Sulphonamides are widely used in agriculture as potent and effective fodder additives. But in case of breaking the regimen of their use for prevention and treatment of cattle diseases, or if the required wash-out period before slaughtering is not adhered, sulphonamides may be present in food products made from meat. Intake of sulphonamide-containing foodstuffs may lead to inhibition of intestinal microflora, disbacteriosis and appearance of antibiotic-resistant pathogenic microflora. sulphonamides amy also cause allergic reactions, in some cases – in a very severe form (exfoliative dermatitis). Besides, chronic intake of sulphonamides may lead to renal insufficiency, impairment of hemopoesis, and CNS pathology. There are some data demonstrating hematotoxic and cancerogenic properties of some sulphonamides – e.g., sulphamethasine. Significant adverse effects intrinsic to sulphonamides lead to a general acknowledgement that a strict control of its use in food industry is requried. sulphonamide content in foodstuffs is regulated by international regulations (Codex Alimentarius), EU Directives and regulations of Ukraine, Russia and other CIS countries. >
50
0,5 ?g/l
2
/60/60/10-20'
37°C
12
ÈÔÀ
002
0
K902
Laevomycetin (Chloramphenicol) EIA
96
Laevomycetin (Chloramphenicol) is a potent antibiotic drug which is widely used in veterinary. Laevomycetin admixture may be potentially harmful for human consumption. Laevomycetin is an undesirable component for foodstuff, it can cause allergic reactions, irritation of mucous membranes of a mouth. Also it leads to hematotoxic side effects in humans. Children of early age are most sensitive to a preparation. Therefore the control of content of this antibiotic over a feed is necessary. Using this test, it is possible to detect chloramphenicol in Meat, Honey, Milk, Shrimps. >
50
0,035 ?g/l
1
//60/25-35'
37 °C
12
ÈÔÀ
909
0
K366
PORK EIA
96
Consumption and handling of pork meat is strictly prohibited by certain religious and/or legal prescriptions. Pork meat may also cause allergy and food intolerance. PORK EIA test is based on immunometric determination of porcine specific proteins by highly specific monoclonal antibodies. The test is highly sensitive and detects trace amounts of pork meat. Sensitivity does not depend on culinary processing - it is roughly the same for fresh pork meat and for prepared pork meat, including boiling, frying, stewing, smoking. >
50
5 U/ml
2
60//60/10-20'
37°C
24
ÈÔÀ
901
0
X366
ÕÅÌÀtåst PORK
5
Consumption and handling of pork meat is strictly prohibited by some religious confessions. Pork meat may also cause allergy and food intolerance. >
500-1000*
0,1 %
1
5-10///-'
18-25°C
24
ÈÔÀ
006
0
K380
Gliadin EIA
96
Celiac disease (CD) is a complex autoimmune pathology characterized by intolerance to a major reserve protein of rye and wheat grains – gluten. Prevalence of this disease varies greatly in different geographic regions and may come to 1:300. If a patient with CD consumes food products containing gluten, a crypt hyperplasia accompanied by total or partial atrophy of intestinal villi develops; at the same time, the risk of development of oncological pathology of the intestine rises significantly. CD may be manifested both as acute and as quiescent disease with occult symptoms. The only treatment for CD by now is a strict adherence of a patient to a gluten-free diet. Apart from obvious exclusion of bread products made from rye and wheat, those food products which may contain gluten due to technological reasons should also be controlled. The current technologies used for production of meat-based, soured milk-based and some other products often use wheat êëåéêîâèíà? As a stabilizer and çàãóñòèòåëü? Besides, contamination of the main substitutes of rye and wheat – e.g., corn, rice, buckwheat - with gluten-containing cereals may also take place during their harvesting, transportation and/or storage. >
100*
0,1 µg/ml
2
30//30/10-20'
37°C
12
ÈÔÀ
001
0
K381
Durum EIA
96
The quality of pasta products (both physical texture and characteristic flavor) is fully dependent on the starting material used by the manufacturer. Durum wheat (Triticum durum), or “hard” wheat is the best choice for pasta production. Common wheat (Triticum aestivum), or “soft” wheat, may be also used in pasta production. This gives a substantial economical advantage for the manufacturer but the use of this wheat variety results in a sticky texture and inferior flavor. The elevated content of common wheat in pasta product may also reflect the field pre-harvest contamination of the seed, or faulty cleaning of processing equipment. In different countries and international communities, the legislation may set the maximal allowed threshold content of common wheat in pasta products (e.g. 3%, 10% or 15% of total weight). Durum EIA is based on the XGY20 monoclonal antibody which recognizes the common wheat specific epitope on gliadin molecule. This epitope is encoded by D-genome of common wheat and is never expressed in durum wheat species. Common wheat specific epitope recognized by XGY20 antibody is resistant to the high temperature (up to 100 C); it allows to detect common wheat admixture in pasta products prepared by modern technology.>
100
0,1 %
3
30/30/30/10-20'
18-25°C
12
ÈÔÀ
711
0
K101
Toxoplasma IgG EIA
96
Toxoplasmosis is a widespread infection caused by the intracellular protozoan parasite Toxoplasma gondii. In most of cases, toxoplasmosis is a mild or asymptomatic disease; however, in immunocompromised patients this disease may be very severe and even life-threatening. Another risk group is pregnant women in whom primary toxoplasmosis can be transfected to the fetus, causing abortion, and severe malformations. The non-immune status is revealed by the absence of specific IgG-antibodies in blood serum or plasma. Specific management of non-immune (specific IgG-negative) pregnant women reduces the risk of primary infection. Therefore, the determination of specific IgG-antibodies in young women plays an important role in prophylaxis of damage caused by Toxoplasma gondii. >
100*
K
2
30//30/10-20'
18-25°C
12
ÈÔÀ
909
0
K101M
Toxoplasma IgM EIA
96
TToxoplasmosis is a widespread infection caused by the intracellular protozoan parasite Toxoplasma gondii. In most cases, toxoplasmosis is a mild or asymptomatic disease; however, in immunocompromised patients this disease may be very severe and even life-threatening. Another risk group is pregnant women in whom primary toxoplasmosis can be transfected to the fetus, causing abortion and severe malformations The presence of IgM antibodies to Toxoplasma gondii indicates a primary infection, reactivation of the existing infection or reinfection with T. gondii. It does not differentiate active from resolving or resolved infection as Toxoplasma gondii -specific IgM may persist for a long time. To differentiate these stages of infection, additional testing, including IgG avidity testing, antigen detection, or PCR needs to be done. >
10
K
2
60//30/10-20'
37 °C
12
ÈÔÀ
906
0
K101CF
Toxoplasma IgG-CF EIA
96
Toxoplasmosis is a widespread infection caused by the intracellular protozoan parazite Toxoplasma gondii. Pets (cats and dogs) may serve as intermediate host for T. gondii and transmit infection to humans. In most of cases, toxoplasmosis is a mild or asymptomatic disease; however, in immunocompromised patients this disease may be very severe and even life-threatening. Another risk group is pregnant women in whom primary toxoplasmosis can be transfected to the fetus, causing abortion, and severe malformations. Testing of cats and dogs for toxoplasmosis is used to detect carrier state and thus to reveal the risk for humans. >
100*
K
2
30//30/10-20'
37 °C
12
ÈÔÀ
604
0
K102
Rubella IgG EIA
96
Rubella virus infection in children causes a mild disease with skin rash and enlargement of occipital lymph nodes, followed by a stable life-long immunity. In adults the infection may exert in more severe forms with transitory arthritis and in some cases - lethal encephalitis. Rubella infection in pregnant women may cause serious inborn defects in newborns (cardiac insufficiency, meningoencephalitis, retinopathy), especially if infection develops during the 1st trimester. Rubella infection during the 1st trimester of pregnancy is an indication for abortion. Determination of protective anti-Rubella IgG-antibodies may be used for estimation of immune status in adolescent and pregnant women. >
100*
K
2
30//30/10-20'
18-25°C
12
ÈÔÀ
003
0
K102M
Rubella IgM EIA
96
10
Ê
2
60//30/10-20'
37 °C
12
ÈÔÀ
003
0
K103
Cytomegalovirus IgG EIA
96
Cytomegalovirus (CMV) belongs to herpesviruses and often causes clinically asymptomatic or mild infection, mostly in young children. It can be transmitted via stool, saliva, and breast milk. CMV can also be transmitted via the placenta and cause severe fetal malformations. Specific IgG-antibodies to CMV are evaluated in women before or during pregnancy to assess and manage the risk of transplacental fetus involvement. In immunocompromised hosts, CMV reactivation or primary infection may have serious and even life-threatening consequences. Therefore, the absence of specific IgG-antibodies to CMV (seronegativity) in organ transplant recipients requires the seronegativity of the donor. Specific IgG-antibodies to CMV do not protect from virus reactivation, and usually raise in titer during reactivation caused by decrease of immune system capacity to control the virus replication. >
100*
K
2
30//30/10-20'
18-25°C
12
ÈÔÀ
910
0
K103M
Cytomegalovirus IgM EIA
96
10
Ê
2
60//30/10-20'
37 °C
12
ÈÔÀ
906
0
K104
HSV 1,2 IgG EIA
96
Herpes simplex virus (HSV) is one of the most common pathogens in humans. HSV is transmitted by all secretions of infected body, especially via saliva, semen and cervical fluid. Acute HSV infections appear as a vesicular rash of labial or genital area. In immunocompromised hosts, HSV may cause life-threatening sequela in central nervous system. HSV is rarely fully eradicated after acute infections and persists in human organism lifelong, showing the periodic reactivation. In case of acute infection or reactivation during pregnancy, HSV may cross the placental barrier and cause severe fetal malformations. Specific IgG-antibodies to HSV are not protective; their titer usually raise in response to the reactivation of virus and therefore may be used to monitor the actual status of HSV activity. In pregnant women, the absence of specific IgG-antibodies (seronegativity) requires tight restrictions of the lifestyle during the pregnancy minimizing contacts to seropositive humans. The seronegative individuals should not receive the blood transfusions and organ transplants from seropositive donors. There are two very similar serotypes of HSV – HSV I and HSV II, showing different distribution in affected human tissues and organs. The present test system does not detect the differences between these two serotypes. >
100*
K
2
30//30/10-20'
18-25°C
12
ÈÔÀ
910
0
K104M
HSV 1, 2 IgM EIA
96
10
Ê
2
60//30/10-20'
37 °C
12
ÈÔÀ
906
0
K104CF
HSV 1/2 IgG-CF EIA
96
Herpes simplex virus (HSV) is one of the most common pathogens in mammals. HSV is transmitted by all secretions of infected body, especially via saliva, semen and cervical fluid. Latency and re-activation are characteristic for HSV infection. Specific IgG-antibodies to HSV are protective to some extent - they help to prevent the disease and limit latency, although do not provide a complete protection. A high titer of anti-HSV IgG-antibodies may suggest either a recent acute infection or reactivation of a latent one. Specific anti-viral treatment as well as non-specific activation of the immune system inhibit production of viral antigens and, therefore, induce decline of anti-HSV-IgG antibodies to their normal values. >
100*
K
2
30//30/10-20'
37 °C
12
ÈÔÀ
604
0
K105
Chlamydia IgG EIA
96
Chlamydia are obligate intracellular parasites closely related to Gram negative bacteria. The genus Chlamydia contains three known species: C.trachomatis, C.psittaci and C.pneumoniae (TWAR) which share most of their immunoreactive antigens. C.trachomatis has been recognised as a frequent cause of sexually transmitted diseases, which may lead to serious malfunction in reproductive function both in men and women (chronic pelvic inflammation and infertility). This species may also cause conjunctivitis and keratitis in adults and ophthalmia neonatorum in children born to an infected mother. C.psittaci is transmitted from birds to humans and causes an atypical pneumonia (ornitosis); C.pneumoniae is the causative agents of both acute pneumonia and chronic bronchitis. Due to intracellular ‘depot’ of the microorganism, Chlamydia infections may be asymptomatic and recurrent. Specific IgG-antibodies to Chlamydia are not protective; their titer usually raise in response to the reactivation of Chlamydia and therefore may be used to monitor the actual status of infectious activity. The elevation of these antibodies persist for at least 3-4 weeks after the reactivation, and is not directly related to antimicrobial therapy. The present test system does not detect the differences between species of Chlamydia. >
100*
K
2
30//30/10-20'
18-25°C
12
ÈÔÀ
909
0
K105CF
Chlamydia IgG-CF EIA
96
Chlamydiosis is an infection disease affecting both animals and humans. Clinical manifestations may be the following: abortion, endometritis, vaginitis, mortinatality, nonviable offspring, encephalomyelitis, polyarthritis, conjunctivitis, pneumonia, enteritis, mastitis, orchitis, urethritis, balanoposthitis. A wide spread of infectious agents in natural surrounding (wild animals, especially – birds) represent a constant threat for humans. According to a new classification, Chlamydiaceae family is divided into 2 genera: Chlamydia and Clamydophila. Chlamydia include the following species: C. trachomatis (affects humans and laboratory animals), C. suis (affects pigs), C. muridarum (affects mice, hamsters). Chlamydophila include the following species: C. pneumoniae (affects humans and horses), C. pecorum (affects large horn cattle, sheep, goats, pigs), C. psittaci (affects birds, dogs and large horn cattle), and C. psittaci subspecies: C. abortus (affects large horn cattle, sheep, goats, horses, pigs, dogs), C. caviae (affects guinea pigs), C. felis (affects cats). Both genera of Chlamydiaceae share common antigens. Ca. 18-38% of dogs are infected with Chlamydia with clinical manifestations seen only sporadically. In cats, ca. 65-70% are Chlamydia carriers (mostly, asymptomatic) with living Chlamydia organisms found in saliva, urine, on pads. Various authors report ca. 5-10% cats having chronic chlamydiosis. Chlamydiosis is accompanied by a low production of neutralizing antibodies – they are produced in low titers and not constantly. Elevated IgG antibody titer indicates a persisting infection or recent reactivation.>
100*
K
2
30//30/10-20'
37 °C
12
ÈÔÀ
604
0
K106
Mycoplasma IgG EIA
96
Mycoplasma represent a separate class of microorganisms. Unique metabolic properties of Mycoplasmae determine their poor growth on standard microbiological media and require the application of serological methods in diagnostics. Among large variety of speciei, M.hominis, M.genitalium, M.pneumoniae and closely immunologically related Ureaplasma urealiticum, play the most considerable role in medical practice. All these microorganism share common antigenic epitopes. M.pneumoniae causes pneumonia, bronchitis and bullous meningitis; other mycoplasmae can cause acute or chronic pelvic inflammations and may contribute to male and female infertility. Specific IgG-antibodies to Mycoplasmae do not possess protective properties; however their serum titer reflects the degree of microbial growth. Therefore, the detection of serum IgG antibodies may be used for disease and treatment monitoring. Elevated serum IgG antibody titers are detected after 3-4 weeks from the onset of the disease in spite of successful antibiotic treatment. >
100*
K
2
30//30/10-20'
18-25°C
12
ÈÔÀ
810
0
K106CF
Mycoplasma IgG-CF EIA
96
Mycoplasmae represent a separate class of microorganisms. Unique metabolic properties of Mycoplasmae determine their poor growth on standard microbiological media and require the application of serological methods in diagnostics. All Mycoplasmae share common antigenic epitopes; the microbes cause pneumonia, bronchitis and bullous meningitis; acute or chronic pelvic inflammations and may contribute to male and female infertility. Specific IgG-antibodies to Mycoplasmae do not possess protective properties; however their serum titer reflects the degree of microbial growth. Therefore, the detection of serum IgG antibodies may be used for disease and treatment monitoring. Elevated serum IgG antibody titers are detected after 3-4 weeks from the onset of the disease in spite of successful antibiotic treatment. >
100*
K
2
30//30/10-20'
37 °C
12
ÈÔÀ
604
0
K122C
Candida IgG-C EIA
96
Candidosis is a rare pathology affecting skin and mucous surfaces and caused by fungi of Candida species. Various Candida species are pathogenic, C. albicans and C. tropicalis being the most common. Alteration of normal microflora and/or immune status due to other pathology or drugs intake facilitates disease progression. The main symptoms are: erosive non-healing lesions covered by a greyish-white layer and surrounded by a red hem. Erosions are found on mucous surfaces of the mouth, throat, esophagus, on praeputium, in the anus and on skin-mucous borders. Various Candida species may also be the causative agents of erosive skin lesions, chronic and acute diarrhea, otitis externa, abscesses of interdigital folds, and inflammation of the nail bed. Substantial alteration of cellular immunity may lead to more serious pathologies, such as lesions of the intestine, gall bladder and ducti, bronchi and urinary tract as well as systemic candidosis (sepsis) with living Candida fungi found in circulation and Candida antigens detected in urine. Specific IgG-antibodies to Candida antigens are not protective (they do not protect animals from recurrent or repeated infection), but their titer usually reflects activity of fungal growth and therefore may be used to monitor such infections. Despite effective antifungal therapy, elevated serum levels of IgG-antibodies may be found 3-4 weeks after the onset of the disease. >
100*
K
2
30//30/10-20'
37 °C
12
ÈÔÀ
604
0
K121
Aspergillus IgG EIA
96
The fungi of Aspergillus species are important human pathogens and established causative agents of systemic and local infections as well as allergic diseases. The isotypic pattern of antibody response to Aspergillus is variable and depends on the form of the disease. Low titre IgG-antibody response reflects anamnestic infection and has little or no clinical significance. However, in allergic broncho-pulmonary aspergillosis (ABPA) the level of Aspergillus-IgG is significantly elevated and is used as one of diagnostic criteria of this nosological form. Higher levels of Aspergillus-IgG can be detected in aspergilloma and invasive aspergillosis. The latter form of aspergillosis is a life-threatening disease mostly affecting immunosuppressed patients. The elevation of Aspergillus-specific IgG antibody titres in above mentioned diseases is very dramatic and these antibodies can be detected by immunoprecipitation (double immunodiffusion, DID). Our studies showed that in pulmonary diseases, e.g. chronic bronchitis, bronchial asthma, pulmonary fibrosis etc. the titres of Aspergillus-IgG are significantly elevated, but do not reach the sensitivity threshold of immunoprecipitation (DID). This milder form of aspergillosis (so called ‘fungal bronchitis’) is underdiagnosed and the specific anti-fungal treatment is not applicated. The EIA test for Aspergillus-IgG is designed for the detection of moderately elevated concentrations of specific antibody to Aspergillus specific antigens. >
100*
K
2
30//30/10-20'
18-25°C
12
ÈÔÀ
810
0
K131
aTPO EIA
96
Anti-TPO antibodies (formerly - thyroid microsomal antibodies) are directed against a target protein - thyroid peroxidase (TPO) - located in the smooth endoplasmic reticulum of thyroid cells. The presence of anti-TPO antibodies in serum is associated with thyroid autoimmune diseases (Graves' disease and Hashimoto's thyroiditis). Anti-TPO antibodies mostly belong to the IgG class. Low to moderate levels of serum anti-TPO antibodies can be found in some other autoimmune pathology (eg systemic lupus erythematosus or Sjogren syndrom) and, rarely, in apparently healthy subjects (especially elderly women). Anti-TPO antibodies are more sensitive in diagnosis of thyroid autoimmune diseases than anti-thyroglobulin (anti-TG) antibodies. However, in some cases anti-TG positive sera may be negative for anti-TPO. Therefore, combined determination of both types of anti-thyroid antibodies (anti-TPO + anti-TG) provides a more sensitive laboratory diagnostic tool for thyroid autoimmunity. >
100*
5 IU/ml
2
30//30/10-20'
18-25°C
12
ÈÔÀ
802
DE/CA37/IVD/13/44
K132
aTG EIA
96
Thyroglobulin (TG) is a well known target for autoantibodies occurring in thyroid autoimmunity (Graves' disease and Hashimoto's thyroiditis). Anti-TG antibodies mostly belong to the IgG class. Low to moderate levels of anti-TG antibodies can be found in sera of other autoimmune patients (eg systemic lupus erythematosus or Sjogren syndrome). In some cases anti-TG positive sera may show negativity for other type of anti-thyroid antibodies - anti-TPO. Therefore, combined determination of both types of anti-thyroid antibodies (anti-TPO + anti-TG) provides most sensitive laboratory diagnostic tool for thyroid autoimmunity. Separately from autoimmunity, anti-TG antibodies may develop in patients suffering from thyroid cancer. High level of anti-TG in such patients may interfere with correct determination of serum thyroglobulin which serves as tumour marker for therapy control in this group of patients. >
100*
10 IU/ml
2
30//30/10-20'
18-25 °C
12
ÈÔÀ
812
0
K133
aMPO EIA
96
Antibodies to myeloperoxidase (aMPO) are one of the two main members of anti-neutrophilic-cytoplasm antibodies (ANCA). ANCA are directed towards cytoplasmic components of neutrophilic granulocytes and monocytes. The classical method for determination of ANCA is immunofluorescense. Indirect immunofluorescense (IF) reveal two main patterns: perinuclear (p-ANCA) type and cytoplasmatic (c-ANCA) type. The main antigen for p-ANCA is myeloperoxidase (MPO) while for c-ANCA the main antigen is proteinase 3 (PR3). A similar fluorescent p-ANCA pattern may accompany the presence of autoantibodies to other antigens –e.g., elastase, catepsin G, lactoferrin and lysozyme. Besides, indistinguishable from p-ANCA pattern may be caused by different granulocyte specific antinuclear antibodies (GS-ANA) with atypical pattern. Therefore, an exact interpretation of IF patterns is difficult, and every positive p-ANCA pattern should be confirmed by EIA methods using purified antigens. aMPO are mostly found in patients with eosinophilic vasculitides, including Takayasu syndrom, Churg-Strauss syndrom and periarteriitis nodosa (PAN). Combined positivity with anti-PR3 is observed in ca.70% of the patients with microscopic polyangiitis. >
100*
3 U/ml
2
30//30/10-20'
18-25 °C
12
ÈÔÀ
912
DE/CA37/IVD/13/42
K151C
Parvo-IgG EIA
96
Parvovirus genus includes several specii, the canidae Parvovirus (CPV) type 2 being defined as a causative agent of parvoviral enteritis affecting Canidae and Mustelidae. CPV induces a rapid and serious disease with high mortality, especially in non-immunized animals. The symptoms are not specific to CPV infection and include chronic diarrhoea, dehydration, aphasia, vomiting and panleucopenia. In newborn puppies myocardial damage is also often seen. The female dog antibodies give protection to puppies until 5-6 weeks of age. The latter get their own immunological protection after week 8 only. Serum IgG antibodies to CPV appear on day 4-6 after infection with their maximal titre being reached on day 10-12. Anti-CPV IgG antibodies are protective. That is why vaccination is widely used to prevent infection. Quantitative determination of IgG-antibodies to CPV is used to estimate effectiveness of vaccination and to diagnose the infection in non-immunized animals. >
100*
5 U/ml
2
30//30/10-20'
37 °C
12
ÈÔÀ
711
0
K152C
CDV-IgG EIA
96
canidae/mustelidae Distermer disease is caused by a virus of the Pramyxoviridae family. Very contagious, it affects mainly young animals by direct contamination through the respiratory tract. The disease course may be divided into two stages: fever stage and nervous stage. Fever stage is comparatively easy to cure and rarely leads to death. Nervous stage develops if the animal is not cured and is characterized by damage of the CNS caused by autoimmune reactions. This stage usually ends with animal’s death. Among dogs, most sensitive to the disease are huskies, poodles, German sheepdogs and some other breeds. A part of dogs (ca. 20%) are genetically deficient for anti-CDV immune response, such animals being very reluctant to treatment and usually dying. CDV-IgG plays a protective role – that is why prophylaxis of this infection is based on vaccination. This test may be used both to estimate effectiveness of vaccination and to detect infection in non-immune animals. >
100*
10 U/ml
2
30//30/10-20'
37 °C
12
ÈÔÀ
711
0
K160
anti-TGlu IgG EIA
96
Celiac disease (CD) or gluten-sensitive entheropathy is a chronic disease characterized by impaired intestinal absorption due to mucosal lesions. The exact ethiology of CD is unknown but it is clearly shown that gliadin - the alcohol soluble fraction of wheat gluten - is the toxic agent. Gliadin serves as a substrate for tissue Transglutaminase (tTG) – a calcium-dependent enzyme which is a constituent of the intestine mucosa. Gliadin-tTG complex antigen induces formation of IgA- and – later on – IgG-autoantibodies in patients with acute CD. Previously, anti-tTG antibodies were called “endomisium antibodies” and were detected by immunofluorescense methods on smooth muscle slides. After gluten exclusion from the diet, anti-tTG antibodies level in blood gradually decreases. To further confirm the diagnosis, a mucosal biopsy of the duodenal-jejunal junction is used, with characteristic lesions (“flat” mucosa) indicating presence of severe/moderate CD. Thus, determination of anti-tTG may be used for screening while mucosal biopsy – for confirmation of CD diagnosis. Usually, CD onset occurs in early childhood after implementing additional feeding, but later on the symptoms may spontaneously disappear notwithstanding continuing malabsorption. Nevertheless, even such mild pathology may lead to retardation of growth, puberty and even to dwarfness. Normally, following such a “remission”, an onset of classical symptoms of CD occurs again during 3rd-6th decades of life, and the correct diagnosis in such patients is made too late. Usually, mild and asymptomatic CD in adults manifests as unexplained anemia, hyposplenism or osteoporosis. It is rational (from economical point of view as well) to screen the following patient groups for CD: children with growth retardation, unexplained anemia, unexplained hypocalcaemia or osteomalation, retardation of puberty, patients with insulin-dependent diabetes, persons having close relatives suffering from CD, patients with autoimmune thyroiditis, systemic connective tissue pathology, selective IgA deficiency. >
100*
2 U/ml
2
30//30/10-20'
37 °C
12
ÈÔÀ
602
DE/CA37/IVD/13/41
K161
anti-TGlu IgA EIA
96
Celiac disease (CD) or gluten-sensitive entheropathy is a chronic disease characterized by impaired intestinal absorption due to mucosal lesions. The exact ethiology of CD is unknown but it is clearly shown that gliadin - the alcohol soluble fraction of wheat gluten - is the toxic agent. Gliadin serves as a substrate for tissue Transglutaminase (tTG) – a calcium-dependent enzyme which is a constituent of the intestine mucosa. Gliadin-tTG complex antigen induces formation of IgA- and – later on – IgA-autoantibodies in patients with acute CD. Previously, anti-tTG antibodies were called “endomisium antibodies” and were detected by immunofluorescense methods on smooth muscle slides. After gluten exclusion from the diet, anti-tTG antibodies level in blood gradually decreases. To further confirm the diagnosis, a mucosal biopsy of the duodenal-jejunal junction is used, with characteristic lesions (“flat” mucosa) indicating presence of severe/moderate CD. Thus, determination of anti-tTG may be used for screening while mucosal biopsy – for confirmation of CD diagnosis. Usually, CD onset occurs in early childhood after implementing additional feeding, but later on the symptoms may spontaneously disappear notwithstanding continuing malabsorption. Nevertheless, even such mild pathology may lead to retardation of growth, puberty and even to dwarfness. Normally, following such a “remission”, an onset of classical symptoms of CD occurs again during 3rd-6th decades of life, and the correct diagnosis in such patients is made too late. Usually, mild and asymptomatic CD in adults manifests as unexplained anemia, hyposplenism or osteoporosis. It is rational (from economical point of view as well) to screen the following patient groups for CD: children with growth retardation, unexplained anemia, unexplained hypocalcaemia or osteomalation, retardation of puberty, patients with insulin-dependent diabetes, persons having close relatives suffering from CD, patients with autoimmune thyroiditis, systemic connective tissue pathology, selective IgA deficiency. >
100*
2 U/ml
2
30//30/10-20'
37 °C
12
ÈÔÀ
602
DE/CA37/IVD/13/41
K180
Gliadin IgG EIA
96
Celiac disease (CD) or gluten-sensitive entheropathy is a chronic disease characterized by impaired intestinal absorption due to mucosal lesions. The exact ethiology of CD is unknown but it is clearly shown that gliadin - the alcohol soluble fraction of wheat gluten - is the toxic agent. High concentrations of antigliadin antibodies (AGA) found in blood, saliva and intestinal secretions are characteristic for untreated celiac patients. These antibodies gradually disappear after gluten exclusion from the patient’s diet. AGA testing is a simple and inexpensive method to efficiently select candidates for mucosal biopsy of the duodenal-jejunal junction, the latter method being essential for the confirmation of the diagnosis of CD. Early detection of AGA in high risk populations would contribute to prevent the insidious consequences of chronic malabsorption. Individuals at risk include short-stature children, unexplained anemia, unexplained hypocalciemia or osteomalacia, delayed puberty, insulin-dependent diabetes mellitus, autoimmune thyroiditis and selective IgA deficiency. It is well established that IgA-AGA are more specific than IgG-AGA. Nevertheless, combined IgG/IgA screening might be more effective since there is an unexplained but clear association between CD and selective IgA deficiency. In treated celiac patients without this deficiency IgA-AGA is the test of choice for monitoring diet compliance. Serum IgA-AGA level responds very quickly to the admission of gluten-free diet (levels drop below the cut-off level within two to six months) while IgG-AGA may take more than one year to become negative; breaking the diet causes more prompt elevation of IgA-AGA compared to IgG-AGA. Herpetiform dermatitis is a disease entity strongly associated to gluten-sensitive enteropathy, and AGA serology is not capable to distinguish between these two diseases. Separately, there are well reported clinical conditions showing positive IgG-AGA and, rarely, IgA-AGA nonrelated to histologically proven CD, eg all kind of malapsortion syndromes, including Crohn's disease, ulcerative colitis, galactosidase deficiency, post-infection malapsorption etc. The patients with rheumatoid arthritis, Sjogren syndrome, systemic sclerosis and other connective tissue diseases show abnormally high prevalence of moderately elevated gliadin IgA and IgG. These findings may be considered as non-relevant to GI pathology; however, gliadin free diet may be implemented for their treatment. According to data obtained by XEMA, first degree relatives of CD children patients (especially their parents) show very frequent positivity for both IgG-AGA and IgA-AGA while displaying virtually no symptoms of gastrointestinal diseases, herpetiform dermatitis, or other diseases supposed to cause this positivity. >
100*
5 U/ml
2
30//30/10-20'
18-25°C
18
ÈÔÀ
903
DE/CA37/IVD/13/40
K181
Gliadin IgA EIA
96
Celiac disease (CD) or gluten-sensitive entheropathy is a chronic disease characterized by impaired intestinal absorption due to mucosal lesions. The exact ethiology of CD is unknown but it is clearly shown that gliadin - the alcohol soluble fraction of wheat gluten - is the toxic agent. High concentrations of antigliadin antibodies (AGA) found in blood, saliva and intestinal secretions are characteristic for untreated celiac patients. These antibodies gradually disappear after gluten exclusion from the patient’s diet. AGA testing is a simple and inexpensive method to efficiently select candidates for mucosal biopsy of the duodenal-jejunal junction, the latter method being essential for the confirmation of the diagnosis of CD. Early detection of AGA in high risk populations would contribute to prevent the insidious consequences of chronic malabsorption. Individuals at risk include short-stature children, unexplained anemia, unexplained hypocalciemia or osteomalacia, delayed puberty, insulin-dependent diabetes mellitus, autoimmune thyroiditis and selective IgA deficiency. It is well established that IgA-AGA are more specific than IgG-AGA. Nevertheless, combined IgG/IgA screening might be more effective since there is an unexplained but clear association between CD and selective IgA deficiency. In treated celiac patients without this deficiency IgA-AGA is the test of choice for monitoring diet compliance. Serum IgA-AGA level responds very quickly to the admission of gluten-free diet (levels drop below the cut-off level within two to six months) while IgG-AGA may take more than one year to become negative; breaking the diet causes more prompt elevation of IgA-AGA compared to IgG-AGA. Herpetiform dermatitis is a disease entity strongly associated to gluten-sensitive enteropathy, and AGA serology is not capable to distinguish between these two diseases. Separately, there are well reported clinical conditions showing positive IgG-AGA and, rarely, IgA-AGA nonrelated to histologically proven CD, eg all kind of malapsortion syndromes, including Crohn's disease, ulcerative colitis, galactosidase deficiency, post-infection malapsorption etc. The patients with rheumatoid arthritis, Sjogren syndrome, systemic sclerosis and other connective tissue diseases show abnormally high prevalence of moderately elevated gliadin IgA and IgG. These findings may be considered as non-relevant to GI pathology; however, gliadin free diet may be implemented for their treatment. According to data obtained by XEMA, first degree relatives of CD children patients (especially their parents) show very frequent positivity for both IgG-AGA and IgA-AGA while displaying virtually no symptoms of gastrointestinal diseases, herpetiform dermatitis, or other diseases supposed to cause this positivity. >
100*
5 U/ml
2
30//30/10-20'
18-25 °C
18
ÈÔÀ
903
DE/CA37/IVD/13/40
K200
Total IgE EIA
96
Total immunoglobulin E (IgE) serum level is widely reported as the laboratory marker of atopic diseases such as atopic asthma, atopic dermatitis, and pollenosis. Separately, high levels of total serum IgE are characteristic for parasitic infestations and some other clinical disorders including superficial and systemic mycosis. Decreased levels of IgE are found in cases of hypogammaglobulinemia, autoimmune diseases, ulcerative colitis, and primary biliary cirrhosis. In allergic patients, serum total IgE level in general corresponds to the severity of the allergic disease and may be therefore used for monitoring of all kinds of anti-allergic therapy or allergen elimination. >
50
6 IU/ml
2
30//30/10-20'
37 °C
12
ÈÔÀ
210
DE/CA37/IVD/13/39
K201
TSH EIA
96
Thyroid stimulating hormone (TSH) is a glycoprotein with molecular weight ca.30 kDa which is secreted by hypophysis. A molecule of TSH consists of two noncovalently bound subunits: ?- and ?-HCG. ?-subunit determines biological activity and immunological specificity of TSH. TSH stimulates thyroid gland to secrete thyroid hormones. TSH secretion in hypophysis is controlled by a negative feedback regulation by thyroid hormones. TSH secretion is subject to circadian rhythms with highest levels seen early in the morning (6 a.m.). Changes of TSH blood level during a day are not significant; nevertheless, if the results do not correspond with clinical status and other laboratory data, it is recommended to take and test another blood sample. Determination of TSH level in serum is recommended in the following states and conditions: 1. Diagnostics of dysfunction of the thyroid gland; 2. Hypothyroidism (TSH level is increased. The diagnosis is confirmed by low concentrations of total and free T4 and T3. In mild subclinical forms when T4 and T3 levels are within normal ranges, determination of TSH concentration is critical); 3. Hyperthyroidism (synthesis and secretion of TSH are inhibited); monitoring of replacement therapy; 4. Screening for inherited hypothyroidism (on day 5 after birth TSH level in blood is determined). TSH level is elevated just after birth but it comes within the normal range in several days (both in boys and in girls). Serum TSH level is elevated during pregnancy, after physical stress, in individuals with lowered blood pressure and lowered temperature. Secretion of TSH is inhibited by Cortisol and Growth hormone. Low TSH levels are often seen in elderly people, in patients with chronic renal insufficiency, liver cirrhosis, in retardation of sexual development, in secondary amenorrhea, Cushing syndrome, acromegaly. In a present test system, ?- chain specific monoclonal antibody XTB1 is used as capture reagent; enzyme-labelled (Fab2)-fragment of another ?- chain specific monoclonal antibody XTB2 is used as tracer. This combination enables to minimize both cross-reactive reactions with other pituitary hormones and false positivity caused by anti-species antibodies.>
50
0,08 mIU/l
1
//60/10-20'
37 °C
12
ÈÔÀ
608
DE/CA37/IVD/13/38
K201A
TSH plus EIA
96
Thyroid stimulating hormone (TSH) is a glycoprotein with molecular weight ca.30 kDa which is secreted by hypophysis. A molecule of TSH consists of two noncovalently bound subunits: ?- and ?-HCG. ?-subunit determines biological activity and immunological specificity of TSH. TSH stimulates thyroid gland to secrete thyroid hormones. TSH secretion in hypophysis is controlled by a negative feedback regulation by thyroid hormones. TSH secretion is subject to circadian rhythms with highest levels seen early in the morning (6 a.m.). Changes of TSH blood level during a day are not significant; nevertheless, if the results do not correspond with clinical status and other laboratory data, it is recommended to take and test another blood sample. Determination of TSH level in serum is recommended in the following states and conditions: 1. Diagnostics of dysfunction of the thyroid gland; 2. Hypothyroidism (TSH level is increased. The diagnosis is confirmed by low concentrations of total and free T4 and T3. In mild subclinical forms when T4 and T3 levels are within normal ranges, determination of TSH concentration is critical); 3. Hyperthyroidism (synthesis and secretion of TSH are inhibited); monitoring of replacement therapy; 4. Screening for inherited hypothyroidism (on day 5 after birth TSH level in blood is determined). TSH level is elevated just after birth but it comes within the normal range in several days (both in boys and in girls). Serum TSH level is elevated during pregnancy, after physical stress, in individuals with lowered blood pressure and lowered temperature. Secretion of TSH is inhibited by Cortisol and Growth hormone. Low TSH levels are often seen in elderly people, in patients with chronic renal insufficiency, liver cirrhosis, in retardation of sexual development, in secondary amenorrhea, Cushing syndrome, acromegaly. >
100
0,025 mIU/l
2
60//60/10-20'
37 °C
12
ÈÔÀ
506
DE/CA37/IVD/13/38
K202
LH EIA
96
Luteinizing hormone (LH) is produced in both men and women by the anterior pituitary gland in response to luteinizing hormone-releasing hormone (LH-RH or Gn-RH), which is released by the hypothalamus. LH, also called interstitial cell-stimulating hormone (ICSH) in men, is a glycoprotein with a molecular weight of approximately 30,000 daltons. It is composed of two noncovalently associated amino acid chains: alpha and beta. The basal secretion of LH in men is episodic and has the primary function of stimulating the interstitial cells (Leydig cells) to produce testosterone. The variation in LH concentrations in women is subject to the complex ovulatory cycle of healthy menstruating women, and depends on sequence of hormonal events along the gonado-hypothalamus-pituitary axis. During the cycle, LH level is low except for the middle of the cycle when its concentration may increase up to 5-10 fold. LH peak is preceeded by a peak of Estradiol which occurs approximately 12 hours earlier. Ovulation occurs 12-120 hrs after LH peak. When the ovum is released, the corpus luteum is formed which secretes progesterone and estradiol, these latter exerting negative feedback effects on LH and FSH levels through hypothalamo-pituitary axis. LH concentration in blood is subject to circadian rhythms; therefore blood sample for LH assay should always be taken at the same time of the day. Circadian variations of LH level are more pronounced in women depending of the stage of menstrual cycle: they become less frequent at the end of luteinic phase and less pronounced – at the end of follicular stage. Increased LH levels are found in primary dysfunction of gonadal glands, in amenorrhea caused by ovarian insufficiency, in Stein-Leventhal syndrome, after menopause. Increased concentrations of LH are also present during renal failure, cirrhosis, hyperthyroidism, and severe starvation. Decreased LH concentrations are seen in dysfunction of hypophysis or hypothalamus, in galactorrhea-amenorrhea syndrome, in isolated decrease of gonadotropins, in isolated LH decrease; in neurotic anorexia, in patients with retardation of growth and sexual development, after intake of digoxin, phenotiazine, progesterone, estrogens. In the differential diagnosis of hypothalamic, pituitary, or gonadal dysfunction, assays of LH concentration are routinely performed in conjugation with FSH assays since their roles are closely interrelated. Furthermore, the hormone levels are used to determine menopause, pinpoint ovulation, and monitor endocrine therapy.>
50
0,3 IU/l
1
//60/10-20'
37 °C
18
ÈÔÀ
610
DE/CA37/IVD/13/37
K203
FSH EIA
96
Follicle stimulating hormone (FSH) is a glycoprotein with molecular weight 28 kDa secreted by basophil cells in hypophysis. Gonadotropin releasing hormone (GnRH) produced by the hypothalamus controls the release of FSH from anterior pituitary. Follicle-stimulating hormone (FSH) and Luteinizing hormone (LH) are intimately involved in the control of the growth and reproductive activities of the gonadal tissues, which synthesize and secrete male and female sex hormones. The levels of circulating FSH and LH are controlled by these sex hormones through a negative feedback. Like LH, TSH and HCG, FSH consists of two subunits – alpha and beta, its biological and immunological properties being dependent on the hormone-specific beta subunit. In females, FSH stimulates the growth and maturation of ovarian follicles. At the beginning of normal menstrual cycle FSH level is higher that at the final stage of follicular phase. Peak FSH levels are seen in the middle of the cycle concomitantly with LH peak levels. Increased estradiol and progesterone production during luteinic phase leads to decreased FSH blood concentrations by negative feedback mechanism. The same mechanism leads to elevation of FSH levels at the end of the cycle due to decreased estrogen and progesterone concentrations, and the new cycle is initiated. In men, FSH regulates growth of seminiferous tubules and maintenance of spermatogenesis. However, androgens, unlike estrogen, do not lower FSH level, therefore demonstrating a feedback relationship only with serum LH. High levels of FSH in women are seen in menopause, preliminary ovarian failure, agenesia of ovaries; in men elevated FSH levels may be found in primary testicular failure, dysgenesia of seminiferous tubules, delayed sexual maturation, and Klinefelter syndrome. Elevated concentrations are also found in cases of starvation, renal failure, hyperthyroidism, cirrhosis and after intake of clomifen, l-DOPA. Decreased FSH levels are found in hypopituitarism and after intake of oral contraceptives, phenotiazine, estrogens. >
50
0,3 IU/l
1
//60/10-20'
37 °C
12
ÈÔÀ
610
DE/CA37/IVD/13/36
K204
GH EIA
96
Human growth hormone (GH) is a monomeric protein with molecular weight of 21.5 kDa which is secreted by hypophysis. GH stimulates growth and possesses anabolic activity. GH takes part in regulation of various metabolic processes but its main activity is directed towards regulation of protein metabolism and growth. Normally, secretion of GH is not even – it occurs as 5-10 discharges a day giving peak levels. Between these peaks, concentration of GH in blood may be rather low. Due to this, estimation of GH level in blood for diagnostics of acromegaly or gigantism is recommended to be done at fasting serially, during 2-3 days, with calculation of average value. If GH levels are near normal range, serial determination during a day is necessary to confirm diagnosis and to determine a stage of a disease. Elevation of GH concentration in blood is found in acromegaly and gigantism, after starvation , in stress conditions and alcoholic states, in chronic renal insufficiency, hyperglycemia, hyperpituitarism, after physical stress. Decreased blood levels of GH are seen in dwarfism due to hypophysis insufficiency (circadian rhythms of GH secretion are also absent in this condition), hypercorticism, Cushing syndrome, hypopituitarism. >
50
0,25 mIU/l
1
//60/10-20'
37 °C
12
ÈÔÀ
807
DE/CA37/IVD/13/35
K205
hCG EIA
96
Human chorionic gonadotropin (HCG) is a glycoprotein hormone secreted by trophoblastic cells of placenta. A molecule of HCG consists of two noncovalently bound subunits: alpha- and beta-HCG. Beta-subunit is specific for HCG hormone. Determination of HCG is widely used for early diagnosis of pregnancy. Multiple pregnancy results in correspondent elevation of serum HCG; while ectopic pregnancy and placental insufficiency cause decreased serum HCG levels. Determination of HCG in serum during second trimester is used for pregnancy monitoring, especially in screening for Down syndrome, along with other laboratory tests (AFP and Estriol). Serum HCG is also a laboratory marker of trophoblastic tumours - chorionepitheliomas, some seminomas and theratomas. Serial determination of serum HCG can be used for therapy monitoring in these cancers. The present test system uses beta (?)-chain specific monoclonal antibody as the capture, and alpha (?)-chain specific monoclonal antibody as the tracer; therefore only the whole intact HCG molecule is detected. >
50
2,5 IU/l
1
//60/10-20'
37 °C
12
ÈÔÀ
805
DE/CA37/IVD/13/34
K206
Prolactin EIA
96
Prolactin is a 198 aminoacids polypeptide with molecular weight ca. 22.5 kDa which is secreted by eosinophil cells of hypophysis. Hyperplasia and adenomas of hypophysis are the main causes of infertility. Functional changes in regulation of reproductory function are also caused by alterations in secretion of hormones of hypophysis. One of markers of such alterations is changes in Prolactin secretion. That is why WHO recommended to use determination of Prolactin level as a screening test in primary laboratory investigation of couples claiming for infertility. In women Prolactin level remains low before menarche and elevates during puberty. During this period, Prolactin stimulates development of mammary glands. Prolactin level changes during menstrual cycle with elevations up to 900 mIU/l seen during periovulatory period and the second stage of luteinic phase. That is why it is recommended to evaluate Prolactin level during the first stage of the cycle. Besides, physiological hyperprolactinemia is seen in stress conditions and after physical exercises. Prolactin secretion is subject to circadian rhythms with maximal levels found during the night (3-7 fold higher than during the day). That is why time of sampling is extremely important. Elevated Prolactin levels are seen in Prolactin-producing tumours of hypophysis, idiopathic hyperprolactinemias (symptoms: in women – alteration of menstrual cycle, in men – impotence), hypofunction of the thyroid gland, renal insufficiency, after intake of phenothiazine derivatives, haloperidol, estrogens, oral contraceptives, histamine preparations, opiates, in hypoglycemia caused by insuline intake. Low Prolactin levels are found after surgical resection of hypophysis, after X-ray therapy, after bromocriptin therapy, after intake of T4.>
50
10 mIU/l
1
//60/10-20'
37 °C
12
ÈÔÀ
702
DE/CA37/IVD/13/33
K207
Progesterone EIA
96
Progesterone is a gestagen with a MW of 314.5 Dalton. Progesterone is secreted by corpus luteum, adrenals and testis; it plays a role of a precursor for corticosteroids and androgens. Being an estrogen antagonist, Progesteronó induces characteristic changes in endometrium necessary for implantation of an impregnated ovum. During normal menstrual cycle, Progesterone level remains low until LH peak level begins to drop: only slight but statistically significant elevation of Progesterone level occurs concomitantly with LH peak followed by a decrease of Progesterone concentration. During second stage of the cycle, Progesterone and Estradiol levels increase again to complete luteinization. By the end of the cycle, Progesterone level drops again up to levels seen during follicular phase. This quick drop causes menstrual bleeding. During pregnancy, Progesterone concentration continuously increases, and it induces proliferation and development of mammary glands and inhibits ovulation. During the first trimester, Progesterone is secreted by corpus luteum while from month 3-4 – by mitochondria of the trophoblast. Progesterone level in maternal blood increases rapidly – by week 7-8 it increases 2-fold and continues to increase by week 37-38. Decreased Progesterone levels indicate pathology of pregnancy while elevated levels suggest renal insufficiency. Elevated Progesterone levels are found in pregnancy, tumours of adrenals or testicles, chorionepithelioma, in lipid tumours of ovaries as well as after intake of preparations of Progesterone or its analogues. Decreased Progesterone levels are seen in galactorrhea-amenorrhea syndrome, in pregnant women at risk of premature delivery, and in persons taking some drugs such as oral contraceptives, ampicilline, ethynilestradiol.>
25
0,5 nmol/l
1
//120/10-20'
37 °C
12
ÈÔÀ
111
DE/CA37/IVD/13/32
K207CF
Progesterone-CF EIA
96
Progesterone is a gestagen with a MW of 314.5 Dalton. Progesterone is secreted by corpus luteum, adrenals and testis; it plays a role of a precursor for corticosteroids and androgens. Being an estrogen antagonist, Progesteron induces characteristic changes in endometrium necessary for implantation of an impregnated ovum. >
50
0,5 nmol/l
1
//120/10-20'
37 °C
12
ÈÔÀ
606
0
K207M
Progesterone milk EIA
96
Progesterone is a gestagen with a MW of 314.5 Dalton. Progesterone is secreted by corpus luteum, adrenals and testis; it plays a role of a precursor for corticosteroids and androgens. Being an estrogen antagonist, Progesteron induces characteristic changes in endometrium necessary for implantation of an impregnated ovum. During pregnancy, Progesterone concentration continuously increases at least by week 10-12, and it induces proliferation and development of mammary glands and inhibits ovulation. A certain proportion of serum Progesterone penetrates into milk; this enables to detect pregnancy in cows using non-invasive sample collection method. >
25
0,3 ng/ml
1
//60/10-20'
37 °C
12
ÈÔÀ
611
0
K208
Estradiol EIA
96
Estradiol (E2) is a steroid hormone with molecular weight 272.4 Da. In humans, E2 shows the highest physiological activity among the estrogens. In males, minor quantities of E2 are producód by adrenals and testicles. In females, E2 is produced by ovarian follicles. The physiological activity of E2 involves multiple functions in female reproductive system. Regulation of E2 production and secretion is complex and depends on pituitary and ovarian hormones. Serum E2 level is low in follicular phase of the menstrual cycle; 3-5 days before serum LH peak, serum E2 level begins to rise and reaches a maximum ca. 12 hours before LH peak. After LH peak, E2 level drops dramatically to the minimal level and starts to rise again. The maximal E2 level in serum is observed in luteal phase, at day 9 after ovulation; then the decline of serum E2 reflects the degradation of corpus luteum. During pregnancy, the determination of serum E2 reflects the status of fetoplacental system. In first trimester, serum E2 level is in the range corresponding to the ovulation levels. Sharp increase of serum E2 in pregnant women is observed between 9th and 10th week; then the increase continues less sharply by the end of pregnancy. Increased levels of serum estradiol are characteristic for metrorrhagias in post-menopausal age; adrenal hyperplasia; estrogen-secreting tumours; liver cirrhosis; feminization in children and males; intake of gonadotropins and estrogens. Decreased levels of serum estradiol are observed in Turner syndrome, primary or secondary hypogonadism; germaphroditism; post-climacteric syndrome; fetal dysfunctions; intake of oral contraceptives.>
25
0,05 nmol/l
1
//120/10-20'
37 °C
12
ÈÔÀ
612
DE/CA37/IVD/13/31
K209
Testosterone EIA
96
Testosterone is a steroid with a MW of 288.4 Dalton. The main sites of testosterone secretion are Leidig cells in interstitial tissue of testicles in men. In women testosterone is secreted in the adrenals and is controlled by luteinizing hormone. Testosterone stimulates development of male genital organs and formation of secondary sexual features. In males, Testosterone secretion undergoes circadian rhythms with maximal concentrations seen in the morning (6 am) and minimal – in the evening (8 pm). In females, Testosterone secretion is regulated by menstrual cycle with maximal levels found in luteinic phase and during ovulation. Leidig cell tumours producing high levels of serum testosterone in young boys lead to development of “little Hercules” syndrome. Elevated testosterone level in women causes the clinical signs of masculinization. In men, decreased Testosterone levels may lead to female habitus or underdevelopment of male genital organs in boys. To differentiate between primary and secondary hypogonadism, Testosterone should be assayed in conjunction with LH and FSH. >
25
0,3 nmol/l
1
//120/10-20'
37 °C
12
ÈÔÀ
611
DE/CA37/IVD/13/30
K209S
Salivary Testosterone EIA
96
Testosterone is a steroid with a MW of 288.4 Dalton. The main sites of testosterone secretion are Leidig cells in interstitial tissue of testicles in men. In women testosterone is secreted in the adrenals and is controlled by luteinizing hormone. Testosterone stimulates development of male genital organs and formation of secondary sexual features. In males, Testosterone secretion undergoes circadian rhythms with maximal concentrations seen in the morning (6 am) and minimal – in the evening (8 pm). In females, Testosterone secretion is regulated by menstrual cycle with maximal levels found in luteinic phase and during ovulation. In serum, testosterone is found both in free and bound form, the latter being a complex with transport proteins (SHBG, albumin). But only free form exerts biological activity, although its proportion is lt 1% of total testosterone. Currently, there are no reliable immunochemical method for quantitative determination of free testosterone in serum. At the same time, complicated reference laboratory methods (e.g., dialysis) are not suitable for everyday use. That is why the only method of direct determination of free testosterone is its determination in saliva. Follow-up of salivary testosterone level is a very informative and non-traumatic method widely used in endocrinology, physiology, sport medicine, veterinary, etc. for estimation of masculine status. Elevated salivary testosterone in females is characteristic for hirsutism, polycystosis of ovaries and serves as a laboratory marker of masculinization. Stably low levels of salivary testosterone in males suggest primary or secondary hypogonadism. >
100
0,015 pg/ml
1
//60/10-20'
37 °C
12
ÈÔÀ
805
0
K210
Cortisol EIA
96
Cortisol is a glucocorticoid with a MW of 362.5 Dalton. Cortisol is the major hormone secreted by adrenals. In blood, cortisol is found mostly in a bound form, transcortin being the carrier. Cortisol secretion undergoes circadian rhythms with maximal (up to 700 nmol/l) concentrations seen in the morning (6-9 am) and minimal (up to 55 nmol/l) – in the midnight. During pregnancy, Cortisol blood level is continuously increasing by up to 5-fold of initial concentration before delivery, its circadian rhythm being altered. Cortisol plays an important role in development of alveolar epithelium and surfactant secretion, this being of major importance for the first inhale of a newborn. Elevated Cortisol concentrations in blood are found in secreting tumours of adrenals, in virilizing hyperplasia of adrenals, in Cushing syndrome, in ACTH-producing tumours, during surgical stress, in cardiac insufficiency, diabetes, burns, pains, during pregnancy, during estrogen therapy, etc. Cortisol blood level may be increased by intake of ACTH, Cortisol, alcohol, nicotine, oral contraceptives. Decreased Cortisol levels are found in Addison syndrome, adrenogenital syndrome, hypopituitarism. Some drugs may decrease Cortisol level in blood, such as: L-DOPA, dexamethasone, etc. Decreased Cortisol level during pregnancy may indicate anencephaly of the fetus. >
25
12 nmol/l
1
//60/10-20'
37 °C
12
ÈÔÀ
711
DE/CA37/IVD/13/29
K210CF
Cortisol-CF EIA
96
10
25 nmol/l
1
//60/10-20'
37 °C
12
ÈÔÀ
603
0
K210S
Salivary Cortisol EIA
96
Cortisol is a glucocorticoid with a MW of 362.5 Dalton. Cortisol is the major hormone secreted by adrenals. Cortisol secretion undergoes circadian rhythms with maximal (up to 700 nmol/l) concentrations seen in the morning (6-9 am) and minimal (up to 55 nmol/l) – in the midnight. In serum, cortisol is found both in free and bound form, the latter being a complex with transport proteins (transcortin, albumin). But only free form exerts biological activity, its proportion being ca. 10% of total cortisol. Currently, there are no reliable immunochemical method for quantitative determination of free cortisol in serum. At the same time, complicated reference laboratory methods (e.g., dialysis) are not suitable for everyday use. That is why the only method of direct determination of free cortisol is its determination in saliva. Follow-up of salivary cortisol level is a very informative and non-traumatic method widely used in endocrinology, physiology, sport medicine, veterinary, etc. for estimation of adrenal glands function, differential diagnostics of Cushing syndrome with its characteristic alteration of circadian rhythm of cortisol secretion being a good example. Elevated Cortisol concentrations in blood are found in secreting tumors of adrenals, in virilizing hyperplasia of adrenals, in Cushing syndrome, in ACTH-producing tumors, during surgical stress, in cardiac insufficiency, diabetes, burns, pains, during pregnancy, during estrogen therapy, etc. Cortisol blood level may be increased by intake of ACTH, Cortisol, alcohol, nicotine, oral contraceptives. Decreased Cortisol levels are found in Addison syndrome, adrenogenital syndrome, hypopituitarism. Some drugs may decrease Cortisol level in blood, such as: L-DOPA, dexamethasone, etc. Decreased Cortisol level during pregnancy may indicate anencephaly of the fetus. >
50
0,07 ng/ml
1
//60/10-20'
37 °C
12
ÈÔÀ
805
0
K211
T3 EIA
96
Thyroid hormones thyroxin (T4) and 3,5,3’-triiodothyronine (T3) exert regulatory influences on growth, differentiation, cellular metabolism and development of skeletal and organ systems. T4 and T3 in blood are found both in free and bound form – mostly, they are bound to thyroxin binding globulin (TBG). Only free forms of T3 and T4 exert hormonal activity also their percentage is very low – 0.3% for T3 and 0.03% for T4. The concentration of T3 is much less than that of T4 but its metabolic activity is about 3 times greater. About 80% of T3 is produced in peripheral tissues by deiodination of T4, and only 20% is secreted by thyroid gland. That is why in hypothyroid patients T3 level may for a long time remain on the lower limit of the normal range, because its loss may be compensated by enhanced conversion of T4 into T3. Determination of T3 level is most useful in T3-hyperthyroidism because 5-10% of such patients do not show significant changes in T4 level while concentration of T3 is highly elevated. Elevated T3 levels are seen in early thyroid hypofunction, after intake of estrogens, oral contraceptives, heroin, methadone, during pregnancy. Decreased concentrations of T3 are found in initial stage of hyperthyroidism, acute and subacute thyroiditis, after intake of androgens, dexamethasone, salycilates.>
50
0,4 nmol/l
1
//30/10-20'
37 °C
12
ÈÔÀ
702
DE/CA37/IVD/13/28
K212
T4 EIA
96
Thyroid hormones thyroxin (T4) and 3,5,3’-triiodothyronine (T3) exert regulatory influences on growth, differentiation, cellular metabolism and development of skeletal and organ systems. T4 and T3 in blood are found both in free and bound form – mostly, they are bound to thyroxin binding globulin (TBG). Only free forms of T3 and T4 exert hormonal activity also their percentage is very low – 0.3% for T3 and 0.03% for T4. The concentration of T4 is generally accepted as an index of thyroid function which provide enough information to differentiate between hyper-, hypo- and euthyroidism. Elevation of total T4 is found in hyperthyroidism, in patients with tumours of pituitary gland, in subjects with elevated TBG level (pregnancy, acute or chronic active hepatitis, estrogen-secreting tumours or estrogen intake, hereditary elevation of TBG), in patients taking oral contraceptives, heroin, methadone, thyroid preparations, TSH, thyroliberin. Low total T4 is found in hypothyroidism, in patients with panhypopituitarism, in subjects with low TBG level (acromegaly, nephritic syndrome, hypoproteinemia, chronic liver diseases, androgen-secreting tumours, hereditary reduction), in patients taking aminosalicylic and acetylsalicylic acids, cholestyramine, reserpine, potassium iodide, triiodothyronine. >
25
6 nmol/l
1
//60/10-20'
37 °C
12
ÈÔÀ
611
DE/CA37/IVD/13/27
K213
fT3 EIA
96
Thyroid hormones thyroxin (T4) and 3,5,3’-triiodothyronine (T3) exert regulatory influences on growth, differentiation, cellular metabolism and development of skeletal and organ systems. T4 and T3 in blood are found both in free and bound form – mostly, they are bound to thyroxin binding globulin (TBG). Only free forms of T3 and T4 exert hormonal activity also their percentage is very low – 0.3% for T3 and 0.03% for T4. The concentration of T3 is much less than that of T4 but its metabolic activity is about 3 times greater. About 80% of T3 is produced in peripheral tissues by deiodination of T4, and only 20% is secreted by thyroid gland. That is why in hypothyroid patients T3 level may for a long time remain on the lower limit of the normal range, because its loss may be compensated by enhanced conversion of T4 into T3. Determination of T3 level is most useful in T3-hyperthyroidism because 5-10% of such patients do not show significant changes in T4 level while concentration of T3 is highly elevated. Elevated T3 levels are seen in early thyroid hypofunction, after intake of estrogens, oral contraceptives, heroin, methadone, during pregnancy. Decreased concentrations of T3 are found in initial stage of hyperthyroidism, acute and subacute thyroiditis, after intake of androgens, dexamethasone, salycilates.>
50
1 pmol/l
1
//60/10-20'
37 °C
12
ÈÔÀ
304
DE/CA37/IVD/13/26
K214
fT4 EIA
96
Thyroid hormones thyroxin (T4) and 3,5,3’-triiodothyronine (T3) exert regulatory influences on growth, differentiation, cellular metabolism and development of skeletal and organ systems. T4 and T3 in blood are found both in free and bound form – mostly, they are bound to thyroxin binding globulin (TBG). Only free forms of T3 and T4 exert hormonal activity also their percentage is very low – 0.3% for T3 and 0.03% for T4. The concentration of T4 is generally accepted as an index of thyroid function which provide enough information to differentiate between hyper-, hypo- and euthyroidism. Elevation of total T4 is found in hyperthyroidism, in patients with tumours of pituitary gland, in subjects with elevated TBG level (pregnancy, acute or chronic active hepatitis, estrogen-secreting tumours or estrogen intake, hereditary elevation of TBG), in patients taking oral contraceptives, heroin, methadone, thyroid preparations, TSH, thyroliberin. Low total T4 is found in hypothyroidism, in patients with panhypopituitarism, in subjects with low TBG level (acromegaly, nephritic syndrome, hypoproteinemia, chronic liver diseases, androgen-secreting tumours, hereditary reduction), in patients taking aminosalicylic and acetylsalicylic acids, cholestyramine, reserpine, potassium iodide, triiodothyronine. >
25
1,5 pmol/l
1
//60/10-20'
37 °C
12
ÈÔÀ
803
DE/CA37/IVD/13/25
K215
DHEAS EIA
96
Dehydroepiandrosterone (DHEA) is an androgen with a MW of 288.4 Dalton secreted in adrenals. The main derivate of DHEA present in human tissue is DHEA sulfate (DHEAS). Since birth, DHEAS serum concentration is increasing continuously showing a pronounced peak after puberty and maximal levels at the age of 20. After that, serum DHEAS level continuously decreases. As DHEAS is the main component of 17-ketosteroids in serum, this test may substitute for column tests for determination of 17-ketosteroids in urine. Elevated DHEAS concentrations are found in adrenogenital syndrome, hirsutism, acne, benign hyperplasia of adrenals and adrenal tumors, Stein-Leventhal syndrome, polycystic ovary syndrome. Decreased levels of DHEAS are found in hyperlipidemia, psychotic states, psoriasis, adrenal insufficiency. >
25
0,05 µg/ml
1
//60/10-20'
37 °C
12
ÈÔÀ
803
DE/CA37/IVD/13/24
K217
17-OH-progesterone EIA
96
17-ÎÍ-progesterone (17-ÎÍ-P) is a steroid with molecular weight 330 Da, an intermediate precursor in biosynthesis of glucocortiosteroids, estrogens and androgens. 17-OH-P is secreted by adrenals, ovaries and testicles by the enzyme 21-hydroxylase. 17-ÎÍ-Ð is secreted by ovaries during follicular phase; its serum level remains stable by the end of luteal phase. In case of non-fertile cycle, the serum level of 17-OH-P decreases; in case of fertilization, this hormone is secreted by corpus luteum. The determination of 17-OH-P is important for diagnosis of inborn adrenal hyperplasia which causes elevated secretion of androgens and the development of adrenogenital syndrome (AGS). In AGS, the deficient 21-hydroxylase activity causes blocked steroid synthetic pathway and correspondent dramatic increase in serum 17-OH-P level. If the deficiency of 21-hydroxylase is acquired in mature age, or in case of delayed inborn defect, the serum 17-OH-P may remain normal. >
50
0,25 nmol/l
1
//90/10-20'
37 °C
12
ÈÔÀ
803
DE/CA37/IVD/13/22
K218
free Estriol EIA
96
Free (non-conjugated) Estriol (E3) is a steroid hormone with a MM of 288 Da. Production of Estriol in non-pregnant women and men is negligible with no sex-related differences. During pregnancy, Estriol is produced in placenta by a multistep metabolic pathway, and its serum level is continuously growing up to delivery. Due to wide normal ranges of Free E3 at different pregnancy terms, serial determinations to monitor Estriol level are recommended. Estriol biological function is to maintain blood flow in maternal blood vessels and to provide for differentiation of mammary ducts. During 2nd trimester, E3 determination in conjunction with other tests (AFP, beta-HCG) is used to estimate risk of Down syndrome in fetus: a tendency of serum E3 level to decline is indicative of Down syndrome. Besides, a decline of E3 serum level during the 2nd trimester may indicate dangerous feto-placental insufficiency (an increased risk of miscarriage, intra-uterine infections, etc.). Increased E3 levels are seen in multifetal pregnancy and in case of a fetus bigger than normal. >
25
0,25 nmol/l
1
//90/10-20'
37 °C
12
ÈÔÀ
802
0
K221
tPSA EIA
96
Prostate specific antigen (PSA) is a serin-like protease with molecular weight ca. 34 kDa and was initially found exclusively in normal prostatic gland as well as in prostatic fluid and seminal plasma. Later it was localized also in breast milk and, according to its enzymological properties, was classified as human prekallikrein 3. In human serum, most of PSA forms complexes with serine protease inhibitor proteins (mostly alpha-1-antichymothripsin, alpha-2-macroglobulin and antithripsin). A minor proportion of PSA (free PSA) is circulating outside these complexes. Elevated serum PSA levels are found in patients with prostatic adenocarcinoma even at early stages of the disease. Values of 1000 ng/ml and even more may be found in patients with profound disease. Clinical value of this parameter is due to possibility of clinical monitoring and prognosis of the disease. Continuous elevation of PSA level is indicative of tumour progression and ineffective therapy. Nevertheless, interpretation of the results obtained should be made in the context of other clinical data. According to data obtained in University of Turku, Finland, the pair of monoclonal antibodies used in present test system (PS2-PS6), recognizes both free and complex-bound forms of PSA with equal affinity (equimolar binding). Elevations of serum PSA levels are characteristic to prostatic hyperplasia, inflammation and tumours. Serum PSA level can be used for monitoring and treatment control of all diseases involving prostatic tissue, especially prostatic tumours. Additional information valuable for differential diagnosis between benign and malignant prostate hyperplasia may be obtained by estimation of free PSA/total PSA ratio. In this case, age and case history of patients should be considered: that is, free PSA/total PSA ration in patients under 60 years is to be estimated if total PSA level is above 4 ng/ml while in males over 60 years when benign prostatic hyperplasia is common this ratio is rational to be estimated when total PSA level is above 7 ng/ml. Besides, it should be kept in mind that significant elevation of total PSA level may be found in patients with prostatitis as well as after massage of prostatic gland and the next day after ejaculation (according to ÕEMA data, up to 20 ng/ml and 80 ng/ml, respectively). Please, note, that free PSA/total PSA ratio should be estimated using EIA kits of the same manufacturer. This kit is intended for use with ÕEMA fPSA EIA, Cat.# Ê231.>
50
0,3 ng/ml
1
//60/10-20'
37 °C
12
ÈÔÀ
612
0
K222
CA125 EIA
96
CA125 is an antigen (an epitope) associated with ovarian carcinoma and some other tumors. Quantitative determination of CA125 in serum and plasma is used for follow-up of patients with primary invasive ovarian carcinoma. The CA125 epitope is found on a heterogeneous group of glycoproteins with a high molecular weight (MW 200.000 to over 1.000.000). CA125 can be detected in a high percentage of nonmucinous epithelial ovarian tumours. In addition, CA125 is detectable in some fetal tissues and in adult tissues in the epithelium of the phallopian tubes, apocrine sweat glands, breast glands, endometrium and endocervix. Elevated serum concentrations of CA125 are found in most patients with epithelial ovarian cancer, including those with stage 1 disease. CA125 determination is useful for therapy control and follow-up of ovarian cancer patients treated by any type of therapy. However, the CA125 values obtained should always be interpreted in the context of the results obtained by other clinical procedures. Internal data obtained by XEMA suggest that serial determination of CA125 may be helpful for diagnosis of adenocarcinoma development in fibrotic lung tissue in patients with interstitial lung diseases. In a present test system, monoclonal antibodies X306 (epitope group A) is used to capture the antigen, and monoclonal antibodies X52 (epitope group B) are used as a tracer. The epitope specificity of both antibodies were confirmed by an independent expert group (TD1 workshop 2000, International Society of Oncodevelopmental Biology and Medicine). Determination of CA125 is not suitable for early diagnosis of malignancies because elevated CA125 values may also be found in patients with uterine carcinoma, hepatoma and pancreatic adenocarcinoma as well as in non-malignant conditions such as liver cirrhosis, interstitial lung diseases, severe endometriosis and during pregnancy. >
50
3 U/ml
1
//60/10-20'
37 °C
12
ÈÔÀ
802
DE/CA37/IVD/13/23
K223
CA19.9 EIA
96
ÑA19.9 or sialyl-Lewisa is an antigen (an epitope) associated with tumours of the gastrointestinal tract, such as pancreatic, liver, stomach and colorectal carcinoma. Quantitative determination of ÑA19.9 in serum and plasma is helpful in monitoring of patients where such tumours have been diagnosed, especially together with determination of carcinoembryonic antigen (CEA, XEMA Cat# K224). Increasing levels of ÑA19.9 may indicate a progression of disease or poor therapeutic response while decreasing values point to the efficacy of treatment. However, the ÑA19.9 values obtained should always be interpreted in the context of the results obtained by other clinical procedures. Determination of ÑA19.9 is not suitable for early diagnosis of malignancies because elevated ÑA19.9 values may also be found in patients with pancreatitis, cystic fibrosis as well as liver cirrhosis and other severe hepatic diseases, especially accompanied by cholestasis as the antigen is excreted with bile. Some individuals lack the enzyme responsible for synthesis of sialyl-Lewisa antigen and therefore cannot respond by antigen elevation even to progressive tumour growth. >
50
2 U/ml
2
30//30/10-20'
37 °C
12
ÈÔÀ
810
DE/CA37/IVD/13/21
K224
CEA EIA
96
Carcinoembryonic antigen (CEA) represents a family of heavily glycosylated glycoproteins with MW 180-200 kDa which is expressed and secreted by normal human gastrointectinal mucosa. Serum CEA elevation may serve as the early laboratory marker of relapsing or metastatic colon or rectal carcinoma. Elevated serum CEA is observed in many other adenocarcinomas, including mammary, gastric, pulmonary, esophageal and ovarian; in some of these patients serum CEA may be used for disease monitoring. In blood circulation, there are the substances showing high degree of similarity to CEA (NCA, NCA2); this fact requires the use of highly specific anti-CEA reagents. In a present test-system, we use for capturing CEA the monoclonal antibody 3C6 directed towards domain A3/B3, epitope Gold group I. Due to high prevalence of serum CEA elevation in benign diseases (mucosal inflammations), this test system is not recommended for screening for malignant tumours. >
50
1 ng/ml
1
//60/10-20'
37 °C
12
ÈÔÀ
806
DE/CA37/IVD/13/20
K225
AFP EIA
96
Alpha-fetoprotein (AFP) is a glycoprotein with a MW ca. 65 kDa which is secreted by fetal liver and yolk sac. AFP represents the main protein of fetal serum while being found in trace quantities in adults. Serum AFP quantitative determination is used in primary diagnostics and monitoring of hepatocellular liver cancer, trophoblastic tumours of testicles and ovary as well as theratomas and theratocarcinomas. Quantitative determination of AFP in serum of pregnant women or in amniotic fluid during week 15-20 of gestation is widely used for laboratory screening of Down syndrome and defects of spinal cord. >
50
2 U/ml
1
//60/10-20'
37 °C
12
ÈÔÀ
611
DE/CA37/IVD/13/19
K226
CA15.3 (M12) EIA
96
CA15-3 or MUC1 is a heterogenous glycoprotein with a molecular mass ca. 300-450 kD. Elevation of serum CA15-3 is associated with mammary carcinomas. Quantitative determination of CA15-3 in serum and plasma is helpful in monitoring of patients with such tumours to estimate the course of the disease, effectiveness of its treatment and to reveal recurrence or metastases. However, CA15-3 values obtained should always be interpreted in context of results obtained by other diagnostic and clinical procedures. Besides mammary carcinomas, CA15-3 levels in blood may rise in lung tumours, prostate cancer, ovarian carcinomas, gastro-intestinal tumours. Elevation of CA15-3 level in blood can be also found in benign tumours of the mammary gland and the ovary, endometriosis, hepatitis, liver cirrhosis and lung fibrosis. Pregnancy and lactation may also cause elevation of CA15-3 level in serum. All CA15-3 test systems are usually not very sensitive (not more than 75% even at stage III mammary carcinoma). Therefore, in monitoring of tumours, we recommend to use this test in conjunction with two other test systems designed by XEMA for diagnostics and monitoring of mammary carcinomas – M20 (analogous to BR27.29 developed by Biomira) and M22 (analogous to MCA, Roche). All three systems should be used to evaluate MUC1 concentration before and after surgery; the test system showing the most pronounced postsurgery decline should be then used for further monitoring. NOTE: the patients that have received murine monoclonal antibodies for radioimaging or immunotherapy may develop high titered anti-mouse antibodies (HAMA). The presence of these antibodies gives false results in the present assay. Sera from HAMA positive patients should be treated by depleting adsorbents before assaying. >
50
1,5 U/ml
2
30//30/10-20'
18-25°C
12
ÈÔÀ
302
DE/CA37/IVD/13/18
K227
MUC1 (M22) EIA
96
CA15-3 or MUC1 is a heterogenous glycoprotein with a molecular mass ca. 300-450 kD. Elevation of serum CA15-3 is associated with mammary carcinomas. Quantitative determination of CA15-3 in serum and plasma is helpful in monitoring of patients with such tumours to estimate the course of the disease, effectiveness of its treatment and to reveal recurrence or metastases. However, CA15-3 values obtained should always be interpreted in context of results obtained by other diagnostic and clinical procedures. Besides mammary carcinomas, CA15-3 levels in blood may rise in lung tumours, prostate cancer, ovarian carcinomas, gastro-intestinal tumours. Elevation of CA15-3 level in blood can be also found in benign tumours of the mammary gland and the ovary, endometriosis, hepatitis, liver cirrhosis and lung fibrosis. Pregnancy and lactation may also cause elevation of CA15-3 level in serum. All CA15-3 test systems are usually not very sensitive (not more than 75% even at stage III mammary carcinoma). Therefore, in monitoring of tumours, we recommend to use this test in conjunction with two other test systems designed by XEMA for diagnostics and monitoring of mammary carcinomas – M20 (analogous to BR27.29 developed by Biomira) and M22 (analogous to MCA, Roche). All three systems should be used to evaluate MUC1 concentration before and after surgery; the test system showing the most pronounced postsurgery decline should be then used for further monitoring. NOTE: the patients that have received murine monoclonal antibodies for radioimaging or immunotherapy may develop high titered anti-mouse antibodies (HAMA). The presence of these antibodies gives false results in the present assay. Sera from HAMA positive patients should be treated by depleting adsorbents before assaying. >
50
1,5 U/ml
2
30//30/10-20'
18-25°C
12
ÈÔÀ
206
DE/CA37/IVD/13/17
K228
MUC1 (Ì20) EIA
96
MUC1 is a heterogenous glycoprotein with a molecular mass ca. 300-450 kD. Elevation of serum MUC1 is associated with mammary carcinomas. Quantitative determination of MUC1 in serum and plasma is helpful in monitoring of patients with such tumours to estimate the course of the disease, effectiveness of its treatment and to reveal recurrence or metastases. However, MUC1 values obtained should always be interpreted in context of results obtained by other diagnostic and clinical procedures. Besides mammary carcinomas, MUC1 levels in blood may rise in lung tumours, prostate cancer, ovarian carcinomas, gastro-intestinal tumours. Elevation of MUC1 level in blood can be also found in benign tumours of the mammary gland and the ovary, endometriosis, hepatitis, liver cirrhosis and lung fibrosis. Pregnancy and lactation may also cause elevation of MUC1 level in serum. The M20 kit is based on a principle of competitive immunoassay. The labelled monoclonal antibody X19 recognizing the peptide determinant TRPAPGS binds the natural purified mammary carcinoma-derived antigen on the solid phase Such test systems (e.g., BR27.29 developed by Biomira) may give a higher sensitivity for tumour specific forms of MUC1 compared to kits based on sandwich principle. However, due to considerable heterogeneity of tumour derived forms of MUC1 antigen, we recommend to use this test in conjunction with two other test systems designed by XEMA for diagnostics and monitoring of mammary carcinoma – M22 (analogous to MCA, Roche) and M12 (analogous to CA15-3 developed by Centocor). All three systems should be used to evaluate MUC1 concentration before and after surgery; the test system showing the most pronounced postsurgery decline should be then used for further monitoring. >
50
1 U/ml
1
//60/10-20'
37 °C
18
ÈÔÀ
002
DE/CA37/IVD/13/17
K231
fPSA EIA
96
Prostate specific antigen (PSA) is a serin-like protease with molecular weight ca. 34 kDa and was initially found exclusively in normal prostatic gland as well as in prostatic fluid and seminal plasma. Later it was localized also in breast milk and, according to its enzymological properties, was classified as human prekallikrein 3. In human serum, most of PSA forms complexes with serine protease inhibitor proteins (mostly alpha-1-antichymothripsin, and alpha-2-macroglobulin). A minor proportion of PSA (free PSA) is circulating outside these complexes. In a present test system, monoclonal antibodies PS2 capture both free and bound forms of PSA with an equal affinity (“equimolar” binding”). To detect captured free form of PSA, we use labelled monoclonal antibody PS1 which is highly specific for free PSA. The specificities and epitope mapping of these two antibodies were confirmed by independent laboratory (University of Turku, Finland). It is generally accepted now that the ratio free PSA/ total PSA may help in differential diagnosis between benign diseases of prostatic gland (adenomas, inflammatory diseases) and carcinomas. This ratio should be measured when the total PSA level exceeds the used populational threshold level (usually, 4 ng/ml). In sera with lower concentrations of total PSA, especially in women, the correct measurement of free to total PSA ratio is not recommended by present test system. >
50
0,07 ng/ml
2
30//30/10-20'
18-25 °C
12
ÈÔÀ
105
0
K232
Thyroglobulin EIA
96
Thyroglobulin (TG) is a high MW (ca. 650-700 kDa) glycoprotein synthesized by the thyroid epithelial cells. In normal thyroid gland, TG is secreted to the follicular lumen and undergoes iodination of tyrosine residues leading to formation of thyroid hormones (T3 and T4). Minor quantities of TG penetrate to the circulation in normal donors. Synthesis of TG is regulated by hormones (TSH, TRH, exogenous thyroid therapy). In differentiated thyroid carcinoma, serial determination of serum TG is used for post-treatment monitoring. An elevation of serum TG in such patients indicates a presence of residual thyroid tissue, relapse or metastatic growth of the tumour. The elevated serums TG are also observed in benign thyroid diseases, e.g. thyroiditis, hyperthyroidism and non-toxic goiter. The monitoring of serum TG is also used for prognostic evaluation of thyrostatic treatment of Graves’ disease. >
50
1 ng/ml
1
//60/10-20'
37 °C
12
ÈÔÀ
512
DE/CA37/IVD/13/16
K235
free?-HCG EIA
96
Human chorionic gonadotropin (HCG) is a glycoprotein hormone secreted by trophoblastic cells of placenta during pregnancy. HCG appears in blood and urine in about 7-13 day after fertilization, reaching its maximum by the end of the first trimester. An intact molecule of HCG consists of two non-covalently bound polypeptide chains: ?- and ?-subunits. ?-subunit is specific for HCG hormone while ?-chain is identical in TSH, LH, FSH and HCG.. Normally, blood levels of free ?- and ?-chains reach not more than 0.5-1.0% of intact HCG level and during pregnancy vary in parallel with intact HCG. Recently, it was shown that, compared to control, a significant elevation of free ?-chain is found in trisomy 21 (Down syndrome), the most pronounced difference being found during weeks 8-9 of pregnancy. That is why determination of free ?-chain of HCG in conjunction with other markers (PABB-A, AFP) may be used to estimate risk of congenital pathology of the fetus. In oncology, a marked rise of free ?-chain in blood is found in trophoblastic and germinal tumours (choriocarcinoma, carcinoma of ovaries, etc.). >
50
2 ng/ml
2
30//30/10-20'
37 °C
12
ÈÔÀ
707
DE/CA37/IVD/13/15
K238
PAPP-A EIA
96
PAPP-A (pregnancy-associated plasma protein A) is a high molecular weight glycoprotein consisting of two subunits. In normal pregnancy, PAPP-A level in maternal blood increases during the first two trimesters. Functional significance of PAPP-A during pregnancy remains unclear. Lowered levels of PAPP-A are observed in Down’s syndrome (trisomy 21) during weeks 8-12; after week 14, PAPP-A levels become similar to those in normal pregnancies. Low PAPP-A levels are also found in other trisomies (18 and 13) and chromosomal abnormalities in the fetus and in complicated pregnancies. Determination of PAPP-A level in the first trimester is used in the following combinations of tests: 1. PAPP-A + free beta-HCG 2. PAPP-A + free beta-HCG + USI of nuchal translucency In men and non-pregnant women, PAPP-A level is extremely low – usually, it is below the sensitivity level of most immunoassays. Recently, some evidence has appeared to confirm a link between raised PAPP-A levels and increased risk of complications in patients with coronary disease. >
10
20 mU/l
1
//60/10-20'
37 °C
12
ÈÔÀ
902
DE/CA37/IVD/13/14
K240
Alveomucin EIA
96
Alveomucin (AM) or mucin antigen 3EG5 is produced by alveolocytes of type 2. Elevated serum levels of AM were found in patients with interstitial lung diseases (ILD), the degree of elevation correlating to the severity of clinical symptoms. AM determination may be of use for ILD diagnostics and monitoring. >
50
20 U/ml
2
30//30/10-20'
18-25°C
12
ÈÔÀ
301
DE/CA37/IVD/13/13
K244
CA72-4 EIA
96
CA72-4 is a carbohydrate antigen (an epitope) with a MM ca. 230 kD associated with gastric cancer, ovary carcinoma and some other tumors. Quantitative determination of CA72-4 in serum or plasma – especially, in conjunction with CA19-9 (XEMA Cat.# K223) - is helpful to monitor the course of gastric cancer and to evaluate effectiveness of its therapy. Together with CA125 (XEMA Cat.# K222), CA72-4 is useful for monitoring of ovarian cancer. Normally, CA72-4 is not expressed in adults. Elevated CA72-4 concentrations are found in most patients with gastric cancer, ovarian cancer and lung cancer. Rarely, elevated CA72-4 levels are also found in patients with various benign tumours. However, CA72-4 values obtained should always be interpreted in the context of the results obtained by other diagnostic procedures and clinical data. >
10
2 U/ml
2
120//60/10-20'
37 °C
12
ÈÔÀ
901
0
K250
CRP EIA
96
C-reactive protein (CRP) is a member of penthraxin family with the MW ca. 100 kDa. In evolution of vertebrates, CRP was one of the first developed factors of inborn humoral immunity. CRP efficiently binds both endogenous (phosphoethanolamine, phosphorylcholine, histones, fibronectin, laminin) and exogenous (cell walls of Gram positive bacteria) ligands. The binding of these ligands as well as the debris of apoptotic and necrotic cells by CRP facilitates the phagocytosis. CRP is capable to activate classic pathway of complement activation and phagocytic activity of macrophages. Dramatic (up to 1000 fold) elevation of serum CRP level is highly sensitive but nonspecific marker of inflammation induced by interleukin 6. Recently, there was observed a correlation between moderately elevated serum CRP (3-10 mg/l) and risk of ischemic heart disease. Elevated serum CRP is also observed in smokers and post-menopausal women receiving substitution hormonal therapy. >
25*
0,2 mg/l
2
30//30/10-20'
37 °C
12
ÈÔÀ
5072
DE/CA37/IVD/13/12
K271
total IgG EIA
96
Immunoglobulin G (IgG) is the main part of serum ? – globulin fraction. IgG is secreted during secondary immune response and plays a key role in humoral immunity. Decrease of serum IgG concentration below 5 g/l is a marker of severe life-threatening immunodeficiency. Determination of serum IgG concentration and IgG/IgA/IgM ratios can be used for monitoring of humoral immune status. Marked elevation of serum IgG may be observed in chronic inflammation, autoimmune diseases and myeloma.
IgG2 subclass plays a pivotal role in immune response to polysaccharide antigens of incapsulated bacteria. Selective IgG2 deficiency is characterized by low or absent serum IgG2 and may lead to higher probability of infections caused by Meningococcus, Pneumococcus, Haemophilus and related pathogens. In this case the risk of chronical infectious diseases of respiratory system is increased. Low serum IgG2 is also observed in common variable immunodeficiency (CVID). IgG2 serum content comprises 20 % of total serum IgG. Serum IgG2 determination may be used for monitoring of humoral immune status. >
100*
0,12 g/l
2
30//30/10-20'
37 °C
18
ÈÔÀ
506
DE/CA37/IVD/13/8
K274
IgG4 EIA
96
IgG4 subclass represents ca. 3% of total serum IgG. IgG4-antibodies are developed after long term antigen stimulation, eg in chronic fungal infections, parasitic invasions and autoimmunity. IgG4 plays a special role in atopic allergy. Elevated serum total and venom specific IgG4 is observed in honey bee keepers. The development of IgG4 response is suggested to correlate with successful treatment of allergy patients by modified allergens (immunotherapy). Serum IgG4 is also elevated in atopic diseases (atopic asthma, atopic dermatitis) even in the patients showing normal serum IgE. IgG4 deficiency is frequently associated with IgG2 deficiency and lead to decreased immune response to bacterial antigens. >
5*
0,02 g/l
2
30//30/10-20'
37 °C
18
ÈÔÀ
509
DE/CA37/IVD/13/8
K275
total IgA EIA
96
Immunoglobulin A (IgA) is a main factor of mucosal immune response to bacteria and viruses. Selective IgA deficiency is one of the most frequent hereditary disorders causing chronic infections inflammation in gastrointestinal, urinary and respiratory systems. Determination of IgA concentration in serum and other biological fluids can be used as screening for selective IgA deficiency and other immunodeficiency syndromes. Marked elevation of serum IgA is observed in some autoimmune diseases and IgA myeloma. >
5*
0,12 g/l
2
30//30/10-20'
37 °C
12
ÈÔÀ
506
DE/CA37/IVD/13/7
K276
secretory IgA EIA
96
Secretory IgA (sIgA) is the main immunoglobulin present on mucosal surfaces. Ca. 90% of sIgA is produced locally and does not penetrate into blood circulation. sIgA is considerably different from serum IgA, as this complex protein consists of 3 completely different molecules. Two or four molecules of immunoglobulin A with molecular weight 160 kDa are joined by J-chain (16 kDa) and attached to the secretory component (80kDa); the formation of this complex occurs during transepithelial transport of polymeric IgA. sIgA plays a pivotal role in local immunity by blocking bacterial and viral adhesion and invasion through epithelial tissues. Determination of sIgA concentration allows to evaluate the local immunity status in stomatology, ophthalmology, respiratory diseases, gastroenterology, gynaecology. The sIgA in saliva can be also used as noninvasive mass screening for selective IgA deficiency. Elevation of sIgA in serum is occasionally observed in soautoimmune diseases and several tumours. >
10*
1,2 ?g/ml
2
90//30/10-20'
37 °C
12
ÈÔÀ
505
DE/CA01/181/144
K277
total IgM EIA
96
Immunoglobulin M (IgM) is secreted during primary immune response and exists in monomeric and pentameric forms. Elevated serum IgM is observed in chronic inflammation, macroglobulinemia and IgM myeloma. Decreased IgM level may occur in some immunodeficiency syndromes. >
5*
0,12 g/l
2
30//30/10-20'
37 °C
12
ÈÔÀ
506
DE/CA37/IVD/13/6
K279K
free K-chain EIA
96
Apart from normal immunoglobulins, free immunoglobulin light chains (k, ? – chains) are also present in serum, cerebrospinal fluid and urine of healthy individuals. Normally, small amounts of free k, ? – chains are produced by B-cells as well as by proteolysis of normal immunoglobulins. Recently, it was found that free k, ? – chains exert proteolytic and anti-angiogenic activity, and can specifically bind to mast cells receptors to induce hypersensitivity reactions. Extremely high levels of free immunoglobulin light chains in biological fluids are found in multiple sclerosis, lymphoproliferative disorders, rheumatoid arthritis, SLE, acute nephritis. Free k, ? – chains have short half-life in comparison with normal immunoglobulins – that is why determination of their concentration should be recommended as useful diagnostic tool to control treatment efficiency. >
40*
1 ?g/ml
2
30//30/10-20'
37 °C
18
ÈÔÀ
000
0
K279L
free L-chain EIA
96
Apart from normal immunoglobulins, free immunoglobulin light chains (k, ? – chains) are also present in serum, cerebrospinal fluid and urine of healthy individuals. Normally, small amounts of free k, ? – chains are produced by B-cells as well as by proteolysis of normal immunoglobulins. Recently, it was found that free k, ? – chains exert proteolytic and anti-angiogenic activity, and can specifically bind to mast cells receptors to induce hypersensitivity reactions. Extremely high levels of free immunoglobulin light chains in biological fluids are found in multiple sclerosis, lymphoproliferative disorders, rheumatoid arthritis, SLE, acute nephritis. Free k, ? – chains have short half-life in comparison with normal immunoglobulins – that is why determination of their concentration should be recommended as useful diagnostic tool to control treatment efficiency. >
40*
0,1 ?g/ml
2
30//30/10-20'
37 °C
18
ÈÔÀ
000
0
K291
Troponin I EIA
96
During the last decade cardiac TnI has been proved to be one of the most specific and sensitive markers of acute myocardial infarction (AMI), perioperative myocardial infarction, and other types of myocardial tissue damage. TnI is a protein with MW 22.5 kDa and comprises a component of troponin complex, or simply troponin. Troponin plays an important role in the regulation of striated and cardiac muscle contraction and consists of three components - troponin C (TnC), troponin I (TnI) and troponin T (TnT), each of them performing specific roles. Three isoforms of TnI are known for human muscular tissue - two isoforms are characteristic for skeletal muscles and one isoform is strictly cardiac-specific. The structural differences enable to discriminate between skeletal and cardiac isoforms of TnI by immunological methods. TnI appears in the bloodstream within 4-6 hours after onset of the chest pain attack and reaches its peak level during the first 16-20 hours. Within the first day after AMI cardiac TnI is released from necrotic myocardial tissue showing similar pattern to CKMB - the 'golden' AMI marker of the 1990s. However, while CKMB remains elevated for two-three days after onset of the chest pain, TnI can be detected in serum or plasma for up to one week after the first symptoms of the AMI. Therefore, TnI can be used not only for rapid diagnostics of AMI, but also for late evaluation, if serum testing was non-available during the acute phase. This property of TnI assay makes TnI to resemble TnT - another representative of the troponin family among cardiac markers. However, it has been demonstrated that TnT (as well as CKMB) concentrations may be increased in chronic dialysis patients and in patients with chronic skeletal muscle disease even in the absence of ischaemic heart disease. This fact is explained by expression of cardiac isoform of TnT and CKMB in abnormal skeletal muscle in such groups of patients. On the contrary, no expression of cardiac TnI was detected in skeletal muscles of the patients with chronic renal and skeletal muscle diseases and the concentration of this analyte in such groups of patients mostly remains within the cut-off level. >
50
0,25 ng/ml
1
//60/10-20'
37 °C
12
ÈÔÀ
608
0
KH302
IHC visualization kit MIG
100
0
0
3
20/30/20/10-20'
18-25°C
12
ÈÖÕ
406
0
KQ13
AutoQon-Ab-Control
5 óðîâíåé/levels x 1 øò/pcs; 1 ìë/ml
The set is intended for use to estimate within-laboratory and laboratory-to-laboratory repeatability of quantitative determination of the above autoantibodies by immunometric assays. This set may also be used for QC of immunoassays for determination of anti-thyroid antibodies. >
0
///-'
0
36
0
512
DE/CA37/IVD/13/5
KQ14
AutoQon-ANA/ENA-Control
5 óðîâíåé/levels x 1 øò/pcs; 0.5 ìë/ml
The set is intended for use to estimate within-laboratory and laboratory-to-laboratory repeatability of quantitative determination of the ANA\ENA antibodies by immunometric assays. >
0
///-'
0
36
0
512
0
KQ15
AutoQon-ACL-Control
óðîâíåé/levels x øò/pcs; 0.5 ìë/ml
The set is intended for use to estimate within-laboratory and laboratory-to-laboratory repeatability by immunometric assays. >
0
///-'
0
36
0
512
0
KQ21
HormoQon-Control
2 óðîâíÿ/levels x 2 øò/pcs; 2 ìë/ml
0
///-'
0
36
0
510
DE/CA37/IVD/13/4
KQ22
OmaQon-Control
2 óðîâíÿ/levels x 2 øò/pcs; 2 ìë/ml
0
///-'
0
36
0
510
DE/CA37/IVD/13/3
KQ23
PrenaQon-Control
2 óðîâíÿ/levels x 2 øò/pcs; 1 ìë/ml
0
///-'
0
36
0
510
NO
#N003
Adhesive Tapes Sheet
0
0
0
///-'
0
0
0
610
NA
#XA161
1
10
0
1
5///-'
18-25°C
18
ÈÕ
006
IMPORTED
#XA291
Biocard Troponin I Test
1
15
0
1
5///-'
18-25°C
18
ÈÕ
006
IMPORTED
#XB026C
Speed Giardia
5
0
0
1
5///-'
18-25°C
24
ÈÕ
806
IMPORTED
#XB039C
Speed Diro
5
40-80
0
1
20///-'
18-25°C
24
ÈÕ
806
IMPORTED
#XB116C
Speed Brucella
5
40
0
1
20///-'
18-25°C
24
ÈÕ
806
IMPORTED
#XB128C
Speed Leish
6
40-80
0
1
20///-'
18-25°C
24
ÈÕ
806
IMPORTED
#XB129C
Speed Ehrli
6
40-80
0
1
20///-'
18-25°C
24
ÈÕ
806
IMPORTED
#XB153F
Speed FIP
10
40-80
0
1
20-40///-'
18-25°C
24
ÈÕ
801
IMPORTED
#CPRS
0
0
0
0
///-'
0
0
ÈÔÀ
610
IMPORTED
#K3T
0
0
0
0
///-'
0
0
ÈÔÀ
610
IMPORTED
#K3xxxx
0
0
0
0
///-'
0
0
ÈÔÀ
610
IMPORTED
#K3xxxxA
0
0
0
0
///-'
0
0
ÈÔÀ
610
IMPORTED
#DS1033C
0
0
0
0
///-'
0
0
ËÀ
610
IMPORTED
#DS1039R
0
0
0
0
///-'
0
0
ËÀ
610
IMPORTED
Z001
0
0
0
0
///-'
0
0
ÈÔÀ
610
IMPORTED
#N001
Plate Maxi sorb
0
0
0
///-'
0
0
ÈÔÀ
610
NA
#N002
Plate Normal sorb
0
0
0
///-'
0
0
ÈÔÀ
610
NA
#XV017F
SensPert FeLV Test
10
40
0
1
5-10///-'
18-25°C
24
ÈÕ
806
IMPORTED
#XV039C
SensPert Heartworm test
10
40
0
1
5-10///-'
18-25°C
24
ÈÕ
806
IMPORTED
#XV052C
SensPert CDT test
10
90-120
0
1
5-10///-'
18-25°C
24
ÈÕ
806
IMPORTED
#XV112F
SensPert FIV
10
40
0
1
5-10///-'
18-25°C
24
ÈÕ
510
IMPORTED
E235
?-HCG LIFA
96
Thyroid stimulating hormone (TSH) is a glycoprotein with molecular weight ca.30 kDa which is secreted by hypophysis. A molecule of TSH consists of two noncovalently bound subunits: ?- and ?-HCG. ?-subunit determines biological activity and immunological specificity of TSH. TSH stimulates thyroid gland to secrete thyroid hormones. TSH secretion in hypophysis is controlled by a negative feedback regulation by thyroid hormones. TSH secretion is subject to circadian rhythms with highest levels seen early in the morning (6 a.m.). Changes of TSH blood level during a day are not significant; nevertheless, if the results do not correspond with clinical status and other laboratory data, it is recommended to take and test another blood sample. Determination of TSH level in serum is recommended in the following states and conditions: 1. Diagnostics of dysfunction of the thyroid gland; 2. Hypothyroidism (TSH level is increased. The diagnosis is confirmed by low concentrations of total and free T4 and T3. In mild subclinical forms when T4 and T3 levels are within normal ranges, determination of TSH concentration is critical); 3. Hyperthyroidism (synthesis and secretion of TSH are inhibited); monitoring of replacement therapy; 4. Screening for inherited hypothyroidism (on day 5 after birth TSH level in blood is determined). TSH level is elevated just after birth but it comes within the normal range in several days (both in boys and in girls). Serum TSH level is elevated during pregnancy, after physical stress, in individuals with lowered blood pressure and lowered temperature. Secretion of TSH is inhibited by Cortisol and Growth hormone. Low TSH levels are often seen in elderly people, in patients with chronic renal insufficiency, liver cirrhosis, in retardation of sexual development, in secondary amenorrhea, Cushing syndrome, acromegaly. >
50
0,5 ng/ml
1
//60/10-'
37°C
0
ËÈÔÀ
901
0
E238
PAPP-A LIFA
96
Thyroid stimulating hormone (TSH) is a glycoprotein with molecular weight ca.30 kDa which is secreted by hypophysis. A molecule of TSH consists of two noncovalently bound subunits: ?- and ?-HCG. ?-subunit determines biological activity and immunological specificity of TSH. TSH stimulates thyroid gland to secrete thyroid hormones. TSH secretion in hypophysis is controlled by a negative feedback regulation by thyroid hormones. TSH secretion is subject to circadian rhythms with highest levels seen early in the morning (6 a.m.). Changes of TSH blood level during a day are not significant; nevertheless, if the results do not correspond with clinical status and other laboratory data, it is recommended to take and test another blood sample. Determination of TSH level in serum is recommended in the following states and conditions: 1. Diagnostics of dysfunction of the thyroid gland; 2. Hypothyroidism (TSH level is increased. The diagnosis is confirmed by low concentrations of total and free T4 and T3. In mild subclinical forms when T4 and T3 levels are within normal ranges, determination of TSH concentration is critical); 3. Hyperthyroidism (synthesis and secretion of TSH are inhibited); monitoring of replacement therapy; 4. Screening for inherited hypothyroidism (on day 5 after birth TSH level in blood is determined). TSH level is elevated just after birth but it comes within the normal range in several days (both in boys and in girls). Serum TSH level is elevated during pregnancy, after physical stress, in individuals with lowered blood pressure and lowered temperature. Secretion of TSH is inhibited by Cortisol and Growth hormone. Low TSH levels are often seen in elderly people, in patients with chronic renal insufficiency, liver cirrhosis, in retardation of sexual development, in secondary amenorrhea, Cushing syndrome, acromegaly. >
50
20 mIU/l
1
//60/10-'
37°C
0
ËÈÔÀ
901
0
K236
CYFRA 21-1 EIA
96
Antigen CYFRA 21-1 is an established name for the epitopes expressed on soluble fragments of cytokeratin 19. Cytokeratin 19 and related cytokeratin 8 molecules are the members of cytokeratin family proteins with molecular weight range ca 25 to 45 kDa which are ubiquitously expressed in all connective tissue cells. Some tumors show elevated production of cytokeratin 19 which iin turn may result in increased serum CYFRA 21-1 levels. Most important examples are squamous cell carcinomas (SCC) of the lung and bladder carcinomas. Therefore, the determination of CYFRA 21-1 antigen in patients’ serum or plasma may help in monitoring of tumor growth and efficiency of anti-cancer therapy. >
50
1 ng/ml
1
//30/10-20'
37 °C
12
ÈÔÀ
912
0
K174CF
Nematoda IgG-CF EIA
96
100*
K
2
30//30/10-20'
37 °C
12
ÈÔÀ
002
0
K175CF
Eucestoda IgG-CF EIA
96
100*
K
2
30//30/10-20'
37 °C
12
ÈÔÀ
004
0
K200SCB
Specific IgE CB EIA
16
Specific IgE (sIgE) mediates type I (immediate) allergic reactions, with usual onset of symptoms (allergic rhinitis, conjunctivitis, urticaria, asthma, anaphylactic shock) within 30 minutes after exposure. If allergen-specific IgE is found, it helps to make a diagnosis of type I allergy. >
0
0
///-'
0
12
ÈÔÀ
001
0
K200SP
Specific IgE P EIA
96
Specific IgE (sIgE) mediates type I (immediate) allergic reactions, with usual onset of symptoms (allergic rhinitis, conjunctivitis, urticaria, asthma, anaphylactic shock) within 30 minutes after exposure. If allergen-specific IgE is found, it helps to make a diagnosis of type I allergy. >
0
0
///-'
0
12
ÈÔÀ
001
0
K200ST
Specific IgE T EIA
96
Specific IgE (sIgE) mediates type I (immediate) allergic reactions, with usual onset of symptoms (allergic rhinitis, conjunctivitis, urticaria, asthma, anaphylactic shock) within 30 minutes after exposure. If allergen-specific IgE is found, it helps to make a diagnosis of type I allergy. >
0
0
///-'
0
12
ÈÔÀ
001
0
K200STx
Specific IgE-Tx EIA
40
Specific IgE (sIgE) mediates type I (immediate) allergic reactions, with usual onset of symptoms (allergic rhinitis, conjunctivitis, urticaria, asthma, anaphylactic shock) within 30 minutes after exposure. If allergen-specific IgE is found, it helps to make a diagnosis of type I allergy. >
*
0
///-'
0
12
ÈÔÀ
001
0
K200SD1
Specific IgE-D1 EIA
40
Specific IgE (sIgE) mediates type I (immediate) allergic reactions, with usual onset of symptoms (allergic rhinitis, conjunctivitis, urticaria, asthma, anaphylactic shock) within 30 minutes after exposure. If allergen-specific IgE is found, it helps to make a diagnosis of type I allergy. >
*
0
///-'
0
12
ÈÔÀ
001
0
K200SE1
Specific IgE-E1 EIA
40
Specific IgE (sIgE) mediates type I (immediate) allergic reactions, with usual onset of symptoms (allergic rhinitis, conjunctivitis, urticaria, asthma, anaphylactic shock) within 30 minutes after exposure. If allergen-specific IgE is found, it helps to make a diagnosis of type I allergy. >
*
0
///-'
0
12
ÈÔÀ
001
0
K200SE2
Specific IgE-E2 EIA
40
Specific IgE (sIgE) mediates type I (immediate) allergic reactions, with usual onset of symptoms (allergic rhinitis, conjunctivitis, urticaria, asthma, anaphylactic shock) within 30 minutes after exposure. If allergen-specific IgE is found, it helps to make a diagnosis of type I allergy. >
*
0
///-'
0
12
ÈÔÀ
001
0
K200SGx
Specific IgE-Gx EIA
40
Specific IgE (sIgE) mediates type I (immediate) allergic reactions, with usual onset of symptoms (allergic rhinitis, conjunctivitis, urticaria, asthma, anaphylactic shock) within 30 minutes after exposure. If allergen-specific IgE is found, it helps to make a diagnosis of type I allergy. >
*
0
///-'
0
12
ÈÔÀ
001
0
K200SW56
Specific IgE-W56 EIA
40
Specific IgE (sIgE) mediates type I (immediate) allergic reactions, with usual onset of symptoms (allergic rhinitis, conjunctivitis, urticaria, asthma, anaphylactic shock) within 30 minutes after exposure. If allergen-specific IgE is found, it helps to make a diagnosis of type I allergy. >
*
0
///-'
0
12
ÈÔÀ
001
0
K470
CIC-ÕÅÌÀ
96x4
Immune complexes are clusters of interlocking antigens and antibodies. Under normal conditions immune complexes are rapidly removed from the bloodstream by macrophages in the spleen and Kupffer cells in the liver. In some circumstances, however, immune complexes continue to circulate. Eventually they become trapped in the tissues of the kidneys, lung, skin, joints, or blood vessels. Just where they end up probably depends on the nature of the antigen, the class of antibody - IgG, for instance, instead of IgM - and the size of the complex. Deposition of circulating immune complexes (CIC) in tissues or in vascular endothelium can produce immune complex-mediated tissue injury by activation of complement (if CIC include complement-activating Igg: IgM or IgG – subclasses 1, 2 or 3), generation of anaphylatoxins, chemoattraction of polymorphonuclear leukocytes, and tissue injury. The commonly affected organs include skin (urticaria, vasculitis), joints (arthritis), and kidney (nephritis). Immune complexes work their damage in many diseases. Sometimes, as is the case with malaria and viral hepatitis, they reflect persistent low-grade infections. Sometimes they arise in response to environmental antigens such as the moldy hay that causes the disease known as farmer's lung. Frequently, immune complexes develop in autoimmune disease, where the continuous production of autoantibodies overloads the immune complex removal system (e.g., Lupus erythematosis). High levels of CIC are found in diffuse connective tissue disease, systemic vasculitis, subacute infectious endocarditis, HIV infection, Crohn’s disease, autoimmune hepatitis, etc. Usually, a selective polyethylene glycol precipitation technique is used for determination of CIC. But, keeping in mind heterogenic nature of CIC, it is rational to use several techniques simultaneously, C1q-binding technique being considered the most informative. Diagnostic value of the test: CIC level in blood is an indicator of intensity of inflammatory processes and autoimmune diseases. Indications for CIC determination are: autoimmune diseases, rheumatism, collagenoses, viral, bacterial and mold infections, glomerulonephritis, arthritis, allergy. >
20
0
1
120///-'
18-25°C
36
ÊÕ
001
0
K201N
TSH-Neo EIA
96
TSH-Neo ELISA is intended for the quantitative determination of Thyroid Stimulating Hormone (TSH) in newborn blood specimens dried on filter paper and used as a screening test for congenital hypothyroidism in babies. TSH is a glycoprotein with MM ca. 30 kDa which is secreted by the anterior lobe of the pituitarty gland. TSH molecule is combined from two non-covalently bound polypeptide chains: alpha-chain and beta-chain. Specificity and biological activity of TSH is caused by its beta-chain. Congenital hypothyroidism is a hereditary pathology expressed in altered thyroid function and found with prevalence ca 1:3500 – 1:4000. Congenital hypothyroidism is characterized by a decreased secretion of thyroid hormons – T3 and T4, this in turn upregulating TSH secretion and leading to elevated TSH levels in blood. Screening of newborns with congenital hypothyroidism is based on cut-off TSH value. If TSH value obtained is higher that the cut-off, it indicates a possible pathological state and requires additional laboratory investigations. To confirm the diagnosis, quantification of TSH and T4 in serum is required. >
