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home - Liver - Clinical Presentations - Bloods Written by Dr Sebastian Zeki

Bloods

Serum aminotransferases.These measure liver cell injury.ALT, (=SGPT) ) and AST(=SGOT) are the most commonly measuredThey catalyze the transfer of alpha-amino groups of alanine+ aspartate, respec., to alpha-keto group of ketoglutarate, forming pyruvate and oxaloac-etate.ALT levels are increased in males, higher BMI and serum lipid levels.Caffeine can lower ALT.AST source includes liver, cardiac and skeletal muscle, kidneys, brain,pancreas, lungs, leukocytes, and erythrocytes and is less specific than ALT for liver disease.ALT is only found in the cytosol;AST occurs in the cytosol(20% in liver 100% elsewhere) and mitochondria (different forms).Neither ALT nor AST has isoenzymes that are tissue specific so isoenzyme analysis is usually pointless unless for MI- get large increases in mitochon-drial AST. Written by Dr Sebastian Zeki Isocitrate dehydrogenase It is a cytoplasmic enzyme; in the liver, heart, kidneys, and skeletal muscle.It parallels serum aminotransferases in acute and chronic hepatitis, but is less sensitive.Serum aminotransferases are more sensitive. Glutamate dehydrogenase It is a mitochondrial enzyme, primarily in the liver (esp in centrilobular hepato-cytes.), heart, muscle and kidneys.It is hardly ever measured. Lactate dehydrogenase It is a cytoplasmic enzyme throughout the body.- 5 isoenzymes.It has a poor diagnostic specificity, even when isoenzyme analysis is used.It is more useful as a marker of myocar-dial infarction and haemolysis. Step 1Review possible link to medications, herbal therapies or recreational drugs Screen for alcohol abuse (screening instru-ments, AST/ALT ratio >2:1) Serology for hepatitis B and C (HBsAg, HBsAb, HBcAb, HCV Ab) Screen for hemochromatosis (FE/TIBC >45 percent) Evaluate for fatty liver (AST/ALT usually < 1, obtain a RUQ ultrasound) Step 2: Confirm hepatic source Exclude muscle disorders (CK) Obtain thyroid function tests.Consider celiac disease.Consider adrenal insufficiency Step 3: Less common causes of liver disease Consider autoimmune hepatitis.Consider Wilson's disease if<40.Consider alpha-1-antitrypsin deficiency.Step 4: Obtain a liver biopsy or observe Observe if ALT and AST are <2x inc.Otherwise consider a liver biopsy Causes of a raised ALT without liver disease:False positive if on erythromycin.Muscle disease.Macro AST.Hypo/ hyperthyroid.Addisons.Coeliac. Rarely..... Measurement —Clearance AST >ALT.Activity of both measured via lactate and malate (byproduct of pyruvate and oxaloacetate formation in the aminotransferase reactions); results in NADH (absorbs light at 340nm to NAD (doesnt absorb light at 340nm).False readings:False +ve: Erythromycin and para-aminosalicylic acid .False -ve AST: renal failure probably reflects interference with the assay uraemia.Clinical significance —Liver necrosis correlates badly with necrosisRapid decrease in plasma AST and ALT levels, together with rise in [plasma bilirubin] and prolongation of the PT indicates poor prognosis in acute fulminant hepatitis. Clinical significance —A prolonged prothrombin time usually reflects one of two disorders:1.Vit K deficiency2. Parenchymal liver disease- unable to use vit K- supplementation usually doesnt work. Albumin —Total body albumin is 500 g distributed in the body fluids.Liver synthesises 5 g per day and can double if needed.Inhibition caused by inflammatory states, such as tumor necrosis factor and interleukin-1, impede albumin synthesis.Its half-life is approximately 20 days, with 4 % of the total albumin pool being degraded daily. Liver Bloods: Tests of the liver's biosynthetic capacity Moderately elevated ALT levels (upto 4x normal) Markedly elevated ALT causes:Viral hepatitis.Shock liver (ischaemic hepatitis).Acute drug- or toxin-induced liver injury.During an acute exacerbation of autoim-mune chronic active hepatitis.Spontaneous reactivation of chronic type B hepatitis.Superimposition of delta hepatitis in a chronic carrier of hepatitis B virus infection.Miscellaneous disorders such as acute Budd-Chiari syndrome (especially those with concomitant portal vein thrombosis), veno-occlusive disease, HELLP syndrome, acute fatty liver of pregnancy, and hepatic infarction. Coagulation factors —The liver is the major site of synthesis of 11 blood coagulation proteins.Liver produces I (fibrinogen) II (prothrombin), 5, 7, 9, 10, 11,13Clotting factor deficiency frequently occurs during the course of liver disease. Sorbitol dehydrogenase —It is cytoplasmic.It reflects aminotransferases in hepat-biliary disorders.It is not sensitive for cirrhosis and other chronic liver disorders.It is not useful.

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