The condition of destruction of a petite cells, disruption of hepatic architecture, overgrowth of fibrous issues, proliferation of the remaining cells associated with features of progressive hepato-cellular failure and portal hypertension arising out of diverse aetiology is called the cirrhosis of liver.
In general there are three types of cirrhosis of liver. Those are –
1) Micronodular: the nodules vary from 3 to 4 mm in diameter. Chronic alcoholism is the most common causes of it.
2) Macronodular: the nodules in this case measure several centimeters in diameter. Chronic active hepatitis is the most common cause.
3) Mixed type: both of the above types.
ii) Alcohol: this is an important cause of cirrhosis in temperate climate. It is responsible for hepatocellular damage and indirectly hepatic damage is produced by the associated deficiency of Lipotropic factors and high calorie diet. Alcoholic-hyaline is very suggestive of alcoholic cirrhosis of liver and micronodular seriously usually develops.
iii) Post hepatic and post-necrotic cirrhosis: hepatitis B, non-A, non-B, hepatitis D may lead. Almost all cases of chronic active hepatitis lead to cirrhosis.
iv) Immunological: auto immune chronic active hepatitis may cause the cirrhosis.
v) Metabolic disorder and inherited disorder: cirrhosis of liver may develop in cases of haemochromatosis, Kinnier Wilson’s disease, glycogen storage disease, fibrocystic disease of the pancreas, alpha antitrypsin deficiency, Fanconi syndrome, and galactosaemia.
vi) Cholestasis: prolonged biliary stasis either primary or secondary may cause cirrhosis.
vii) Hepatic congestion: as in cardiac cirrhosis, Budd-Chiari syndrome et cetera.
viii) Drug: Alpha-methyl dopa, Methotrexate, arsenic, oral contraceptive may cause cirrhosis.
ix) Idiopathic or cryptogenic: diabetes, sarcoidosis.
After necrosis and disintegration of liver cells the reticulin framework collapses and portal and Central Jones are approximated. Fibrous septae develop in the portal Jones and proceed towards lobular parenchyma dissecting them into various sizes. In the meantime some cells regenerate to form nodules of various sizes giving a macroscopic appearance of macronodular, micronodular or mixed type of cirrhosis of liver.
i) Age-group is above 30 years and mainly affected.
ii) Hepatic facies is present. These consist of sunken eyes, prominence of malar Bones, icteroid conjunctivae, dirty complexion of the face and spider angioma.
iii) Anaemia is generically present.
iv) Jaundice is usually absent but in the case of cholestasis jaundice may be prominent.
v) Spider angioma is observed in the upper part of the chaste specially in the necklace area.
vi) Oedema is present and it is pitting type. This is due to low protein level, excess of aldosterone and antidiuretic hormones in the blood, pressure of ascitic fluid over inferior vena cava and low glomerular filtration rate.
vii) In 35% of cases fever is present due to secondary infection.
viii) Cutaneous haemorrhages may be present.
ix) Cyanosis may be present in more than 35% of cases due to hypoxaemia.
x) Tongue is pale and dry, it may be red due to avitaminosis or glossitis.
xi) Abdomen is bloated, umbilicus is everted, abdominal veins are prominent particularly in the epigastric region.
xii) Liver may be palpable in early-stage due to fatty infiltration but the latter on it shrinks.
xiii) Spleen is palpable due to portal hypertension.
xiv) Apex beat is displaced upwards due to ascites and they are maybe a soft sisterly murmur over mitral and pulmonary area.
xv) Falling of pubic and axillary hairs may also be seen due to lack of detoxification of oestrogen in the liver.
i) Anorexia, nausea, vomiting and flatulence are common symptoms.
ii) Gradual weakness and weight loss.
iii) Gradual swelling of the abdomen and feet.
iv) Haematemesis and melaena from ruptured oesophageal varices.
v) Diarrhoea or constipation.
vi) Amenorrhoea in female patients.
vii) Loss of libido, impotence.
viii) Bleeding piles is not uncommon.
i) Test of blood: – lab examination shows moderate leucopenia, thrombocytopenia and anaemia. HBs Ag or its antibody may be found in blood.
ii) Liver function test: – plasma protein level is low and albumin globulin ratio is altered. Prolonged prothrombin time unaffected by administration of vitamin K. Serum alkaline phosphate is increased moderately. S.G.O.T. and S. G.P.T. Levels are elevated usually up to hundreds unit. Serum bilirubin level may be normal or raised.
iii) Liver biopsy will show multilobular fibrosis and complete disorganisation of hepatic architecture.
iv) Urine shows excess of urobilinogen but the bile may be present in biliary cirrhosis.
In the case of cirrhosis of liver rest is particularly advisable when there is haemorrhage, oedema, ascites or other complications. Nutritious diet containing more carbohydrate and moderate protein and fat are maybe given to the patient. Too much restriction of fat is possibly not required alcohol is to be avoided totally. Diet should be very much restricted regarding protein when the patient has just recovered from encephalopathy.
It is very well decision to treat the cirrhosis homeopathically. There are various homeopathic remedies for symptomatic treatment of cirrhosis of liver but treatment should be done under proper guidance of experienced physician. For this treatment some important homeopathic remedies are Hydrastis can, Chelidonium, Carduus meri, Bryonia alb, Nux vom, Arsenic, Calc Flour, Lycopodium etc. Magnetized water of mixture of both pole should be given four times in a day.