Transaminase determinations are basic tests for the diagnosis, differentiation, progression and therapeutic evaluation of: – Liver and biliary tract disease – myocardial infarction – skeletal muscle damage – in initial internal medicine and pediatric examinations There is no evidence that transaminase synthesis is increased in liver or skeletal muscle disease. AST is present in a variety of tissues, including liver, cardiac and skeletal muscle, kidney, brain, pancreas, lung, leukocytes, and erythrocytes. Liver, heart and skeletal muscle have relatively high specific activity of AST compared to other organs. Parallel increase of AST and ALT always indicates hepatocellular necrosis. AST is of essential importance in the differential diagnosis of liver diseases and in the assessment of the course of myocardial infarction.
Reagent is used for the quantitative in vitro determination of alanine aminotransferase (ALT) (also: GPT, glutamate pyruvate transaminase) with and without pyridoxal phosphate (Pyp) in human serum and plasma according to the IFCC method.
Transaminase determinations are basic tests for diagnosis, differentiation, progression and therapy assessment of: – Disease of the liver and bile ducts – myocardial infarction – skeletal muscle damage – in initial internal medicine and pediatric examinations. There is no evidence that transaminase synthesis is increased in liver or skeletal muscle disease. ALT is a liver-specific enzyme. Greater than 15-fold increased ALT activities, or parallel increase in ALT and AST, are indicative of hepatocellular necrosis. However, lower ALT activities also occur in other tissues e.g. kidney, heart, skeletal muscle, pancreas, spleen and lung.
Pyridoxal-5-phosphate (PYP) is required for the determination of GOT/GPT activity by the IFCC method with pyridoxal phosphate activation. PYP is important as a coenzyme for the activation of transaminases. In patients with vitamin B6 deficiency or in samples with insufficient endogenous pyridoxal phosphate, e.g., in patients with myocardial infarction, liver disease, or in intensive care patients, falsely low activities may be measured without pyridoxal phosphate supplementation. Depletion of NADH would occur in the AST approach if pyruvate were not removed in the pre-incubation step. would be removed. Therefore, activation with PYP is recommended for optimal determination and stabilization of transaminases.
BIOMED Reagent for Total Protein is used for the quantitative in vitro determination of total protein in human serum and plasma according to the Biuret method.
Total protein consists of more than 100 structurally known proteins, and the biological function of about 50 is known in more detail. For example, plasma proteins are mainly composed of immunoglobulins, transport proteins (such as albumin), enzymes, lipoproteins, proteohormones, and coagulation factors. Serum is somewhat lower in protein because clotting factors have been depleted for blood clotting. Albumin, α1, α2, and β-globulins are produced by the parenchymal cells of the liver, and the proteins of the γ-globulin fraction and immunoglobulins are produced by plasma cells. There are known diseases that either increase the total protein concentration (hyperproteinemia) or decrease it (hypoproteinemia). Indications for the determination of TP are e.g. pathological blood sedimentation reaction, proteinuria, edema, polyuria, chron. Kidney disease, chron. Liver disease, chron. Diarrhea, malignant tumor, susceptibility to infections, bone pain, rheumatism that cannot be localized, lymphoma, external and internal bleeding, pregnancy, pre- and postoperative, severe trauma, shock, burns, intensive care patients, for clarification of an acute hemoglobin drop.
The BIOMED Creatine Kinase (CK-NAC) Reagent is used according to the IFCC method for the determination of total creatine kinase in human serum and plasma.
Total CK activity predominantly corresponds to the activity of the muscle-specific isoenzyme CK-MM and can therefore serve as a lead enzyme for the detection of cardiac and skeletal muscle damage. Nevertheless, on the one hand, activities remaining within the reference range do not exclude muscle disease with certainty, and on the other hand, increased activities may also have physiological causes. Follow-up examinations (enzyme-time curves), as well as the determination of CK isoenzymes and variants or exercise tests in the case of unclear images, facilitate interpretation in any case.
Elevated total CK levels are indicative of cardiac or skeletal muscle disease: – Progressive muscular dystrophy – Post-polio syndrome – Myositis (inflammatory disease of skeletal muscle) – Heart muscle inflammation – Myocardial infarction – Coronary heart disease (CHD) – Rhabdomyolysis (muscle disintegration)
BIOMED Cystatin C Reagent is used as a turbidimetric immunoassay for the quantitative in vitro determination of Cystatin C in human serum and plasma.
Cystatin C is a low molecular weight, non-glycosylated, basic protein that belongs to the cystatin superfamily as a protease inhibitor in blood. Cystatin-C is endogenously produced at a constant rate by almost all nucleated cells of the human body. Its serum concentration depends exclusively on the glomerular filtration capacity of the kidney; tubular secretion does not occur. Unlike the determination of GFR by creatinine, age, sex, muscle mass, and diet do not affect the result, nor do inflammatory processes (except autoimmune diseases) influence the value of cystatin C. Cystatin C becomes conspicuous at a GFR of less than 88 mL/min/1.73 m², whereas creatinine only increases at a GFR of less than 75 mL/min/1.73 m². With a decreased GFR, the concentration of cystatin C increases.
An increase in cystatin C in the blood is an indication of impaired renal function. The level of cystatin C measured in the blood can be used to draw conclusions about renal performance. In particular, the so-called glomerular filtration rate (a measure of kidney performance) can be estimated.
Cystatin C is elevated in: – renal insufficiency – autoimmune diseases
BIOMED α-HBDH Reagent is used for the quantitative in vitro determination of α-HBDH (alpha-hydroxybutyrate dehydrogenase) in human serum and plasma by the optimized standard method (DGKC).
The α-HBDH is isoenzyme 1 of LDH and catalyzes the conversion of lactic acid to pyruvic acid. LDH 1, unlike the other isoenzymes, can convert 2-oxobutyrate to hydroxybutyrate and is therefore also called hydroxybutyrate dehydrogenase (HBDH) and can thus be measured separately. It is mainly localized in the myocardium and the hematopoietic system. Increased α-HBDH activities can therefore be detected in myocardial infarction, but also in hemolytic processes of all kinds.
BIOMED hsFerritin Reagent is used as a turbidimetric immunoassay for the quantitative in vitro determination of ferritin in human serum and plasma.
The protein ferritin is the most important iron store in the human body, and its normal values vary greatly according to age and sex. Plasma ferritin shows a direct and quantitative correlation with mobilizable storage iron in healthy individuals and in patients with iron deficiency or iron overload. In its function as an acute-phase protein, increased concentrations of ferritin can be detected in the context of inflammatory and necrotic processes, such as hepatitis or myocardial infarction. Serum ferritin concentration is pathologically elevated in a number of solid tumors (hepatomas, pancreatic carcinomas, bronchial carcinomas, neuroblastomas) and in lymphomas and leukoses and correlates with tumor activity and spread. However, with regard to desirable tumor specificity, clinical data to date are controversial.
Since ferritin can also be present in very high concentrations during inflammation caused, for example, by acute, chronic diseases or infections, a high ferritin concentration is possible although iron deficiency is present. In this case, determination of the inflammatory marker C-reactive protein (CRP) or the iron transport molecule transferrin may be useful to rule out misinterpretation of the measurement results due to high serum levels of ferritin.
Low ferritin levels are indicative of: – Diseases that prevent iron absorption (sprue, Crohn’s disease). – malnutrition (e.g. alcoholism or vegan diet) – Malabsorption syndrome – Increased iron requirement (e.g. during pregnancy, lactation and growth phase) – Iron loss (e.g. menstrual bleeding, bleeding due to gastric ulcer) – Transferrin deficiency (e.g. in certain kidney diseases)
Elevated ferritin levels occur in: – Hemochromatosis (iron storage disease). – iron overload – Iron distribution disorders (e.g. due to hepatitis, infections, tumors, uremia, liver damage, hemolysis) – Iron utilization disorders (e.g. due to anemia, folic acid or vitamin B21 deficiency, hemoglobinopathies) – Overdoses of iron supplements – Frequent blood transfusions
BIOMED Transferrin Reagent is used as a turbidimetric immunoassay for the quantitative in vitro determination of transferrin in human serum.
Transferrin is the major transport protein for iron in the blood and for tissue function. Iron is provided either from the storage iron reserve or from absorbed food. The transferrin concentration in plasma is controlled by the iron content in tissues, especially hepatocytes. If their iron content is low, transferrin synthesis is increased; if it is high, downregulation occurs. Indication: – Suspected deficiency of functional iron – Suspicion of iron overload By determining iron and transferrin from one sample, transferrin saturation (TfS) can be calculated. Compared to the determination of serum iron concentration, TfS has the advantage that the half-life of transferrin is much longer than that of iron. Rapid fluctuations in serum iron concentration are therefore less likely to be reflected in TfS. Limitations of TfS: In the acute phase reaction, transferrin synthesis is suppressed. Transferrin is released from the hepatocyte into the plasma during parenchymal injury. In pregnancy, transferrin synthesis is higher than the decrease in total body iron. An increase in TfS occurs only when there is a drop in hemoglobin of at least 2 g/dL with an empty storage iron reserve.
BIOMED Reagent HDL is used as a homogeneous enzymatic assay for the quantitative in vitro determination of HDL (high density lipoprotein cholesterol) in human serum and plasma.
HDL (High Density Lipoprotein-Cholesterol) is a high density transport protein responsible for the transport of the membrane component cholesterol. Since HDL mediates the removal of cholesterol from the tissues and is able to remove excess cholesterol that has been deposited in the vessel walls, HDL has a principally anti-atherogenic effect. HDL concentration is determined when the physician wants to assess the risk of atherosclerosis or coronary heart disease (CHD). This risk is increased when HDL cholesterol is too low. Low HDL cholesterol is thus considered a risk marker for the occurrence of cardiovascular events. In particular, the importance of HDL cholesterol has increased with the introduction of direct determination methods. The simplified measurement principle as well as the much more precise determination allow routine diagnostics of this analyte.
BIOMED Reagent LDL is used as a homogeneous enzymatic assay for the quantitative in vitro determination of LDL (low density lipoprotein cholesterol) in human serum and plasma.
Elevated LDL concentrations are of causal importance in atherosclerosis development. The atherogenic potential of this lipoprotein fraction has been demonstrated in numerous epidemiological and clinical studies. Among all lipid and lipoprotein variables, LDL cholesterol showed the strictest association with coronary mortality in the Göttingen Risk, Incidence and Prevalence Study (GRIPS). LDL cholesterol thus represents an important risk determinant, if not the most important one next to HDL cholesterol, for the detection of individuals at increased coronary risk.
Indication: – Early detection of atherosclerosis risk. – Follow-up of therapy with lipid-lowering drugs
BIOMED Triglyceride Reagent is used according to the GPO-PAP method for the quantitative in vitro determination of triglycerides in human serum and plasma.
Triglycerides (triacylglycerols, glycerol esters, neutral fats, glycerides) are esters of glycerol with 3 fatty acid residues. Exogenous triglycerides are ingested with food and endogenous ones are synthesized mainly in liver, kidney and heart muscle from L-glycerol-3-phosphate via phosphatidic acid u. diglyceride. Transport in the blood takes place in lipoproteins, especially chylomicrons and VLDL. Free fatty acids can be formed by hydrolysis, monoglycerides are formed by degradation (pankr. triglyceride lipase). Physiological significance: mainly as an energy supplier. Indication: – Early detection of atherosclerosis risk and classification of hyperlipoproteinemia. – Control of dietary and drug lipid-lowering therapy.
Reagent is used for the quantitative in vitro determination of glucose in human serum, plasma and CSF by the PAP method.
The determination of blood glucose can be performed in capillary and venous whole blood, plasma or serum. In the different specimens, different glucose concentrations are determined in the same person, at the same time of collection. This must be taken into account in the clinical evaluation. In Europe, glucose determination is mainly performed in capillary whole blood, in the USA in venous whole blood or venous plasma. Determination in serum should be used only in exceptional cases. Intraindividual variations in blood glucose concentrations are greater than for other blood parameters due to dependence on muscle work and time interval from food intake. Dysregulations such as insulin deficiency or hyperinsulinism magnify the fluctuations.
Consequences of hypoglycemia (“low blood sugar”): – Decreased brain performance – Seizures – Increased adrenaline secretion – Shaky hands and sweating – Shock Causes may include the rare insulinoma or the early phase of type 2 diabetes. It can also be a side effect of medication in the treatment of diabetes mellitus. Hormonal imbalances due to hypofunction of the pituitary gland, thyroid gland, or adrenal cortex can also cause low blood glucose levels.
Hyperglycemia (excessive blood glucose) occurs with: – Diabetes mellitus – Gestational diabetes (also: pregnancy diabetes) – Diseases of the pancreas – Hormone disorders caused by tumors in the adrenal medulla or tumors of the pituitary gland – Rare hereditary diseases – As a side effect of medication Consequences may include feeling thirsty, increased urination and visual disturbances. In the long term, hyperglycemia leads to vascular damage (resulting in atherosclerosis, stroke and kidney weakness) and tissue damage; life-threatening coma can also occur.
BIOMED IgE Reagent is used as a turbidimetric immunoassay for the quantitative in vitro determination of immunoglobulin E – IgE in human serum and plasma.
Immunoglobulins consist of two light (L-) and two heavy (H-) chains. IgE occurs predominantly as a monomer and is also known as reagin. IgE antibodies mediate the type I immediate-type hypersensitivity reaction. Polyvalent antigens, such as grass pollen, house dust mite, components of food, parasites or insect stings, stimulate B cells of the mucous membranes at the port of entry to produce spec. IgE with mediation of CD4+ cells. This binds via Fc receptors to mast cells, which are now sensitized. At the next contact of the antigen with the mast cell, bound IgE antibodies are cross-linked, the cell is degranulated and mediators are released, which e.g. cause the symptoms of hay fever, asthma and atopic eczema. IgE is not placental and does not activate complement.