Morbidity due to serum hepatitis and toxic hepatitis is increasing all over the world. Under homeopathic treatment, 90% of VBH (Viral B Hepatitis) will be cured in 6 months. ALFALFA tincture is one of the best tools for chronic hepatitis. It is available from all homoeopathic doctors.
The liver is the largest organ in body. It is situated in the right upper abdomen largely under the right lower ribs. It is a dark brown, highly vascular soft organ and retains the shape of a blunt wedge. It weighs 1200 to 1500 gm or about 2% of the total adult body weight.
The liver is both a secretory and an excretory gland. It secretes about 1000 ml to 1500 ml of bile in 24 hours, of which 80% to 90% is reabsorbed. Normal secretion of bilirubin is about 5 to 16µml / liter.
Functionally, the liver has 2 lobes which are subdivided into many lobules and the later are composed of a radial column of hepatic cells arranged around the central vein. Between the columns of liver cells are sinusoid lined in places by kupffers cells which are of a polyhedral structure about 30µ in diameter. The sinusoids are drained to a central vein. The sinusoid are supplied by both the portal and hepatic arteries and through them blood enter the central vein. Liver cells are separated from sinusoid by a space contain tissue fluids draining to hepatic lymphatics. Lymph flow through the liver is about 75 ml /minute.
Intercellular canaliculi arise between liver cells and radiate outwards from the central axis of lobules, while vascular capillaries at the side of hepatic cells are going inwards and join to the central vein. The bile canaliculi are devoid of endothelial lining and contain numerous mast cells. Bile ductules are surrounded by collagen fibers.
The portal tract lies at the periphery of the lobules, and consists of inter lobar branches of the hepatic artery, inter lobar vein, and bile ductules, all being layered with fibrous capsules.
Liver cells: Cytoplasm contains glycogen, fat, and basophilic material. Mitochondria, the site of energy production contain phospholipids, cytochrome oxidase and succinoxidase. Endoplasmic reticulum similar to basophils is the site of detoxification of drugs, conjugation of bilirubin, synthesis of steroids and synthesis of protein. Acid phosphatase is formed in lysosomes. It is the site of deposition of ferritin, lipofusin, copper and bile pigments. It also contains hydrolytic enzymes. Bile is formed in the vacuoles of hepatic cells.
The liver receives blood from two sources, the portal vein (70 %) and the hepatic artery (30 %). The blood from the superior mesenteric vein (60 %) and splenic vein (40 %) are drained to portal vein.
The left lobe receives blood mainly from splenic vein while right lobe receives the blood (contain food) from the mesenteric vein.The left lobe is relatively larger in infants. Cirrhosis by nutritional deficiency is more likely to occur in the left lobe.
Blood flow through liver is about 1.5 l / minute (Blood flow/ minute through the heart and liver per 100 gm are about 85 ml and 100 ml respectively). The liver is also a reservoir of blood and thus can control the systemic blood pressure (Sympathetic sinusoidal constrictions cause portal and systemic hypertension).
Normal pressure in the portal vein is about 5mm to15mm of Hg, as compared with about 6mm in hepatic vein, thus an adequate flow through sinusoid takes place. Mixing of blood is takes place in sinusoids.
Oxygen saturation in the hepatic artery and portal vein is about 95% and 50% respectively. Oxygen saturation is less in the center portion of lobules. So, hepatic artery thrombosis, portal obstruction, emphysema, cardiac failure, and severe anemia etc. affect mostly in the center of liver lobules. The liver is always very susceptible to viruses and toxins due to this borderline supply of oxygen.
Each portion of lobules has a different susceptibility.
Diffuse necrosis: HAV, toxins (lead, arsenic, phosphorous, chloroform, sulphonamide, carbon tetra chloride. mushroom; hyperthyroidism)
Focal necrosis: Bacteria (diphtheria, salmonella and streptococcus)
Peripheral necrosis: Virus infection, eclampsia of pregnancy, bleeding diathesis
Mid zone necrosis: Spirochete, streptococcus, yellow fever
Central zone necrosis: Toxins
The liver performs the following vital functions:-
Derangements of hepatic function do not begin simultaneously; it progresses in a parallel fashion.
1. Formation and destruction of RBC
2. Manufacture and elimination of bile: Bile is a complex, alkaline, yellowish green fluid, formed in vacuoles of liver cells and discharged to bile canaliculi. Chief constituents are water (98%) and solids (2%) which include
A. Inorganic salt- chlorides, carbonates and phosphates of Na, Ca, and K; NaHCo3.
B. Bile salts – sodium taurocholate, sodium glycocholate.
C. Pigments – bilirubin, biliverdin
D. Cholesterol, lecithin, fatty acids and mucin.
Bile too has many functions. It acts as a lubricant and promotes peristalsis. It neutralizes the duodenal and gastric acidity. It is involved in the excretion of zinc, mercury, copper, pigments, cholesterol, lecithin, toxins and bacteria. Bile salts aid emulsification, digestion and absorption of fat. 80% of bile salts are reabsorbed to the liver. The normal ratio of bile salts and cholesterol is about 20:1. When the ratio is reduced to 13:1 precipitation takes place.
3. Formation of glycogen, neoglucogenesis and glycogenolysis
4. Metabolism of protein (Gama globulin are not synthesized in liver but from plasma cells. Its level is increased in chronic liver damage due to RE system activity.), deamination of amino acids, formation of plasma albumin and alpha & beta globulin. A normal individual produces 1 to 16 gm of albumin daily.
5. Synthesis of prothrombin (bile salts insufficiency in the intestine is due to obstruction in the bile duct which affects the absorption of fat soluble vitamin K thus synthesis of prothrombin in the liver is inhibited. Prothrombin time may be increased > 22 seconds both in the hepatic damage and in biliary tree obstruction), heparin (which prevents intravascular clotting) and fibrinogen.
6.Metabolism of lipid and cholesterol: 2 gm of cholesterol is synthesized in the liver and about 1gm is excreted through bile daily. Esterification occurs in liver cells. 25% of cholesterol should be esterified. Total cholesterol is increased in biliary obstruction and esterified cholesterol is lowered in cellular damage. So the ratio of total and free cholesterol is lowered.
7.Storage of fat, absorption of fat soluble vitamins; formation of the phospholipids from phosphoric acid, glycerol, and choline etc
Normal fat content of liver is less than 5%. Liver converts the free fatty acid derived from depot fat and food fat into triglycerides.
8. Storage of copper, iron, folic acid, vitamin B12, A, D etc:
9. Synthesis of urea, uric acid, zinc enzyme (dehydrogenase -essential for alcohol metabolism)
10 Production of immune bodies
11. Detoxification by the process of hydrolysis, oxidation, reduction and conjugation
12. Inactivation of hormoneslike estrogen, adrenal corticoids, testosterone, thyroxine, ADH, insulin and glucagon: Hormones conjugate with liver protein & glucuronic acid and excreted to bile. If this is impaired hyper hormonal activity may manifest.
14. Production of heat
15. Enzymatic functions: ALP is found abundantly in osteoblast of bone, bile canaliculi, small intestinal epithelium, proximal tubules of kidney, placenta and in the breast during lactation. Normal alkaline phosphatase is removed from blood by hepatic cells and excreted through bile. Normal serum level in adults is 4-13 king Armstrong units/100ml and in children is 10 to 20 KA units/100ml. It’s level is primarily elevated due to obstruction in the icteric phase. Acetyl cholinesterase is exclusively produced by liver cells.
The icterus (yellow discoloration) is associated hemoglobin – haemosiderin, haematozoin, bilirubin and haematoidin). 1 gm of RBC yields 35 mg of bilirubin.
Hyperbilerubinemia occurs in case of excess of destruction of RBC, liver damage, or obstruction in biliary ducts.
Conjugation is essential for bilirubin excretion. Bilirubin conjugates with glucuronic acid and becomes soluble. Unconjugated bilirubin is fat soluble. Unconjugation also occurs in deficiency of glucoronyl transferase. The conjugated bilirubin can pass only through the glomerular membrane and can be identified in urine by color.
Hyperbilerubinemia occurring in hemolytic jaundice is the unconjugated type. Sulphonamide can convert conjugate bilirubin to the unconjugated one. Testosterone and steroids can inhibit transfer of pigments across the liver cells.
Insoluble and soluble bilirubins are excreted to the intestine and expelled through the feces as stercobilnogen. Soluble bilirubin is reabsorbed partly through the gallbladder and intestinal lining and excreted through urine as urobilinogen.
The urobilinogen may be absent in urine either due to lack of conjugation in liver or failure in transportation through the bile canal system. The urobilinogen in urine will be high in hemolytic and hepatocellular damage (re excretion failure).
with an increase in serum bilirubin. Bilirubin is derived from hemoglobin. Normally 6 gm of hemoglobin per day is broken down from RE cells of various parts especially in bone marrow, the spleen and liver. (4 types of pigments are derived from the breakdown of
Hepatitis means inflammation of the liver, due to infection or toxic substances. Infectious agents include viruses, bacteria (Klebs loeffler bacillus, salmonella, streptococcus), richettsia (Q fever), spirochete (leptospirosis, canicola fever, relapsing fever), parasites (liver fluke in Africa and China), toxic agents including drugs, anesthetics, industrial chemicals, insecticides, aflatoxin, yeasts, metallic compounds and alcohol. Hepatitis may also develop following the congestion which occurs from emphysema, RVF, bile duct obstruction or by allergic reactions.
Deficiency hepatitis may occur rarely due to either lack of lipotropic factors like choline and sulphur containing amino acids (cystine and methionine), or following mal-absorption syndrome. It may develop in alcoholics due to magnesium deficiency.
Viral hepatitis is the 4th among the 30 leading communicable diseases.
Several viruses cause hepatitis. The most common types are classified alphabetically as HAV, HBV, HCV, Delta virus and HEV.
Arbo viruses (yellow fever, dengue fever and kayasanur fever), Epstein Barr virus (infective mononucleosis), inclusion of cytomegalovirus viruses, rubella virus, herpes simplex virus, Cox Sakie virus etc. can cause hepatitis in susceptible individuals.
VHA is a common disorder in India. HAV is present in stool and semen during pre icteric and early icteric phases of diseases. Transmission of HAV usually occurs following fecal contamination of water and milk, although infusion of infected blood obtained from a virimic donor may cause sporadic infection. It may be carried by flies. Occurrence is dependent on the susceptibility of exposed population and distribution of infected material.
Epidemics are common in poverty groups, military forces, summer camps, and institutions. Outbursts may also take place following the consumption of polluted shellfish or sea foods. Recovery generally occurs within 4 weeks. There is no carrier state following VHA. Mortality rate is about 2/1000. Incubation period is 2 to 4 weeks.
Hepatitis Bis the most serious form of hepatitis found throughout the world. It is spread as HIV through sexual contact, blood transfusion, infective blood products (albumin solutions, Plasminogen, and gamma globulin are free of risk), exposure to an infected person’s blood via surgical and dental instruments, immunization, acupuncture, ear piercing, tattooing, shared needles, piercing tools, cuts, bites, open wounds, tooth brushes, razors etc.
About 85% of homosexual men have it.Potent sources are massive transfusions such as those used in a heart lung bypass, renal dialysis, pooled human plasma, or through blood products like fibrinogen and anti hemophilic globulin. Inoculation of as little as 0.01ml of infected blood may transmit HBV.
HBV is present in blood, all physiological fluids, with the exception of stool, urine, vomit, sputum, nasal secretion, sweat and tears. HBV can survive outside the body for at least 7 days and can be still capable of causing infection. HBV replication may follow after immunosuppressive drugs or chemotherapy.
VBH in children occurs through vertical transmission from mother and through injection procedure in early childhood. It is estimated that about 90% of infants are infected at birth, 30%of children are infected at age of 1-5years and 2%-6% of adults don’t clear the virus from their bodies and remain able to spread the virus.
VBH may take 6 months to produce symptoms. About 50% of adults with VBH have no jaundice when the infection first develops.
Individuals who remain HBV surface antigen positive for at least 6 months are considered to be HBV carriers. The children can become active carriers in early adulthood. Incubation period: 1 to 6 months.
Hepatitis Cis the most common cause of chronic hepatitis. It is transmitted by blood transfusion (90%) and blood contact. Incidence is more common in developing countries. Vertical and sexual spreads are uncommon. VCH may take 6 months to produce symptoms.
About 80% of these people have no jaundice when the infection first develops. They develop chronic hepatitis and show no specific symptoms for up to 20 to 30 years. It is estimated that there are > 300million carriers.
Hepatitis D is an ongoing infection of HBV and is required before HDV is capable of replication. It is the most serious and the rarest form of hepatitis. VDH takes 1-2 months to produce symptoms
Hepatitis Eis generally contracted from drinking sewage-contaminated water. The mortality rate among pregnant women is high, at about 20%.
Symptoms of acute hepatitis
Pre icteric phase: Early symptoms are anorexia, nausea, vomiting and tenderness in the liver region. Fever lasts 3 to 7 days. Skin rashes, arthralgia, arthritis, pruritus, neck stiffness also occur in pre icteric stage. Urine may show bilirubin before the patient is icteric. Pain in upper abdomen occurs due to over stretching of liver capsule by passive congestion.
Icteric phase: Fever and jaundice occur more when the liver is apparently damaged. Temperature returns to normal and jaundice develops. Jaundice disappears shortly after 10 days, but it may last longer in older patients. Spleen and lymph glands at the right side of neck may be enlarged.
Symptoms of obstructive jaundice may develop in some cases of viral hepatitis due to bile thrombi blocking, in minute biliary ducts. Early stage of hepatitis may be evidenced by enlargement of the liver but atrophy is the common feature later. Acuteness of diseases is less marked in VBH. Viral hepatitis is infective in the early days of acute symptoms. Mortality rate is about10-20% .
Complications are cholestatic hepatitis, chronic active hepatitis, liver failure, cirrhosis (20% HCV), hepato cellular carcinoma and death. VAH does not lead to chronic hepatitis or a carrier state and only rarely does it cause massive liver necrosis. All individuals with chronic liver disease are more susceptible to viral hepatitis.
|DIFFERENT TYPES OF JAUNDICE|
|Distribution of pigment||Conjunctivararely affected||Seen in the skinbefore conjunctiva||Seen in conjunctiva before the skin|
|Pruritus||Not present||May be present||Severe +|
|Color of stool||Normal||Normal or pale||Pale +|
|Urine||No bilirubin; Urobilinogen andurobilin present||Often no bilirubin||bilirubin present +|
|Liver||Little or large,but not palpable||Normal/large/small||Large|
|Spleen||Palpable||Rarely palpable||rarely palpable|
|Anemia||Severe +||Usually not severe||may or may not be present|
|Serum alkaline phosphatase||Little increased||Little increased||Increased +|
|Thymol turbidity||Variable||Positive +||Negative|
|Albumin/globulin ratio||Normal||Low albumin,raised globulin +||Normal|
|Prothrombin time||Normal||Decreased||Normalexcept in late stage|
|Van den Bergh reaction||No direct reaction||Indirect reaction +||Direct reaction +|
|Serum bilirubin||High serum bilirubin +||Moderate bilirubin and serumurobilinogen||Steadily rising|
Fulminant acute hepatitis (1%)
Certain adults develop acute hepatitis within 4 weeks of onset of initial illness, and manifested as acute encephalopathy without history of pre existing liver diseases. This type of acute hepatitis occurs more in association with VCH.
Predisposing factors are multi viral infection, leptospirosis, septicemia, liver abscess, malaria, hepatotoxins, amino oxidase inhibitors, Halothane anesthetic, over dose of paracetamol, drug hyper sensitivity, certain foods which include mycotoxin, senecioses etc.
Symptoms: Pre icteric symptoms are short with a high fever, abdominal pain, and vomiting. The icteric phase is with rapid onset of coma, focal fits, hyperpyrexia, cramps, flapping tremor, plantar extension, dilated pupisl, changes in electrolyte balance, generalized bleeding, ascitis, hypotension, hypoglycemia, leucocytosis, and hypoxia. Prothrombin time is increased. Urine may show crystals of leucine and tyrosine. The liver shrinks rapidly. This illness may last 6-8 weeks. Mortality rate in this group is 70% to 80%. The victims of fulminant hepatitismay die within 2 weeks of onset of illness.
Sub acute hepatitis
Usually occurs in the right lobe
Symptoms: Fever, anorexia, nausea, abdominal pain etc. lasts up to the first few week of the icteric stage. Hypo albuminemia, hyperglycemia, hyper bilirubinemia are seen. Patient remains icteric for a long time or hepatic failure may develop within 12 months. Aplastic anemia (due to changes in bone marrow) and neurasthenia are also common.
Other causes are allergies, eosinophilic infiltration and toxicity due to arsenic, testosterone, or Para amino salicylic acid. Frothy, bulky and clay colored stool due to absence of bile salts, increased serum cholesterol, conjugated hyper bilirubinemia, raised alkaline phosphatase >30 KA units, absence of urobilinogen in urine, itching, xanthelasma are the main features. Hyper gamma glubinemia, raised SGOT, A.N.F and L.E cell tests may be positive in certain allergic individuals.
The degree to which the liver was exposed to toxins, determines the amount of damage. Toxins find a favorable environment for the replication of viruses within hepatic cells. Long consumption of antibiotics and steroids can promote the opportunistic infections. Chloroform and arsenic affect the liver enzyme system by neutralizing the lipotropic amino acids (cystine and methionine).
List of hepatotoxic drugs
Hepatitis: Halothane, paracetamol, phenytoin, carbon tetra chloride, iproniazid, phenyl butazone, acetazolemide, sulpha group
Cholangitis: Chlorpromazine, arsphenamine, thiouracils, para amino salicylate
Fatty degeneration: Steroids.
Encephalopathy: Ammonium salts (they can pass through damaged liver cell and may precipitate a coma).
Other drugs: Pethidine, PABA, and Chloramphenicol.
Other toxic agents: Phosphorus, benzenes, aluminum, mercury, phenol, picric acid, sulphuric acid, benzoic acid, barium salts and lead.
Various Blood tests are valuable in identifying symptomless carriers as well as determining the etiology of some form of chronic liver diseases.
Plasma protein: Plasma albumin level is lowered even in mild hepato cellular disease. The normal level of 3.6 gm to 4.7 gm/100 ml may fall to 2 gm in severe liver disease. The globulin fraction is elevated > about 2.8gm/100 ml.
Thymol turbidity test (normal value is 0 to 4 units.): It is increased in viral hepatitis, but it is normal in obstructive jaundice.
Amino transferases are present in all cells, but the concentration is greatest in heart, liver and striated muscles. Normal level of both aspartate amino transferase (SGOT) and alanine amino transferase (SGPT) are less than 18 IU / liter of serum (40 spectro photo metric unit/ml). Alanine amino transferase (SGPT) is increased in cellular hepatitis specifically.
Vanden Bergh test: Direct is positive in obstructive and indirect (adding alcohol) in hepatic and hemolytic jaundice.
Antibodies are proteins produced by WBC which can be detected in blood within weeks of infection and remain detectable in blood for long periods.
Antibodiestests are HAV antibody serum, HB surface antigen antibody serum, HB envelop antigen antibody serum, HB core antigen antibody; HC core antigen antibody and HDV antibody.
Viral protein tests are HB surface antigen, HB envelope antigen, HB DNA and HC RNA.
Other investigations: Avoid unnecessary biopsies because of bleeding and secondary acute inflammations.
|BLOODNORMAL PHYSIOLOGICAL VALUES|
|NORMAL VALUES||INCREASE IN||DECREASE IN|
|Serum amylase80 -160 |
Somogyi units / 100 ml
|Acute surgical disorder(above 160 units)|
(above 200 units)
Biliary tract disorder
(above 1000.S units)
|Serum Alkaline phosphatase5 – 13 KA units||Obstructive jaundiceMyeloid leukaemia|
|Serum bilirubinDirect 0.4 mg-1mg %|
Indirect 0.2 – 0.7 mg %
Total 0.3 to 1.1 mg %
|Obstructive jaundiceHaemolytic jaundice|
|Serum Chloride100 mEq / L||NephritisUrinary tract obstruction||Vomiting, DiarrhoeaDiuretics|
|Serum cholesterol150 – 250 mg/100 ml||Familial cholestrolaemia HypothyroidismNephrotic syndrome|
|Blood creatinine0.7-1.5 mg %||Renal insufficiency, Shock,Dehydration, G.I. bleeding||CachexiaHepatic failure|
|Serum fibrinogen200- 400 mg %||Infectious diseaseInflammation|
|Hepatic -insufficiencyPost partum|
|Serum folic acid7-16 nano gm/ml||Haemolytic anemiaMegaloblastic anemia|
|Serum globulin2.5 -3.0 gm/100 ml||Chronic infection, MyelomaRheumatoid arthritis|
Cirrhosis of liver
80-140 mg %
80 – 120 mg %
|Diabetes mellitusMyocardial infarction|
|AlcoholDrugs like salicyclates|
Sulphonilurea, PABA, Insulin., Myxoedema
|Serum iron75 – 175 micro gram / 100 ml|
45 mg %
|Lactic dehydrogenase90 – 200 I.U||Myocardial infarctionAcute haemolysis|
|Serum albumin3.0 -5.5 gm/ 100 ml|
6.0 – 8.0 gm/ 100 ml
|Blood potassium3.5 – 4.5 mEq / L||Renal insufficiencyCell necrosis|
|Steroids, DiarrhoeaRenal tubular acidosis|
|Serum sodium135 – 145 mEq / L||Excessive sweatingInsufficient water intake|
|Water intoxicationExcess of ADH|
|S.G.O.T5 – 40 units / ml||Hepatitis, InfarctionAcute infection|
|S.G.P.T5 – 35 units / ml||Myocardial infarctionHepatitis|
Liver cirrhosis is the 12th leading cause of death by disease.
Causes of cirrhosis
VBH & VCH, alcoholism, auto immune liver disease, inherited alpha-1 antitrypsin deficiency, galactosemia, glycogen storage diseases, Wilson diseases; cardiomyopathy, corticosteroid, childhood biliary atresia, biliary obstruction, hepatotoxins, haemochromatotosis, chronic venous congestion, schistosomiasis, diabetes, protein malnutrition and obesity.
Feature of portal hypertension: Haematemesis, spleenomegaly with pan cypocytopenia, ascitis
Other features: parotid enlargement, prostatic enlargement, opportunistic infection, female breast atrophy, gynacomastia, testicular atrophy, scanty body hair, Dupuytren’s contracture,Xanthomatosis, steatorrhoea, osteomalacia & osteoporosis due to vitamin D deficiency, fluid retention, edema, low serum sodium, clubbing and hyperkinetic circulation.
Features of hepatic failure: Fatigue, low grade fever, weight loss, indigestion, offensive breath, bleeding tendency, white nails, palmar erythema, spider naevi, jaundice in later stage, firm hepatomegaly
Encephalopathy: Lethargy, slurred speech, flapping tremor dementia, delirium and coma.
Fatty Lymphocytes and monocytes may be lowered in peripheral blood owing to excessive infiltration of the same at the portal zone of lobules. Acetylcholine esterase is decreased in hepatic injury. So symptoms of parasympathetic over activity may develop. Persistent swelling of liver cells may obstruct the hepatic capillaries and aggravate the hypoxia. The Hyperthyroidism worsens this condition if present.
Liver cancer is the 5th most common cancer globally. It may originate either as solitary nodules which spread to other lobules or as multi focal nodules simultaneously. Multi nodular hyperplasia is seen more in post viral cirrhosis (20%) than alcoholic cirrhosis. The adeno carcinoma originating from bile duct epithelium is not associated with cirrhosis. The course is more rapid in this case.
Secondary liver nodules occur more in surface of the liver and are originated directly from the stomach or the gall bladder. It is also developed mainly through the portal vein, hepatic artery and retrograde lymphatic permeations. These nodules are more than 2cm in size and have an umbilication in the center. Sinusoidal hepatic circulation provides a favorable site for the growth of malignant cells. Melanoma of the liver also occurs as metastasis.
Metastasis: It usually metastasizes to the lymph glands of the supra clavicular fossa, lungs, ribs, spinal column or brain.
Predisposing causes : inborn susceptibility, elevated hereditary alpha-fetoglobulin level, chronic serum hepatitis, cirrhosis (20%), alcohol use, aflatoxin (the incidence is highest in oriental races due to aflatoxin which is a product of mold found in rice, soybeans, wheat, peanuts, and corn), pesticides, industrial toxins, thorium dioxide, steroid abuse, male gender ((less in female due to iron loss through the menses), haemochromatosis ((20 %), tobacco smoking, fatty liver, hypothyroidism, old age, schistosomiasis, clonorchiasis and nutritional deficiency etc.
Common symptoms are non specific fever, abdominal pain, weight loss, sudden appearance of ascites, symptoms of portal hypertension, and jaundice. Pain is due to peri hepatitis. Deposits on the hepatic porta also cause jaundice. Pressure symptoms may occur by obstruction on the inferior vena cava or portal vein. Some children may show precocious puberty in hepatoma. Other features are similar to symptoms of chronic hepatitis.
Pruritus usually occurs due to presence of histamine, bile salts or insufficiency of circulating testosterone. A vascular noise may be heard over the tumor.
Differential diagnosis: hepatic artery thrombosis, cirrhosis, yellow fever and toxic hepatitis. Many of homeopathic tinctures and minerals have an influence on liver cancer.
Prevention of VAH: Improve sanitary habits and personal hygiene. Eat only fresh and cooked foods. Restrain from eating processed foods.Water should be boiled before using in epidemic area. Other measures are isolation of the patient and proper disposal of night soiling.
Prevention of VBH: This can be achieved by increasing health, a better diet and hygiene. Use deep breathing exercises (exhale through lips slowly first, then inhale through nose rapidly; avoid other non physiological patterns) to get adequate Oxygen to the center part of lobules. Practice massage and physical exercise. Promote early elimination all body toxins (macro miasm) through the nearest natural orifices. Abstain from alcohol, toxic drugs, processed foods, pickled foods and bakery items.
Don’t share personal items like drug solutions, syringes, needles, shavers, masks, gloves, tooth brushes and manicure tools. Disinfect contaminated materials and sterilize all surgical instruments properly. Remain monogamous. Practice safe sex. Use barrier contraceptive if a carrier. The avoidance of injecting drugs for both patients as well as doctors. The avoidance of blood and blood products by hospitals. Avoid professional blood donors.
Treatment of acute hepatitis and chronic hepatitis is different than the other liver diseases. It should be in proportion to the degree of liver damage, causes and its natural prognosis.
Pre icteric phase: Take bed rest until the acute stage has past. Lie down in a prone position for few hours daily. Wash hands with soap after using the toilet and before fixing food or eating. Sterilize utensils after each meal.
Take plenty of fluids. Promote rapid digestion with light, palatable and a non fatty diet. Drink apple, pear, grape, or pineapple juice. Try a grapefruit mono diet for 7 days. Take 15 gm of Epsom salt in 150 ml of warm water. Avoid bitter items if nausea is present. Drink sweet and slightly sour (fresh butter milk) beverages.
Icteric stage: Eat bitter and astringent foods. Avoid salt and spicy foods.Ensure adequate nutrition and hydration. Drink barley, coconut or rice water.
Undue physical exertion, applying oil to the scalp, hot humid environments and sleeping during the day etc. are contraindicated in the acute phase.
Food allowed: figs, ribbed gourd, bitter gourd, snake gourd, ash gourd,green gram, unpolished rice, ripe mango, grapes, banana, yellow fruits, and cumin seed.
Stop modern hepatotoxic drugs like oral contraceptive pills, non steroidal anti inflammatory drugs, oral hypoglycemic, anticoagulants, diuretics, anti epileptics, anti tubercular drugs, hepatic activators, alcohol etc for one month in acute hepatitis if taking these.