ed, reduce concentrations indicate reduce cardiovascular risk and values two.three mmol/l (200 mg/dl) have already been thought of an indication for pharmacological reduction [8, 9]. Failure to set the TG target results in the lack of proof from randomised clinical trials that would make its determination doable. Probably the most critical therapy target in prevention of cardiovascular ailments remains low LDL-C concentration, and in patients with TG concentrationArch Med Sci six, October /PoLA/CFPiP/PCS/PSLD/PSD/PSH recommendations on diagnosis and therapy of lipid problems in PolandTable XIX. Classification of major hypertriglyceridaemia Types of HTG Monogenic chylomicronaemia (familial chylomicronaemia syndrome, FCS) mutation of on the list of five genes: most frequently lipoprotein lipase, apolipoprotein CII, apolipoprotein CV, LIMF1, or GPIHBP1 Multifactorial or polygenic chylomicronaemia (multifactorial chylomicronaemia syndrome, MCS) accumulation of genes linked with enhanced TG IL-15 Compound concentration Risk Risk of recurrent acute pancreatitis Diagnostic evaluation Clinical Laboratory Xanthomata or yellow Higher TG and total papules (xanthomas) on cholesterol (TC) the skin, retinal lipaemia concentration it is in homozygotes chylomicron cholesterol Paroxysmal abdominal LDL-C and pains may possibly happen apolipoprotein B not elevated Milky fasting serum Positive cold flotation test (chylomicron layer at the serum surface) Paroxysmal abdominal pains could occur High TG and TC concentrations that is chylomicron cholesterol and VLDL cholesterol LDL-C, typically not elevated Milky fasting serum Constructive cold flotation test (chylomicron layer at the surface, cloudy serum beneath chylomicron layer due to enhanced VLDL-TG TG and TC (from remnants) HDL-C Apo Bnotelevated DNAtesting(genotype apo E2/apo E2) Considerably elevated TG concentration (VLDL-TG) LDL-C standard or slightly elevated Cold flotation test negative cloudy to milky serum with out a chylomicron layer on the surface following 102 h of refrigerated storage Generally elevated concentration of TG, LDL-C and apo BRisk of acute pancreatitis Threat of CVD may be increasedDysbetalipoproteinaemia (formerly kind III HLP or dysbetalipoproteinaemia or remnant disease) apo E2/apo E2 homozygosity Multifactorial or polygenic hypertriglyceridaemia (formerly sort IV HLP or familial HTG)Pretty higher danger of CVDCharacteristic palmar tendon xanthomasIncreased danger of CVD. May be a risk element of AP with higher VLDL-TG concentrationCombined hyperlipoproteinaemia (formerly sort IIb HLP or familial combined hyperlipoproteinaemia). This is a polygenic disorderHigh risk of CVDPremature CVD and/or combined hyperlipidaemia in firstdegree relatives Intraindividual and interindividual (relatives, phenotypic variation), i.e. periodically elevated TG and LDL-C, or elevated TG alone or LDL-C aloneArch Med Sci 6, October /M. Banach, P. Burchardt, K. Chlebus, P. Dobrowolski, D. Dudek, K. Dyrbu, M. Gsior, P. Jankowski, J. J iak, L. Klosiewicz-Latoszek, I. Kowalska, M. Malecki, A. Prejbisz, M. Rakowski, J. Rysz, B. Solnica, D. Sitkiewicz, G. Sygitowicz, G. Sypniewska, T. Tomasik, A. Windak, D. Zozuliska-Zi kiewicz, B. CybulskaTable XX. Secondary causes of hypertriglyceridaemia Obesity Diabetes mellitus Excessive alcohol consumption CDK13 Accession Hypothyroidism Renal diseases (proteinuria, uraemia, glomerulonephritis) Paraproteinaemia, systemic lupus erythematosus Pregnancy (especially third trimester) Eating plan wealthy in monosaccharides Medicines: glucocorticosteroids, oral oestro