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LipoPrint tests

Patient 1 | Patient 2

Patient 1

A 35-year-old woman from Bratislava with newly diagnosed mixed hyperlipoproteinemia. In November of 2008 (fig.1), the first LipoPrint LDL assessment was performed, which found an extremely elevated concentration of VLDL particles and a significant proportion of small dense LDL fraction (red range of the profile), in turn indicating a major derangement in the metabolism and structure of the lipoproteins. The device assessed the patient’s profile as type B atherogenic lipoprotein.


After three months of successful treatment, which was ordered by the attending physician, the patient’s lipoprotein profile improved significantly (Fig. 2). We found a marginally elevated concentration of the VLDL (candy addiction) and traces of small dense LDL.


After another five months of treatment, the level of VLDL was reduced to within the reference range and the highly atherogenic small dense LDLs were eliminated completely. The elevated LDL-1 and LDL-2 as the non-atherogenic sub-fractions of the LDL lipoprotein class resulted from the structural transformation of the atherogenic small dense LDLs into non-atherogenic LDL sub-fractions. (Fig. 3). The device assessed the patient’s profile as a type A non-atherogenic lipoprotein profile, in turn significantly reducing the risk of acute cardiovascular events (acute myocardial infarction or stroke).


Patient 2

47-year-old man from Banská Bystrica with combination hyperlipoproteinemia. In April of 2008 (Fig 4), the first LipoPrint LDL assessment was performed, finding extremely elevated levels of VLDL, IDL-1 and IDL-2; a major proportion of small LDL parts (red part of the profile) and a significant reduction of HDL. This finding confirmed a combination of a genetic fat metabolism disorder and poor lifestyle and nutrition. The device assessed the patient’s profile as type B atherogenic lipoprotein profile.


After 5 months of hypolipidemic treatment, the patient’s lipoprotein profile partially improved (fig. 5). The VLDL concentration was reduced by more than one-third and the level of small dense LDL, which contributes to the development of cardiovascular diseases, was reduced by more than fourfold. Even with an increased HDL concentration, these values are still below normal. Even though the patient’s lipid levels are now normal, his lipoprotein profile remained atherogenic. The persistence of the type B atherogenic lipoprotein profile, in spite of the achieved normal lipid levels, can be interpreted as an insufficient coordination between the demonstrably effective pharmacologic treatment and the required modification of the lifestyle and dietary habits of the respective patient.