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Download Evaluation of Liver Function tests
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Evaluation of Liver Function tests in Primary Care Abid Suddle Institute of Liver Studies, KCH Liver Function tests • Markers of hepatocellular damage • Cholestasis • Liver synthetic function Markers of Hepatocellular damage Transaminases • AST‐ liver, heart skeletal muscle, kidneys, brain, RBCs • In liver 20% activity is cytosolic and 80% mitochondrial • Clearance performed by sinusoidal cells, half‐life 17hrs • ALT – more specific to liver, v.low concentrations in kidney and skeletal muscles. • In liver totally cytosolic. • Half‐life 47hrs Markers of Cholestasis • ALP – liver and bone (placenta, kidneys, intestines ) • Hepatic ALP present on surface of bile duct epithelia and accumulating bile salts increase its release from cell surface. • ALP isoenzymes, 5‐NT or gamma GT may be necessary to evaluate the origin of ALP • Gamma‐GT – hepatocytes and biliary epithelial cells, pancreas, renal tubules and intestine • Very sensitive but Non‐specific • Confirm hepatic source for a raised ALP • Alcohol Markers of liver synthetic function Bilirubin, Albumin and PT (INR) • Useful indicators of liver synthetic function • In primary care when associated with liver enzyme abnormalities should raise concern • Thrombocytopaenia is a sensitive indicator of liver fibrosis Patterns of liver enzyme alteration • Hepatic vs cholestatic • Magnitude of enzyme alteration (ALT >10x vs minor abnormalities) • Rate of change • Nature of the course of the abnormality (mild fluctuation vs progressive increase) COMMON CAUSES OF ABNORMAL LFTS IN THE UK • • • • • Transient mild abnormalities Drugs – eg Statins Alcohol excess Viral hepatitis Non‐Alcoholic Fatty Liver Disease (NAFLD) Investigation of Abnormal LFTs • • • • • • • • PRINCIPLES 2.5% of population have raised LFTs Normal LFTs do not exclude liver disease Interpret LFTs in clinical context Take a careful history for risk factors, drugs, alcohol, comorbidity, autoimmunity Physical examination for liver disease Chase likely diagnosis rather than follow algorithm unless there are no clues If mild abnormalities and no risk factors or suggestion of serious liver disease , repeat LFTs after an interval (with lifestyle modification) Synthetic impairment/ signs of decompensation URGENT evaluation Acute hepatitis (ALT>10xULN) • Viral • Drugs/ Toxic • Ischemia • Autoimmune Investigation of acute hepatitis • Urgent evaluation especially if jaundiced/ synthetic impairment • Evaluation RFs viral hepatitis, drug exposure • Discontinue potential candidate drugs • Hep A IgM, HBV cIgM + SAg, HCV IgG, HEV IgM • Ultrsound Acute alcoholic hepatitis Spectrum: abnormal LFTs → ACLF History: malaise, abdo pain anorexia Examination: PSCLD, Hepatomegaly Investigations: AST never >10xULN; AST:ALT>2; Bilirubin, PT • Urgent evaluation if jaundiced • Steroids/ DF • • • • ALT/AST 2‐5x ULN • • • • • • • Transient Drug effect Chronic viral hepatitis Alcohol NAFLD Autoimmune Metabolic liver disease Common medication • • • • • • Statins NSAIDs Antibiotics Antituberculosis drugs Herbal remedies Alternative medications NAFLD • • • • • Hepatic manifestation of metabolic syndrome Therefore risk factors ALT, AST 2‐4x ULN GGT Fat on USS Chronic viral hepatitis • Hepatitis B Ethnic group, Risks for BBV HBSAg • Hepatitis C Blood product transfusion before 1992 IDU HCV Ab, RNA, genotype Autoimmune • • • • • Female sex Young Previous/ family history AI disease Elevated globulin/ serum IgG Positive AAs: ANA, SMA, anti‐LKM Metabolic liver disease • Haemochromatosis Arthralgia, DM Elevated serum ferritin and TFS genetics • Wilsons Young, undiagnosed liver disease Psychaitric/ Neurologic symptoms Caeruloplasmin Cholestasis • • • • • • Transient Drugs Biliary Obstruction PBC PSC Infiltration Biliary obstruction • Gallstones • Cancer head of pancreas • Cholangiocacinoma • Ultrasound CT Medications elevation of bilirubin and ALP • • • • • • • • • • • • • Anabolic steroid Allopurinol Amoxicillin‐clavuronic acid Captopril Carbamazepine Chlorpropamide Cyproheptadine Diltiazem Erythromycin Estrogens Floxuridine Flucloxacillin Fluphenazine • • • • • • • • • • • • • Gold salts Imipramine Indinavir Iprindole Nevirapine Methytestosterone Methylenedioxymethamphetamine Oxaprozin Pizotyline Quinidine Tolbutamide TPN Trimethoprim‐sulfamethoxazole PBC • Female predominant • Elevated cholestatic enzymes, no biliary obstruction, pruritis, xanthelasma • AMA positive, IgM PSC • Young, IBD • ANCA • Secondary care evaluation Diagnostic approach in elevated serum alkaline phosphatase elevated ALP History and PE normal bilirubin, ALT, AST GGT or 5’nucleotidase positive negative not hepatobiliary U/S review medication AMA abnormal liver chemistries yes Cholangiography CT no AMA negative no duct dilatation liver biopsy U/S observation > 6 months as elevated ALT evaluation, liver biopsy, ERCP γ‐glutamyltransferase (GGT) • Sensitive but not specific • increase – alcohol – drug • anticonvulsant (CBZ, phenytoin, and barbiturate), OC – almost all type of liver diseases Important points • Investigate abnormalities in light of clinical context • Abnormalities associated with synthetic impairment or signs of decompensation require emergent evaluation
