Abbott Alinity c Cedia assay

Urine Clean plastic or glass container

2-8℃: 5 days      

-20℃: longer

24 hours

ng/mL

Positivity Cut-Off: 10

Stago Compact Max, Stago Satellite Max

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Sodium Citrate Plasma 3.2%

Temperature: 4 hours Room temperature or 2 weeks -20ºC

Miscellaneous: N/A

Collection: Cf. Special requirement for Coagulation test

Whole blood:  4 hours, unless centrifuged at room temperature at 1500g for 15 min, separated and the plasma frozen. Can only be thawed once. If an expected delay from collection time to receipt in the laboratory, suggest send frozen plasma.

(BD Ref. VS5966 Evaluation of 0.109M BD Vacutainer® Plus Plastic and 0.105M BD Vacutainer® Glass Sodium Citrate Tubes for PT and APTT Using the Sysmex CA - 1500 Analyzer. BD, Franklin Lakes, NJ, USA June 2002; CSLI H21- A5)

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Dacie and Lewis, Practical Haematology 12th edition, 2017

This test is also known as the Partial Thromboplastin Time with Kaolin (PTTK) and the Kaolin Cephalin Clotting Time (KCCT) reflecting the methods used to perform the test. The APTT is the main screening test for the Intrinsic clotting system and is the second most common coagulation test being exceeded in frequency only by the prothrombin time. The Partial Thromboplastin of the APTT is a phospholipid extract of animal tissue or from vegetable sources. The phospholipids act as a platelet substitute in the Intrinsic system. The test incorporates an activator, in the absence of added Thromboplastin, which shortens the test and increases the precision and reproducibility by eliminating the variable effects of contact from glass surfaces and by effecting maximum activation. The activator is used to stimulate the production of FXIIa by providing a surface for the function of high molecular weight Kininogen, Kallikrein and FXIIa. The contact activation occurs for a time at 37oC. Calcium is then added to trigger further reactions and the time required for clot formation measured. Standardised Phospholipids are required to form complexes, which activate FX and Prothrombin, which allows the test to be conducted in patient Platelet poor plasma (PPP). The test depends not only on the contact factors and factors VIII and IX, but also on the reactions with factors X, V, Prothrombin and Fibrinogen. It is also sensitive to the presence of circulating anticoagulants (inhibitors) and Heparin.

Preparation of patients: Patients should be relaxed pre-venepuncture. Excessive stress and exercise will increase Factor VIII, vWF antigen and fibrinolysis. Veno-occlusion should be avoided.

Precautions: APTT results may be affected by many commonly administered drugs and further studies should be made to determine the source of unexpected abnormal results. Oral contraceptive and Oestrogen therapy in males have been found to decrease APTT in vivo. Conversely, Heparin, Warfarin, Lupus anticoagulant and radio therapy have been found to increase APTT in vivo.

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24 Hours

26.0 – 40 seconds

Abbott Alinity c Spectrophotometry NADH(without P-5'-P)

Serum: Serum Separator

Plasma: Di potassium EDTA Lithium heparin Lithium heparin separator Sodium heparin

Abbott:

20-25℃: 3 days              

2-8℃: 7 days      

-20℃: 60 days

Abbott IFU

24 hours

U/L

Abbott:

Adult Male < 45

Adult Female < 34

Abbott Alinity c Spectrophotometry (Bromocresol Green)

Serum : Serum tubes (with or without gel barrier)

Plasma: Acceptable anticoagulants are:

Lithium heparin

Potassium EDTA

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Abbott:

20-25°C: 7 days

2-8°C: 7 days

-20°C: 3months

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Abbott IFU

24 Hours

g/L

Abbott:

Adults: 35 - 50

60 – 90 years: 32 - 46

> 90 years: 29 - 45

CALCULATION based on Abbott Alinity methodologies for Microalbumin and Urinary creatinine.

Urine spot/ timed/24hr: Clean, unused plastic or glass container with preservatives

20-25℃: 7 days                

2-8℃: 7 days      

-20℃: 1 year

NICE Guideline NG203, August 2021

24 Hours

ACR (Albumin/Creatinine Ratio): <3.0

Abbott Alinity c Spectrophotometry Hydrolysis of Para- Nitrophenyl phosphate

Serum:

Serum separator

Plasma:

Lithium heparin

Lithium heparin separator

Sodium heparin

20-25℃: 7 days                

2-8℃: 7 days      

-20℃: 7 days

Abbott IFU

24 hours

U/L

16 to 21 years (Male): 56 - 167

22 to 79 years (Male): 50 - 116

16 to 29 years (Female):44 - 107

30 to 79 years (Female): 46 - 122

Fluoroenzyme immunoassay on Phadia 250.

Serum (Red and gold cap); Heparin or EDTA Plasma (Green and Lavender cap)

Temperature: + 4ºC

Whole blood: RT unknown.

7 days @ + 4°C

Phadia Instructions for Use

Immunoglobulin E (IgE) specific to individual allergens is measured to determine which allergens are responsible for atopic symptoms and signs in an individual. The concentration of the specific IgE frequently correlates with the severity of symptoms. The following individual allergen specific IgEs are assayed at Eurofins Biomnis: E1, E3, E4, E5, D1, D2, F1, F2, F3, F4, F13, F14, F17, F18, F20, F25, F26, F27, F36, F44, F75, F81, F82, F83, F201, F245, F284, F343. The following panels are assayed: EX1, FX1, FX2, FX5, FX7, FX13, FX15, GX3, MX1, MX2, TX8, WX1, WX2. For details on these tests, see the Phadia Allergy website at http://www.phadia.com/Products/Allergy-testing-products/ImmunoCAPAllergen-Information/ (Accessed 22/05/20).

4 working days

Panels are reported as Positive or Negative only. Individual allergens are reported in kIU/L, ranging from less than 0.10 to greater than 100. A result of > 0.10 kIU/L is interpreted as positive.

Abbott Alinity c Immunoturbidimetry

Serum :

Serum tubes (with or without gel barrier)

Plasma: Acceptable anticoagulants are:

Sodium heparin

Potassium EDTA

Sodium citrate

2-8℃: 2 days      

-20℃: not specified

24 hours

g/L

0.9 - 2.0

Abbott Alinity i Chemiluminescent Microparticle Immunoassay (CMIA)

Serum:

Serum, Serum separator.

Plasma:

Sodium heparin, Lithium heparin,

Dipotassium EDTA

Sodium EDTA

20-25℃: 3 days              

2-8℃: 7 days      

-20℃: longer

Abbott IFU

24 hours

IU/mL

Adult: 0.74 - 7.29

Abbott Alinity c Homogeneous particle enhanced turbidimetric inhibition immunoassay (PETINIA).

Serum:

Serum tubes (with or without gel barrier)

Plasma: Acceptable anticoagulants are:

Lithium heparin, Sodium heparin

K2-EDTA, K3-EDTA

2-8℃: 7 days      

-20℃: 14 days

24 hours

mg/L

Trough: 4 - 8

Severe Infection (Peak): 25 - 35

Toxic Levels (Peak): >35

Abbott Alinity c Enzymatic Immunoassay

Urine Clean plastic or glass container

2-8℃: 5 days      

-20℃: longer

Abbott IFU

24 hours

ng/mL

Positivity Cut-off: 1000

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Abbott Alinity c Enzymatic + Colorimetric

Serum:

Serum tubes (with or without gel barrier)

20-25°C: 7 days

2-8°C: 7 days

Abbott IFU

24 hours

U/L

Adults: 25 - 125

> 70 years: 20 - 160

Abbott Alinity c Enzymatic/ Colorimetric Hydrolysis of Furylacryloylphenylalanylglyclglycine (FAPGG)

Serum is the preferred specimen.

Plasma:

Lithium heparin

Lithium heparin separator

Sodium heparin

20-25℃: 7 days              

2-8℃: 7 days      

-20℃: 1 year

Glenbio IFU

24 hours

U/L

>14 years: 8 - 65

Fluoroenzyme immunoassay (Phadia 250)

Tube Type: Serum (Gold and red cap); Plasma (green and lavender cap)

Temperature: + 4ºC

Whole blood: unknown.

Separated: RT unknown;

14 days @ + 4ºC

Yes

The antiphospholipid syndrome (APS), also known as “Hughes syndrome”, is characterized by typical clinical features such as arterial/venous thromboses or recurrent miscarriages together with persistently positive tests for antiphospholipid antibodies. The criteria for classification of the APS have been revised in 2004 in Sydney. Besides the clinical criteria, three different laboratory tests are listed: lupus anticoagulant, anticardiolipin antibodies (IgG and IgM) and anti-β2-Glycoprotein I antibodies (IgG and IgM). The latter was not included in the former Sapporo criteria. However, by majority, the Sydney committee agreed that they are an independent risk factor for thrombosis and pregnancy complications. For APS diagnosis, β2-Glycoprotein I antibody tests show higher specificity than anticardiolipin assays. In 3-10% of APS patients, β2-Glycoprotein I antibodies may be the only positive test. The association of β2-Glycoprotein I antibodies with pre-eclampsia and/or eclampsia in unselected pregnant women who tested negative for anticardiolipin antibodies implies that the inclusion of β2-Glycoprotein I antibodies may also help clarify this type of pregnancy morbidity. Outside the context of clinical studies, testing for β2-Glycoprotein I antibodies can be helpful for APS diagnosis, particularly when anticardiolipin antibodies and lupus anticoagulant are negative and APS is strongly suspected.

4 working days

Negative: < 7.0 U/mL

Weak Positive: 7.0 U/mL to 10.0 U/mL

Positive: > 10.0 U/mL

Fluoroenzyme immunoassay (Phadia 250)

Serum (Gold and red cap); Plasma (green and lavender cap)

Temperature: + 4ºC

Whole blood: unknown.

Separated: RT unknown;

14 days @ + 4ºC

Source: Phadia IFU

The antiphospholipid syndrome (APS), also known as “Hughes syndrome”, is characterized by typical clinical features such as arterial/venous thromboses or recurrent miscarriages together with persistently positive tests for antiphospholipid antibodies. The criteria for classification of the APS have been revised in 2004 in Sydney. Besides the clinical criteria, three different laboratory tests are listed: lupus anticoagulant, anticardiolipin antibodies (IgG and IgM) and anti-β2-Glycoprotein I antibodies (IgG and IgM). The latter was not included in the former Sapporo criteria. However, by majority, the Sydney committee agreed that they are an independent risk factor for thrombosis and pregnancy complications. For APS diagnosis, β2-Glycoprotein I antibody tests show higher specificity than anticardiolipin assays. In 3-10% of APS patients, β2-Glycoprotein I antibodies may be the only positive test. The association of β2-Glycoprotein I antibodies with pre-eclampsia and/or eclampsia in unselected pregnant women who tested negative for anticardiolipin antibodies implies that the inclusion of β2-Glycoprotein I antibodies may also help clarify this type of pregnancy morbidity. Outside the context of clinical studies, testing for β2- Glycoprotein I antibodies can be helpful for APS diagnosis, particularly when anticardiolipin antibodies and lupus anticoagulant are negative and APS is strongly suspected.

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4 working days

Negative: < 7.0 U/mL

Weak positive: 7.0 U/mL to 10.0 U/mL

Positive: > 10.0 U/mL

Chemiluminescent microparticle immunoassay (CMIA)

Chemiluminescent microparticle immunoassay (CMIA) technology

Serum (Gold and red cap); Plasma (lavender cap)

Temperature: + 4ºC

Miscellaneous: Non fasting

Serum (Gold and red cap);

Plasma (lavender cap)

Temperature: + 4ºC

Miscellaneous: Non fasting

≤3 days at 15-30 ºC

≤14 days at 2-8 ºC

>14 days at -20 ºC or colder.

≤3 days at 15-30 ºC

≤14 days at 2-8 ºC

>14 days at -20 ºC or colder.

Source: Abbott IFU

Source: Abbott IFU

Anti-HBc determinations can be used to monitor the progress of hepatitis B viral infection. Anti-HBc is found in serum shortly after the appearance of Hepatitis B Surface Antigen (HBsAg) in acute hepatitis B infections. It will persist after the disappearance of HBsAg and before the appearance of detectable antibody to HBsAg (anti-HBs).

In the absence of information about any other hepatitis B virus (HBV) markers, it must be considered that an individual with detectable levels of anti-HBc may be actively infected with HBV or that the infection may have resolved, leaving the person immune. Anti-HBc may be the only serological marker of hepatitis B viral infection and potentially infectious blood. The presence of anti-HBc does not differentiate between acute or chronic hepatitis B infections.

Preparation of Patient: There is no special physical preparation for the test.

1 working day

1 working day

Specimens with S/CO values < 1.00 are considered Non-reactive (NR).

Specimens with S/CO values >= 1.00 are considered reactive (R).

This is a screening test and reactive samples will be referred to NVRL for confirmatory testing.

Chemiluminescent microparticle immunoassay (CMIA)

Chemiluminescent microparticle immunoassay (CMIA)

Serum (Gold and red cap);

Plasma (lavender cap)

Temperature: + 4ºC

Miscellaneous: Non-fasting

Serum (Gold and red cap);

Plasma (lavender cap)

Temperature: + 4ºC

Miscellaneous: Non fasting

Whole blood ≤ 14 days at 2-8°C.

Separated: >14 days frozen (-20°C or colder)

Whole blood ≤ 14 days at 2-8°C.

Separated: >14 days frozen (-20°C or colder)

Source: Abbott IFU

For further guidance re. immunisation protocols and testing see https://www.hse.ie/eng/health/immunisation/hcpinfo/guidelines/chapter9.pdf

Source: Abbott IFU

For further guidance re. immunisation protocols and testing see https://www.hse.ie/eng/health/immunisation/hcpinfo/guidelines/chapter9.pdf

Anti-HBs is a specific antibody directed against the hepatitis B surface antigen. Anti-HBs can be formed following a Hepatitis B infection or after a Hepatitis B vaccination. This test is used within the scope of hepatitis B vaccination to check the necessity and success of vaccination. Moreover, anti-HBs tests are used to monitor the course of disease following acute hepatitis B infection.

Preparation of Patient: There is no special physical preparation for the test.

1 working day

1 working day

mIU/ml <10 : Non reactive /Non-Immune

If post-vaccination, patient is a nonresponder. Test for Anti-HBc. If anti-HBc negative, give booster dose of the same hepatitis B vaccine. Recheck anti-HBs 2 months later and if anti-HBs remains <10

mIU/ml, give two further doses of the same hepatitis B vaccine (i.e. complete a second course of the same hepatitis B vaccine).

Recheck anti-HBs 2 months later and if anti-HBs remains <10 mIU/ml, person is susceptible to HBV.

≥ 10: Reactive/Immune

Based on the World Health Organisation and NIAC recommendations, an Anti-HBs concentration ≥ 10 mIU/mL is regarded as being protective against Hepatitis B viral infection.

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Abbott Alinity i Chemiluminescent Microparticle Immunoassay (CMIA)

Serum: Serum, Serum separator

Plasma: Lithium heparin

Potassium EDTA

20-25℃: 8hours            

2-8℃: 72 hours              

-20℃: 30 days

Abbott IFU

24 hours

IU/mL

Adults: < 4.11

Abbott Alinity i Chemiluminescent Microparticle Immunoassay (CMIA)

Serum: Serum, Serum separator

Plasma: Lithium heparin

Potassium EDTA

20-25℃: 8 hours              

2-8℃: 72 hours      

-20℃: 30 days

Abbott IFU

24 hours

IU/mL

Adults: < 5.61

Fluoroenzyme immunoassay (Phadia 250)

Serum (Gold and red cap); Plasma (EDTA, Citrate).

Heparin plasma is NOT suitable.

Temperature: + 4ºC

Whole blood: unknown.

Separated: RT unknown.

14 days @ + 4ºC

Phadia IFU

Celiac disease is a life-long condition in which ingestion of gluten, the water insoluble wheat gliadin and the prolamins in rye and barley, leads to chronic inflammation and damage of the small intestinal mucosa. Tissue transglutaminase has been identified as the major autoantigen in celiac disease. IgA antibodies against tTG are highly disease specific serological markers for celiac disease and dermatitis herpetiformis. tTG IgG antibodies are less specific for these diseases but are helpful markers in patients with IgA deficiency.

Preparation of Patient: No special preparation.

4 working days

Negative: less than 7 U/mL

Weak Positive: 7 - 10 U/mL

Positive: greater than 10 U/mL

Fluoroenzyme immunoassay (Phadia 250)

Serum (Gold and red cap); Plasma (green and lavender cap)

Temperature: + 4ºC

Whole blood: unknown.

Separated: RT 1 day.

14 days @ + 4ºC

Source: Phadia IFU

Anti-cardiolipin antibodies (ACA) belong to the group of anti-phospholipid antibodies (aPL). Their occurrence was first demonstrated in sera of syphilis patients, but later they have also been described frequently in SLE (systemic lupus erythematosus) patients (prevalence 30-40%) and in patients with other rheumatic diseases. The antiphospholipid syndrome (APS), also known as “Hughes syndrome”, is characterized by typical clinical features such as arterial/venous thrombosis or recurrent miscarriages together with persistently positive tests for aPL. In contrast to “secondary APS” which occurs in association with SLE or other rheumatic disorders, there is no evidence for another relevant underlying disease in primary APS. New criteria for classification of the antiphospholipid syndrome have been defined recently.

Anti-cardiolipin antibodies in infectious diseases and in APS can be distinguished with respect to their dependence on cofactors: whereas ACA from patients with infectious diseases recognize the pure phospholipid as antigen, binding of ACA from patients with APS requires β2-glycoprotein I as a cofactor. For this reason, ACA ELISAs need β2- glycoprotein I to be incorporated into the assay.

The so-called ‘lupus anticoagulant' (LA) describes a phenomenon that is related to the presence of antiphospholipid antibodies. It is defined by the measurement of antibody dependent coagulation inhibition in vitro. ACA/LA are considered to be of significant diagnostic relevance, as a correlation has been found between these antibodies and a tendency towards thromboses. This results in an increased incidence of venous/arterial thromboses, thrombocytopenia, livido reticularis, habitual abortion and neurological manifestations in ACA/LA-positive patients. Elevated levels of ACA/LA may also be found in patients with cerebrovascular insufficiency or myocardial infarction. aPL are thought to play a direct role in the pathogenesis of APS.

Preparation of Patient: No special preparation.

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4 working days

Negative: < 10.0 GPL-U/mL

Weak positive: 10.0 - 40.0 GPL-U/mL

Positive: > 40.0 GPL-U/mL

Fluoroenzyme immunoassay (Phadia 250)

Serum (Gold and red cap); Plasma (green and lavender cap)

Whole blood: unknown.

Separated: RT 1 day.

14 days @ + 4ºC

Phadia IFU

Anti-cardiolipin antibodies (ACA) belong to the group of anti-phospholipid antibodies (aPL). Their occurrence was first demonstrated in sera of syphilis patients, but later they have also been described frequently in SLE (systemic lupus erythematosus) patients (prevalence 30-40%) and in patients with other rheumatic diseases. The antiphospholipid syndrome (APS), also known as “Hughes syndrome”, is characterized by typical clinical features such as arterial/venous thrombosis or recurrent miscarriages together with persistently positive tests for aPL. In contrast to “secondary APS” which occurs in association with SLE or other rheumatic disorders, there is no evidence for another relevant underlying disease in primary APS. New criteria for classification of the antiphospholipid syndrome have been defined recently.

Anti-cardiolipin antibodies in infectious diseases and in APS can be distinguished with respect to their dependence on cofactors: whereas ACA from patients with infectious diseases recognize the pure phospholipid as antigen, binding of ACA from patients with APS requires β2-glycoprotein I as a cofactor. For this reason, ACA ELISAs need β2- glycoprotein I to be incorporated into the assay.

The so-called ‘lupus anticoagulant' (LA) describes a phenomenon that is related to the presence of antiphospholipid antibodies. It is defined by the measurement of antibody dependent coagulation inhibition in vitro. ACA/LA are considered to be of significant diagnostic relevance, as a correlation has been found between these antibodies and a tendency towards thromboses. This results in an increased incidence of venous/arterial thromboses, thrombocytopenia, livido reticularis, habitual abortion and neurological manifestations in ACA/LA-positive patients. Elevated levels of ACA/LA may also be found in patients with cerebrovascular insufficiency or myocardial infarction. aPL are thought to play a direct role in the pathogenesis of APS.

Preparation of Patient: No special preparation.

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4 working days

Negative: < 10.0 MPL-U/mL

Weak positive: 10.0 - 40.0 MPL-U/mL

Positive: > 40.0 MPL-U/mL

Abbott Alinity. CMIA.

Serum (Gold and red cap); Plasma (green and lavender cap)

Temperature: + 4ºC

Serum/Plasma: RT 22 hours,

2-8ºC 7 days.

>7 days @ -20ºC

Abbott IFU‍

Rheumatoid Arthritis (RA) is a common, systemic autoimmune disease affecting 0.5-1% of the population. It is characterized by chronic inflammation of the synovium, which commonly leads to progressive joint destruction and in most cases, to disability and reduction of quality of life. Evidence gained over the last few years suggests that aggressive therapy given early in the disease has the greatest therapeutic potential.

The serum of RA patients contains a variety of antibodies directed against self-antigens. The most widely known of these autoantibodies is the rheumatoid factor (RF) antibody directed against the constant domain of IgG molecules. The presence of RF is one of the American College of Rheumatology’s criteria for the classification of RA. Although the RF test has good sensitivity for RA, it is not very specific for the disease as it can also be detected in the serum of patients with other rheumatic or inflammatory diseases and even in a substantial percentage of the healthy (elderly) population. For several years it has been recognized that antibodies to anti-perinuclear factor and anti-keratin are highly specific for RA. It was subsequently reported that both of these antibodies reacted with native filaggrin and are now referred to as anti-filaggrin antibodies. More recently it has been shown that all of these antibodies are directed to citrulline-containing epitopes. Citrulline is a nonstandard amino acid, as it is not incorporated into proteins during protein synthesis. It can, however, be generated via post-translational modification of arginine residues by the enzyme peptidyl arginine deiminase. In 1998, Schellekens and colleagues reported that linear peptides containing citrulline (CP) were very specific for RA antibodies (96%) in an ELISA based assay. Subsequent work demonstrated that cyclic variants of these peptides, termed cyclic citrullinated peptides (CCP), were equally specific for RA, but with a higher sensitivity than linear peptides. To improve the sensitivity of the CCP test further, several dedicated libraries of citrulline-containing peptides were screened with RA sera and a new set of peptides (CCP2) were discovered which gave superior performance compared to the CCP1 test. Over the last few years, many independent studies have confirmed the diagnostic performance of the CCP2 test. In 2007, the European League against Rheumatism (EULAR) published guidelines for the diagnosis of early RA, and the measurement of antibodies to anti-CCP was included as a serology marker.

Preparation of Patient: No special preparation.

‍

4 working days

Negative: < 5.0 U/mL

Positive: ≥ 5.0 U/mL

Fluoroenzyme immunoassay (Phadia 250) EliA GliadinDP IgA

‍

Serum (Gold and red cap); Plasma (green and lavender cap)

Temperature: + 4ºC

‍

Whole blood: unknown

Separated: RT unknown,

14 days @ + 4ºC

‍

Phadia IFU

Coeliac disease is a life-long condition in which ingestion of gluten, the water insoluble wheat gliadin and the prolamins in rye and barley, leads to chronic inflammation and damage of the small intestinal mucosa. The disease is multifaceted in nature with clinical presentation ranging from gastrointestinal manifestations to asymptomatic, silent and extraintestinal forms. It is widely accepted that dermatitis herpetiformis, a bullous skin disease, is induced by gluten. The term gluten refers to a whole set of proteins in the socalled endosperm, the nutritive tissue of the grain seed of wheat, rye, oats and barley. The alcohol-soluble polypeptides of gluten, the gliadins, are solely responsible for the toxic effects to the intestinal mucosa. More recent research revealed that gliadin peptides deamidated by tissue transglutaminase represent more specific B-cell epitopes than native peptides.

‍

4 working days

Negative: < 7.0 U/mL

Borderline: 7.0 - 10.0 U/mL

Positive: > 10.0 U/mL

Fluoroenzyme immunoassay (Phadia 250) EliA GliadinDP IgG

‍

Serum (Gold and red cap); Plasma (green and lavender cap)

Temperature: + 4ºC

‍

Whole blood: unknown

Separated: RT unknown,

14 days @ + 4ºC

Phadia IFU

Coeliac disease is a life-long condition in which ingestion of gluten, the water insoluble wheat gliadin and the prolamins in rye and barley, leads to chronic inflammation and damage of the small intestinal mucosa. The disease is multifaceted in nature with clinical presentation ranging from gastrointestinal manifestations to asymptomatic, silent and extraintestinal forms. It is widely accepted that dermatitis herpetiformis, a bullous skin disease, is induced by gluten. The term gluten refers to a whole set of proteins in the socalled endosperm, the nutritive tissue of the grain seed of wheat, rye, oats and barley. The alcohol-soluble polypeptides of gluten, the gliadins, are solely responsible for the toxic effects to the intestinal mucosa. More recent research revealed that gliadin peptides deamidated by tissue transglutaminase represent more specific B-cell epitopes than native peptides.

‍

4 working days

Negative: < 7.0 U/mL

Weak positive: 7.0 - 10.0 U/mL

Positive: > 10.0 U/mL

Fluoroenzyme immunoassay (Phadia 250)

Serum (Gold and red cap); Plasma (green and lavender cap)

Temperature: + 4ºC

Whole blood: unknown.

Separated: RT unknown

14 days @ + 4ºC

Phadia IFU

GBM antibodies occur in patients suffering from Goodpasture syndrome, anti-GBMdisease and ANCA associated vasculitis. Goodpasture syndrome is defined by the combined occurrence of progressive glomerulonephritis, lung haemorrhage and antibodies to the glomerular basement membrane (GBM). A more limited form only involving the kidney or the lung is referred to as anti-GBM disease. For the diagnosis of both, Goodpasture syndrome and anti-GBM-disease, the presence of GBM antibodies is required. Furthermore up to 10 % of ANCA positive patients show GBM antibodies, which indicate a more severe course of renal damage.

‍

4 working days

Negative: < 7.0 U/mL

Weak positive: 7.0 - 10.0 U/mL

Positive: > 10.0 U/mL

Fluoroenzyme immunoassay (Phadia 250)

Serum (Gold and red cap); Plasma (green and lavender cap)

Temperature: + 4ºC

‍

Whole blood: unknown.

Separated: RT 8 hours;

14 Days @ + 4ºC

Phadia IFU

Pernicious anaemia (also known as Biermer’s disease) is an autoimmune atrophic gastritis, predominantly of the fundus, and is responsible for a deficiency in vitamin B12 (cobalamin) due to its malabsorption. Its prevalence is 0.1% in the general population and 1.9% in subjects over the age of 60 years. Pernicious anaemia represents 20%–50% of the causes of vitamin B12 deficiency in adults. Anti intrinsic factor antibodies do not appear to have a clearly defi ned pathogenic role in the development of gastritis. By contrast, they have a well-documented role in the onset of pernicious anaemia, via the vitamin B12 deficiency they induce. The finding of a low total serum cobalamin level may be further evaluated by testing for anti-intrinsic factor antibodies. If positive, the antibodies have a high positive predictive value (95%) for the presence of pernicious anaemia with a concurrent low false positive rate (1–2%) i.e. a high specificity. It identifies those patients with a need for lifelong cobalamin replacement therapy.2 With regard to diagnostic performance sensitivity is low for anti-intrinsic factor antibodies, in the most recent studies while specificity is 100%. In combination with anti-parietal cell antibodies they yield 73% sensitivity and 100% specificity.

Preparation of Patient: No special preparation.

‍

4 working days

Negative: less than 7 U/mL

Equivocal: 7 - 10 U/mL

Positive: greater than 10 U/mL

‍

Fluoroenzyme immunoassay (Phadia 250)

Serum (Gold and red cap); Plasma (green and lavender cap)

Temperature: + 4ºC

‍

Whole blood: unknown.

Separated: RT 8 hours;

14 Days @ + 4ºC; months at - 20 ºC

Phadia IFU

Primary biliary cirrhosis (PBC) is a chronic, cholestatic liver disease which affects mainly middle-aged women. It starts with an inflammatory process of the small and middle-sized interlobular bile ducts leading first to a proliferation and then to a loss of bile ducts, to portal inflammation and in late stages to liver cirrhosis.

PBC occurs all over the world but with varying incidence, ranging from 0.7-49 per million per year. In most recent studies the point prevalence was estimated to range from 6.7 to 402 per million.

Typical clinical features of PBC are fatigue, pruritus and Sicca-syndrome. However, nowadays at diagnosis, the majority of patients are asymptomatic and present for other reasons, e.g. for workup of elevated serum levels of AP or cholesterol. A diagnosis of PBC is made “with confidence” when biochemical markers of cholestasis, particularly alkaline phosphatase, are elevated persistently for more than 6 months in the presence of antibodies against mitochondria and in the absence of an alternative explanation.

PBC-related antibodies against mitochondria react with subunits of the 2-oxoaciddehydrogenase complex (2-OADC) and, in most cases, recognize the E2-subunit of pyruvate dehydrogenase (PDH-E2). Individuals, who are positive for these so-called antiM2 antibodies, even if they have no signs of cholestasis and/or liver inflammation, are very likely to develop PBC.

Anti-M2 antibodies are present in about 95% of PBC-patients.

Preparation of Patient: No special preparation.

4 working days

Negative: < 4.0 IU/mL

Equivocal: 4.0 IU/mL to 6.0 IU/mL

Positive: > 6.0 IU/mL

Chemistry – Fluoroenzyme immunoassay.

Serum (Red and gold cap); Plasma (Green and lavender cap). Lipaemic and haemolysed samples are unsuitable.

Temperature: + 4ºC

Whole blood: unknown

Separated: RT unknown;

14 days @ + 4ºC

Phadia IFU

First described in patients with necrotizing crescentic glomerulonephritis (NCGN) without immune deposits (pauci-immune), the clinical spectrum associated with anti-MPO includes also NCGN associated with systemic vasculitis, either Granulomatosis with polyangiitis (GPA) or a microscopic polyangiitis (MPA). Indeed, anti-MPO are detectable in 65% of patients with idiopathic NCGN, 45% of patients with MPA and 20% to 30% of patients with GPA. Additionally, anti-MPO are present in some 60% of patients with the eosinophilic granulomatosis with polyangiitis (EGPA). Antibodies to PR3 are highly sensitive (81%) and specific (97%) for GPA. The sensitivity is dependent on the phase and on the activity of the disease. Despite the strong association between PR3 antibodies and GPA, there is a small percentage of patients with microscopic polyangiitis and about 30% of EGPA patients who are PR3 antibodies positive. PR3 antibodies may also occur in 20% to 30% of patients with necrotizing glomerulonephritis with no obvious extrarenal manifestations of small vessel vasculitis.

Preparation of Patient: There is no special physical preparation required.

4 working days

Anti-MPO: less than 3.5 IU/mL (<3.5 = negative; 3.5-5.0 = equivocal; >5.0 = positive)

Anti-PR3: less than 2.0 IU/mL (<2.0 = negative; 2.0-3.0 = equivocal; >3.0 = positive)

Fluoroenzyme immunoassay (Phadia 250)

Serum (Gold and red cap); Plasma (green and lavender cap).

Temperature: + 4ºC

Whole blood: unknown

Separated: RT unknown;

14 days @ + 4ºC

Phadia IFU

The determination of antinuclear antibodies (ANA) is of central importance for the clinical diagnosis of connective tissue diseases, which are systemic inflammatory diseases with a chronic course of disease. Connective tissue diseases exhibit overlapping symptomatic features that render an accurate diagnosis difficult.

The Phadia EliA ANA CTD screen wells are coated with human recombinant U1RNP (RNP70, A, C),SS-A/Ro (60 kDa, 52 kDa), SS-B/La, Centromere B, Scl-70, Jo-1, Fibrillarin, RNA Pol III, Rib-P, PM-Scl, PCNA, Mi-2 proteins, Sm proteins and native purified DNA. This ANA screen is more specific than traditional IF ANA methods, which show a high false positive rate.

A positive ANA CTD screen requires the specific quantification of the antibodies listed above: ds-DNA and the individual anti-extractable nuclear antigen (ENA) antibodies.

For the diagnosis of systemic lupus erythematosus (SLE), dsDNA antibodies are considered to be a highly specific marker representing one of the diagnostic criteria for SLE (ACR criteria). More than 90 % of sera from patients with active SLE contain dsDNA antibodies. Additionally, the determination of dsDNA antibodies is a tool to monitor the clinical course of a defined SLE patient, because a clear-cut relationship exists between anti-dsDNA titre and disease activity, in particular renal involvement. Sm antibodies offer a highly specific, but comparatively insensitive, clinical marker for SLE. Indeed, their presence constitutes one of the revised ACR criteria for diagnosis, even though their overall prevalence ranges from 20 % to 30 % in SLE. U1-snRNP antibodies typically appear in both SLE and mixed connective tissue disease (MCTD, Sharp Syndrome).

In MCTD, the presence of U1-snRNP antibodies is required for diagnosis, whereas they occur in only 30 to 40 % of SLE patients. Detection of SS-A/Ro antibodies is of interest and significance for the clinical diagnosis of SLE (prevalence 40-50%) and Sjögren's syndrome (prevalence 60-75% for primary Sjögren's syndrome). They have been reported to occur in tight association with certain disease subsets, such as subacute cutaneous LE, neonatal lupus erythematosus or vasculitis in Sjögren's syndrome. As anti-SS-A/Ro may be the only antibody present in many patients with SLE or Sjögren's syndrome, failure to measure antiSS-A/Ro leaves a diagnostic void which cannot be filled by other tests. SS-B/La antibodies are the serological hallmark of Sjögren's syndrome but a small proportion of patients remains anti-SS-B/La negative. La antibodies are found in 6-15 % of sera from SLE patients. Here, they are associated with a lower prevalence of dsDNA antibodies and renal disease.

Although a strong association of neonatal lupus erythematosus (NLE) with Ro antibodies was recognized first, the majority of mothers with babies with NLE are now known to have La antibodies as well.

CENP antibodies are found in 70-90 % of patients with CREST Syndrome, a limited form of scleroderma with a comparatively favourable prognosis. However, they may also occur in Raynaud's phenomenon and primary biliary cirrhosis (about 10-20 %).

Antibodies against Scl-70 are characteristic and specific for scleroderma (particularly the diffuse form; frequency up to 70%). Jo-1 antibodies can be found as markers in dermatomyositis/polymyositis (prevalence of about 25%), but also in patients with polymyositis overlap syndrome. They are associated with interstitial pneumonitis (in the context of myositis) and occur in a far smaller proportion of children with myositis than of adults. Patients with Jo-1 antibodies tend to have a severe form of the disease with a tendency to relapse and a poorer prognosis. Fibrillarin antibodies produce a nucleolar pattern in immunofluorescence. They occur in less than 15% of patients with scleroderma and seem to be associated with internal organ involvement including pulmonary hypertension, myositis, and renal disease. The presence of fibrillarin antibodies in diseases other than scleroderma and their clinical relevance requires further investigation. RNA polymerase III antibodies are highly specific for scleroderma and are here more frequent in patients with diffuse cutaneous scleroderma than in those with limited cutaneous scleroderma. Among patients with diffuse cutaneous involvement, RNA polymerase III antibody was the most common antibody detected (35-45%).

Antibodies against Ribosomal P proteins react with the specific ribosomal proteins (P0, P1 and P2). These autoantibodies occur in SLE during active disease and are associated with neuropsychiatric, renal and hepatic involvement. They are found in 23% of SLE patients.

Autoantibodies to the polymyositis/scleroderma (PM-Scl) complex were the first antinucleolar antibodies identified in systemic sclerosis. Anti-PM-Scl are associated with a specific form of scleroderma; indeed, only 2% of the patient population with scleroderma, but 24% of the patients with myositis-scleroderma overlap syndrome produce these antibodies. They correlate with a benign course of disease and a positive response to steroid therapy. Antibodies against PCNA (proliferating cell nuclear antigen) occur in 2 to 10% of SLE patients but seem to be not very specific for SLE as it was found in 12.3% of hepatitis B and 18.7% of hepatitis C patients, respectively.

Autoantibodies targeting the Mi-2 nuclear antigen represent one of the serologic hallmarks of polymyositis/dermatomyositis, with a diagnostic sensitivity and specificity of approximately 4-18% and 98-100%, respectively. They are strongly associated with dermatomyositis with a frequency of up to 31%.

‍

Preparation of Patient: No special preparation.

‍

Reflex testing: The Phadia EliA ANA CTD wells are coated with human recombinant U1RNP (RNP70, A, C),SS-A/Ro (60 kDa, 52 kDa), SS-B/La, Centromere B, Scl-70, Jo-1, Fibrillarin, RNA Pol III, Rib-P, PM-Scl, PCNA, Mi-2 proteins, Sm proteins and native purified DNA. A positive ANA CTD screen will lead to analysis of specific ds-DNA antibodies and ENA antibody typing.

‍

4 working days

ANA: ratio less than 0.7

ds-DNA: less than 10 IU/mL

Anti-Sm, anti-SSA/RO, anti-SSB/La, anti-Scl-70, anti-Jo-1 and anti-centromere Antibodies: each less than 7 EliA U/mL.

Anti-U1 RNP: less than 5 EliA U/mL.

Fluoroenzyme immunoassay (Phadia 250)

Serum (Gold and red cap); Plasma (green and lavender cap)

Temperature: + 4ºC

Whole blood: unknown.

Separated: RT 8 hours;

14 Days @ + 4ºC

Phadia IFU

Pernicious anaemia (also known as Biermer’s disease) is an autoimmune atrophic gastritis, predominantly of the fundus, and is responsible for a deficiency in vitamin B12 (cobalamin) due to its malabsorption. Its prevalence is 0.1% in the general population and 1.9% in subjects over the age of 60 years. Pernicious anaemia represents 20%–50% of the causes of vitamin B12 deficiency in adults. Parietal cell antibodies are found in about 90% of Caucasian patients with pernicious anaemia. In the later stages of the disease, the incidence of these antibodies decreases due to the progression of autoimmune gastritis and a loss of parietal cell mass, as a result of the decrease in antigenic rate. In recent studies, an average incidence of 55% of anti-parietal cell antibodies was documented in patients with advanced pernicious anaemia. Parietal cell antibodies are present in 7.8–19.5% of the general healthy adult population. A not fully explained question is whether parietal cell antibodies presence is related to Helicobacter pylori infection. Anti-parietal cell antibodies are found in up to 20.7% of these patients.

Preparation of Patient: No special preparation.

4 working days

Negative: less than 7 U/mL

Equivocal: 7 - 10 U/mL

Positive: greater than 10 U/mL

Turbidimetric/Immunoturbidimetric

Serum (Gold and red cap).

Temperature: + 4ºC

Miscellaneous: Non fasting

Serum

‍≤2 days at 2-8 ºC

> 2 days -20 ºC

Source: Abbott IFU

The group A β-haemolytic streptococci produce various toxins that can act as antigens. One of these exotoxins is streptolysin-O. The affected organism produces specific antibodies against these exotoxins, among which concentration of Anti-Streptolysin-O in the patient’s serum will enable to establish the degree of infection due to the β-haemolytic streptococcus.

A positive test can indicate recent or current group A, C, and G streptococcal infection (e.g., upper airway infections, scarlet fever, toxic shock syndrome) and may support the diagnosis of post-streptococcal infection complication (e.g., glomerulonephritis and rheumatic fever).

The test is positive in only 80-85% of group A streptococcal infections, so a negative test does not necessarily exclude the diagnosis.

Preparation of Patient: There is no special physical preparation for this test.

1 working day

Up to 7 years: less than 100 IU/mL

Greater than 7 years: less than 200 IU/mL

Abbott Alinity c Spectrophotometry

Serum:

Serum Separator

Plasma:

Lithium heparin

Lithium heparin separator

Sodium heparin

20-25℃: 4 days                

2-8℃: 7 days        

-20℃: 3 months

Abbott IFU

24 hours

U/L

Adults: 11- 34

Abbott Alinity c Enzymatic Immunoassay

Urine Clean plastic or glass container

2-8℃: 5 days        

-20℃: longer

Abbott IFU

24 hours

ng/mL

Positivity Cut-off: 200

Abbott Alinity c Enzymatic Immunoassay

Urine Clean plastic or glass container

2-8℃: 5 days        

-20℃: longer

Abbott IFU

24 hours

ng/mL

Positivity Cut-off: 200

Abbott Alinity c Turbidimetric/ Immunoturbidimetry

Plasma Collection tubes Acceptable anticoagulants are: EDTA Sodium heparin

20-25℃: 7 days                

2-8℃: 7 days      

-20℃: 1 year

Abbott IFU

24 hours

mg/L

Adults: 0.97 - 2.64

Abbott Alinity c Cyclic-enzymatic/ colorimetric

Serum Plastic tubes (with or without gel barrier)

20-25°C: 1 day

2-8°C: 7 days

Abbott IFU

24 hours

µmol/L

Adult: 1.0 - 6.0

Pregnancy: 1.3 - 9.0

Abbott Alinity c Spectrophotometry, Diazo-Reaction

Serum:

Serum tubes (with or without gel barrier)

Plasma: Acceptable anticoagulants are:

Lithium heparin (with or without gel barrier)

Sodium heparin

EDTA

‍

20-25℃: 2 days              

2-8℃: 7 days        

-20℃: 3 months

Abbott IFU

24 hours

µmol/L

Adult: 0.0 - 8.6

Abbott Alinity c Spectrophotometry, Diazonium salt

Serum Plastic tubes (with or without gel barrier)

20-25°C:8 hours

2-8°C: 7 days

-20°C: 3 months

Abbott IFU

24 Hours

µmol/L

Adult: 1.0 - 6.0

Pregnancy: 1.3 - 9.0

CALCULATION based on Abbott Alinity methodologies for Total Bilirubin and Direct Bilirubin

Serum:

Serum tubes (with or without gel barrier)

Plasma: Acceptable anticoagulants are:

Lithium heparin, Sodium heparin, EDTA

20-25℃: 8hours                

2-8℃: 7 days            

-20℃: 3months

Abbott IFU

24 hours

Adult: 3.0 - 12.0

Haematology – Thick & Thin Blood film & CareStart Malaria Rapydtest antigen kit (Kit Insert:

APACOR CareStart RAPYDTEST- APA059 V7 04/2017)

Whole Blood K2/K3 EDTA (Lavender cap)

Temperature: + 2-8ºC

Miscellaneous: Observe periodicity where applicable.

‍

Blood films Thick & thin need to be made less than 2 hours after the blood EDTA was drawn.

WHO Guideline: ‘The Laboratory Diagnosis of Malaria’. J.W Bailey, B.J Bain, J Parker-Williams and P.Chiodini for the General Haematology Task Force of the British Committee for Standards in Haematology. http://www.bcshguides.com/documents/malaria-bcsh.2005.pdf

Malaria Reference Laboratory. www.malaria-reference.co.uk

‍

Malaria is caused by a group of related intracellular protozoan pathogens of the genus Plasmodium. These species exhibit a complex life cycle reliant on a mammalian host and anopheles mosquito vector. In the human host they are obligate intracellular pathogens infecting initially the liver in the sporozoite form. In the liver the parasites replicate and develop into merozoites which are then released into the blood stream. These infect the erythrocyte and begin a restricted life cycle. Each parasite may develop into a schizont (a cluster of infectious units which may invade further erythrocytes) or a gametocyte (the sexual form which may be transferred to the anopheles mosquito upon taking a blood meal). Re-infection of the liver does not occur. Suspected malaria is a medical emergency. Sampling and processing of the blood sample must not be delayed if malaria is suspected. Five primary species of malaria have been identified in humans: P.falcparum, P.vivax, P.ovale P.malariae and P.knowlesi. Their geographic distribution is unique for each species. Blood should ideally be taken direct from the patient’s finger or ear & the films prepared at the bedside or in the clinic. When this is not possible blood taken into anticoagulant (EDTA) can be used. Thick & thin blood films should be made as soon as possible, certainly less than 2 hours after the EDTA blood was drawn, to minimise morphological changes in the parasites. Parasite and red cell morphology can be seriously affected if the blood has been in anticoagulation for too long. Where there is a strong clinical suspicion if the first films are negative, blood should be taken and films made and checked at least two times over the first 24 hours and further films examined every 12 hours after that if strongly clinically indicated.

24 Hours Mon - Fri

% parasitaemia (applicable to P. falciparum & P. knowlesi infection)

No reference ranges applicable. Genus and species reportable.

Abbott Alinity i Chemiluminescent Microparticle Immunoassay (CMIA)

Serum:

Serum, Serum separator.

Plasma:

Potassium EDTA, Lithium heparin, Sodium heparin, Ammonium heparin

20-25℃: 24 hrs                

2-8℃: 48 hrs        

-20℃: 3 months

Abbott IFU

24 hours

ug/L

Adult (fasting, 12hours): 0.80-5.20

Adult (postprandial): 2.0 - 9.0

Abbott Alinity c, Turbidimetric/ Immunturbidimetric

Serum:

Serum tubes (with or without gel barrier)

Plasma: Acceptable anticoagulants are:

Lithium heparin (with or without gel barrier)

Sodium heparin

EDTA

20-25℃: 15 days                

2-8℃: 2 months                

-20℃: 1 year

Pearson TA et al, Circulation 2003; 107:499-511

24 hours

mg/L

Adult: < 5.0

Lowest relative CVD risk: < 1.0

Average relative CVD risk: 1.0 - 3.0

Highest relative CVD risk: > 3.0

Abbott Alinity i Chemiluminescent Microparticle Immunoassay (CMIA)

Serum:

Serum, Serum separator.

Plasma:

Tripotassium EDTA, Sodium Heparin,

Lithium Heparin

2-8℃: 7 days        

-20℃: longer

Abbott IFU

24 Hours

U/mL

Adult: < 35

Abbott Alinity i Chemiluminescent Microparticle Immunoassay (CMIA)

Serum:

Serum, Serum separator.

Plasma:

Tripotassium EDTA, Sodium Heparin,

Lithium Heparin

2-8℃: 7 days        

-20℃: longer

Abbott IFU

24 hours

U/mL

Adult: < 31.3

Abbott Alinity i Chemiluminescent Microparticle Immunoassay (CMIA)

Serum:

Serum, Serum separator.

Plasma:

Tripotassium EDTA, Sodium Heparin,

Lithium Heparin

2-8℃: 7 days        

-20℃: longer

Abbott IFU

24 hours

U/mL

Adult: <37

Abbott Alinity c Spectrophotometry, Arsenazo III

Serum :

Serum tubes (with or without gel barriers)

Plasma: Acceptable anticoagulants:

Lithium heparin, Sodium heparin

20-25°C: 7 days

2-8°C: 3 weeks

-20°C: 8months

Abbott IFU

24 Hours

mmol/L

Adult: 2.1 - 2.55

CALCULATION based on Abbott Alinity methodologies for Calcium and Albumin. FORMULA:

Serum:

Serum tubes (with or without gel barriers)

Plasma: Acceptable anticoagulants:

Lithium heparin, Sodium heparin

20-25℃: 7 days                

2-8℃: 3 weeks              

-20℃: 8 months

Abbott IFU

24 hours

mmol/L

Adult: 2.1 - 2.55

Abbott Alinity c Spectrophotometry, Arsenazo III

Spot Urine

or

Timed Specimen (24hours)

20-25℃: 2 days                

2-8℃: 4 days        

-20℃: 3 weeks

Abbott IFU

24 hours

mmol/L

mmol/24hr

Adult Male: 0.23 to 9.47

Adult Female: 0.13 to 8.92

Calcium free: 0.13 to 1.00

Low to average: 1.25 to 3.75

Average (20 mmol/day): 2.5 to 7.5

Fluoroenzyme immunoassay on Phadia 250 - Phadia EliA 2nd Generation

At least 20g stool sample.

Temperature: + 4ºC or room temp or frozen

Stool: 8 days RT or at 2°C to 8°C.

The stool extract can be stored at room temperature for a max 3 days, at +4℃ for 7 days and at <=20℃ for 3 months.

1. Phadia Calprotectin 2 IFU
2. “EliA Calprotectin Assay Background Technical & Clinical 15.11.2012”, presentation from ThermoFisher.
3. NICE guideline DG11.

Calprotectin is a calcium- and zinc-binding protein which is predominantly present in the cytoplasm of cells involved in pathogen defence, such as neutrophil granulocytes, monocytes and macrophages. In neutrophil granulocytes it accounts for as much as 60% of the cytosolic protein. In intestinal inflammation neutrophil granulocytes migrate through the intestinal wall into the intestinal lumen, which leads to an elevated calprotectin level in the stool. The level of faecal calprotectin correlates directly with the number of neutrophil granulocytes in the intestinal lumen and is thus specifically elevated in inflammatory bowel diseases (IBD), such as Crohn's disease and ulcerative colitis, and to a much smaller extent in other entities such as neoplasia and polyps. Faecal calprotectin measurement is an easy, non-invasive first line test which clearly differentiates IBD from IBS (irritable bowel syndrome) and other functional disorders. It has been shown to be the most sensitive and most specific test for this discrimination; clearly outperforming blood tests such as CRP or ESR. Faecal calprotectin correlates with disease activity and is able to predict relapses in IBD. This makes faecal calprotectin useful for both diagnosis and monitoring of IBD patients.

‍

2 weeks maximum (batched).

<50 ug/g: Negative. Calprotectin level not suggestive of organic pathology.

50-100 ug/g: Gray Zone. Organic pathology cannot be excluded. A repeat sample in 4 to 6 weeks is suggested.

>100 ug/g: Positive. Calprotectin level is consistent with organic pathology.

‍

Abbott Alinity c Enzymatic Immunoassay

Urine Clean plastic or glass container

2-8℃: 5 days      

-20℃: longer

Abbott IFU

24 hours

ng/mL

Positivity Cut-off: 50

Abbott Alinity c Spectrophotometry, PEP Carboxylase

Serum :

Serum tubes (with or without gel barrier)

20-25°C: 2 hours

2-8°C: 2 days

Abbott IFU

24 Hours

mmol/L

Adult: 22 to 29 > 60 years 23 to 31

Abbott Alinity i Chemiluminescent Microparticle Immunoassay (CMIA)

Serum:

Serum, Serum separator.

Plasma:

Sodium heparin, Lithium heparin,

Potassium EDTA

2-8℃: 7 days        

-20℃: longer

Abbott IFU

24 hours

ng/mL

Adult: <5

Abbott Alinity c Turbidimetric/ Immunturbidimetric

Serum:

Serum tubes

Plasma: Acceptable anticoagulants are:

Lithium heparin

EDTA

20-25℃: 8 days            

2-8℃: 2 weeks      

-20℃: 3 months

Abbott IFU

24 hours

g/L

Adult: 0.2 to 0.6 g/L

The cobas® 4800 CT/NG Test is an in vitro nucleic acid amplification test for the qualitative detection of Chlamydia trachomatis (CT) and/or Neisseria gonorrhoeae (NG) in patient specimens. The test allows for detection of CT/NG DNA in endocervical and vaginal swab specimens, and male and female urine in cobas® PCR Media. The intended targets for the cobas® 4800 CT/NG Test include all fifteen major Chlamydia trachomatis serovars, the Swedish C. trachomatis mutant (nvCT), and both wild-type and variant DR-9 sequences of N. gonorrhoeae.

Urine or urine in cobas PCR Urine Media (cobas® PCR Urine Sample Kit).

Endocervical or Vaginal swabs in cobas PCR Media (cobas® Media Dual Swab Kit).

Urine specimens should be transferred into the cobas PCR media tube as soon as possible. If specimens cannot be transferred immediately, they can be stored at 2-30℃ for up to 24 hours. Stabilised urine specimens are stable at 2-30o℃for up to 12 months.

Swabs collected with the cobas PCR Media Swab Kit may be stored at 2-30℃ for up to 12 months.

Chlamydia trachomatis (CT) is the second most leading cause of sexually transmitted diseases worldwide, with approximately 89.1 million cases occurring annually worldwide. CT is the causative infectious agent for a variety of diseases in men, including urethritis, proctitis, conjunctivitis and epididymitis. In women, the consequences of infection with CT are severe if left untreated. Infection can lead to endometriosis, salpingitis (with subsequent infertility and ectopic pregnancy) and perihepatitis. Additionally, infants from infected mothers can develop conjunctivitis, pharyngitis, and pneumonia.

Neisseria gonorrhoeae (NG) is the causative agent of gonorrhoeae. Acute urethritis is seen in the majority of men with gonorrhoeae, and acute epididymitis is the most common complication, particularly in young men. In women, the primary site of infection is the endocervix, there’s a high prevalence of coinfections with CT, Trichomonas vaginalis, and bacterial vaginosis. Many women remain asymptomatic; when symptoms do occur, the most common are increased discharge, dysuria, and intermenstrual bleeding. Additionally, NG may cause pelvic inflammatory disease, endometriosis, tubo ovarian abscess, and pelvic peritonitis.

Preparation of patient: Prior to the collection of urine, the patient should not have urinated for at least one hour. For best results, female patients should not cleanse the labial area prior to collection.

There is no physical preparation for the vaginal swab.

Precautions: None for patient. Media contains Guanidine Thiocyanate, adequate PPE for the person taking the sample.

Note: Chlamydia trachomatis and Neisseria Gonorrhoeae are notifiable diseases under the Infectious Diseases (Amendment) Regulations 2020 (S.I. No. 53/2020).

4 working days from sample receipt

CT and/or NG Detected

Not Detected

Invalid

Abbott Alinity c Indirect ISE

Serum:

Serum tubes (with or without gel barrier)

For Potassium, hemolyzed specimens must not be used.

Plasma: Acceptable anticoagulants are:

Lithium heparin (with or without gel barrier)

Sodium heparin

20-25℃: 7 days                

2-8℃: 7 days        

-20℃: 1 year

Abbott IFU

24 Hours

mmol/L

Adult: 98 - 107

Abbott Alinity c Indirect ISE

Urine (timed, 24- hour) Without preservatives

OR

Spot urine (random)

20-25℃: 7 days                

2-8℃: 7 days        

-20℃: 7 days

AbbottIFU

24 Hours

Timed:

mmol/ 24hr

‍

Random:

mmol/L

Timed:

Adult <60 years: 110 - 250

Adult >60 years: 95 - 195

‍

Random:

No reference range available

Abbott Alinity c, Selective resolution of LDL-Particles under dye formation

Serum :

Serum tubes (with or without gel barrier)

Plasma: Acceptable anticoagulants are:

Lithium heparin, Sodium heparin, EDTA Anticoagulants containing citrate should not be used.

2-8℃: 5 days        

-80℃: 3 months

Source: ESC/EAS Guidelines for the management of dyslipidaemias. http://www.eassociety.org/guidelines-2.aspx

24 Hours

mmol/L

0.0 – 3.0

Abbott Alinity c Enzymatic

Serum: Serum separator

Plasma Lithium heparin

Lithium heparin separator

Sodium heparin

‍

20-25℃: 7 days                

2-8℃: 7 days        

-20℃: 3 months

Source: ESC/EAS Guidelines for the management of dyslipidaemias. http://www.eassociety.org/guidelines-2.aspx

24 hours

mmol/L

Adult: < 5.0

Abbott Alinity c, Accelerated enzymatic Reaction/selective solvent

Serum :

Serum tubes (with or without gel barrier)

Plasma Collection tubes Acceptable anticoagulants are:

Lithium heparin, Sodium heparin, EDTA

20-25℃: 7 days                

2-8℃: 7 days      

-20℃: 1 year

National Cholesterol Education Program (NCEP) Adult Treatment Panel III Report and European Guidelines http://www.eassociety.org/guidelines-2.aspx

24 Hours

mmol/L

Adult: >1.0

Abbott Alinity c, Enzyme immunoassay

Urine Clean plastic or glass container

2-8℃: 5 days          

-20℃: longer

Abbott IFU

24 hours

ng/mL

Positivity Cut-off: 300

Abbott Alinity c Immunoturbidimetry

Serum: Serum tubes (with or without gel barrier)

Plasma - Acceptable anticoagulants are: Lithium heparin (with or without gel barrier) Sodium heparin

2-8℃: 3 days        

-20℃: 8 days

Abbott IFU

24 hours

g/L

Adult Male 14 - 80 years: 0.82 - 1.85

Adult Female 14 - 80 years: 0.83 - 1.93

Abbott Alinity c Immunoturbidimetry

Serum:

Serum tubes (with or without gel barrier)

Plasma: Acceptable anticoagulants are:

Lithium heparin (with or without gel barrier)

Sodium heparin

EDTA

2-8℃: 2 days        

-20℃: 2 days

Abbott IFU

24 hours

g/L

Adult Male 14 - 80 years: 0.15 - 0.53

Adult Female 14 - 80 years: 0.15 - 0.57

Abbott Alinity i Chemiluminescent Microparticle Immunoassay (CMIA)

Serum:

Serum, Serum separator.

Plasma: Lithium Heparin, Sodium Heparin,

Potassium EDTA

Plasma separator tubes with Lithium Heparin.

2-8℃: 14 days                

-20℃: 30 days

Blood: Handbook of Diagnostic Endocrinology, 2nd Edition, 2008. William E Winter & al. AACC Press

24 hours

nmol/L

Morning 08:00H: 171 - 800

Afternoon: Approx. half the morning values

In the evaluation of Adrenal

Highly Unlikely: >550

Virtually Diagnostic <138

Evening 24H00:

Virtually excludes: <138

Highly suggestive: <207

Abbott Alinity i Chemiluminescent Microparticle Immunoassay (CMIA)

Urine: The urine sample must be collected in a clean, previously unused container.

Preservatives are not required; however, ten grams of boric acid per liter of urine may be used.

2-8℃: 14 days                  

-20℃: 30 days

Abbott IFU

24 hours

nmol/24hr

Adult: 12 - 486

Abbott Alinity c, NAC (N-Acetyl-L-Cystein)

Serum:

Serum tubes (with or without gel barrier)

Plasma: Acceptable anticoagulants:

Lithium heparin

20-25℃: 2 days                

2-8℃: 7 days

Abbott IFU

24 Hours

U/L

Adult Male: 30 - 200

Adult Female: 29 - 168

Abbott Alinity c, Enzymatic

Serum:

Serum tubes (with or without gel barrier)

Plasma: Acceptable anticoagulants are:

Lithium heparin

20-25℃: 7 days                

2-8℃: 7 days        

-20℃: 3 months

Abbott IFU

24 hours

µmol/L

Adult Male: 64 - 104

Adult Female: 49 - 90

Abbott Alinity c, Enzymatic

Urine -Timed specimens collected over intervals shorter than 24 hours

OR

Urine (random/spot specimens) Clean plastic or glass container without preservatives

‍

20-25℃: 2 days            

2-8℃: 6 days        

-20℃: 6 months

Abbott IFU

24 hours

Urine Timed:

mmol/ 24hr

Urine Random:

g/L

Adult Male: 7.7 - 21.3

Adult Female: 5.9 - 14.1

Adult Male: 5.1 - 14.2

Adult Female: 3.9 - 9.4

Cytology Processing. Diagnosis.

• An adequately completed test request form must accompany the specimen.
• Fluid should be freshly collected and placed into:
  • a container with an equal volume of CytoRich Red Collection Fluid, or The specimen container(s) must be adequately labelled.
  • an empty sterile container and kept refrigerated

• Up to 20mls of the fluid is an adequate volume for testing.
• The aspirated material should be spread onto a glass slides and air dried or fixed (fixative available from the lab)
• If a needle rinse is available, it should be collected into a container with CytoRich Red Collection Fluid.
• All slides must be labelled with patient name and date of birth written using pencil on the frosted end of the slide.

If transport of the specimen will be delayed for more than 24 hours, the cytofix should be added at collection. The specimen is stable for 48 hours if stored at 4 degrees .

A range of fluid types can be collected from the body including urine, cyst fluid, pleural fluid, and ascetic fluid.

Cytology specimens can be sent to the laboratory in conjunction with a histopathology specimen or in isolation. Collecting a cytology specimen can be less invasive than sampling for a histopathology specimen, but there are associated limits in the diagnostic value of a cytology specimen.

Fine needle aspiration of mass lesions is commonly utilized in the detection and characterization of a variety of malignant diseases. Obtaining an adequate specimen requires attention to good aspiration technique as well as processing of material obtained. It is highly desirable that several direct smears are prepared (preferably air-dried) for all fine needle aspiration specimens submitted to the laboratory.

10 working days

Chemiluminescent microparticle immunoassay (CMIA)

Chemiluminescent microparticle immunoassay (CMIA)

Serum (Gold and red cap);

Plasma (green and lavender cap)

Temperature: + 4ºC

Miscellaneous: Non fasting

Serum (Gold and red cap);

Plasma (green and lavender cap)

Temperature: + 4ºC

Miscellaneous: Non fasting

Whole blood: RT unknown; ≤14 days 2-8ºC

Separated: RT unknown; ≥14 days -10°C or colder

Whole blood: RT unknown; ≤14 days 2-8ºC

Separated: RT unknown; ≥14 days -10°C or colder

Source: Abbott IFU

Source: Abbott IFU

Infections with CMV (a member of the herpes virus family) are very common and usually mild and asymptomatic. In immunocompromised patients, however, infections can be severe and sometimes fatal. Also, in utero infection of the

foetus can lead to birth defects. If the CMV IgG is positive, CMV IgM is measured to determine if the infection is current or recent.

Preparation of Patient: There is no special physical preparation for these tests.

3 working days

3 working days

CMV IgG:

≥6.0 AU/mL are considered reactive (POSITIVE)

Less than 6.0 AU/mL are nonreactive (NEGATIVE)

CMV IgM:

Index <0.85 are considered nonreactive (NEGATIVE)

Index 0.85 to 0.99: GRAYZONE, Repeat in 7 to 14 days

Index greater than or equal to 1.00: reactive (POSITIVE)

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Stago Compact Max

‍

Sodium Citrate 3.2%,

Temperature: 15-25°C (Do not refrigerate or freeze)

Miscellaneous: N/A

8 hours @ 15-25°C

Konstantinides SV, Meyer G, Becattini C, Bueno H, Geersing GJ, Harjola VP, Huisman MV, Humbert M, Jennings CS, Jiménez D, Kucher N, Lang IM, Lankeit M, Lorusso R, Mazzolai L, Meneveau N, Áinle FN, Prandoni P, Pruszczyk P, Righini M, Torbicki A, Van Belle E, Zamorano JL; The Task Force for the diagnosis and management of acute pulmonary embolism of the European Society of Cardiology (ESC). 2019 ESC Guidelines for the diagnosis and management of acute pulmonary embolism developed in collaboration with the European Respiratory Society (ERS): The Task Force for the diagnosis and management of acute pulmonary embolism of the European Society of Cardiology (ESC). Eur Respir J. 2019 Oct 9;54(3):1901647. doi: 10.1183/13993003.01647-2019. PMID: 31473594.

D-dimer is a degradation product of cross-linked fibrin. The D-dimer concentration is a measure of the fibrinolytic activity of plasmin in the vascular system. Elevated concentrations of D-dimer indicate increased coagulatory and fibrinolytic activity. With a normal D-dimer value, acute deep vein thrombosis and pulmonary embolisms may be ruled out with high reliability.

Preparation of patients: There is no physical preparation for the D-Dimer test.

Precautions: No modifications to change diet, medications, or activity required before this test. Phlebotomists should enquire about any blood thinners or anticoagulant medication any diseases like liver disease and rheumatoid arthritis. There are some herbs that are also able to replicate the effects of blood thinning medication.

SAME DAY

0.0-0.50 µg/mL

Abbott Alinity i Chemiluminescent Microparticle Immunoassay (CMIA)

Serum: Serum, Serum separator.

Plasma: Potassium EDTA,

Sodium citrate

Sodium heparin

2-8℃: 8 days        

-20℃: longer

Abbott IFU

24 hours

µmol/L

Male: 19Y 1.2 -10.4

Male: 24Y 6.5 -14.6

Male: 34Y 4.6 -16.1

Male: 44Y 3.8 -13.1

Male: 54Y 3.7 -12.1

Male: 64Y 1.3 -9.8

Male: >64 6.2 -7.7

Female: 19Y 1.7 -13.4

Female: 24Y 3.6 -11.1

Female: 34Y 2.6 -13.9

Female: 44Y 2 -11.1

Female: 54Y 1.5 -7.7

Female: 64Y 0.8 -4.9

Female: >64 0.9 -2.1

Abbott Alinity c, Particle-enhanced turbidimetric inhibition immunoassay (PETINIA)

Serum :

Serum tubes (with or without gel barrier)

Plasma: Acceptable anticoagulants are:

Lithium heparin

Sodium heparin

Potassium EDTA

Heparin gel plasma separator

2-8℃: 48 hours              

-20℃: 7 days

Therapeutic range for digoxin as recommended by European Society of Cardiology Guidelines for the diagnosis and treatment of acute and chronic heart failure.

European Heart Journal (2008) 29, 2388 - 2442.)

24 hours

ug/L

0.6 – 1.2

>2 associated with toxicity

Abbott Alinity c Immunalysis assay

Urine Clean plastic or glass container

20-25℃: 7 days            

2-8℃: 2months      

-20℃: >2months

Immunalysis EDDP IFU

24 Hours

g/ml

Positivity Cut-off: 100

CALCULATION based on Creatinine methodology and patient demographics.

Serum Serum tubes (with or without gel barrier)

Plasma -Acceptable anticoagulants are: Lithium heparin (with or without gel barrier) Sodium heparin EDTA is not recommended.

20-25℃: 7 days            

2-8℃: 7 days        

-20℃: 3 months

https://kdigo.org/

24 hours

Adults:

> 90: Normal

60 - 89: Normal or Stage 2 CKD

30 - 59: Moderate

‍

Abbott Alinity c, Enzyme immunoassay

Urine Clean plastic or glass container

2-8℃: 5 days        

-20℃: longer

Abbott IFU

24 Hours

ng/mL

Positivity Cut-off: 500

Haematology – Capillary photometric-kinetic technology

Whole Blood K2/K3 EDTA anticoagulated.

2 days @ + 2-8ºC

‍

‍

Reference ranges for the ESR assay are derived in house. Data was obtained from a clinical normal population and statistics generated using the Graph Pad statistics module. Data was analysed for Gaussian distribution and reference ranges derived using either parametric or non-parametric statistics. A copy of the data is kept in the QA department.

The Erythrocyte Sedimentation Rate (ESR) is a traditional test used in Haematology. It is affected by the numbers of erythrocytes present in the blood, changes in plasma protein pattern, age and sex of the patient. Three phases can be distinguished in the sedimentation process: the lag phase (reflects the period in which the individual erythrocytes form rouleaux), the decantation or precipitation phase (the plasma-red cell interface falls more rapidly), and the final packing phase (the red cells aggregates pile up on the bottom of container). The ESR is dependent on the presence of agglomers, such as fibrinogen, IgM, alpha2-macroglobulin and other acute phase proteins. It is a completely non-specific test. It is a measure of the presence and severity of pathological processes. In general, the ESR is elevated in all acute, general infections, in localized, acute, inflammatory conditions, variations in the ESR depend on the nature and severity of the process.  Additionally, the ESR is an important screen for occult disease. The ESR is also useful to differentiate organic disease from functional disorders, or as a guide to the progress of diseases such as rheumatic carditis, rheumatoid arthritis, and certain malignancies, including Hodgkin's disease, and is diagnostic for Temporal Arteritis.

Preparation of patients: There is no physical preparation for the ESR test.

Precautions: The ESR should not be used to screen healthy persons for disease.

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24 Hours

Abbott Alinity i Chemiluminescent Microparticle Immunoassay (CMIA)

Serum: Serum, Serum separator Plasma: Lithium heparin, Plasma separator, Potassium EDTA

2-8℃: 7 days        

-20℃: longer

Abbott IFU

24 Hours

pmol/L

Follicular phase: 77 – 922

Mid Cycle phase: 140 – 2383

Luteal phase: 77 – 1145

Postmeno pausal no HRT: < 103

Postmeno pausal on HRT: < 529

Male: 40 – 161

Abbott Alinity c Enzymatic (Alcohol Dehydrogenase)

Urine Clean plastic or glass container

2-8℃: 30 days      

-20℃: longer

Abbott IFU

24 Hours

mg/dL

Positivity Cut-off: 10

OC-Sensor Pledia, Latex Agglutination Immunoturbidimetry

Faeces sample collected into an analyser specific sampling bottle containing buffer (OC Auto Sampling Bottle 3).

2-8℃: 10 days

BowelScreen Guidelines for Quality Assurance in Colorectal Screening, Second Edition, Published 2017, ISBN 978-1-907487-26-2

24 Hours

ng/ml

Normal range cutoff: <100

NSS Bowel Screen Normal Range Cutoff: <225

Abbott Alinity i Chemiluminescent Microparticle Immunoassay (CMIA)

Serum: Serum, Serum separator  

Plasma: Tri potassium EDTA, Lithium heparin

2-8℃: 7 days        

-20℃: 1 year

Abbott IFU

24 Hours

ng/mL

Adult Male: 22 - 275

Adult Female: 5 - 204

Stago Compact Max, Stago Satellite Max

Sodium Citrate Plasma 3.2% 0.105M

Temperature: 4 hours Room temperature or 2 weeks @ -20ºC. If an expected delay in transporting samples to the laboratory samples should be centrifuge, separated & send as frozen within 4 hours of blood collection.

Miscellaneous: N/A

Collection: Cf. Special requirement for Coagulation test

‍

‍

‍

Whole blood: 4 hours, unless centrifuged at room temperature at 1500g, separated and the plasma frozen. Can only be thawed once. If an expected delay from collection time to receipt in the laboratory, suggest send frozen sample.

(SIEMENS Kit Insert & CSLI H21-A5)

‍

‍

‍

Dacie and Lewis, Practical Haematology 12th edition, 2017

Clauss developed a simple method for the quantitative determination of Fibrinogen by measuring the clotting time of dilute plasma after the addition of Thrombin. The clotting time is inversely proportional to the Fibrinogen concentration. The clotting time obtained in this manner is then compared with that of a standardised Fibrinogen preparation. The plasma must be diluted to provide a low level of potential inhibitors, e.g. FDP’s and Heparin. A strong Thrombin solution is utilised in order to ensure that the clotting time is independent of Thrombin concentration over a broad range.

Preparation of patients: Patients should be relaxed pre-venepuncture. Excessive stress and exercise will increase Factor VIII, vWF antigen and fibrinolysis. Veno-occlusion should be avoided.

Precautions: This test is not recommended for patients with active bleeding, acute infection or illness, or in those patients who have received blood transfusions within four weeks. Drugs that may increase Fibrinogen levels includec estrogens and oral contraceptives. Drugs that may cause decreased levels include anabolic steroids, androgens, Phenobarbital, Urokinase, Streptokinase, and Valproic acid.

‍

‍

24 Hours

Abbott Alinity i Chemiluminescent Microparticle Immunoassay (CMIA)

Folate:

Serum: Serum, Serum separator  

Plasma: Lithium heparin plasma, Lithium heparin plasma separator.

2-8℃: 7 days        

-20℃: 30 days

Abbott IFU

24 hours

ng/mL

Adults: 3.1 - 20.5 ng/mL

Abbott Alinity i Chemiluminescent Microparticle Immunoassay (CMIA)

Serum: Serum, Serum separator

Plasma: Sodium heparin, Lithium heparin, Potassium EDTA

2-8℃: 7 days        

-20℃: 1 year

Abbott IFU

24 Hours

UI/L

Follicular phase: 3.0 - 8.1

Mid Cycle phase: 2.6 - 16.7

Luteal phase: 1.4 - 5.5

Post-Meno pausal: 26.7 - 133

Males: 1.0 - 12.0

Abbott Alinity i Chemiluminescent Microparticle Immunoassay (CMIA)

Serum: Serum, Serum separator

Plasma: Sodium heparin, Lithium heparin, Potassium EDTA

2-8℃: 6 days        

-20℃: longer

Abbott IFU

24 Hours

pmol/L

Adult: 2.42 - 6.01

Abbott Alinity i Chemiluminescent Microparticle Immunoassay (CMIA)

Serum: Serum, Serum separator

Plasma: Sodium heparin, Lithium heparin, Lithium heparin plasma separator, Potassium EDTA

2-8℃: 6 days        

-20℃: longer

Abbott IFU

24 Hours

pmol/L

Adult: 9.01 - 19.05

CALCULATION based on Abbott Alinity methodology for Testosterone and SHBG

Serum: Serum, Serum separator

Plasma: Lithium heparin,

2-8℃: 8 days        

-20℃: 3 months

Abbott IFU

24 Hours

Male: 20.4 - 81.2

Female (Pre-meno pausal): 0.5 - 7.3

Female (Post-meno pausal): 0.6 - 8.0

Sysmex XN2000

Sysmex XN1000

Whole Blood EDTA

Temperature: + 2-8ºC

Miscellaneous: N/A

Whole Blood EDTA

Temperature: + 4ºC

Miscellaneous: N/A

2 Days @ + 2-8ºC

2 Days @ + 2-8ºC

Dacie and Lewis, Practical Haematology 12th edition, 2017

Dacie and Lewis, Practical Haematology 12th edition, 2017

The Full Blood Count (FBC) is one of the most commonly requested laboratory tests and is a very useful indicator of potential problems that require further investigation. Common causes of an abnormal RCC & haematocrit include anaemia, acute blood loss & polycythaemia. Depressed WCC may be seen in AIDS, cancer and overwhelming infections. High WCCs are commonly observed in leukaemia and infections. A high neutrophil count often indicates an infection. A low lymphocyte count can be seen in AIDS patients. A high monocyte count can indicate a bacterial infection and a high eosinophil count indicates an allergic reaction or a parasitic infection. Common causes of a low platelet count include immune system disorders, some leukaemias and patients undergoing cancer treatments.

‍

24 hours

24 Hours

Abbott Alinity c, L-Gammaglutamyl-3-carboxy-4-nitroanilid-Substrate

Serum: Serum separator

Plasma: Lithium heparin, Sodium heparin

20-25℃: 7 days                  

2-8℃: 7 days        

-20℃: 3 months

Abbott IFu

24 Hours

U/L

Male: < 55

Female: < 38

Abbott Alinity c, Particle-enhanced turbidimetric inhibition immunoassay (PETINIA)

Serum:

Serum tubes (with or without gel barrier)

Plasma: Acceptable anticoagulants are:

Lithium heparin (with or without gel barrier)

Sodium heparin

K2-EDTA

K3-EDTA

2-8℃: 7 days      

<-10℃: 14 days

Abbott IFU

24 hours

mg/L

Trough (Less Severe Infection): <1

Trough (Severe Infection): <2 - 4

Peak (Less Severe Infection): 5 - 8

Peak (Severe Infection): 8 - 10

Toxic Levels: >10 - 12

‍

CALCULATION based on Abbott Alinity methodologies for Total Protein and Albumin.

Serum: Serum tubes (with or without gel barrier)

Plasma: Acceptable anticoagulants are:

Sodium heparin

Potassium EDTA

Sodium citrate

Abbott:

20-25°C: 7 days

2-8°C: 7 days

-20°C: 3 months

Abbott IFU

‍

24 hours

g/L

Abbott:

Adults: 21 - 36

Abbott Alinity c, Enzymatic (Hexokinase/ G-6-PDH)

Plasma: Acceptable anticoagulants are:

Sodium Fluoride

Potassium Oxalate

Sodium Fluoride/K2 EDTA

20-25℃: 2 days                    

2-8℃: 7 days        

-20℃: 3 months

WHO criteria for the diagnosis of diabetes mellitus.

24 Hours

mmol/L

Fasting glucose: ≤ 6.00

Molecular Biology – Real-time PCR

Whole blood EDTA

Temperature: + 4ºC

Miscellaneous: Non fasting

Whole blood at room temperature: 7 days.

Long term storage (>10 days) of blood samples intended for nucleic acid isolation should be in EDTA tubes at 4 °C.

DNA extracts: 3 Months at -20˚C

Primary EDTA tube: 3 Months at 4˚C

HLA-B27 is a class I surface antigen strongly associated with seronegative spondyloarthropathies, such as ankylosing spondylitis. Ankylosing spondylitis is a type of arthritis characterised by long-term inflammation of the joints of the spine. 90% of patients diagnosed with Ankylosing spondylitis (AS) test positive for HLA-B27, thus genotyping is suitable for the differential diagnosis of AS. However, only 1-2% of those who test positive for HLA-B27 develop AS. Therefore, the test is not indicated as a screening test.

HLA-B27 has a frequency of approximately 8% in the general Caucasian population.

Preparation of patient: There is no physical preparation for the HLA-B27 test.

Precautions: None.

5 working days from sample receipt

HLA-B27 Positive

HLA-B27 Negative

Invalid

Chemiluminescent microparticle immunoassay (CMIA)

Chemiluminescent microparticle immunoassay (CMIA)

Serum (Gold and red cap);

Plasma (green and lavender cap)

Temperature: + 4ºC

Miscellaneous: Non fasting

Serum (Gold and red cap);

Plasma (green and lavender cap)

Temperature: + 4ºC

Miscellaneous: Non fasting

≤ 3 days at 15-30 ºC

≤ 14 days at 2-8ºC

Separated: ≥ 14 days at -20ºC or colder

≤ 3 days at 15-30 ºC

≤ 14 days at 2-8ºC

Separated: ≥ 14 days at -20ºC or colder

Source: Abbott IFU

Source: Abbott IFU

HTLV-I and HTLV-II are closely related human type C retroviruses. HTLV-I has been etiologically associated with neoplastic conditions and a variety of demyelinating neurologic disorders including adult T-cell leukaemia, tropical spastic paraparesis and/or HTLV-I associated myelopathy and more recently HTLV-I associated polymyositis, arthritis, and infective dermatitis.

Detection of antibodies against HTLV-I and HTLV-II serves to aid in the diagnosis of HTLV infection and to protect the safety of blood supply.

Preparation of Patient: There is no special physical preparation for the HTLV-I/II test.

5 working days

5 working days

Specimens with S/CO values < 1.00 are considered Non-reactive (NR).

Specimens with S/CO values >= 1.00 are considered Reactive (R).

This is a screening test and reactive samples will be referred to NVRL for confirmatory testing.

A negative (non-reactive) test result does not exclude the possibility of exposure to human T-cell lymphotropic virus types I and II.

Levels of total antibodies to these viruses may be undetectable in early infection.

‍

Molecular Biology - Real time PCR

Whole blood EDTA

Temperature: + 2-8ºC

Miscellaneous: Non fasting

Whole blood at room temperature: 7 days.

Long term storage (>10 days) of blood samples intended for nucleic acid isolation should be in EDTA tubes at 4 °C.

DNA extracts: 3 Months at -20˚C.

Primary EDTA tube: 3 Months at 4˚C

‍

Haemochromatosis (HH) is an autosomal recessive disorder of iron metabolism that affects approximately 0.2-0.5% of the Caucasian population, with a higher than average incidence in the Irish population. The disease is characterized by the excessive accumulation of iron in the body and caused by an increased absorption of dietary iron at the intestinal mucosa level. The HFE gene is responsible for the disease and was identified in 1996 (Feder JN et al., 1996); it is localized on the short arm of chromosome 6, near the locus of the HLA-A gene. A mutation of this gene causes the synthesis of an abnormal protein unable to interact with the transferrin receptors, favouring the transport of iron through the intestinal mucosa. However, the exact mechanism with which the mutated HFE protein contributes to the increased intestinal absorption is not completely clear. The two most frequent mutations found in the HFE gene correspond to the C282Y mutation (substitution of a cysteine with a tyrosine in position 282 of the protein) and the H63D mutation (substitution of the histidine with an aspartic acid in position 63).

Preparation of patient: There is no physical preparation for the haemochromatosis test.

Precautions: None.

7 working days from sample receipt.

Homozygous for C282Y and H63D mutations.

Heterozygous for C282Y and H63D mutations.

C282Y and H63D mutations not present.

TOSOH - High Performance Liquid Chromatography (HPLC)

Whole Blood Acceptable anticoagulants are:

Potassium EDTA

20-25°C: 1 day

2-8°C: 14 days

Irish College of General Practitioners "A Practical Guide to Integrated Type II Diabetes Care 2016"

24 Hours

mmol/mol

Adult: 20 - 42

Chemiluminescent microparticle immunoassay (CMIA)

Chemiluminescent microparticle immunoassay (CMIA)

Serum (Gold and red cap);

Plasma (green and lavender cap)

Temperature: + 4ºC.

Miscellaneous: Non fasting

Serum (Gold and red cap);

Plasma (green and lavender cap)

Temperature: + 4ºC.

Miscellaneous: Non fasting

Whole blood:

Up to 24 hours at RT or ≤ 6 days at 2-8ºC

Separated: ≥ 6 days at -20ºC or colder.

Avoid more than 3 freeze/thaw cycles

Whole blood:

Up to 24 hours at RT or ≤ 6 days at 2-8ºC

Separated: ≥ 6 days at -20ºC or colder.

Avoid more than 3 freeze/thaw cycles

Source: Abbott IFU

Source: Abbott IFU

This is a polypeptide component of the Hepatitis B virus particle external envelope. Its presence in the blood indicates infection by the virus; it is the first hepatitis B immunological marker and is present in blood days or weeks before symptoms appear. It may persist in persons who are chronic carriers of hepatitis B.

Preparation of Patient: There is no special physical preparation for this test.

1 working day

1 working day

Specimens with S/CO values < 1.00 are considered nonreactive (NR). Specimens with S/CO values >=1.00 are considered reactive (R).

This is a screening test and reactive samples will be referred to NVRL for confirmatory testing.

Hep B surface antigen alone is not useful during the "window period" of acute hepatitis B infection (i.e. after the disappearance of Hep B surface antigen and before the appearance of Hep B surface antibody). Testing for acute hepatitis B infection should also include hepatitis B core IgM antibody.

Chemiluminescent microparticle immunoassay (CMIA)

Chemiluminescent microparticle immunoassay (CMIA)

Serum (Gold and red cap);

Plasma (green and lavender cap)

Temperature: + 4ºC

Miscellaneous: Non fasting

Serum (Gold and red cap);

Plasma (green and lavender cap)

Temperature: + 4ºC

Miscellaneous: Non fasting

≤ 7 days at 2-8ºC

≤ 3 months at -20ºC or colder.

≤ 7 days at 2-8ºC

≤ 3 months at -20ºC or colder.

Source: Abbott IFU

Source: Abbott IFU

This test detects the presence of antibodies to the Hepatitis C virus. Preparation of Patient: There is no special physical preparation for the Hepatitis C Ab test.

1 working day

1 working day

Specimens with S/CO values < 1.00 are considered Non-reactive (NR).

Specimens with S/CO values >= 1.00 are considered Reactive (R).

This is a screening test and reactive samples will be referred to NVRL for confirmatory testing

‍

Chemiluminescent microparticle immunoassay (CMIA)

Serum (Gold and red cap); plasma (green and lavender cap)

Temperature: + 4ºC

Miscellaneous: Non fasting.

≤ 5 days at 2-8ºC

> 5 days at -20ºC or colder.

Source: Abbott IFU

ARCHITECT HCV Ag is a Chemiluminescent Microparticle Immunoassay (CMIA) using microparticles coated with monoclonal anti-HCV for the detection of HCV Ag. HCV Ag assays are used as an aid in the diagnosis of suspected Hepatitis C viral (HCV) infection and to monitor the status of infected individuals, i.e., whether the patient’s infection has resolved or the patient has become a chronic carrier of the virus. For the diagnosis of acute or chronic hepatitis, HCV Ag reactivity should be correlated with patient history and the presence of other Hepatitis C serological markers.

Preparation of Patient: There is no special physical preparation for the Hepatitis C Ag test.

‍

3 working days

Specimens with concentration values <3.00 fmol/L are considered non-reactive for HCV Ag.

Values ≥3.00 fmol/L are considered reactive for HCV Ag.

Specimens with concentration values ≥3.00 fmol/L to <10.00 fmol/L should be retested after re-centrifuging at 3,000 g for 10 minutes).

If recent contact or exposure risk suggest repeat sample after 6 weeks for Hepatitis C RNA.

Histology Processing. Diagnosis

• The specimen container(s) must be adequately labelled.
• An adequately completed test request form must accompany the specimen.

Specimen(s) are stable at room temperature once fixed in 10% neutral buffered formalin.

Small biopsies: encompass needle tissue cores (prostate, breast, etc) and small surgical tissue pieces measuring less than 5mm.

‍

Endoscopic biopsies: are widely used to diagnose and manage gastro- intestinal disease. They may be taken from the upper gastrointestinal tract (e.g. oesophageal and gastric biopsies) or the lower gastrointestinal tract (e.g. colonic or rectal biopsies). The average size of a GI biopsy ranges from 1-5mm.

‍

Non-biopsy / Other: encompasses a wide range of specimen types. Commonly encountered specimens in this category are: skin excisions, curetting’s, tonsils, gallbladders, appendices.

‍

Malignant resections: are obtained by the therapeutic surgical removal of an entire diseased area or organ. These procedures are often intended as definitive surgical treatment of a disease in which the diagnosis is already known or strongly suspected. However, pathological analysis of these specimens is critically important in confirming the previous diagnosis, staging the extent of malignant disease, establishing whether or not the entire diseased area was removed, identifying the presence of unsuspected concurrent diseases, and providing information for postoperative treatment, such as adjuvant chemotherapy in the case of cancer

‍

10 working days routine specimens.

15 working days dermatology specimens.

Up to 7 days for urgent specimens