Lack of agreement between the plasma lipid-based criteria and apoprotein B for the diagnosis of familial combined hyperlipidemia in members of familial combined hyperlipidemia kindreds

Jarero, Juan Pablo del Rincon; Aguilar-Salinas, Carlos A.; n-Pineda, Luz E. Guill; rez, Francisco J. G; Rull, Juan

doi:10.1053/meta.2002.29993

Cited by 9 publications

(6 citation statements)

References 50 publications

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“…Of note, VLDL cholesterol in those with type IIA phenotype was less than in normals, a finding which is surprising if increased secretion of VLDL3 is the critical pathophysiological mechanism as opposed to impaired clearance. Other reports such as that from Mexico by del Rincon Jarero et al [17] confirm that lipid-based diagnosis of FCHL will diverge importantly from an algorithm incorporating apoB.…”

Section: Studies In Patients With Fchlmentioning

confidence: 92%

Applying apoB to the diagnosis and therapy of the atherogenic dyslipoproteinemias: a clinical diagnostic algorithm

Sniderman

2004

Current Opinion in Lipidology

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Section: Studies In Patients With Fchlmentioning

confidence: 92%

Applying apoB to the diagnosis and therapy of the atherogenic dyslipoproteinemias: a clinical diagnostic algorithm

Sniderman

2004

Current Opinion in Lipidology

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“…Dyslipidemia was defined as either of serum cholesterol >200 mg/dl, triglyceride >150 mg/dl, LDL>110 mg/dl, or HDL<40 mg/dl for men and <50 mg/dl for women [28], [29]. Insulin resistance was estimated by the model of homeostasis model assessment (HOMA) [5], [17], which was derived from fasting insulin (µU/ml) × fasting glucose (mmol/l)/22.5.…”

Section: Methodsmentioning

confidence: 99%

Effects of PPARγ and RBP4 Gene Variants on Metabolic Syndrome in HIV-Infected Patients with Anti-Retroviral Therapy

et al. 2012

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BackgroundPPARγ and RBP4 are known to regulate lipid and glucose metabolism and insulin resistance. The influences of PPARγ (C1431T and Pro12Ala) and RBP4 (−803GA) polymorphisms on metabolic syndrome in HIV-infected patients receiving anti-retroviral therapy were examined in this study.Materials and MethodsA cross-sectional study of HIV-1 infected adults with antiretroviral therapy for more than one year in the National Cheng Kung University Hospital was conducted. The gene polymorphisms were determined by quantitative PCR.ResultsNinety-one patients were included in the study. Eighty-two (90.1%) patients were males with a mean age of 44.4 years. For the C1431T polymorphism in PPARγ, while patients with the T allele (48.4%) had trends toward lower rate of hypertriglyceridemia, the borderline significance together with insignificant power did not support the protective effect of the T allele against development of hypertriglyceridemia. For the Pro12Ala polymorphism in PPARγ, although patients with the Pro/Ala genotype (8.8%) had a higher level of serum LDL (138.0 vs. 111.5 mg/dl, P = 0.04) and trends toward higher rates of hypercholesterolemia and serum LDL>110 mg/dl, these variables were found to be independent of the Pro/Ala genotype in the multivariate analysis. For the −803GA polymorphism in RBP4, patients with the A allele (23.1%) more often had insulin resistance (HOMA>3.8; 33.3 vs. 8.7%, P = 0.01) and more often received anti-hypoglycemic drugs (14.3 vs. 1.4%, P = 0.04). The detrimental effect of the A allele in RBP4 −803GA polymorphism on development of insulin resistance was supported by the multivariate analysis adjusting for covariates.ConclusionThe impacts of PPARγ C1431T and Pro12Ala polymorphisms on metabolism in HIV-infected patients are not significant. RBP4 −803GA polymorphism has increased risk of insulin resistance in HIV-infected patients with anti-retroviral therapy.

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“…Our group found a lack of agreement between the lipid and the apoB diagnostic criteria when studying 217 members of 22 FCHL relatives. 32 No agreement was found, even after analyzing multiple cutoff points for cholesterol, triglycerides, and apoB. Only the combination of triglycerides greater than or equal to 150 mg/dL and cholesterol greater than or equal to 200 mg/dL had an acceptable agreement, with an apoB concentration greater than or equal to 120 mg/dL (kappa ¼ 0.604).…”

mentioning

confidence: 96%

“…In Table 1, the mean lipid concentrations of various studies are shown. [19][20][21][22][23][24][25][26][27][28][29][30][31][32] Large differences are evident between the highest and lowest values for every lipid parameter. In addition, many authors have used differing thresholds for either the lipid or the apoB concentrations.…”

mentioning

confidence: 99%

“…Furthermore, even when using diagnostic criteria that result in similar prevalence rates, there is no concordance between the FCHL definitions used. [32][33][34] Until a genetic marker is found, a better definition resulting in greater homogeneity between affected cases is necessary. In our FCHL patients, an apoB greater than or equal to 120 mg/dL identified subjects with less heterogeneous lipid levels compared with the other populations shown in Table 1 (cholesterol 260 AE 42, triglycerides 257 AE 148 mg/dL, high-density lipoprotein cholesterol 39 AE 9 mg/dL and apoB 142 AE 12 mg/ dL).…”

mentioning

confidence: 99%

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Familial Combined Hyperlipidemia: Controversial Aspects of its Diagnosis and Pathogenesis

Aguilar-Salinas

Zamora

Gómez-Díaz

et al. 2004

Seminars in Vascular Medicine

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Familial combined hyperlipidemia is the most frequent cause of primary dyslipidemia in Mexico. Its manifestations include hypercholesterolemia, hypertriglyceridemia, or a combination of both. Despite its high frequency, a proper diagnosis is rarely made. Assessment of the lipid profiles of at least three first-degree relatives is necessary. The diagnosis of familial combined hyperlipidemia in a family not only leads to the identification of other affected family members but, more important, allows cardiovascular risk stratification of those affected. Prospective studies have confirmed the atherogenicity of the disease. A critical review of the current literature in this field is presented in this article. Although three screenings of the genome have been completed, the genes responsible for this disorder have not been identified. Limitations with respect to the characterization of affected subjects and the heterogeneity of the disease are among possible explanations. However, familial combined hyperlipidemia, because of its high prevalence, must be given greater priority. It represents a great challenge for physicians involved in the treatment of dyslipidemic patients.

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Lack of agreement between the plasma lipid-based criteria and apoprotein B for the diagnosis of familial combined hyperlipidemia in members of familial combined hyperlipidemia kindreds

Cited by 9 publications

References 50 publications

Applying apoB to the diagnosis and therapy of the atherogenic dyslipoproteinemias: a clinical diagnostic algorithm

Applying apoB to the diagnosis and therapy of the atherogenic dyslipoproteinemias: a clinical diagnostic algorithm

Effects of PPARγ and RBP4 Gene Variants on Metabolic Syndrome in HIV-Infected Patients with Anti-Retroviral Therapy

Familial Combined Hyperlipidemia: Controversial Aspects of its Diagnosis and Pathogenesis

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