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Cardio Diabetes Medicine 2017 355

Biochemical Evaluation of Dyslipidemia

Dr.Devaki Nair, BSc, MSc, MBBS, FRCP, FRC (Path)

Consultant and Honorary Senior Lecturer in Clinical Biochemistry
Clinical Lead for Clinical Biochemistry -RFH and NMUH
Clinical Lead for Lipids and CVD Prevention
Director SAS Centre for Cardiovascular Biomarkers
Royal Free London NHS Foundation Trust
London

INTRODUCTION
Genetic, epidemiological and histopathological stud- ified fatty acids (NEFAs) that is available for hepatic
ies have clearly established the primary role of plas- uptake. Some of the NEFAs that are liberated by the
ma lipids and lipoproteins in the development of hydrolysis of chylomicrons releases NEFAs which are
atherosclerotic disease. Lipid disorders, also called hepatically removed and used for VLDL-TG produc-
dyslipidaemia, are abnormalities of lipoprotein me- tion and secretion. Insulin resistance in impairs fatty
tabolism and include elevations of total cholesterol, acid storage and raises plasma NEFAs, which are
LDL cholesterol, or triglycerides; or deficiencies of used for VLDL production accounting for the raised
HDL cholesterol. These disorders can be acquired fasting TG in diabetes as well s post prandial rise
or familial (e.g., familial hypercholesterolemia). The in TG. Increased hepatic lipase divers NEFA to the
preferred screening tests for dyslipidaemia are total liver making VLDL-TG.The structure, production, re-
cholesterol HDL cholesterol levels and triglyceride modeling, and catabolism of HDLs have been more
levels on non-fasting or fasting samples. There is difficult to study than those for the apoB containing
currently sufficient evidence of the benefit of includ- lipoproteins. HDLs are small and heterogeneous with
ing triglycerides as a part of the initial tests used to respect to size and composition. They are involved
screen routinely for dyslipidaemia. Abnormal screen- in Reverse cholesterol transport (RCT) that compris-
ing test results should be confirmed by a repeated es three steps within the context of cardiovascular
sample on a separate occasion, and the average of disease (CVD):
both results should be used for risk assessment. Abnormal lipid profile is common and several termi-

Plasma lipids are transported by lipoproteins, which nologies are used to explain these abnormalities
are defined by the densities at which they are iso- Hyperlipoproteinemia: abnormally elevated concen-
lated, that is, as the high-, low-, intermediate-, and trations of specific lipoprotein particles in the plasma.
very low-density lipoproteins. (HDLs, LDLs, IDLs,
and VLDLs, respectively); chylomicrons, are intesti- Hyperlipidemia: increased plasma cholesterol and/or
nally derived, consists of mainly dietary lipids and triglyceride
small amounts of protein. HDL-C appears in two sub-
classes, HDL and HDL . Through a simple blood test, Dyslipidemia:
2
3
plasma lipoprotein levels, which are among the most abnormal cholesterol (TC, LDL-C, or HDL-C) and/or
important risk factors for coronary artery disease, TG concentrations. Dyslipidaemia includes low HDL
provide clues about the aetiology of lipid disorders concentration as well as abundance of small dense
and about their most prominent pathologic associ- LDL.
ations.VLDL and chylomicrons are assembled and
secreted by hepatocytes and enterocytes in the liver Dyslipidaemia is clinically important because of the
and intestine, respectively. driven by the TG synthesis complications related to atherogenesis ie coronary
from endogenous and exogenous, pathways that is, artery disease, cerebrovascular disease and periph-
dietary, fatty acids. An important determinant of fast- eral vascular disease; however, These disorders may
ing plasma TG concentration is the plasma Nonester- manifest as pancreatitis and fatty liver disease.

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