Clinical Biochemistry – Liver Enzymes and Cytolysis Markers
ALT (ALAT — alanine aminotransferase)
Alanine aminotransferase (ALT) is an intracellular enzyme that catalyzes the reversible transfer of the amino group from alanine to alpha-ketoglutarate, producing pyruvate and glutamate. This transamination reaction is part of the metabolic crossroads between amino acid catabolism and the Krebs cycle. ALT is present in high concentrations in the cytoplasm of hepatocytes, making it the most specific liver marker of all transaminases measured in clinical routine. Unlike AST (aspartate aminotransferase), whose tissue distribution is broad (liver, cardiac muscle, skeletal muscle, kidney, brain, erythrocytes), ALT is almost exclusively hepatic in clinical practice, giving it diagnostic superiority for assessing hepatocyte integrity. Under physiological conditions, serum ALT concentrations are low, as intact hepatocytes retain the enzyme in their cytoplasm. Any hepatocyte injury, whatever the cause (toxic, viral, ischemic, infiltrative, autoimmune or metabolic), alters the membrane integrity of hepatocytes and releases intracellular ALT into the bloodstream, resulting in a serum elevation proportional to the extent and severity of cytolysis. ALT is measured as part of a complete hepatic workup and, along with AST, alkaline phosphatase (ALP), gamma-glutamyl transferase (GGT), total and conjugated bilirubin and prothrombin time, constitutes the standard panel for liver function assessment prescribed in Quebec clinical biochemistry laboratories.
Severe ALT elevation: urgent consultation
An ALT elevation greater than 10 times the upper limit of normal (ULN), let alone 20 to 50 times ULN, constitutes severe acute hepatitis until proven otherwise, and requires urgent medical evaluation the same day. In the presence of a very high ALT (greater than 1,000 to 3,000 IU/L) associated with one or more of the following signs, go to the emergency room without delay: intense or rapidly progressive jaundice, hepatic encephalopathy (confusion, disorientation, asterixis), significant prolongation of prothrombin time or INR (INR greater than 1.5 to 2.0), hypoglycemia, de novo ascites, intense right upper-quadrant abdominal pain, fever. These signs suggest acute liver failure (fulminant hepatitis), whose mortality without emergency liver transplantation can exceed 50 to 80 % in the most severe forms. The main causes of severe acute hepatitis to be ruled out as a matter of urgency include: paracetamol intoxication (excessive single or cumulative dose, treatment with N-acetylcysteine to be instituted without delay), ischemic hepatitis (cardiogenic shock, sepsis, heat stroke), severe acute viral hepatitis A or B, fulminant drug or toxic hepatitis, autoimmune hepatitis in initial flare-up, acute Budd-Chiari syndrome.
Physiological role and tissue localization
ALT is a cytosolic enzyme whose cofactor is pyridoxal phosphate (the active form of vitamin B6, pyridoxine). The reaction it catalyzes occupies a strategic position in hepatic gluconeogenesis: alanine released by skeletal muscle during fasting or exertion is transported to the liver, where ALT converts it into pyruvate, a substrate for gluconeogenesis. This alanine-glucose cycle (Cahill cycle) allows the liver to maintain blood glucose levels during prolonged fasting by using muscle amino acids as glucoformative substrates.
The intrahepatic concentration of ALT is considerable: hepatocytes contain approximately 3,000 to 10,000 times the normal serum concentration. Therefore, even the slightest disruption of hepatocyte membrane integrity is sufficient to release a measurable amount of enzyme into the vascular compartment. The serum half-life of ALT is approximately 47 hours (compared to 17 hours for AST), which explains why ALT remains elevated longer than AST during resolving acute hepatitis and why it is more useful for longitudinal monitoring of liver inflammatory activity.
Reference values
ALT reference values vary depending on the laboratory, assay methods (enzyme kinetics at 37 °C according to IFCC, International Federation of Clinical Chemistry recommendations), and the characteristics of the reference population used to establish the intervals. The values indicated below correspond to the intervals usually used by Quebec laboratories affiliated with the health network.
| Population | Usual reference interval | Comments |
|---|---|---|
| Adult male (18 to 60 years old) | 7 to 56 IU/L (some laboratories: 5 to 40 IU/L) | Men have physiologically higher values than women due to greater muscle mass and hormonal differences (testosterone increases hepatic enzymatic activity) and a higher prevalence of metabolic fatty liver disease. |
| Adult woman (18 to 60 years old) | 7 to 45 IU/L (some labs: 5 to 35 IU/L) | Recent epidemiological studies suggest that the upper limit of normal should be lowered to 19 IU/L in women and 30 IU/L in men for better diagnostic sensitivity in non-alcoholic fatty liver disease; these lowered values are not yet universally adopted in Canadian laboratories. |
| Elderly person over 60 | Slight decrease in normal values compared to young adults; most laboratories keep the same reference intervals | Liver mass decreases with age (a reduction of 20 to 40 % between 20 and 80 years of age) but reference intervals are not systematically adjusted; an ALT at the upper limit of normal in an elderly subject may be relatively more significant than an identical value in a young subject. |
| Pregnant woman | Physiologically stable values in the first and second trimesters; slight decrease in the third trimester due to hemodilution | Any significant elevation of ALT during pregnancy must be taken seriously: intrahepatic cholestasis of pregnancy (moderately elevated ALT with elevated serum bile acids), severe preeclampsia, HELLP syndrome (hemolysis, elevated liver enzymes, low platelets), acute fatty liver of pregnancy (obstetric emergency) |
| Child (0-17 years) | Higher values in newborns and infants (up to 2 times adult norms); gradually decrease to adult values in adolescence; age-specific pediatric ranges provided by laboratories | Pediatric reference intervals are established by laboratories from pediatric reference populations; always refer to the intervals of the laboratory that performed the analysis for interpretation in children. |
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Large-scale population studies (NHANES in the US, CARTaGENE in Quebec) have shown that current ALT reference intervals were established from populations including individuals with subclinical non-alcoholic fatty liver disease and undiagnosed metabolic syndrome, thus overestimating the upper limit of normal. An adult with an ALT between 20 and 40 IU/L, long considered within the normal range, may actually have early-stage metabolic dysfunction-associated steatotic liver disease (formerly NAFLD, now MASLD: Metabolic dysfunction-Associated Steatotic Liver Disease), particularly if this value is associated with abdominal overweight, hypertriglyceridemia, impaired fasting glucose, or insulin resistance. The role of the primary care physician is to interpret ALT within its overall clinical and metabolic context, not solely in relation to the laboratory's reference interval.
Classification of ALT Elevations by Degree
| Angle of inclination | Value (multiple of LSN) | Main diagnostic orientation | Emergency |
|---|---|---|---|
| Slight elevation | 1 to 3 times the LSN | Metabolic steatotic liver disease (MASLD), mild alcoholic hepatitis, hepatotoxic medications, thyroid disease, celiac disease, recent intense physical exercise, physiological variation | Scheduled outpatient follow-up; no urgency if patient is asymptomatic and INR is normal |
| Moderate elevation | 3-10 times the LSN | Chronic viral hepatitis (HBV, HCV), moderate alcoholic hepatitis, drug-induced liver disease, autoimmune hepatitis, Wilson's disease, hereditary hemochromatosis, steatohepatitis (MASH) | Urgent comprehensive liver function test within 1 to 2 weeks; assessment of liver synthesis (Quick time, bilirubin, albumin levels) |
| Severe elevation | 10 to 50 times the ULN (ALT greater than 500 to 2,000 U/L) | Acute viral hepatitis (A, B, E), severe drug-induced or toxic hepatitis (paracetamol), ischemic hepatitis, initial flare-up of autoimmune hepatitis, reactivation of hepatitis B | Urgent medical evaluation on the same day; complete assessment including prothrombin time, bilirubin, blood glucose; hospitalization depending on clinical profile |
| Massive elevation | Greater than 50x ULN (ALT > 2,000 to 3,000 IU/L) | Ischemic hepatitis (shock, acute heart failure), acute acetaminophen poisoning, acute Budd-Chiari syndrome, heatstroke, fulminant toxic or viral hepatitis; rarely, severe rhabdomyolysis with secondary liver involvement | Absolute medical emergency; referral to hospital emergency department; evaluation for liver transplant if criteria for acute liver failure are met (King's College or Clichy criteria) |
Causes of elevated ALT
Most common liver causes in Quebec
| Etiology | Characteristic biological profile | Ancillary diagnostic elements |
|---|---|---|
| Metabolic dysfunction-associated steatotic liver disease (MASLD) and metabolic dysfunction-associated steatohepatitis (MASH) | Moderately elevated ALT (1 to 5 times the ULN); AST/ALT ratio less than 1 (unlike alcoholic hepatitis where this ratio is often greater than 2); elevated GGT; often associated with elevated triglycerides and fasting hyperglycemia | Metabolic context (BMI > 25 to 30, elevated waist circumference, metabolic syndrome, type 2 diabetes, dyslipidemia, PCOS); liver ultrasound (parenchymal hyperechogenicity, «bright liver»); FIB-4 score (age × AST / [platelets × √ALT]) for non-invasive fibrosis assessment; FibroTest or FibroScan (liver elastography) as a second-line option; liver biopsy for histological staging in progressive forms |
| Alcoholic hepatitis and chronic alcoholic liver disease | AST/ALT ratio greater than 2 (De Ritis sign, highly suggestive of alcoholic cause); very high GGT (sensitive marker of recent alcohol consumption, greater than 3 to 5 times the upper limit of normal); high MCV (mean corpuscular volume) greater than 100 fL; elevated bilirubin in severe forms; prolonged INR in alcoholic cirrhosis | Alcohol consumption history (AUDIT-C tool as a first-line assessment); CDT (carbohydrate-deficient transferrin) as a marker for excessive chronic alcohol consumption; liver ultrasound (steatosis, liver dysmorphia, portal hypertension); Maddrey score (bilirubin × INR × factor) to assess the severity of acute alcoholic hepatitis and guide corticosteroid indication |
| Chronic viral hepatitis C (HCV) | ALT fluctuante, élevée de façon chronique ou par poussées (1 à 10 fois la LSN); peut être normale chez 30 % des porteurs chroniques malgré une fibrose active; AST proportionnellement moins élevée que l'ALT | HCV serology (4th generation anti-HCV ELISA); if positive, HCV RNA by quantitative PCR to confirm active viremia; viral genotyping; fibrosis assessment by FibroTest or FibroScan; treatment with pangenotypic direct-acting antivirals (DAAs) (sofosbuvir/velpatasvir, glecaprevir/pibrentasvir) available and reimbursed in Quebec via the RAMQ with a cure rate greater than 95% % |
| Chronic viral hepatitis B (HBV) | ALT variable depending on the phase of infection: normal during the immune tolerance phase (inactive carrier with high viral load), elevated during the immune elimination phase (chronic active hepatitis), fluctuating during the immune escape phase; sudden and massive elevation during reactivation | HBsAg (surface antigen), HBcAb IgG and IgM, HBeAg, HBeAb, HBV viral load (HBV DNA by PCR); HBV genotyping; fibrosis assessment; antiviral treatment (tenofovir disoproxil or alafenamide, entecavir) if indicated according to EASL and AASLD criteria; hepatocellular carcinoma (HCC) screening with bi-annual ultrasound if cirrhosis or chronic active hepatitis B |
| Autoimmune hepatitis (AIH) | Very high ALT during flares (5 to 50 times the normal limit); may mimic acute viral hepatitis on initial presentation; hypergammaglobulinemia (IgG greater than 1.5 times normal); autoantibodies: ANA (antinuclear antibodies), ASMA (anti-smooth muscle antibodies) in Type 1 autoimmune hepatitis; anti-LKM1 in Type 2 autoimmune hepatitis | Simplified scoring system for the diagnosis of AIH (IAIHG criteria) based on autoantibodies, IgG, histology, and absence of viral markers; liver biopsy essential (interface hepatitis, hepatocyte rosettes, plasma cell infiltrate); treatment with prednisone and azathioprine; rapid, often very favorable response (ALT reduction within weeks under corticosteroids) |
| Hereditary Hemochromatosis (HFE) | Moderately elevated ALT (2 to 5 times the ULN) in symptomatic forms; very high ferritin (often >500 to 1,000 µg/L, sometimes several thousand); transferrin saturation coefficient >45% % (early warning sign, first-line screening) | Mutation HFE (C282Y homozygote dans 80 à 85 % des hémochromatoses génétiques en population caucasienne québécoise; H63D/C282Y composé hétérozygote); IRM hépatique (surcharge en fer sans biopsie dans les cas typiques); phlébotomies thérapeutiques (saignées) en traitement de première ligne; dépistage des apparentés au premier degré |
| Wilson's Disease | Elevated ALT in young patients (typically 10-35 years old); paradoxically low or normal alkaline phosphatases despite severe hepatitis (suggestive sign in the context of acute liver failure); frequent associated hemolysis (Coombs-negative hemolytic anemia) | Low serum ceruloplasmin (less than 0.20 g/L in 95 % of cases); high 24-hour urinary copper (greater than 100 µg/24h); Kayser-Fleischer ring on slit-lamp examination (pathognomonic if present, but absent in 50 % of pure hepatic forms); liver biopsy with hepatic copper greater than 250 µg/g dry weight; ATP7B genetic test; chelating treatment (D-penicillamine, trientine) or oral zinc |
Medication and toxic causes of ALT elevation
Drug-induced liver injury (DILI) is the most common cause of acute liver failure in North America, ahead of viral hepatitis. It should be systematically considered in any unexplained elevation of ALT, regardless of the time elapsed between the introduction of the drug and the appearance of the abnormality (which can range from a few days to several months). The LiverTox database (NIH, livertox.nih.gov) lists over 1,300 drugs and substances with their hepatotoxicity profiles.
| Class or substance | Common medications in Quebec | Hepatotoxicity Profile |
|---|---|---|
| Acetaminophen (paracetamol) | Tylenol, Atasol, many combination preparations (cold, flu, opioids); most consumed over-the-counter medication in Quebec | Dose-dependent hepatotoxicity due to accumulation of the reactive metabolite NAPQI (N-acetyl-p-benzoquinone imine) when hepatic glutathione conjugation capacities are exceeded; standard hepatotoxic dose greater than 7.5 to 10 g in a single dose in healthy adults; threshold lowered to 4 to 5 g/day in case of chronic alcohol consumption, prolonged fasting, or enzyme inducers (rifampicin, antiepileptics); ALT may exceed 10,000 to 20,000 IU/L in severe poisoning; antidote treatment: IV N-acetylcysteine (NAC) to be initiated without delay according to the Rumack-Matthew nomogram |
| Statins (HMG-CoA reductase inhibitors) | Atorvastatin (Lipitor), rosuvastatin (Crestor), simvastatin, pravastatin; some of the most prescribed medications in Quebec for cardiovascular prevention. | Asymptomatic and transient elevation of ALT in 1 to 3 % of patients on statins, generally mild (less than 3 times the ULN) and spontaneously reversible even without discontinuing treatment in 70 % of cases; severe symptomatic hepatitis is very rare (less than 1 in 100,000); systematic monitoring of ALT before and during statin therapy is no longer recommended by most cardiology and gastroenterology societies since 2013; in case of persistent elevation greater than 3 times the ULN, consider dose reduction or a change of statin |
| Antitubercular | Isoniazid (INH), rifampicin, pyrazinamide; used for prevention (treatment of latent tuberculosis infection) and treatment of active tuberculosis | Frequent hepatotoxicity (10 to 20 % for mild ALT elevation; clinically apparent hepatitis in 1 to 2 % of cases); pyrazinamide is the most hepatotoxic, followed by isoniazid (slow acetylators CYP2E1 at higher risk) and rifampicin; monthly ALT monitoring recommended during anti-tuberculosis treatment, more frequent if risk factors (pre-existing liver disease, alcoholism, age over 35 years, pregnancy); discontinue treatment if ALT is more than 5 times the asymptomatic ULN or more than 3 times the ULN with symptoms |
| Nonsteroidal anti-inflammatory drugs (NSAIDs) | Ibuprofen (Advil, Motrin), naproxen (Naprosyn, Aleve), diclofenac, celecoxib, indomethacin | Mild to moderate elevation of ALT in 1-5 % of patients; diclofenac has the most pronounced hepatotoxicity profile among common NSAIDs; clinically apparent hepatitis rare but documented; reversible upon discontinuation; mixed mechanism (direct reactive metabolite and immunoallergic component) |
| Antibiotics | Amoxicillin-clavulanate (Clavulin, the leading drug cause of cholestatic DILI in Canada); nitrofurantoin; tetracyclines; fluoroquinolones; cotrimoxazole; isoniazid | Amoxicillin-clavulanate: predominant cholestatic profile (ALP and GGT higher than ALT) but can also produce mixed cytolysis; sometimes occurs 2 to 6 weeks after the end of treatment (delayed DILI); nitrofurantoin: chronic autoimmune hepatitis possible with prolonged use for prophylaxis of recurrent urinary tract infections, to consider in elderly women on long-term nitrofurantoin |
| Natural health products and dietary supplements | Kava (Piper methysticum); valerian; germander (Teucrium chamaedrys); berberine; comfrey (Symphytum officinale, pyrrolizidine alkaloids); certain bodybuilding supplements (contaminated protein powders, «natural» weight loss products); green tea in concentrated extracts (EGCG over 800 mg/day) | Hepatotoxicity is often underreported because patients do not spontaneously mention natural products during medical history; always inquire specifically about all natural products, dietary supplements, herbal teas, and alternative medicine preparations when evaluating unexplained ALT elevation; kava has been banned in Canada since 2002 but is available illegally; bodybuilding and weight loss supplements represent a growing cause of severe DILI in North America. |
Extrahepatic causes of ALT elevation
Although ALT is much more specific to the liver than AST, moderate elevations can be observed in certain extrahepatic conditions, particularly when accompanied by secondary or indirect hepatic damage.
- Undiagnosed or untreated celiac disease: ALT is moderately elevated in 15% to 40% % of celiac disease cases at the time of diagnosis, often being the only indicative biological abnormality; normalization of ALT under a strict gluten-free diet is expected within 6 to 12 months; any unexplained mild hypertransaminasemia in a patient with chronic diarrhea, refractory iron-deficiency anemia, or osteopenia warrants testing for tissue transglutaminase IgA antibodies (tTG-IgA).
- Hypothyroidism: ALT may be mildly to moderately elevated (1 to 3 times the ULN) in severe or prolonged hypothyroidism, due to slowed hepatic catabolism of circulating enzymes and direct hepatocellular damage related to thyroid hormone deficiency; normalization with levothyroxine is expected within 2 to 4 months.
- Intense physical exercise (exercise-induced rhabdomyolysis or simple post-exercise elevation): ALT may moderately increase after very intense or prolonged physical exercise (marathon, intensive weightlifting), partly due to hepatic release from micro-ischemia and partly due to muscle contamination of the measured fraction; AST and CK (creatine kinase) are then proportionally higher than ALT; CK measurement helps distinguish muscle origin from hepatic origin.
- Congestive heart failure and ischemic heart disease: Hepatic venous congestion secondary to right or global heart failure results in moderate to severe ALT elevation (congestive hepatopathy); acute decompensation (massive pulmonary embolism, cardiogenic shock) can cause ischemic hepatitis with very high ALT (greater than 10 times the ULN).
- Severe rhabdomyolysis: ALT is present at low concentrations in skeletal muscle; very severe rhabdomyolysis (CK > 10,000 IU/L) can cause elevated ALT due to direct muscle release and secondary ischemic liver injury from acute kidney injury; the ALT/CK ratio is very low in this context, allowing differentiation of a false elevation of muscular origin from true hepatitis
- Intravascular hemolysis: In severe hemolytic anemias (sickle cell crisis, thrombotic microangiopathy, transfusion hemolysis), the release of red blood cell AST leads mainly to an increase in AST, with ALT being less affected. This distinction is important from true hepatitis and can be confirmed by simultaneous measurement of haptoglobin (decreased), LDH (very elevated), and a blood smear.
AST/ALT Ratio: clinical interpretation
| AST/ALT ratio | Interpretation | Typical clinical setting |
|---|---|---|
| Less than 1 (predominant ALT) | Hepatocyte lysis predominantly in the cytosolic compartment; the liver is the primary source of the enzymatic elevation | Metabolic steatotic liver disease (MASLD); chronic viral hepatitis B or C; cytotoxic drug-induced hepatitis; hereditary hemochromatosis; Wilson's disease (except in acute liver failure); autoimmune hepatitis |
| Equal to 1 (balanced ratio) | Non-specific intermediate profile | Acute viral hepatitis A or B; onset of progression to cirrhosis in chronic liver disease (AST tends to catch up to ALT as fibrosis sets in) |
| Greater than 2 (predominant AST, De Ritis ratio) | Suggestive of alcoholic liver disease or cirrhosis regardless of cause; mitochondrial AST is preferentially released by hepatocytes damaged by alcohol | Acute alcoholic hepatitis (ratio often greater than 2 to 3); cirrhosis of any cause (loss of ALT-rich hepatocytes, predominant fibrosis); acute ischemic hepatitis; rhabdomyolysis (elevated muscle AST) |
| Greater than 3 to 5 (AST very disproportionate) | Muscle damage (cardiac or skeletal) or hemolysis contributing to elevated AST; or very severe alcoholic hepatitis | Myocardial infarction (cardiac AST); severe rhabdomyolysis; massive hemolysis; severe acute alcoholic hepatitis with high Maddrey score |
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The Fibrosis-4 Index (FIB-4) score is a validated non-invasive tool for assessing the degree of hepatic fibrosis in metabolic hepatic steatosis (MASLD) and chronic viral hepatitis B and C. It is calculated according to the formula: FIB-4 = age (years) × AST (IU/L) / [platelets (10⁹/L) × square root of ALT (IU/L)]. A score of less than 1.30 has a negative predictive value of over 90 % for advanced fibrosis (F3-F4), helping to reassure the patient and avoid costly additional tests. A score greater than 2.67 has a significant positive predictive value for advanced fibrosis, and warrants specialized evaluation by liver elastography (Fibroscan) or FibroTest. This score can be calculated at no extra cost from a routine biological work-up (age, AST, ALT, platelets), and is recommended by the American and European gastroenterology societies (AASLD, EASL 2023) as a first-line risk stratification tool for advanced fibrosis in primary care.
Diagnostic approach to elevated ALT
The approach to elevated ALT levels is based on a structured method that integrates the degree of elevation, the complete biological profile of the liver function tests, the clinical context, and the patient's risk factors.
| Step | Contents |
|---|---|
| Targeted medical history | Alcohol consumption (AUDIT-C tool, precise quantification in standard units per week); complete list of prescription medications, over-the-counter medications (paracetamol, NSAIDs), natural health products, dietary supplements, and bodybuilding or weight loss products; history of blood transfusions, tattoos, piercings, HBV/HCV infectious risk behaviors; recent travel to an endemic area for hepatitis A or E; family history of liver disease (hemochromatosis, Wilson's disease, autoimmune hepatitis); associated symptoms (fatigue, jaundice, abdominal pain, pruritus, arthralgias, weight loss) |
| Complete initial biological assessment | AST, ALT, ALP, GGT, total and conjugated bilirubin, prothrombin time/INR, albumin, CBC with platelets (thrombocytopenia suggestive of cirrhosis or hypersplenism); creatinine and electrolytes; fasting blood glucose and HbA1c (metabolic context); ferritin and transferrin saturation index (hemochromatosis); TSH (hypothyroidism); HBV (HBsAg, total HBcAb) and HCV (anti-HCV) serologies; if suggestive context: ANA, ASMA (autoimmune hepatitis), ceruloplasmin (Wilson's in young patient), IgA anti-tTG (celiac disease) |
| First-line imaging | Abdominal ultrasound with hepatic Doppler: assessment of liver echogenicity (steatosis), liver morphology (cirrhotic dysmorphia), gallbladder and bile ducts (dilation), spleen (splenomegaly suggestive of portal hypertension), and portal and hepatic vein vascularization (Budd-Chiari). |
| Non-invasive assessment of fibrosis | FIB-4 score calculated from standard blood test (age, AST, ALT, platelets); if FIB-4 is greater than 1.30: FibroTest (serum fibrosis markers) or FibroScan (liver elastography, available in gastroenterology and hepatology centers in Quebec) as a second-line test; liver biopsy reserved for situations where non-invasive tests are discordant, insufficient, or when histological diagnosis is essential (autoimmune hepatitis, Wilson's disease, atypical DILI). |
| Specialized reference | Gastroenterologist or hepatologist if: ALT persistently above 3 times the upper limit of normal for 3 to 6 months after investigation and correction of modifiable factors; suspicion of autoimmune hepatitis, Wilson's disease, primary or secondary biliary cholestasis; FIB-4 above 2.67; clinical or biochemical signs of cirrhosis; indication for antiviral treatment against HBV or HCV; severe drug-induced hepatitis |
Consult at Clinique Omicron
Clinique Omicron's physicians, at its locations in Quebec, take charge of the evaluation of any ALT elevation discovered incidentally or as part of a health check-up. During the consultation, our practitioners take a structured history, including assessment of alcohol consumption, a complete review of medications and natural products, and calculation of the FIB-4 score. The complete first-line biological work-up is prescribed and interpreted in an integrated manner, taking into account the patient's overall clinical and metabolic profile. Prescribing and monitoring treatment for chronic hepatitis B and C in collaboration with partner hepatologists is part of our practice. Our teams also systematically screen for genetic hemochromatosis, hypothyroidism and celiac disease when assessing unexplained hypertransaminasemia. For metabolic hepatic steatosis, our physicians support the patient in modifying lifestyle habits (diet, physical activity, weight control and cardiovascular risk factors) and coordinate referrals to hepatic ultrasound and elastography when non-invasive evaluation of fibrosis is indicated. Book an appointment at one of our points of service on the South Shore or at one of our branches in Quebec. Teleconsultation is available for interpretation of biological results and follow-up of patients with stable chronic liver disease.
The content of this page is provided for informational purposes only and is not intended to replace the advice of a qualified healthcare professional. Consult a physician for any symptoms, questions or decisions you may have regarding your health.
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