Lipometabolism diagnostics
(fat metabolism diagnostics)
Material: | 2 ml serum (if necessary refrain from food for 12 hours) | Reference range | Target values of individual parameters are dependent of the current risk profile (please refer to ESC guideline, AHA/ACC guideline or ASCVD-/Framingham score). The 10-year risk can be calculated by means of the PROCAM algorithm or the ASCVD score. In case of triglyceride values > 400 mg/dl, a valid measurement of all cholesterol metabolism parameters is no longer possible. In these cases, lipid electrophoresis can be carried out, if required. |
Please note | Diagnostics: As shown in the Framingham study more than 50 years ago, individual blood lipids, with the exception of marked hypercholesterinemia, have only a minor predictive value as to the cardiovascular risk. Decisive is rather the presence of several risk factors, which have a type of multiplier effect. Besides an increased LDL-cholesterol value and a low HDL-cholesterol value, these are especially the familial predisposition, arterial hypertension, nicotine-abuse and diabetes mellitus. When evaluating the individual cardiovascular risk, no assessment should be made of an isolated single risk factor. The relevance of blood lipids lies in their treatability. As part of a screening, total cholesterol, LDL, HDL and triglycerides should be evaluated initially. If secondary hyperlipoproteinemia is suspected, endocrine, metabolic, liver- and kidney diseases should be ruled out in a second stage and the influence of taking medication such as oral contraceptives, betablockers, diuretics, glucocorticoids and retinoids should be evaluated. The third stage of cardiovascular risk evaluation, apart from tests of the lipid metabolism, covers new risk factors, which were added in the last few years. Here, lipoprotein a (see there), CRP ultrasensitive (see there) and, if necessary, homocysteine (see there) are especially important. A thrombophilia test (see there) is also recommended. In most hereditary fat metabolism disorders the genetic defect is known. In the clinical every day life, a more thorough genetic evaluation is usually not required, as therapeutical options are limited anyway. Therefore, the therapeutic consideration in general should deal with the question if LDL, triglycerides or both, as well as homocysteine should be decreased. |
More Results for the letter L
- Lacosamide (LACO)
- Lacrimal gland, autoantibodies to (LACR)
- Lactate in blood (plasma), CSF or synovial fluid (LACT)
- Lactic acid
- Lactoferrin (LACTST)
- also known as lactotransferrin
- Lactose in breast milk (LAKTUMU)
- Lactose in urine (LAKTU)
- Lactose intolerance (LACPCR)
- Genetic testing T13910C, genetic testing for lactose intolerance
- Lamblia (EGIAR, MGIAR)
- Giardia lamblia
- Laminin autoantibodies (LAMIN)
- Lamotrigine (LAMO)
- LAP (LAP)
- Leucine aminopeptidase, leucine arylamidase
- Lassa virus infection (LASSA)
- Laxatives (LAXA)
- LBP (LBP)
- Lipopolysaccharide binding protein
- LC1 autoantibodies (LC1)
- Formiminotransferase cyclodeaminase (FTCD)
- LCM virus (LCMK)
- Lymphocytic choriomeningitis
- LDH (LDH)
- Lactate dehydrogenase
- LDH isoenzymes (LDHISO)
- Lactate dehydrogenase isoenzymes
- LDL cholesterol (LDL)
- Low-density lipoprotein cholesterol
- Lead in the blood (BLEI)
- Pb
- Lead in the urine (BLU)
- Pb
- Legionella (KLEGI)
- Legionella pneumophila
- Leishmaniasis (LEISH)
- Leptin (LEPTI)
- Leptospirosis (LEPGA)
- Leptospira interrogans
- Levetiracetam (LEVET)
- Levomepromazine (LEVO)
- LH (LH)
- Luteinizing hormone
- Lindan (LINDAN)
- Gamma-hexachlorcyclohexane
- Lipase (LIP)
- Pancreatic lipase