Presented by MLS Manuel Jesmi

1. LABORATORY
DIAGNOSTIC APPROACH
TO LIVER
BIOCHEMISTRIES

2.  Summary of liver anatomy
 Function of the liver
 Biochemical parameters of liver function
 Blood picture of hepatic disorder
 Bilirubin metabolism
 Principles used in diagnosis/monitoring of liver
disorders
 Test validation
 Clinical causes of jaundice
 Pre-hepatic jaundice
 Alcoholic liver disease
 Hepatic jaundice
 Post-hepatic jaundice
 Dx of bone disorders
 Early CVA diagnosis
 Portal hypertension
 Test limitations
 Case study

3. At the end of this presentation, clinical laboratory staffs should be able to:
 Relate FBC with LFT
 Understand bilirubin metabolism
 Understand the anatomical location of liver enzymes
 Make the appropriate laboratory diagnosis
 Deduce the actual constituents of parameters for hepato-pathological
diagnosis

5. The liver is a large organ located
at the right hypochondriac region
of the abdominal cavity.

6.  Albumin,A1AT, enzymes and bile
 Vitamins and mineral storage ( Vit B9,B12 etc)
 Coagulation factors (zymogens)
 Immune-regulatory function
 Haemophagocytic action
 Hormone balance
 Glucose metabolism
 TPO synthesis
 Cholesterol metabolism
 Iron storage as hemosiderin/ copper storage
 Blood pressure regulation
 Drug metabolism

7.  Bilirubin
 Albumin
 Globulin
 Alanine transaminase
 Aspartate transaminase
 Lactate dehydrogenase
 Gamma glutamyl transpeptidase
 5’ Nucleotidase
 Alkaline phosphatase
 Prothrombin Time
 Platelet count

8.  Anaemia/erythrocytopaenia ( sequestration )
 Thrombocytopenia
 monocytosis
 Macrocytosis (lipemia/hyperglycaemia/nutritional def. induced)
 Pseudo-Hb (false Absorbance induced)

9. VAN DEN BERG REACTION
Diazotized sulfanilic acid method for
direct bilirubin
Methanol counter for indirect
bilirubin/ detergent (accelerator) for
total bilirubin

10. INDICES
 A/G ratio ( 2:1 )
 De ritis ratio (1.3-1.7)
I.C.U SCORES
 APRI score (0.5-1.5)
 MELD score (6-40)
 MELD-Na score ( each decline of Na corresponds 12% devalued prognosis)
 CTP score (Group A,B,C)
 SAAG score (≤1.1)

11.  A/G ratio
 Albumin/Total protein
 Indirect/direct/delta quantification with Total bilirubin

12. Neonatal Jaundice
 Congenital causes
 Erythroblastosis and rhesus ‘D’ incompatibilities
 Xenoestrogen causes
 Enzymopathies
 Physiological causes due to immature hepatocytes
OTHERS
 Immune-regulatory causes (auto/allo)
 Extravascular/intravascular haemolysis
 Splenomegaly
 Vaso-occlusive crisis of SCD
 Other haemoglobinopathies
 Febrile agglutinins
 Post-hepatic causes

13.  Indirect bilirubin marked increase
 AST marked increase
 ALP Normal/ mild rise (LMR/lytic PMNs )
 GGT (indeterminate)-mild rise if induced by enzymopathies
 Normal ALT
 Normal PT
 Normal A/G ratio in non-inflammatory/malnutrition induced
 Increased urine urobilinogen/ stool stercobilinogen

14.  Preponderant GGT
 AST increase (phase dependent)
 Albumin Normal/decreased (phase dependent)
 ALT Normal/increased (phase dependent)
 De ritis ratio>1.5
Dx OF HEPATIC JAUNDICE
 ALT increased
 AST increased
 Biphasic hyperbilirubinaemia
 GGT intrahepatic(infectious)/extrahepatic dependent
 ALP mild/moderate rise
 Albumin (phase dependent)
 Urine urobilinogen normal/increase
 PT increase
 bilirubinuria

15.  5’Nucleotidase marked increase
 ALP marked increase
 GGT mild/moderate rise
 AST mild increase
 ALT mild increase
 PT increase
 Direct hyperbilirubinaemia
 steatorrhea
 Absolute decrease in UBG and SBG

16. Osteoclasis, osteocytic and osteoblastic activity induced by combined effect of
PTH, Activated vitamin D and estrogen:
 Normal GGT
 Normal Albumin
 Increased ALP
 Normal AST
 Normal ALT
 Normal 5’ Nucleotidase

17. Some CVA causes can be diagnosed using the Globulins and GGT from the
liver biochemistry test in a hyperlipidemic patient.
 Enzymopathy increases free radicals
 Free radicals increase GGT
 Increased GGT induce hepcidin effect
 Immune-regulatory response yields monocytic cells
 Monocytic cells feed on lipid and become oxidized
 Inflammation induction
 Lipid-soluble remnants cross the BBB causing ischemia

18. Increased blood pressure in the hepatic portal system.
Clinical presentation
 Caput medusae
 Splenomegaly
 Marked ascites
 Hematemesis/melenaesis
Laboratory Evaluation
 increased APRI score
 SAAG score >1.1
 Erythrocytopaenia
 Anaemia
 Hypernatremia

19.  Alcoholics with malnutrition falsely present with ESLD
 Non-specific enzyme activity of AST and ALP to the liver
 Normal liver enzymes sometimes in ESLD/Cirrhosis

20. 60 yr old male with 3 month history of fatigue and joint pain. He confessed to drinking 2 beer
per day. His BP was 128/76 mmHg
His brother is a known type 2 diabetes patient.
Physical examination: hepatomegaly, Enlarged and tender knuckles, several tattoos.
Routine Lab work:
6 weeks later
FBS-Normal
Hb – 14.2g/dl
Albumin -43g/l HBV/HAV- Negative
Bilirubin-Normal
ALT-67U/L……………………………………………… Unchanged
AST-73U/L……………………………………………… Unchanged
GGT-92 U/L…………………………………………….. Normal
Na -138 mmol/l…………………………………………..Normal
Blood Ammonia-Normal
Urea – 4.6 mmol/l
Further Blood work:
Stfr -Decreased
Ferritin- 640mcg(N <300)
Transferrin saturation 60% (N <45%)
What is the likely Dx? Explain the potential genetic cause.
Establish the prognosis for this patient.
What effective treatments can better resolve this disorder?