A Study of Blood Fatty Acids Profile in Hyperlipidemic and Normolipidemic Subjects in Association with Common PNPLA3 and ABCB1 Polymorphisms.

Adiponutrin (patatin-like phospholipase domain-containing 3; PNPLA3), encoded in humans by the PNPLA3 gene, is a protein associated with lipid droplet and endoplasmic reticulum membranes, where it is apparently involved in fatty acid redistribution between triglycerides and phospholipids. A common polymorphism of PNPLA3 (I148M, rs738409), linked to increased PNPLA3 presence on lipid droplets, is a strong genetic determinant of non-alcoholic fatty liver disease (NAFLD) and of its progression. P-glycoprotein (Pgp, MDR1, ABCB1), encoded by the ABCB1 gene, is another membrane protein implicated in lipid homeostasis and steatosis. In the past, common ABCB1 polymorphisms have been associated with the distribution of serum lipids but not with fatty acids (FA) profiles. Similarly, data on the effect of PNPLA3 I148M polymorphism on blood FAs are scarce. In this study, a gas chromatography-flame ionization detection (GC-FID) method was optimized, allowing us to analyze twenty FAs (C14: 0, C15: 0, C15: 1, C16: 0, C16: 1, C17: 0, C17: 1, C18: 0, C18: 1cis, C18: 2cis, C20: 0, C20: 1n9, C20: 2, C20: 3n6, C20: 4n6, C20: 5, C23: 0, C24: 0, C24: 1 and C22: 6) in whole blood, based on the indirect determination of the fatty acids methyl esters (FAMES), in 62 hyperlipidemic patients and 42 normolipidemic controls. FA concentrations were then compared between the different genotypes of the rs738409 and rs2032582 (ABCB1 G2677T) polymorphisms, within and between the hyperlipidemic and normolipidemic groups. The rs738409 polymorphism appears to exert a significant effect on the distribution of blood fatty acids, in a lipidemic and fatty acid saturation state-depending manner. The effect of rs2032582 was less pronounced, but the polymorphism did appear to affect the relative distribution of blood fatty acids between hyperlipidemic patients and normolipidemic controls.

The Role of Mean Platelet Volume in Chronic Obstructive Pulmonary Disease Exacerbation.

BACKGROUND: Studies have supported the correlation between mean platelet volume and COPD. However, there are limited data on the relationship between COPD exacerbation and mean platelet volume. We aimed to evaluate the mean platelet volume trend in patients with COPD exacerbation. METHODS: A total of 81 subjects, 62 men and 19 women, who were admitted to the hospital because of exacerbation of COPD during 9 months, were enrolled in this prospective observational study. The levels of mean platelet volume, C-reactive protein, complete blood count, and percent-of-predicted FEV1 were measured in subjects at admission (exacerbation period) and after 3 months (stable period). Thirty-seven age- and sex-matched healthy individuals constituted the control group. RESULTS: Subjects in the exacerbation period had significantly higher levels of C-reactive protein (P = .001), white blood cell count (P = .01), and percentage of neutrophils (P = .01) and lower percent-of-predicted FEV1 than in the stable period (P = .02). Mean platelet volume levels were significantly decreased in the exacerbation period (P = .001). Considering a cut-off point of mean platelet volume levels <8.2 fL for indicating COPD exacerbation showed a sensitivity of 80% and a specificity of 76%. Also, mean platelet volume levels correlated significantly with increase of C-reactive protein level, white blood cell count, and neutrophil percentage in the exacerbation period (P = .01, P = .01, and P = .02, respectively). CONCLUSIONS: Mean platelet volume may be an inflammatory marker in exacerbation of COPD, and the measurement of mean platelet volume values may be useful for identifying patients who are at increased risk for exacerbations of illness.

A Case of Fenofibrate-Induced Immune Thrombocytopenia: First Report.

Fenofibrate is widely prescribed as a hypolipidemic drug and is well tolerated by most patients. We present the case of a 40-year-old woman who developed severe immune thrombocytopenia while on fenofibrate treatment. Clinical features included spontaneous bruising on the feet and hands, a purpuric rash, and menorrhagia. All the laboratory results were normal except for the finding of isolated thrombocytopenia. The subsequent evolution was favorable after fenofibrate removal and with the administration of immunoglobulin G (IgG) plus corticosteroids. Drug-induced thrombocytopenia is briefly reviewed, and a possible mechanism responsible for causing this side effect of fenofibrate is suggested. This is the first reported case of fenofibrate-induced immune thrombocytopenia.