Aims: To critically evaluate the clinical implications of the use of non-fasting rather than fasting lipid profiles and to provide guidance for the laboratory reporting of abnormal non-fasting or fasting lipid profiles. Methods and Results: Extensive observational data, in which random non-fasting lipid profiles have been compared with those determined under fasting conditions, indicate that the maximal mean changes at 1-6 h after habitual meals are not clinically significant [+0.3 mmol/L (26 mg/dL) for triglycerides; -0.2 mmol/L (8 mg/dL) for total cholesterol; -0.2 mmol/L (8 mg/dL) for LDL cholesterol; +0.2 mmol/L (8 mg/dL) for calculated remnant cholesterol; -0.2 mmol/L (8 mg/dL) for calculated non-HDL cholesterol]; concentrations of HDL cholesterol, apolipoprotein A1, apolipoprotein B, and lipoprotein(a) are not affected by fasting/nonfasting status. In addition, non-fasting and fasting concentrations vary similarly over time and are comparable in the prediction of cardiovascular disease. To improve patient compliance with lipid testing, we therefore recommend the routine use of non-fasting lipid profiles, whereas fasting sampling may be considered when non-fasting triglycerides are >5 mmol/L (440 mg/dL). For nonfasting samples, laboratory reports should flag abnormal concentrations as triglycerides ≥2 mmol/L (175 mg/dL), total cholesterol ≥5 mmol/L (190 mg/dL), LDL cholesterol ≥3 mmol/L (115 mg/dL), calculated remnant cholesterol ≥0.9 mmol/L (35 mg/dL), calculated non-HDL cholesterol ≥3.9 mmol/L (150 mg/dL), HDL cholesterol ≤1 mmol/L (40 mg/dL), apolipoprotein A1 ≤1.25 g/L (125 mg/dL), apolipoprotein B ≥1.0 g/L (100 mg/dL), and lipoprotein(a) ≥50 mg/dL (80th percentile); for fasting samples, abnormal concentrations correspond to triglycerides ≥1.7 mmol/L (150 mg/dL). Life-threatening concentrations require separate referral for the risk of pancreatitis when triglycerides are >10 mmol/L (880 mg/dL), for homozygous familial hypercholesterolemia when LDL cholesterol is >13 mmol/L (500 mg/dL), for heterozygous familial hypercholesterolemia when LDL cholesterol is >5 mmol/L (190 mg/dL), and for very high cardiovascular risk when lipoprotein(a) >150 mg/dL (99th percentile). Conclusions: We recommend that non-fasting blood samples be routinely used for the assessment of plasma lipid profiles. Laboratory reports should flag abnormal values on the basis of desirable concentration cutpoints. Non-fasting and fasting measurements should be complementary but not mutually exclusive.

Objetivos: Evaluar criticamente las implicaciones clinicas de la utilizacion del perfil lipidico sin ayuno en lugar de perfiles de lipidos con ayuno y proporcionar orientacion para la elaboracion de informes de laboratorio sobre perfiles lipidicos anormales con ayuno y sin ayuno. Metodos y Resultados: Abundantes datos observacionales, en los que perfiles lipidicos medidos aleatoriamente sin ayuno se han comparado con perfiles lipidicos determinados en condiciones de ayuno, indican que las variaciones medias maximas de 1-6 h despues de ingestas habituales no son clinicamente significativas [+0,3 mmol/L (+26 mg/dL) para trigliceridos; -0,2 mmol/L (-8 mg/dL) para colesterol total; -0,2 mmol/L (-8 mg/dL) para colesterol-LDL; +0,2 mmol/L (+8 mg/dL) para colesterol de remanentes calculado; -0,2 mmol/L (-8 mg/dL) para el colesterol no-HDL calculado]; las concentraciones de colesterol-HDL, apolipoproteina A1, apolipoproteina B, y lipoproteina(a) no se ven afectados por el estado de ayuno/ no ayuno. Ademas, las concentraciones en ayunas y sin ayuno varian de manera similar con el tiempo y son comparables en la prediccion de la enfermedad cardiovascular. Para mejorar el cumplimiento del paciente con las condiciones para la determinacion del perfil lipidico, por lo tanto, se recomienda el uso rutinario de los perfiles lipidicos sin ayuno, mientras que se puede considerar la toma de muestra en ayunas cuando los trigliceridos sin ayuno son >5 mmol/L (440 mg/dL). Para las muestras sin ayuno, los informes de laboratorio deberian marcar como concentraciones anormales a trigliceridos ≥2 mmol/L (175 mg/dL), colesterol total ≥5 mmol/L (190 mg/dL), colesterol-LDL ≥3 mmol/L (115 mg/dL), colesterol remanente calculado ≥0,9 mmol/L (35 mg/dL), colesterol no-HDL calculado ≥3.9 mmol/L (150 mg/dL), HDL colesterol ≤1 mmol/L (40 mg/dL), apolipoproteina A1 ≤1,25 g/L (125 mg/dL), apolipoproteina B ≥1,0 g/L (100 mg/dL), y lipoproteina(a) ≥50 mg/dL (percentil 80); para muestras con ayuno, las concentraciones anormales corresponden a trigliceridos ≥1,7 mmol/L (150 mg/dL). Aquellas concentraciones que ponen en peligro la vida requieren derivacion inmediata debido al riesgo de pancreatitis cuando los trigliceridos son >10 mmol/L (880 mg/dL), de hipercolesterolemia familiar homocigotica cuando el colesterol-LDL es >13 mmol/L (500 mg/dL) o hipercolesterolemia familiar heterocigota cuando el colesterol-LDL es >5 mmol/L (190 mg/dL), y debido al riesgo cardiovascular muy alto cuando la lipoproteina(a) es >150 mg/dL (percentil 99). Conclusiones: Recomendamos la utilizacion de rutina de muestras de sangre sin ayuno para la evaluacion del perfil lipidico plasmatico. Los informes de laboratorio deberian marcar resultados anormales basandose en valores de corte deseables. Las determinaciones con ayuno y sin ayuno deben ser complementarias, pero no se excluyen mutuamente.

Myelodysplastic syndromes represent a group of heterogeneous hematopoietic neoplasms derived from an abnormal multipotent progenitor cell, characterized by a hyperproliferative bone marrow, dysplasia of the cellular hemopoietic elements and ineffective erythropoiesis. Anemia is a common finding in myelodysplastic syndrome patients, and blood transfusions are the only therapeutic option in approximately 40% of cases. The most serious side effect of regular blood transfusion is iron overload. Currently, cardiovascular magnetic resonance using T2 is routinely used to identify patients with myocardial iron overload and to guide chelation therapy, tailored to prevent iron toxicity in the heart. This is a major validated non-invasive measure of myocardial iron overloading and is superior to surrogates such as serum ferritin, liver iron, ventricular ejection fraction and tissue Doppler parameters. The indication for iron chelation therapy in myelodysplastic syndrome patients is currently controversial. However, cardiovascular magnetic resonance may offer an excellent non-invasive, diagnostic tool for iron overload assessment in myelodysplastic syndromes. Further studies are needed to establish the precise indications of chelation therapy and the clinical implications of this treatment on survival in myelodysplastic syndromes.

In this work, we examined the impact of polymorphism in the cytochrome P450 (CYP) 3A5 gene, CYP3A5*1 (6986A > G, rs 776746), on the reduction in the lipid levels caused by simvastatin and atorvastatin. We studied 350 hyperlipidemic patients who received 10-40 mg of atorvastatin (n = 175) or simvastatin (n = 175) daily. Genotyping for CYP3A5 was done by PCR-RFLP analysis. Differences in the lipid profile before and after treatment were expressed as the % difference. The frequency of CYP3A5 polymorphism was 13.4% for heterozygotes and 86.6% for homozygotes. Comparison of the responses to same dose of each drug showed that the highest % difference was associated with total cholesterol (TC) in subjects receiving atorvastatin 40 mg compared with simvastatin 40 mg (p = 0.048). However, comparison of the responses to equivalent doses of atorvastatin vs. simvastatin revealed no difference in the % change in any of the lipid parameters examined. In individuals with the same CYP3A5 genotype, a head to head comparison of the efficacy of the same dose of simvastatin vs. atorvastatin revealed an advantage for atorvastatin. For equivalent doses of atorvastatin vs. simvastatin there was no difference in the % change in any of the lipid parameters examined. Within the same genotype there was a significant difference in the % change related to the drug treatment.