Hepatogenic gastric disease and hepatogenic peptic ulcer are both extra-hepatic clinical manifestations of chronic hepatic disease. Male patients are more than female, the proportion being 2-4:1. Peptic ulcer can be seen in all ages, but mostly between 20 to 50 years. Duodenal ulcers are mostly seen at about thirty and gastric ulcers at about forty. Its incidence at different age groups coincides with the high incidence age groups of Hepatophilic virus disease (see figure 1 statistics of age groups in 2000 cases of abnormal liver margin).
Patients with virus hepatitis frequently show gastrointestinal symptoms such as loss of appetite, anorexia, nausea, vomiting, distention and pain of upper abdomen, dyspepsia, acid regurgitation and belching, and these presentations often times may be mistaken for simple peptic ulcer. Although the above symptoms may be recognized by some as the clinical manifestations of hepatitis, but it is not enough to ascertain that it is the involvement of the gastrointestinal tract by hepatophilic virus. Gastroscopy had been performed in researches concerning virus hepatitis and it was found that the gastric mucosa (粘膜) of patients with hepatic disease presented abnormalities of variable degrees; the incidence of severe hepatitis complicated with acute hemorrhage of gastric mucosa was high.
The cause in the formation of hepatogenic gastric disease and hepatogenic peptic ulcer may be the following:
(1) the Hepatophilic virus can invade the gastrointestinal mucosa directly and produce virus gastrointestinal disease. The lesion in the gastrointestinal mucosa shows mucosal edema, inflammation and erosion, leading to acute or chronic gastroenteritis, which produces clinical symptoms of hepatogenic gastric disease and induces peptic ulcer.
(2) Hepatophilic virus can also directly activate the immunologic system to produce antibodies in fighting against the reproduced antigens and thus, it may lead to abnormality of the gastrointestinal mucosa tissues, dysfunction of the mucosal barrier, decrease of gastric mucosal blood flow, disorder of endocrines and therefore increase of aggressive factors.
(3) Hepatophilic virus can produce inflammatory edema of liver tissues and metabolic disorder of the liver may lead to imbalance of related endocrines and media causing redistribution of blood circulation and decrease of effective blood flow. The mucosal circulation and nutrition are compromised; the ability of gastric tissues to neutralize acids is decreased. The barrier function of the gastric mucosa is weakened. This promotes the hydrogenions (氫離子) to spread in the opposite direction and causes damage to the mucosa resulting in ulcer formation.
(4) Chronic hepatitis and early cirrhosis of liver may produce compression of the portal vein, the blood of which flows back into the liver and forms a hypertensive state of the portal vein and inferior vena cava. This in turn, causes local congestion of the stomache, circulatory disturbance and hypoxia, leading to the production of clinical gastric symptoms or even to venous varicosities of the lower esophagus and hemorrhoids and profuse hemorrhage from the gastrointestinal mucosa.
(5) In virus hepatitis, hepatic dysfunction causes decrease of the inactivation of gastrin (胃泌素) and enterogenic histamine (腸源性組胺), leading to increase blood concentration of the latter and increase secretion of gastric acid. Alteration of gastrin also causes decrease gastric peristalsis, prolonged retention of food and increase of damage to the gastric mucosa.
(6) In chronic hepatitis or cirrhosis of liver, disorder of the automomic nervous system (植物神經系統紊亂), spirobacteria infection of the pylorus (幽門螺旋菌感染) and pharmaceutical injury may all play a role in the pathological changes of the gastric mucosa.
It is worthwhile to pay attention to the following :
According to the literature, inflammatory cell in infiltration of gastric mucosa in chronic hepatitis is more marked then acute hepatitis and most of the peptic ulcers occurred during the course of hepatitis. In other words, patients diagnosed as chronic hepatitis (for example, positive findings of various types of antigens and antibodies, abnormal liver function, ultrasonic or CT scan showing liver disease or abnormal margin of liver dullness diagnosed by clinicians) complicated with gastric disease or peptic ulcer symptoms, should be treated as hepatogenic gastric disease or hepatogenic peptic ulcer, and they should receive early systemic TCM management.
Case 1
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Law (code No. 664) male, age 34 years. For a long time, he suffered from duodenal ulcer and bacterial disease of the gastric pylorus and although he was treated with anti-inflammatory drugs, stomache ache still occurred repeatedly. He also had insommia, fatigue, became dreamful and perspired during sleep for years. On march 1998, he first visited our clinic with the chief complaint of stomache ache which caused him to take gastric drugs for a long period. He was susceptible for common cold and three days before he had throat itching, cough, profuse sputum and headache during coughing. Physical examination : tongue enlarged, coating whitish and thin, tongue proper red, abdomen soft and distended percussion tenderness over hepatic region, liver 1.5 cm below costal margin. After 3 parcels of TCM drugs, sleeping was good and there was relief of coughing and headache. The liver retracted to the costal margin. After another 3 parcels, the symptoms of exogenous insult disappeared; stomache ache was relieved. The enlarged tongue did not show teeth-prints and the liver was 1.5 cm above costal margin. Forty-five parcels of drugs were taken for the completement of the TCM course and cessation of therapy was undertaken only after disappearance of the symptoms. The gastric drugs were stopped during the TCM course. |
Written by Wong Kwok Hung
published on 27th February 2001
(translated by Professor ZHENG Hua En in August 2002)