باليني شناسي آنزيم

Transaminases

• GOT or AST

• GPT or ALT

AST ALTHeart 7800 450

Liver 7100 2850

Sk-muscle 5000 300

Kidneys 4500 1200

Pancrease 1400 130

Spleen 700 80

Lungs 500 45

RBC 15 7

serum 1 1

گيري اندازه هاي روش

كالريمتريك•فتومتريك•

نرمال مقادير

adults infants Newborn

AST 8-20 9-80 47-150

ALT 10-40 7-40

CPK

• Mg coenzyme

• Inhibitors: Ca, Zn, Cu, Mn, iodoacetate

• Activators: N-acetylcysteine

• CK-MB- α2 glubolin

CK

Ck activity Ck3-MM %

Ck2-MB %

Ck1- BB %

SK-muscle

2500 98.9 1.1 0.06

brain 555 0 2.7 97.3

heart 473 78.7 20 1.3

liver ~ 1 0 0 100

Aldolase

• ALD A : FDP• ALD B : F1P• ALD C : ?• Disease of Skeletal muscle 10-50 times• Duchenne disease • Myasthenia gravis & MS • In MI 5-8 times• Pattern parallel AST• Injection of cortisone & ACTH 10-18 times

LDH

• pH optimum in L P = 8.8-9.8

• pH optimum in P L = 7.8

• Inhibitors: reagents against thiol (Hg), Borate & Oxalate, EDTA

• HBDH = LD1

ALP

• Isoenzyme: liver, bonebone, intestinal, placental, renal

• Activators: Mg, Co, Mn• Inhibotors: phosphate, borate, oxalate, cyanide• 56º & 65º• Urea inhibition• Phe inhibited intestinal & placental•

5‘-Nucleotidase (NTP)

• Localized in cytoplasmic cell membrane

• pH optimum = 6.6 – 7• In hepatobiliary disease increased 2-6 times

• increase: stone, tumor, biliary cirrhosis• In early hepatitis NTP normal or slightly elevated• In hepatobiliary disease ALP & NTP elevated similarly

Comparison of ALP & NTP

• In hepatobiliary disease ALP & NTP elevated similarly

• In Skeletal disease, late pregnancy, childhood ALP increased & NTP normal

Gamma-glutamyl transferase (GGT)

• GGT present in all cells except muscle

• Small in cytosol & large fraction in cell membrane

• GGT elevated in all liver disease

• GGT more sensitive than ALP, NTP, LAP, GOT, GPT in obstructive jaundice

• Normal: skeletal disease, children older than 1 y, pregnancy

Comparison of GGT, ALP & NTP

ALP NTP GGT

Biliary tract disease

4.0 6.2 11.9

Acute & chronic hepatitis

1.5 1.1 2.3

Amylase

• Amylase hydrolased α-1,4 linkage

• Types of amylase:– Beta: plant & bacterial. Terminal reducing,

splits a maltose at a time– Alpha: animal & human. Random hydrolased

α-1,4 linkage

Human amylase

• pH optimum = 6.9 – 7

• Q10 =1.6 , up to 50° active

• Calcium metalloenzyme

• Activator ions: chloride, bromide, nitrate, phosphate

• MW= 55000 – 60000

• Electrophoresis: β & γ globulins

Types of human amylase

• P – type & S – Type (ptyalin)

• Macroamylase : usually S-type with IgA, IgG or other normal proteins

Causes of hyperamylasemia

• Pancreatic disease (P)

• Renal insufficiently (mixed)

• Mumps (s)

• Diabetic ketoacidosis (M)

• Acute alcoholism (M)

• Medicinal opiates (p)

• Heroin lung (s)

Amylase/creatinine clearance ratio (ACCR)

• ACCR (%) = (urine clearance of amylase/ urine clearance of creatinine) X 100

• ( urine amylase (U/L) X serum creatinine (mg/L) / serum amylase (U/L) X urine creatinine (mg/L) X 100

• Normal ACCR = 2 – 5 %• Acute pancreatitis > 8%• Macroamylasemia < 2%

Lipase

• Glycoprotein

• MW = 54000

• Concentration lipase in pancreas ~ 20000 serum

• alpha position carbons

• Lipase activated by NaCl

Cholinesterase

• Choline esterase I = true cholinesterase– RBC, lung, spleen, nerve endings, gray matter of the

brain

• Choline esterase II = pseudocholinesterase– Serum, Liver, pancreas, heart, white matter of the

brain

Cholinesterase

• Liver function

• Insecticide poisoning

• Normal range – 4000-12000 U/L– Level at birth = ¼ adults– In 2 month = adults

Cholinesterase

• 30-50% decrease– Acute & chronic hepatitis

• 50-70% decrease– Advanced cirrhosis & carcinoma

• Decrease slightly in pregnancy

Acid phosphatase

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است تارتارات به حساس پروستاتیک .ایزوآنزیمفعالیت کاهش سبب یخچال در حتی سرم نگهداری

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باشد می سرم کردن اسیدی اسیدفسفاتاز

Angiotensine converting enzyme (ACE)