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About Your Liver

The liver is the largest organ in the body and divided into left and right lobes. The right lobe is larger. The blood supplied to the liver via two main vessels namely the hepatic artery (is a branch of the coeliac axis and supplies 25% of the total blood flow) and the portal vein (drains the gastrointestinal tract and the spleen). 50% of the oxygen is supplied via the portal venous system.

Functions of Liver

  • Protein Metabolism
    • Principal site of synthesis of all circulating proteins with gamma globulins produced in the reticuloendothelial system
    • Key proteins include albumin, globulin and fibrinogen
    • Albumin has a half-life of 16-24 days and 10-12g are synthesized daily with its main function to maintain colloid osmotic pressure and to transport water-insoluble substances such as bilirubin, hormones, fatty acids and drugs. Reduced synthesis of albumin is seen in chronic liver disease and malnutrition.
    • Transport or carrier proteins like transferring and ceruloplasmin, and other proteins such as alpha-1-antitrypsin and alpha-fetoprotein are also produced in the liver
    • Synthesizes all coagulation factors apart from factor VIII, such as fibrinogen, prothrombin, factors V, VII, IX, X, XIII and components of the complement system.
  • Degradation (nitrogen excretion)
    • Convert amino acids into ammonia and excreted by the kidneys to eleminate nitrogenous waste. Failure of this process occurs in severe liver disease
  • Carbohydrate metabolism
    • Glucose homeostasis and maintenance of the blood sugar. It stores ~80g of glycogen. During fasting, blood glucose is maintained either by glucose released from the breakdown of glycogen (glycogenolysis) or by newly synthesized glucose (gluconeogenesis) using lactate, pyruvate, amino acids from muscles, glycerols from lipolysis of fat stores. In prolonged starvation, ketone bodies and fatty acids are used as alternative sources of fuel and the body tissues adapt to a lower glucose requirement.
  • Lipid metabolism
    • Synthesize s very low density lipoproteins (VLDL) and high density lipoproteins (HDL). The liver and kidney are the major sites of HDL catabolism whilst LDLs are degaraded by the liver after uptake by specific cell surface receptors.
    • Triglyceride and cholesterol synthesis
  • Bile acid metabolism
    • Bile acids (cholic acid and chenodeoxycholic acid) are synthesized in hepatocytes from cholesterol with its main function as fat emulsifier
  • Bilirubin metabolism
    • Bilirubin is produced from the breakdown of mature red cells in the Kupffer’s cells of the liver and in the reticuloendothelial system.
    • 250-300mg of bilirubin is produced daily
  • Hormone and drug inactivation
    • The liver is the major site of drug metabolism
    • Catabolizes hormones such as insulin, glucagons, estrogens, growth hormone, glucocorticoids and parathormone.
    • Most important site for the metabolism of drugs and alcohol. Fat-soluble drugs are converted to water-soluble substances, which facilitates their excretion in the bile or urine.
  • Immunological function
    • Antibody production
    • The liver acts as a ‘sieve’ for the bacteria and other antigens carried to it via the portal tract from the gastrointestinal tract
    • The reticuloendothelial system is thought to play a role in tissue repair, T and B cell interaction, and cytotoxic activity in disease processes

Key Indicators for Normal Liver Functions

Most liver function tests are just markers of liver disease rather than actual tests of “function” per se. A primary routine blood sample sent to the laboratory will produce serum levels of bilirubin, aminotransferases (ALT, AST and G-GT), alkaline phosphatase, gamma glutamyl transferase and serum proteins. Secondary tests include antinuclear factor, antimitochondrial antibody, antismooth muscle antibody, viral markers (IgG and IgM), alpha-fetoprotein, serum iron, serum and urinary copper and alpha1-antitrypsin.

Common Tests What to Predict Normal Levels Causal Factors
Bilirubin Normal bilirubin metabolism   Increased serum bilirubin is usually accompanied by other abnormalities of liver function, alcoholic hepatitis
AST (aspartate aminotransferase)/SGOT Liver cell damage   Hepatic necrosis, cardiac infarction, muscle injury and congestive heart failure, hepatitis
ALT (alanine aminotransferase)/SGPT Liver cell damage   Alcoholic hepatitis
G-GT (gamma glutamyl transferase) Liver cell damage   Diabetes and certain drugs and alcohol
Alkaline Phosphatase Liver cell damage   Cholestasis from any cause, primary biliary cirrhosis
Serum Proteins Severity of chronic liver disease   Biliary cirrhosis, autoimmune chronic active hepatitis
Alpha-fetoprotein Fetal liver   Hepatocellular carcinoma, neural-tube defects of the fetus

Types of liver disease

  • Acute liver disease
    • Jaundice and enlarged liver
    • Pale stools and dark urine
    • Spider naevi and liver palms in severe acute disease
  • Chronic liver disease
    • The skin: The chest and upper body may show spider naevi of which consist of a central arteriole with radiating small vessels. The hands may show palmar erythema. Xanthomas (cholesterol deposition) may be seen in the palmar creases or above the eyes in primary biliary cirrhosis
    • The abdomen: Enlarged liver and spleen
    • The endocrine system: Gynaecomastia and testicularatrophy in males which is probably related to altered estrogen metabolism or to treatment with spironolactone.
  • Jaundice
    • Jaundice (icterus) is detectable when the serum bilirubin is more than 30-60 mmol/L. Jaundice can be classified as
      1. Haemolytic jaundice
        1. Increased breakdown of red cells leads to an increase in production of bilirubin
        2. Main cause is due to haemolytic anaemia
      2. Congenital hyperbilirubinaemias
        1. a. Gilbert’s syndrome is the commonest
        2. Asymptomatic and is usually detected during a routine check
        3. Not a serious disease
      3. Cholestatic jaundice (including parenchymal liver disease and large duct obstruction)
        1. Intrahepatic cholestasis – caused by swelling of hepatocytes and edema in parenchymal liver damage or to an excretory dysfunction of the bile canaculi at a cellular level
        2. Extrahepatic cholestasis – caused by large duct obstruction of bile flow at any point in the biliary tract distal to the bile canaculi
  • Viral Hepatitis
    • Hepatitis A
      • Commonest type of viral hepatitis due to Hepatitis A Virus (HAV)
      • Arises from the ingestion of contaminated food (e.g. shellfish, clams) or water
      • Last up to 2 weeks and affects other parts of the body besides liver such as the heart, pancreas, gastrointestinal tract and spleen
      • Symptoms include nausea, vomiting, feel unwell, diarrhea, anorexia, headaches, malaise and a distaste for cigarette
      • Fever is usually mild and there may be upper abdominal discomfort
      • Liver is tender but not enlarged initially
      • Hepatitis A never progresses to chronic liver disease and there is no specific treatment thus prevention is more important by an injection of normal immunoglobulin, good hygiene and improved sanitation. The virus is killed by boiling water for 10 minutes.
    • Hepatitis B
      • The Hepatitis B Virus can only be transmitted within the human population
      • Spread is usually through the intravenous route such as transfusion of infective blood, contaminated needles used by drug addicts, tattooists or acupunturists, or by close personal contact e.g. sexual intercourse, particularly in homosexuals and from mother to child during parturition or soon after birth
      • The virus is found in semen and saliva
      • The virus only replicates in the liver and may be an important link in the development of hepatoma
      • Clinical features similar to Hepatitis A
      • Vaccination should be considered for people at special risk e.g doctors, patient with hemophilia or on dialysis, spouses and sexual partners of chronic hepatitis B carriers, drug addicts and homosexuals
    • Non- A no-B hepatitis
      • Accounts for 15-20% of cases
      • Transmitted by blood and blood products
      • Hepatoma can occur as chronic liver disease may develop
  • Cirrhosis
    • Resulted from the necrosis of liver cells followed by fibrosis and nodule formation
    • Alcohol is the commonest cause
    • Indicators:
      • Low albumin (<25 g/L)
      • Low serum sodium (<120mmol/L
      • Prolonged prothrombin time
      • Persistent jaundice
      • Failure of response to therapy
      • Haemorrhage from varices
      • Neuropsychiatric complications developing with progressive liver failure
      • Small liver
      • Persistent hypotension
  • Carcinoma/ Liver Tumours
    • Commonest is a secondary (metastatic ) tumour particularly from the gastrointestinal tract, breast or bronchus
    • Primary liver tumours either benign (haemangioma) or malignant (hepatocellular carcinoma/hepatoma) but usually malignant will be the case
    • Carriers of hepatitis B have an extremely high risk of developing hepatoma of which 90% of patients with this cancer are hepatits B positive
    • Other factors are aflatoxin (a metabolite of a fungus found in groundnuts), contraceptic pills and androgenic steroids
    • Hepatoma normally presents below the age of 50 years
    • The clinical features include weight loss, anorexia, fever, an ache in the right hypochondrium , enlarged liver and ascites
    • Alpha-fetoprotein is usually raised
  • Alcoholic liver disease
    • Alcoholic hepatitis
      • Necrosis of liver cells and infiltration with polymorphonuclear leucocytes
      • Become cirrhosis if alcohol consumption continues
      • Clinical features include abdominal pain, jaundice, hepatomegaly, ankle edema, ascites and sometimes splenomegaly
      • Branched chain amino acids e.g. leucine, isoleucine and valine is helpful
      • Patients are advised to stop drinking for life
    • Alcoholic cirrhosis
      • Destruction and fibrosis with regenerating nodules produces cirrhosis
      • Fatty liver may be present
      • Elevated bilirubin, aspartate and alanine aminotransferases, alkaline phosphatase and prothrombin time

Drugs those are potential for hepatic damage

Type of Reaction Drug
Dose-dependent Paracetamol, Salicylates, Tetracycline
Dose- independent Antidepressants: Monoamine-oxidase inhibitors, Tricyclic antidepressantsAntituberculous drugs: Isoniazid, Para-aminosalicylic, Pyrazinamide or ethambutol, RifampicinAnticonvulsants and Antispasmodics: Phenytoin, Carbamazepine, Phenobarbitone, Sodium Valproate, DantroleneAnti-inflammatory Drugs: Indomethacin, Non-steroidalsAntibiotics: Penicillins, Sulphonamides Anaesthetics: HalothaneCardiovascular drugs: Amiodarone, Methyldopa, Perhexiline maleateAntifungal drugs: Ketoconazole
Cholestasis Pure cholestasis Cholestatic hepatitis Oral contraceptics, synthetic anabolic steroidsChlorpromazine, Erythromycin estolate, Antirheumatic drugs (sodium aurothiomalate), Antithyroid drugs (carbimazole), Hypoglycaemic drugs (chlorpropamide)
Fatty change Tetracycline
Hepatic fibrosis Methotrexate
Chronic active hepatitis Methyldopa, Nitrofurantoin, Sulphonamides, Oxyphenisatin
Granulomatous reaction Sulphonamides, Methotrexate, Hydralazine, Allopurinol, Chlorpropamide
Liver tumours and peliosis hepatitis 17-alpha-Alkylated synthetic androgens (hepatocellular carcinomas), Oral contraceptives (benign adenomas)

How to keep our liver healthy?

Prevention is always better than cure. Nutrition plays very important role in keeping the liver to function normally and healthily. Basically, the liver needs nutrients for detoxification, cell rejuvenation and elimination of toxic waste. EnerFlex® has been found to be a suitable candidate to take care of liver health as it contains most of the key nutrients required by the liver. Clinical study showed that besides regulating cholesterol disorders, hypertension, EnerFlex® also helped to reduce/normalize elevated liver enzymes. For best result, we suggest that EnerFlex® plus AFA 20g-40g per day should be included in the liver rejuvenation program as AFA helps in detoxification.

Liver Detox Pathway
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