients were excluded if they were treated for medical disorders or prescribed medications known to increase their risk of hyperlipidemia. Cases were ages 18 to 64 years with schizophrenia, major depression, bipolar disorder, or other affective psychoses and incident hyperlipidemia. Cases were matched to up to six control subjects by age, sex, race, and psychiatric diagnosis. Both groups were prescribed either no antipsychotic medication or had two or more prescriptions for one and only one antipsychotic medication during the 60 days prior to the first indication of hyperlipidemia (cases) or matched index date (controls) in the billing record. Conditional logistic regressions were used to derive odds ratios and 95% confidence intervals (95% CIs) of each antipsychotic medication in relation to no antipsychotic medication. RESULTS: A total of 13,133 incident cases of hyperlipidemia were matched to 72,140 control subjects. As compared with no antipsychotic medication, treatment with clozapine (odds ratio: 1.82, 95% CI: 1.61-2.05), risperidone (odds ratio: 1.53, 95% CI: 1.43-1.64), quetiapine (odds ratio: 1.52, 95% CI: 1.40-1.65), olanzapine (odds ratio: 1.56, 95% CI: 1.47-1.67), ziprasidone (odds ratio: 1.40, 95% CI: 1.19-1.65), and first-generation antipsychotics (odds ratio: 1.26, 95% CI: 1.14-1.39), but not aripiprazole (odds ratio: 1.19, 95% CI: 0.94-1.52) was associated with a significant increase in risk of incident hyperlipidemia. CONCLUSIONS: These findings suggest that most commonly prescribed antipsychotic medications increase the risk of developing hyperlipidemia in patients with schizophrenia or mood disorders.

Adolescent↗
PubMed2001

Hearing improvement after therapy for hyperlipidemia in patients with chronic-phase sudden deafness.

Hearing in patients with chronic-phase sudden deafness and associated hyperlipidemia tends to improve with therapy for hyperlipidemia. We studied 12 patients with unilateral sudden deafness and hyperlipidemia in whom more than 1 month had elapsed since the onset of the hearing disturbance. The disturbance was considered to be irreversible without therapy. The 4 men and 8 women ranged in age from 32 to 73 years, with a mean age of 54.3 years. The hearing disturbance was evaluated by measuring the air conduction thresholds at 125 to 8,000 Hz with pure tone audiometry. Hyperlipidemia was diagnosed when the total blood cholesterol level was 230 mg/dL or greater. The therapy for hyperlipidemia consisted of diet therapy and the administration of antilipemic agents. The hearing level was measured both before therapy and when the total blood cholesterol level had decreased to less than 230 mg/dL. After therapy, the mean hearing level had improved significantly (Wilcoxon's test, p < .05) at each of 125, 250, 500, and 2,000 Hz, but the changes in the level were not significant at 1,000, 4,000, or 8,000 Hz. Our results suggest that with therapy for hyperlipidemia, hearing tends to improve in patients with chronic-phase sudden deafness and associated hyperlipidemia, even when more than 1 month has elapsed since the onset of the presumably otherwise-irreversible hearing disturbance.

Adult↗
PubMed2006

Prevalence of hyperlipidemia and its risk factors for the middle-aged and elderly in the Guangxi Hei Yi Zhuang and Han populations.

BACKGROUND: Han is the largest and Zhuang is the second largest among the 56 nationalities in China. Geographically and linguistically, Zhuang can be classified into 43 ethnic subgroups, among which Hei Yi (which means "black worship" and "black dressing") Zhuang is the most conservative group, according to its unique culture and customs. Little is known about the lipid profiles and corresponding risk factors of hyperlipidemia in this population. Therefore, the aim of this study was to compare the effects of demographic characteristics, health-related behaviors, and lifestyle factors on the prevalence of hyperlipidemia for the middle-aged and elderly in the Guangxi Hei Yi Zhuang and Han populations. METHODS: A sample of 657 people of Hei Yi Zhuang aged 40 years and over was randomly selected from 7 villages in Napo County, Guangxi, China. Information on demographic characteristics, health-related behaviors, and lifestyle factors was collected by questionnaire. Blood pressure, height, weight, waist circumference, and serum lipid and apolipoprotein (apo) levels were measured, and body mass index (BMI) was calculated as a measure of weight relative to height. The results were compared with those in 520 people of Han living in the same region. RESULTS: The prevalence of hyperlipidemia in the Hei Yi Zhuang was significantly lower than that in the Han (36.2% vs 42.3%; p < .05). The levels of total cholesterol, triglyceride, low-density lipoprotein cholesterol, and apo B in Hei Yi Zhuang were also significantly lower than those in the Han (p < .05 to .001), but the levels of high-density lipoprotein cholesterol and the ratio of apo A-I to apo B in the Hei Yi Zhuang were significantly higher than those in the Han (p < .01 and < .001, respectively). There were no significant differences in apo A-I levels between the two ethnic groups (p > .05). The prevalence of hyperlipidemia was positively correlated with BMI and blood pressure in the Hei Yi Zhuang. Hyperlipidemia was positively associated with age, BMI, and blood pressure and negatively associated with gender (female higher) in the Han. CONCLUSIONS: In the present study of the middle-aged and elderly population, the Hei Yi Zhuang have a more favorable lipid profile and a lower prevalence of hyperlipidemia than do the Han, and there is also a significant difference in the risk factors for hyperlipidemia between the two ethnic groups, which might result from the effects of different demographic characteristics, health-related behaviors, and lifestyle factors.

Adult↗
PubMed2001

[The relationship of low density lipoprotein receptor gene polymorphism and hyperlipidemia].

OBJECTIVE: To study the relationship of low density lipoprotein receptor gene polymorphism and hyperlipidemia in the population with essential hypertension. METHODS: People with different lipid levels including 107 hyperlipidemia, 104 at margin level and 108 normal were recruited in the study. Their polymorphisms of LDL-R gene were analyzed using PCR-RFLP. RESULTS: There were three kinds of genotype: (+/+), (+/-), (-/-). In male, the frequencies of the (+/-) in three study groups were shown as follows: 41.18% in hyperlipidemia, 46.15% in margin level, 19.05% in normal lipid. The frequency of (+) allele was significantly higher in hyperlipidemia than that in normal lipid (24.51%, 25.00% and 11.11%, respectively). In women, the differences were not statistically significant. The nonconditional univariate and multivariate logistic regression analysis demonstrated that (+) allele of Ava II polymorphism of LDL-R was a genetic marker of male's hypercholesterolemia. CONCLUSIONS: The frequency of (+/-) hyperlipidemia in males was higher than that in normal lipid group and the (+) allele in male hyperlipidemia was significantly more frequent seen than that in normal lipid group. These results suggested that polymorphisms of LDL-Rgene might play an independent role of risk factor for hyperlipidemia.

Female↗
PubMed1988

[Hemostatic changes during pregnancy in reference to hyperlipidemia].

Blood coagulation and fibrinolysis in pregnancy with or without hyperlipidemia were studied. Blood samples were taken from 36 cases with early pregnancy, 59 cases with late pregnancy, and the relationship between the hemostatic changes and the concentrations of lipids was examined. The following results were obtained: 1. In early pregnancy, all cases were non-hyperlipidemic, but in 41% of late pregnancy cases, hyperlipidemia was found. 2. In late pregnancy without hyperlipidemia, shortening of prothrombin time and activated partial thromboplastin time, increases in platelet epinephrine, collagen aggregation, fibrinogen, and plasminogen, and a decrease in alpha 2-plasmin inhibitor were marked compared with those in early pregnancy without hyperlipidemia. 3. In late pregnancy with hyperlipidemia, the platelet count and fibrinogen were increased, and prothrombin and activated partial thromboplastin time were shortened compared with late pregnancy without hyperlipidemia. The platelet epinephrine aggregation was slightly decreased. Antithrombin III was increased and alpha 2-plasmin inhibitor was slightly decreased. 4. In the same subjects, the relationship between changes in blood coagulation and fibrinolysis in early and late pregnancies and total cholesterol was studied by the independent matched pair test. There were significant correlations (p less than 0.02, p less than 0.05) between activated partial thromboplastin time (r = -0.5998) and fibrinogen (r = 0.6230). From these results the author concluded that late pregnancy was a hypercoagulable state and this tendency was more obvious in late pregnancy with hyperlipidemia.

Blood Coagulation↗
PubMed1995

[Progress in the diagnosis of endocrine and metabolic disorders: hyperlipidemia].

Hyperlipidemia is one of the risk factors for coronary atherosclerosis and the establishment of its simple etiological diagnosis is crucial. Hyperlipidemia can be classified into primary and secondary hyperlipidemia. Primary hyperlipidemia includes familial lipoprotein lipase (LPL) deficiency, familial hypercholesterolemia (FH), familial type III hyperlipidemia, and familial combined hyperlipidemia. Many genetic mutations have been identified in patients with familial LPL deficiency and FH. An ELISA kit has been established to determine LPL mass levels, using monoclonal antibodies against LPL. FH is a deficiency of LDL receptor and is characterized by marked hypercholesterolemia and Achilles tendon xanthomas. It can be diagnosed by an LDL receptor assay, using 125I-LDL in skin fibroblasts. However, the diagnosis can be made easily by measuring the uptake of DiI-LDL by peripheral lymphocytes. Familial type III hyperlipidemia is a genetic disorder characterized by the presence of a broad beta pattern in lipoprotein electrophoresis and is based upon the abnormality of apo E isoform (apo E2/2). Apo E4 has been shown to be associated with late-onset Alzheimer's disease. Cholesteryl ester transfer protein (CETP) deficiency is characterized by a marked hyperalphalipoproteinemia and various abnormalities in the size and composition of LDL and HDL. Two common mutations in the CETP deficiency have been identified; an intron 14 splicing defect and D442: G missense mutation. These mutations account for at least one half of hyper-HDL-cholesterolemia in the Japanese. We have recently identified an area (Omagari City, Akita) where the frequency of heterozygotes for the intron 14 splicing defect is approximately 28% of the general population.(ABSTRACT TRUNCATED AT 250 WORDS)

Carrier Proteins↗
PubMed1995

MR imaging of Achilles tendon in patients with familial hyperlipidemia: comparison with plain films, physical examination, and patients with traumatic tendon lesions.

OBJECTIVE: The purpose of this study was to evaluate the MR imaging characteristics of Achilles tendons in patients at risk for tendon xanthomas because of familial hyperlipidemia and to compare these findings with those seen on plain radiographs and physical examination. We also wished to determine if MR imaging could be used to differentiate xanthomas from traumatic tendinopathy in a second group of patients who had no history of hyperlipidemia but who had a history of trauma to the Achilles tendon. SUBJECTS AND METHODS: We evaluated the MR imaging studies of 26 Achilles tendons in 13 patients with heterozygous familial hypercholesterolemia (n = 11) and type III dysbetalipoproteinemia (n = 2). The size, shape, and signal characteristics of the Achilles tendon were recorded. A tendon was considered abnormal by MR if there was high signal, a convex anterior border, or an anteroposterior measurement greater than 7 mm. Findings on plain radiographs and physical examination of the Achilles tendons were evaluated in the same group of patients. In the group of patients with hyperlipidemia, palpable abnormalities of the Achilles tendon were present in 14 of 26 tendons. Plain radiographs were interpreted as showing abnormalities in 18 of the 26 tendons. In a second group of 21 tendons in patients with no history of hyperlipidemia but with traumatic tendinopathy, studies were evaluated for the size, shape, and signal characteristics of the Achilles tendon. RESULTS: On MR images, 24 of 26 tendons showed signal abnormalities, and 19 of 26 were enlarged. Abnormal signal was a diffuse stippled pattern with many low-signal round structures of equal size surrounded by high-signal material on all pulse sequences. Abnormal signal was seen in tendons of both normal and abnormal size. Bilateral and symmetric changes were found in all but one patient. Tendinopathy in patients without known hyperlipidemia appeared indistinguishable from tendon xanthomas in six (29%) of 21 tendons. The other tendons (71%) were distinctly different from xanthomas without a uniform stippled signal pattern. CONCLUSION: MR imaging of patients with familial hyperlipidemia showed an abnormal stippled signal pattern with or without enlargement or abnormal configuration of the tendon. MR imaging is a more sensitive method than physical examination and plain films for detecting abnormalities in Achilles tendons of patients with hyperlipidemia. Although the MR signal pattern of xanthomas is often different from that of partial tendon tears, tendon degeneration, or tendinitis, a significant overlap in appearance can be observed and the MR appearance of a xanthoma is not pathognomonic.

Achilles Tendon↗
PubMed2001

Familial dyslipidemic hypertension syndrome: familial combined hyperlipidemia, and the role of abdominal fat mass.

Familial combined hyperlipidemia (FCHL) is the most frequent genetic lipid abnormality in humans, with a 5- to 10-fold increased risk of early myocardial infarction. Familial combined hyperlipidemia has been proposed as the leading cause of dyslipidemia in familial dyslipidemic hypertension (FDH). It was the objective of this study to quantify and analyze the simultaneous occurrence of hypertension and hyperlipidemia in FCHL families. We assessed blood pressure (BP) and hyperlipidemia in 27 families with FCHL (235 relatives and 140 spouses, aged 30 to 60 years). Hypertension was defined as a BP more than 140/90 mm Hg, or the use of antihypertensive medication. Multiple backward linear regression analysis was used to derive a biological formula describing BP in FCHL families. One-third of 27 FCHL families were diagnosed with FDH. Sixty-four of 235 (27.2%) relatives had dyslipidemic hypertension (DH), compared to 20 of 140 (14.3%) spouses (P = .005); odds ratio = 2.25 (95% confidence interval 1.29-3.91). Multiple linear regression analysis showed that age, FCHL status, and waist circumference significantly contributed to systolic blood pressure (SBP) in female FCHL relatives. In conclusion, in FCHL we defined age, waist circumference, and hyperlipidemia as predictors of SBP. This study indicates that visceral adipose tissue strongly contributes to the high prevalence of DH in FCHL families. Reduction of visceral fat should be tested as a potential therapeutic intervention for hyperlipidemia and hypertension in FCHL individuals.

Abdomen↗
PubMed1997

[Familial combined hyperlipidemia: detection and characterisation of the hyperlipidemic profile among children and adolescents].

BACKGROUND: Familial combined hyperlipidemia is the commonest genetic form of hyperlipidemia among survivors of myocardial infarction and, therefore, its early detection is crucial for the prevention of coronary artery disease. The aim of the study was to establish the prevalence of hyperlipidemia in the offspring of affected families and to characterize their lipid, lipoprotein and apolipoprotein profile. PATIENT AND METHODS: Forty five subjects below the age of 19 were studied from which 30 were from affected families and 15 from healthy control families. Cholesterol and triglycerides in plasma, VLDL, IDL, LDL and HDL as well as apolipoproteins AI, B, C-II and C-III were measured. RESULTS: Hyperlipidemia was detected in 13 children (43%) from affected families. They also presented significantly elevated concentrations of cholesterol in plasma (p < 0.0001), LDL (p < 0.0001) and HDL (p < 0.05); triglycerides in plasma (p < 0.007), VLDL (p < 0.05) and LDL (p < 0.008), together with significantly increased concentrations of apolipoproteins AI (p < 0.02), B (p < 0.0004), C-II (p < 0.0005) and C-III (p < 0.03). No changes were observed in the IDL fraction. CONCLUSIONS: There is an elevated prevalence of hyperlipidemia among the offspring of patients with familial combined hyperlipidemia. On the contrary to that observed in adults, no alterations of the IDL fraction are present among affected children.

Adolescent↗
PubMedDate not supplied

Hyperinsulinemia in hypertension: associations with race, abdominal obesity, and hyperlipidemia.

OBJECTIVE: To determine the relative contributions of race, sex, abdominal obesity, and hyperlipidemia to the development of hyperinsulinemia among patients with hypertension. DESIGN: Cross-sectional survey. SETTING: A large family practice ambulatory care unit in Winston-Salem, NC. PATIENTS: One hundred and forty adult patients with essential hypertension (systolic blood pressure > or = 160 mm Hg or diastolic blood pressure at or above 90 mm Hg on 2 or more occasions) or who were receiving antihypertensive treatment. MAIN OUTCOME MEASURES: Fasting insulin, lipid, and glucose levels; glycosylated hemoglobin; waist-hip ratio; and resting blood pressure. METHODS: Among 4 patient subgroups (hypertension alone; hypertension and abdominal obesity; hypertension and hyperlipidemia; and hypertension, abdominal obesity, and hyperlipidemia) logistic regression analysis was used to determine correlates of elevated fasting insulin levels. RESULTS: Controlling for age and blood pressure, black males had the highest fasting insulin levels (135 +/- 70 pmol/L [18.8 +/- 9.6 microU/mL] and 265 pmol/L [37.0 +/- 0.0 microU/mL] [mean +/- SD] for obese and nonobese black males, respectively); nonobese white males had the lowest fasting insulin levels (23 +/- 22 pmol/L [3.2 +/- 3.0 microU/mL]). Multivariate logistic regression indicated that the addition of abdominal obesity or hyperlipidemia to pure hypertension more than doubled the risk of hyperinsulinemia (adjusted odds ratio, 2.69; 95% confidence interval, 1.04-6.89; and adjusted odds ratio, 2.62; 95% confidence interval, 0.37-8.6, respectively). The combination of abdominal obesity and hyperlipidemia exerted additive effects among patients with hypertension for elevated insulin levels (adjusted odds ratio, 5.1; 95% CI, 1.59-16.4). CONCLUSIONS: Race, sex, abdominal obesity, and hyperlipidemia interact to produce increases in fasting insulin levels. This knowledge may help physicians prevent sequelae from hyperinsulinemia syndrome among their patients with hypertension.

Adult↗
PubMed2001

Clozapine use in patients with schizophrenia and the risk of diabetes, hyperlipidemia, and hypertension: a claims-based approach.

BACKGROUND: Numerous case reports have linked clozapine to the development of diabetes mellitus and hyperlipidemia in patients with schizophrenia. However, investigators have been unable to clearly demonstrate this association when compared with a control group receiving conventional antipsychotics. METHODS: Medical and pharmacy claims from the Iowa Medicaid program were used to compare incidence rates for diabetes, hyperlipidemia, and hypertension in 552 patients receiving clozapine and 2461 patients receiving conventional antipsychotics (eg, haloperidol, chlorpromazine hydrochloride), with the use of a retrospective cohort design. Logistic regression was used to compare incidence rates adjusting for age, sex, and duration of available follow-up. RESULTS: No significant differences in overall incidence rates for diabetes, hyperlipidemia, or hypertension were observed in patients receiving clozapine vs conventional antipsychotics. However, among younger patients (aged 20-34 years), clozapine administration was associated with a significantly increased relative risk of diabetes (2.5 [95% confidence interval, 1.2-5.4]) and hyperlipidemia (2.4 [95% confidence interval, 1.1-5.2]), but not hypertension (0.9 [95% confidence interval, 0.4-2.0]). CONCLUSIONS: These data suggest that clozapine may not be an independent cause of diabetes or hyperlipidemia, but instead acts as an effect modifier in susceptible populations by increasing weight or affecting insulin secretion and resistance. This finding requires confirmation in other settings and patient populations and with the other atypical antipsychotics (risperidone, olanzapine, and quetiapine fumarate). The potential long-term medical and economic implications of the early induction of diabetes and hyperlipidemia in patients with schizophrenia warrant further study.

Adult↗