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Interpretation of Laboratory Tests - A Case-Oriented Review of Clinical Laboratory Diagnosis.ppt

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					Interpretation of Laboratory Tests:
A Case-Oriented Review of Clinical
       Laboratory Diagnosis



            Roger L. Bertholf, Ph.D.
             Associate Professor of Pathology
 University of Florida Health Science Center/Jacksonville


                                                            1
Case 1: Oliguria and hematuria




                                 2
              Case 1: Oliguria and hematuria

   A 7-year-old boy was brought to the pediatrician because of vomiting
   and malaise. On physical examination he was slightly flushed, and had
   some noticeable swelling of his hands and feet. The patient was
   uncomfortable, and complained of pain “in his tummy”. He had a
   slight fever. Heart was normal and lungs were clear. His past medical
   history did not include any chronic diseases. The mother noted that he
   had a severe sore throat “about two weeks ago”, but that it had cleared
   up on its own. The child was not taking any medications. There were
   no masses in the abdomen, and lymphadenopathy was not present. The
   child had some difficulty producing a urine specimen, but finally was
   able to produce a small amount of urine, which was dipstick-positive
   for blood and protein.


R. Bertholf            American Society of Clinical Pathologists             3
                        Questions. . .


    • What is the differential diagnosis in this case?

    • What laboratory tests might be helpful in
      establishing the diagnosis?




R. Bertholf        American Society of Clinical Pathologists   4
                What do the kidneys do?


    •   Regulate body fluid osmolality and volume
    •   Regulate electrolyte balance
    •   Regulate acid-base balance
    •   Excrete metabolic products and foreign substances
    •   Produce and excrete hormones




R. Bertholf         American Society of Clinical Pathologists   5
              The kidneys as regulatory organs


  “The kidney presents in the highest degree the phenomenon
   of sensibility, the power of reacting to various stimuli in a
direction which is appropriate for the survival of the organism;
 a power of adaptation which almost gives one the idea that its
     component parts must be endowed with intelligence.”

                          E. Starling (1909)




R. Bertholf          American Society of Clinical Pathologists   6
    Review of Renal Anatomy and Physiology


    • The kidneys are a pair of fist-sized organs that are
      located on either side of the spinal column just
      behind the lower abdomen (L1-3).

    • A kidney consists of an outer layer (renal cortex)
      and an inner region (renal medulla).

    • The functional unit of the kidney is the nephron;
      each kidney has approximately 106 nephrons.

R. Bertholf        American Society of Clinical Pathologists   7
                            Renal anatomy


                                                                     Cortex



               Pelvis                                                   Capsule


                                                                      Medulla



              To the bladder
R. Bertholf              American Society of Clinical Pathologists                8
                            The Nephron

                                                                   Proximal tubule
Afferent arteriole
                                                                     Distal tubule
         Glomerulus
Bowman’s capsule
                                                                    Collecting duct


Renal artery

               Henle’s Loop


 R. Bertholf           American Society of Clinical Pathologists                 9
                      Glomerular filtration

                                       Glomerlular
 Vascular space
 Vascular space                         capillary                     Bowman’s space
                                                                      Bowman’s space
                                       membrane

                                 Mean capillary blood
                                 pressure = 50 mm Hg


 ~ 2,000 Liters                                                         ~ 200 Liters
                                   BC pressure = 10 mm Hg
    per day                                                               per day
(25% of cardiac output)
                                 Onc. pressure = 30 mm Hg


                            Net hydrostatic = 10 mm Hg
                                                                  GFR @ 130 mL/min
  R. Bertholf             American Society of Clinical Pathologists               10
             What gets filtered in the glomerulus?


• Freely filtered • Some filtered       • None filtered
   – H2O             – b2-microglobulin    – Immunoglobulins
   – Na+, K+, Cl-,   – RBP                 – Ferritin
     HCO3-, Ca++,    – a1-                 – Cells
     Mg+, PO4, etc.    microglobulin
   – Glucose         – Albumin
   – Urea
   – Creatinine
   – Insulin

   R. Bertholf        American Society of Clinical Pathologists   11
                  Then what happens?


    • If 200 liters of filtrate enter the nephrons each day,
      but only 1-2 liters of urine result, then obviously
      most of the filtrate (99+ %) is reabsorbed.

    • Reabsorption can be active or passive, and occurs
      in virtually all segments of the nephron.




R. Bertholf         American Society of Clinical Pathologists   12
          Reabsorption from glomerular filtrate




R. Bertholf        American Society of Clinical Pathologists   13
              How does water get reabsorbed?

    • Reabsorption of water is passive, in response to
      osmotic gradients and renal tubular permeability.
       – The osmotic gradient is generated primarily by
         active sodium transport
       – The permeability of renal tubules is under the
         control of the renin-angiotensin-aldosterone
         system.
    • The driving force for water reabsorption, the
      osmotic gradient, is generated by the Loop of
      Henle.

R. Bertholf         American Society of Clinical Pathologists   14
                                  The Loop of Henle

      Proximal tubule                                                                       Distal tubule

                                                                                              Renal Cortex
         Increasing osmolality




                                                                                      Na+
                                                                                     Na+
                                                                                              300 mOsm/Kg

                                                  Descending loop

                                                                    Ascending loop
                                 H2O                                                  Na+
                                 Na+                                                 Na+


                                                                                      Na+
                                                                                     Na+

                                                                                             Renal Medulla
                                                                                             1200 mOsm/Kg
R. Bertholf                        American Society of Clinical Pathologists                                 15
                Regulation of distal tubule Na+
                         permeability

JGA    ¯ Na+
                Renin         Angiotensinogen
       ¯ BP
                              Angiotensin I
                              Angiotensin II                        vasoconstriction
                              Angiotensin III
                                                                    Adrenal cortex
                               Aldosterone

                          Na+                                            Na+



  R. Bertholf           American Society of Clinical Pathologists                16
              Regulation of H2O reabsorption

                            Pituitary
                                       Plasma
                                       hyperosmolality


                                ADH (vasopressin)


                        H2O                                 H2O


              Renal Medulla (osmolality »1200 mOsm/Kg)

R. Bertholf          American Society of Clinical Pathologists    17
              Summary of renal physiology



                       TRPF (Filtered and secreted)


      Filtration - Reabsorption + Secretion = Elimination


          GFR (Filtered but not reabsorbed or secreted)




R. Bertholf           American Society of Clinical Pathologists   18
                  Measurement of GFR




     Cu = Concentration in urine
     Vu(24h) = 24-hour urine volume
     Cp = Concentration in plasma
     0.694 = 1000 mL/1440 min

R. Bertholf         American Society of Clinical Pathologists   19
              Compounds used to measure GFR

   • Should not be metabolized, or alter GFR
   • Should be freely filtered in the glomeruli, but neither
     reabsorbed nor secreted
   • Inulin (a polysaccharide) is ideal
   • Creatinine is most popular
      – There is some exchange of creatinine in the tubules
      – As a result, creatinine clearance overestimates GFR by
        about 10% (But. . .)
   • Urea can be used, but about 40% is (passively)
     reabsorbed

R. Bertholf         American Society of Clinical Pathologists   20
                    Relationship between creatinine and GFR

                    6
                    5
Plasma creatinine




                    4
                    3
                    2
                    1
                    0
                        0   20   40        60   80    100                    120   140
                                         GFR (mL/min)
    R. Bertholf                  American Society of Clinical Pathologists               21
                Measurement of TRPF


    • Para-aminohippurate (PAH) is freely filtered in the
      glomeruli and actively secreted in the tubules.

    • PAH clearance gives an estimate of the total
      amount of plasma from which a constituent can be
      removed.




R. Bertholf        American Society of Clinical Pathologists   22
                             Creatinine




              Creatine                                      Creatinine



      1-2% of creatine is hydrolyzed to creatinine each day


R. Bertholf          American Society of Clinical Pathologists           23
              Jaffe method for creatinine



                                                   Janovsky Complex
                                                   lmax = 490-500 nm




  Max Eduard Jaffe (1841-1911), German physiologic chemist



R. Bertholf       American Society of Clinical Pathologists            24
              Modifications of the Jaffe method


    • Fuller’s Earth (aluminum silicate, Lloyd’s reagent)
       – adsorbs creatinine to eliminate protein interference
    • Acid blanking
       – after color development; dissociates Janovsky
         complex
    • Pre-oxidation
       – addition of ferricyanide oxidizes bilirubin
    • Kinetic methods

R. Bertholf          American Society of Clinical Pathologists   25
   Absorbance (l = 520 nm)                                         Kinetic Jaffe method

                                 (pyruvate, glucose, ascorbate)




                                                                                                                         Slow-reacting
                                         Fast-reacting




                                                                                                                           (protein)
                                                                                                                   DA

                                                                                            Dt

                                                                         creatinine (and a-keto acids)

                             0                                    20                                                80
                                                                                 Time (sec) ®
R. Bertholf                                                            American Society of Clinical Pathologists                         26
              Enzymatic creatinine methods


    • Creatininase
       – creatinine®creatine®CK®ADP®PK®LD
    • Creatinase
       – creatinine®creatine®sarcosine®sarcosine
         oxidase®peroxide®peroxidase reaction
    • Creatinine deaminase (iminohydrolase)
       – most common


R. Bertholf        American Society of Clinical Pathologists   27
                        Creatinine deaminase method

                    Creatinine
                  iminohydrolase                                               ATP
Creatinine           + H 2O           N-Methylhydantoin
                      NCS                                                   NMH amidohydrolase
                  amidohydrolase
Sarcosine          - NH3, CO2
                                   N-Carbamoylsarcosine                       ADP

        Sarcosine oxidase
                                 Formaldehyde + glycine
                 + O2
    H2O                 H2O2                 H2O

  Oxygen receptor                                   Colored product
                                Peroxidase


   R. Bertholf                  American Society of Clinical Pathologists                28
              Measurement of urine protein

    • Specimen
       – Timed 24-h is best
       – Urine protein/creatinine ratio can be used with
         random specimen
    • Normal protein excretion is <150 mg/24h
       – 50-60% albumin
       – Smaller proteins (a1-, b2-microglobulins)
       – Tamm-Horsfall (uromucoid, secreted by tubules)
       – IgA, tubular epithelial enzymes, and other non-
         filtered components
R. Bertholf        American Society of Clinical Pathologists   29
              Dipstick method for urine protein


    • Method is based on protein association with pH
      indicator
    • Test pad contains dye tetrabromphenol blue at
      pH=3
    • If protein binds to the pH indicator, H+ is displaced
      and the color changes from yellow to green (or
      blue)
    • Most sensitive to albumin (poor method for
      detecting tubular proteinuria)


R. Bertholf          American Society of Clinical Pathologists   30
              What causes excess urinary protein?

    • Overload proteinuria
       – Bence-Jones (multiple myeloma)
       – Myoglobin (crush injury, rhabdomyolysis)
       – Hemoglobin
    • Tubular proteinuria
       – Mostly low MW proteins (not albumin)
       – Fanconi’s, Wilson’s, pyelonephritis, cystinosis
    • Glomerular proteinuria
       – Mostly albumin at first, but larger proteins appear
         as glomerular membrane selectivity is lost.
R. Bertholf           American Society of Clinical Pathologists   31
         Classification of proteinuria: Minimal


    • <1 gram of protein per day
    • Chronic pyelonephritis
    • Mild glomerular disease
    • Nephrosclerosis (usually due to hypertension)
    • Chronic interstitial nephritis (usually analgesic-
      related)
    • Renal tubular disease


R. Bertholf        American Society of Clinical Pathologists   32
        Classification of proteinuria: Moderate


    •   1.0 - 4.0 grams of protein per day
    •   Usually associated with glomerular disease
    •   Overflow proteinuria from multiple myeloma
    •   Toxic nephropathies




R. Bertholf        American Society of Clinical Pathologists   33
              Classification of proteinuria: Severe

  • >4 grams of protein per day
                            G
  • Nephrotic syndrome (­ BM permeability)
     – Sx: edema, proteinuria, hypoalbuminemia,
       hyperlipidemia
     – In adults, usually 2° to systemic disease (SLE,
       diabetes)
     – In children, cause is usually primary renal disease
  • Minimal Change Disease (Lipoid Nephrosis)
     – Most common cause of NS in children
     – Relatively benign (cause unknown, not autoimmune)

R. Bertholf            American Society of Clinical Pathologists   34
          Proteinuria due to glomerulonephritis


        • Acute, rapidly progressive, or chronic GN can
          result in severe proteinuria
        • Often the result of immune reaction (Circulating
          Immune-Complex Nephritis)
           – Antigen can be endogenous (SLE) or exogeneous
           – Glomerular damage is mostly complement-
             mediated
           – If antigen is continuously presented, GN can
             become chronic

R. Bertholf         American Society of Clinical Pathologists   35
              How do red blood cells get in urine?


    • Hematuria can result from bleeding anywhere in
      the kidneys or urinary tract
       – Disease, trauma, toxicity
    • Hemoglobinuria can result from intravascular
      hemolysis
       – Disease, trauma, toxicity




R. Bertholf           American Society of Clinical Pathologists   36
              Dipstick method for hemoglobin

                            Heme
H2O2 + chromogen*                           Oxidized chromogen + H2O
                        Peroxidase

      • Ascorbic acid inhibits the reaction, causing a false
        negative test
      • Depends on RBC lysis (may not occur in urine
        with high specific gravity)
      • Detection limit approximately 10 RBC/mL


*tetramethylbenzidine; oxidized form is green
R. Bertholf         American Society of Clinical Pathologists      37
   Microscopic examination of urine sediment




R. Bertholf   American Society of Clinical Pathologists   38
              Significance of RBC casts in urine


    •   Indicative of blood crossing the GBM
    •   Casts form in the distal tubules
    •   Stasis produces brown, granular casts
    •   RBC casts almost always reflect glomerular disease




R. Bertholf          American Society of Clinical Pathologists   39
   Bright’s Disease (acute glomerulonephritis)


    • Characterized by oliguria, proteinuria, and
      hematuria
    • Most common cause is immune-related




    Richard Bright (1789-1858)
R. Bertholf        American Society of Clinical Pathologists   40
              Primary Glomerulonephritis


    • Proliferative GN
       – Acute Post-infectious GN
       – Idiopathic or Crescentic GN
       – a-GBM disease
       – Membranoproliferative GN
    • Focal GN
       – IgA nephropathy


R. Bertholf        American Society of Clinical Pathologists   41
              Primary Glomerulonephritis, cont.


    • Idiopathic membranous GN
       – Histological diagnosis, probably immune complex
    • Chronic GN
       – Clinical Dx; many potential causes
    • Lipoid Nephrosis
       – Histological findings normal; “Nephrosis”
    • Focal Glomerular Sclerosis
       – Probably immune (IgM) related


R. Bertholf          American Society of Clinical Pathologists   42
              Secondary Glomerulonephritis

    • Systemic Lupus Erythematosus
       – Renal failure accounts for 50% of SLE deaths
    • Polyarteritis (inflammatory vasculitis)
    • Wegener’s Granulomatosis (lung and URT)
    • Henoch-Schönlein Syndrome
       – Lacks edema assoc. with post-streptococcal GN
    • Goodpasture’s Syndrome (pulmonary hemorrhage)
    • Hemolytic-Uremic Syndrome
    • Progressive Systemic Sclerosis (blood vessels)

R. Bertholf        American Society of Clinical Pathologists   43
Case 3: Chest Pain




                     44
                  Case 3: Chest Pain

A 63 year old male was brought to the emergency department
after complaining of severe chest pain that had lasted for two
hours. He had been mowing his lawn when the pain developed,
and he became concerned when the pain did not subside after
he stopped the activity. He had no previous history of heart
disease. On presentation he was moderately overweight, dia-
phoretic, and in obvious discomfort. He described his chest
pain as “beginning in the center of my chest, then my arms,
neck, and jaw began to ache too.”

Diagnostic procedures were performed.

R. Bertholf       American Society of Clinical Pathologists   45
                           Questions


    • What is the most important consideration in the
      triage of this patient?

    • What tests should be ordered?




R. Bertholf       American Society of Clinical Pathologists   46
                           Chest pain

    • One of the most common reasons for seeking
      medical attention
    • Characteristics of cardiogenic chest pain (angina)
       – induced by exercise
       – described as “pressure”
       – radiates to extremities
       – MI not relieved by rest or vasodilatory drugs (NG)
    • Only 25% of patients presenting with chest pain as
      the primary complaint will ultimately be diagnosed
      as MI (specificity=25%; sensitivity=80%)

R. Bertholf        American Society of Clinical Pathologists   47
                            The Heart

              Aorta                                       Pulmonary arteries

 Superior vena cava


              RA                                                LA



                                                                 LV

                   RV

R. Bertholf        American Society of Clinical Pathologists               48
                The Heart (posterior view)

                Aorta

                                                                    Superior vena cava
Pulmonary arteries

Pulmonary veins
                                                                      Inferior vena cava




  R. Bertholf           American Society of Clinical Pathologists                 49
              Cardiac physiology




R. Bertholf   American Society of Clinical Pathologists   50
                   Cardiac conduction system




       Sinoatrial (SA) node


                                                                    Left bundle branch
Atrioventral (AV) node
             His bundle



                 Right bundle branch
   R. Bertholf          American Society of Clinical Pathologists               51
              Normal Electrocardiogram


                                      R




                                                             T

                                                                 U
                P
                                  Q

                                          S
R. Bertholf      American Society of Clinical Pathologists           52
                   Myocardial infarction




                                                                    Left coronary artery




                                                                    Anterior left ventricle
Right coronary artery
   R. Bertholf          American Society of Clinical Pathologists                   53
         ECG changes in myocardial infarction


                                       R


                                               S-T elevation

                                                               T


                 P

                                  Q¯
                                           S
R. Bertholf       American Society of Clinical Pathologists        54
              Diagnostic value of ECG


    • ECG changes depend on the location and severity of
      myocardial necrosis
    • Virtually 100% of patients with characteristic Q-
      wave and S-T segment changes are diagnosed with
      myocardial infarction (100% specificity)
    • However, as many as 50% of myocardial infarctions
      do not produce characteristic ECG changes
      (sensitivity @ 50%)
    • ECG may be insensitive for detecting prognostically
      significant ischemia

R. Bertholf       American Society of Clinical Pathologists   55
              History of cardiac markers


   • 1975: Galen describes the use of CK, LD, and
     isoenzymes in the diagnosis of myocardial infarction.
   • 1980: Automated methods for CK-MB (activity) and
     LD-1 become available.
   • 1985: CK-MB isoforms are introduced.
   • 1989: Heterogeneous immunoassays for CK-MB
     (mass) become available.
   • 1991: Troponin T immunoassay is introduced.
   • 1992: Troponin I immunoassay is introduced.

R. Bertholf       American Society of Clinical Pathologists   56
                   Enzyme markers

    • Aspartate transaminase (AST; SGOT)
    • 2-Hydroxybutyrate dehydrogenase
    • Lactate dehydrogenase
       – Five isoenzymes, composed of combinations of H
         (heart) and M (muscle) subunits
    • Creatine kinase
       – Three isoenzymes, composed of combinations of
         M (muscle) and B (brain) subunits



R. Bertholf       American Society of Clinical Pathologists   57
              Lactate dehydrogenase (LD)


                       NADH                  NAD+
               Pyruvate                                 Lactate
                                     LD

    • LD activity is measured by monitoring absorbance
      at l = 340 nm (NADH)
    • Methods can be P ® L or L ® P
       – But. . .reference range is different
    • Total LD activity has poor specificity

R. Bertholf        American Society of Clinical Pathologists      58
              Tissue specificity of LD isoenzymes




R. Bertholf           American Society of Clinical Pathologists   59
           LD isoenzyme electrophoresis (normal)

                  LD-2 > LD-1 > LD-3 > LD-4 > LD-5
                                LD-2


                     LD-1
                                             LD-3
                                                          LD-4
                                                                     LD-5

Cathode (-)                                                                 Anode (+)


    R. Bertholf          American Society of Clinical Pathologists              60
         LD isoenzyme electrophoresis (abnormal)

                  LD-1

                            LD-2                  LD-1 > LD-2



                                         LD-3
                                                      LD-4
                                                                 LD-5
Cathode (-)                                                             Anode (+)


    R. Bertholf      American Society of Clinical Pathologists              61
              Direct measurement of LD-1


    • Electrophoresis is time-consuming and only semi-
      quantitative
    • Antibodies to the M subunit can be used to
      precipitate LD-2, 3, 5, and 5, leaving only LD-1
       – Method can be automated
       – Normal LD-1/LDtotal ratio is less than 40%




R. Bertholf       American Society of Clinical Pathologists   62
              Sensitivity and specificity of LD-1


    • Sensitivity and specificity of the LD 1:2 “flip”, or
      LD-1 > 40% of total, are 90+% within 24 hours of
      MI, but. . .
       – May be normal for 12 or more hours after
         symptoms appear (peak in 72-144 hours)
       – May not detect minor infarctions
    • Elevations persist for up to 10 days
    • Even slight hemolysis can cause non-diagnostic
      elevations in LD-1

R. Bertholf           American Society of Clinical Pathologists   63
                       Creatine Kinase (CK)


                       CK
Phosphocreatine                      Creatine
                            ++
                       Mg
                 ADP             ATP                       ADP
                       Glucose                                  Glucose-6-phosphate
                                               HK
                                                                            NADP+
                                                                    GPD
                                   6-Phosphogluconate                       NADPH
                                                                           l=340 nm
  Oliver and Rosalki method (1967)

   R. Bertholf          American Society of Clinical Pathologists              64
         Tissue specificities of CK isoenzymes




R. Bertholf       American Society of Clinical Pathologists   65
              Measurement of CK isoenzymes

    • Electrophoresis (not used anymore)
    • Immunoinhibition/precipitation
       – Antibody to M subunit
       – Multiply results by 2
       – Interference from CK-1 (BB)
    • Most modern methods use two-site (“sandwich”)
      heterogeneous immunoassay
       – Measures CK-MB mass, rather than activity
       – Gives rise to a pseudo-percentage, often called the
         “CK-MB index”
R. Bertholf         American Society of Clinical Pathologists   66
              Sensitivity/specificity of CK-MB


    • Sensitivity and specificity of CK-MB for
      myocardial infarction are >90% within 7-18 hours;
      peak concentrations occur within 24 hours
    • CK is a relatively small enzyme (MW = 86K), so it
      is filtered and cleared by the kidneys; levels return
      to normal after 2-3 days
    • Sensitivity is poor when total CK is very high, and
      specificity is poor when total CK is low
    • Presence of macro-CK results in false elevations


R. Bertholf          American Society of Clinical Pathologists   67
                          CK isoforms

                             C-terminal lysine

CK-MB2 (tissue)                                             CK-MB1 (circulating)
                   Plasma carboxypeptidase

      • C-terminal lysine is removed from the M subunit--
        therefore, there are three isoforms of CK-3 (MM)
      • t½: CK-MB1 > CK-MB2
      • Ratio of CK-MB2 to CK-MB1 exceeds 1.5 within six
        hours of the onset of symptoms
      • Only method currently available is electrophoresis

  R. Bertholf       American Society of Clinical Pathologists              68
                          Myoglobin

    • O2-binding cytosolic protein found in all muscle
      tissue (functional and structural analog of
      hemoglobin)
    • Low molecular weight (17,800 daltons)
    • Elevations detected within 1-4 hours after
      symptoms; returns to normal after 12 hours
    • Nonspecific but sensitive marker--primarily used
      for negative predictive value
    • Usually measured by sandwich, nephelometric,
      turbidimetric, or fluorescence immunoassay

R. Bertholf       American Society of Clinical Pathologists   69
  Temporal changes in myoglobin and CK-MB




R. Bertholf   American Society of Clinical Pathologists   70
                          Troponin


  Tropomyosin     Actin                         TnT (42 Kd)




                     TnC                             TnI (23 Kd)
                                         Myosin

                       Thick Filament

R. Bertholf     American Society of Clinical Pathologists          71
        Tissue specificity of Troponin subunits


    • Troponin C is the same in all muscle tissue
    • Troponins I and T have cardiac-specific forms,
      cTnI and cTnT
    • Circulating concentrations of cTnI and cTnT are
      very low
    • cTnI and cTnT remain elevated for several days
    • Hence, Troponins would seem to have the
      specificity of CK-MB (or better), and the long-term
      sensitivity of LD-1

R. Bertholf        American Society of Clinical Pathologists   72
      Is cTnI more sensitive than CK/CK-MB?


 79 y/o female with Hx of HTN, CHF, CRI, Type II diabetes




R. Bertholf      American Society of Clinical Pathologists   73
              Measurement of cTnI and cTnT

    • All methods are immunochemical (ELISA, MEIA,
      CIA, ECIA)
    • Roche Diagnostics (formerly BMC) is the sole
      manufacturer of cTnT assays
       – First generation assay may have had some cross-
         reactivity with skeletal muscle TnT
       – Second generation assay is cTnT-specific
       – Also available in qualitative POC method
    • Many diagnostics companies have cTnI methods


R. Bertholf        American Society of Clinical Pathologists   74
           W.H.O. has a Myocardial Infarction?



A patient presenting with any two of the following:

     • A clinical history of ischemic-type chest discomfort
     • Changes on serially obtained ECG tracings
     • A rise and fall in serum cardiac markers


                                                 Source JACC 28;1996:1328-428


 R. Bertholf        American Society of Clinical Pathologists                   75
       Sensitivity/Specificity of WHO Criteria




R. Bertholf      American Society of Clinical Pathologists   76
         What Cardiac Markers do Labs Offer?




R. Bertholf       American Society of Clinical Pathologists   77

				
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