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Surprising Techniques You May Manage With Doxorubicin

Added: (Wed Oct 10 2018)

Pressbox (Press Release) - For example, chronic kidney disease results in an increase in Lp(a) that depends on the type of disease (whether or not there is a nephrotic component) and on the type of treatment (peritoneal dialysis is associated with higher concentrations than haemodialysis, with normalized concentrations after successful kidney transplantation). It is interesting that in patients with end-stage renal disease treated with haemodialysis, Lp(a) is increased only in those with large apo(a) isoforms compared with isoform-specific control subjects. This might explain why the apo(a) isoform is more predictive of CVD risk than Lp(a) concentrations in these patients (for review see [1, 20]). Another example is type 2 diabetes mellitus (T2DM). Recent SCH 772984 studies have described an unexpected association between very low Lp(a) concentrations (<1?mg/dL) and T2DM [21-23]. The best way to confirm the causality of this finding would be to investigate whether very large apo(a) isoforms that are usually associated with low Lp(a) concentrations are more often observed in T2DM patients; https://www.selleckchem.com/ Kamstrup and Nordestgaard found that this was indeed the case [22]. However, the authors did not find any association between the noncarrier status of SNP rs10455872 and T2DM. This might be explained by the observation (not considered by the authors) that the distribution of Lp(a) concentrations is very similar in noncarriers of this SNP and in the entire population, considering that about 86% of the population are noncarriers of the mutated allele of this SNP [24]. Doxorubicin manufacturer The discovery of two SNPs within the LPA gene that have a pronounced effect on Lp(a) concentrations was an important step forward. These SNPs, however, are an inadequate surrogate for the detection of the number of KIV repeats which better determines Lp(a) concentrations. More than half of the carriers of small apo(a) isoforms (i.e. subjects with ��22 KIV repeats) and an increased risk of CVD will not be detected with these SNPs. The findings from SNP analysis alone will therefore result in a large number of patients with a clear underestimation of CVD risk and so should be considered with caution. The search should be extended for further genetic variants that are easy to genotype and that will describe the risk of CVD events to a better extent than currently possible. The use of the two SNPs discussed might be very convenient from a laboratory standpoint but bears a high risk of false-negative risk prediction. Therefore, apo(a) phenotyping, although laborious, is still the method of choice. The author has no conflict of interests to declare. The work presented in this editorial was funded in part by grants from the German Ministry of Education and Research (BMBF) (http://www.gesundheitsforschung-bmbf.de/de/2101.php, grant number 01ER0804), the KfH Foundation for Preventive Medicine (http://www.kfh-stiftung-praevention.de), the Austrian National Bank and the Austrian Genome Project ��GEN-AU��.

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