Ηπατική σκληρότητα από φαρμακευτική χρήση

　　There are many types of drugs that can cause different liver damage, about200 species and more, including non-steroidal analgesics such as acetaminophen, muscle relaxants, anesthetics, anticonvulsants, antibiotics, antifungal drugs, and antiparasitic drugs, antituberculosis drugs, anticancer drugs, and immunosuppressants, hormone drugs, oral hypoglycemic agents, antithyroid agents, H2-Receptor blockers, psychiatric drugs, etc. According to statistics, patients with drug-induced liver damage account for about10％～15%, its incidence rate is second only to skin and mucosal damage and drug fever.

　　Damage caused by drugs can be divided into predictable (usually dose-related) and unpredictable (or idiosyncratic, often unrelated to dose). Predictable damage can be replicated in animal models and often damages specific sites of the liver lobules. Due to its dose-related nature, this type of drug is called 'direct hepatotoxic' drug. Unpredictable damage is often diffuse, and it is speculated to be an allergic reaction to the drug, where the immune mechanism is the direct cause of liver cell damage. Unpredictable damage cannot be replicated in corresponding animal models.

　　The current view is that non-predictable injury is caused by the production of hepatotoxic metabolites in the biological transformation process of some drugs, thereby causing liver lesions. Due to the differences in individual drug metabolism pathways and rates, especially P450 activity variation, detoxification mechanism differences, etc., lead to an increase in toxic metabolites in the liver, thus making some individuals prone to liver damage.

　　Drugs can cause several types of liver cirrhosis: ① Macronodular or postnecrotic cirrhosis, usually developing from drug-induced chronic active hepatitis or subacute liver necrosis. ② Cirrhosis with fatty degeneration, morphologically small nodules or macronodules. ③ Biliary cirrhosis. ④ Congestive cirrhosis, caused by occlusion of hepatic veins or small intrahepatic veins.

　　1、Hepatic encephalopathy is the increase of blood ammonia caused by liver disease, affecting the energy metabolism of the central nervous system and called encephalopathy, usually accompanied by abnormal behavior and consciousness disorders.

　　2、Severe upper gastrointestinal bleeding due to liver cirrhosis and upper gastrointestinal bleeding, most often due to esophageal and gastric fundus varices rupture, but it should be considered whether there are concurrent gastric mucosal lesions such as peptic ulcers, acute hemorrhagic erosive gastritis, and cardiospasm syndrome. Bleeding from ruptured varices is often caused by rough, hard, or angular food traumas, erosion of the esophagus by gastric acid reflux, severe vomiting, etc. Vomiting blood and black stools may occur. If the amount of bleeding is not much, only black stools may occur. If there is a large amount of bleeding, it can cause shock. Under the condition of ischemia and hypoxia of the liver, liver function often deteriorates. Bleeding also causes the loss of plasma proteins, which can lead to the formation of ascites. After decomposition of blood by bacteria in the intestines, ammonia is produced and absorbed by the intestinal mucosa, which can induce hepatic encephalopathy and even lead to death. After bleeding, the previously enlarged spleen can shrink or even cannot be felt.

　　3Infection due to decreased immune function, splenic hyperactivity, and the establishment of collateral circulation between the portal and systemic veins increases the opportunity for pathogenic microorganisms to enter the systemic circulation, hence it is prone to various infections, such as bronchitis, pneumonia, tuberculous peritonitis, primary peritonitis, biliary tract infection, and Gram-negative bacillary sepsis, etc. Primary peritonitis refers to the acute peritoneal inflammation in the peritoneal cavity of liver cirrhosis patients without organ perforation, the incidence rate accounts for3％～10％Mostly occur in patients with a large amount of ascites, mostly caused by Escherichia coli. The reason is that the phagocytic action of phagocytes is weakened during liver cirrhosis, abnormal proliferation of bacteria in the intestines, entering the peritoneal cavity through the intestinal wall. Also, due to changes in the vascular structure inside and outside the liver, bacteria can also cause bacteremia or carry bactericidal lymph through collateral circulation from under the liver capsule or the portal lymph nodes to the peritoneal cavity, causing infection. Clinical manifestations include fever, abdominal pain, abdominal distension, abdominal wall tenderness and rebound pain, increased ascites, increased white blood cells, cloudy ascites, showing exudative fluid or between exudative and transudative fluid. Ascites culture may show bacterial growth. A few patients have no abdominal pain or fever, but manifest with hypotension or shock, refractory ascites, and progressive liver function failure.

　　1History of taking drugs that damage the liver, especially those that can cause chronic active hepatitis, such as diclofenac, methyldopa, acetaminophen, aspirin, amiodarone, sulfonamides, etc., some drugs have an insidious progression to liver cirrhosis, such as methotrexate.

　　2Clinical manifestations of liver cirrhosis, such as portal hypertension and its complications, upper gastrointestinal bleeding, ascites, hepatic encephalopathy, etc.

　　3Liver biopsy confirmed as liver cirrhosis.

　　4Exclude liver cirrhosis caused by other reasons, such as various viral hepatitis, all serum markers are negative, exclude cardiogenic liver cirrhosis, etc.

　　Drug-induced liver cirrhosis focuses on prevention, preventing early drug-induced injury, such as regular liver function tests during the period of drug treatment. For patients with existing liver or kidney disease, more attention should be paid to changes in liver function during the period of medication. For those with a history of drug-induced liver damage, it is necessary to avoid reusing the same or similar drugs in chemical structure. For drug-induced chronic active hepatitis or liver fibrosis, it is advisable to use antifibrotic drugs early, such as Salvia miltiorrhiza, Angelica sinensis, etc.

　　In addition, according to the mechanism of liver injury caused by drugs, it is possible to choose targeted drugs in combination with therapeutic drugs to prevent the occurrence of liver injury, such as aminopyridine can inhibit cytochrome P450 activity, N-acetylcysteine can promote the synthesis of GSH, acetylsalicylic acid can reduce the concentration of calcium ions, etc.

　　Η φαρμακευτική σκληρότητα του ήπατος πρέπει να κάνει ποια εξετάσεις

　　1、Συνταγές για τη σκληρότητα του ήπατος με ηπατική βλάβη

　　（1）Πρωινό γεύμα: ρύζι (ρύζι50 Κιλό), το μαντάτο (μαγιά75Κιλό), το κρέας (κρέας150 Κιλό)

　　（2）Γεύμα ανάγκης: γλυκό γάλα (νερό γάλα250 Κιλό, σοκολάτα10Κιλό), την φράουλα150 Κιλό

　　（3）Μεσημεριανό γεύμα: ρύζι (ρύζι150 Κιλό), τα βραστότατα ψάρι (ψάρι200 Κιλό), τα σπανάκι (σπανάκι150 Κιλό).

　　（4）Γεύμα ανάγκης: τσόκολα (ζάχαρη30 Κιλό, σοκολάτα100 Κιλό)

　　（5）Βραδινό γεύμα: ρύζι (ρύζι150 Κιλό), τα βραστότατα κοτόπουλο (κοτόπουλο100 Κιλό), τα βραστότατα κοτόπουλο (κοτόπουλο50 Κιλό), τα κόκκινα κρεμμύδια100 Κιλό).

　　Ημερήσια χρήση λιπαρών25Κιλό). Η διατροφή περιέχει ενέργεια2422Κιλοκαλόρι (10120 Κιλοκαλόρι).

　　2、Τροφές που πρέπει να φατέ στη σκληρότητα του ήπατος με ηπατική βλάβη

　　（1）Πρέπει να διατηρήσετε τη διατροφή με χαμηλή αλάτι και χωρίς αλάτι για τους ασθενείς με σοβαρή υδροοίδηση ή ασθενείς με ascites;

　　（2）Στην τελική φάση της σκληρότητας του ήπατος με κώμα του ήπατος, πρέπει να διατηρήσετε την κουταροζωία της πρωτεΐνης.

　　（3）Αν υπάρχουν δυσκουλία στη διάρροια, μπορείτε να φάτε περισσότερο σπόρο σιταριού, μέλι, σπόρους σίτου, μπανάνα για να διατηρήσετε την άνετη εκτόνωση των κόπρανων, να μειώσετε την συσσώρευση της αμμώνιας, να αποφύγετε την κώμα του ήπατος.

　　3Τροφές που πρέπει να αποφεύγονται στη σκληρότητα του ήπατος με ηπατική βλάβη

　　Αποφύγετε τα πικάντικα και καυτερά τρόφιμα. Κάντε το κάπνισμα και το ποτό λιγότερο, καλύτερα δεν να τρώτε την αστακό, επειδή το αστακό έχει υψηλή περιεκτικότητα σε πρωτεΐνη, η κατανάλωση του είναι δύσκολη για την πέψη, θα βαρύνει το μεταβολισμό του ήπατος.

　　1、αμέσως να σταματήσουν τα σχετικά ή δυνητικά φάρμακα.

　　2、αύξηση της διατροφής, όπως υψηλή πρωτεΐνη, Β-καροτίνη και βιταμίνη C.

　　3、φαρμακευτική προστασία του ήπατος, όπως η φαρμακευτική κινεζική σοκολάτα, αν ο ασθενής έχει σημαντική αύξηση της αμυλάσης μπορεί να χρησιμοποιηθεί ο αναγεννητικός γλουταθειόνη, γλυκυρρίνη κ.λπ. φαρμακευτική προστασία του ήπατος.

　　4、παράλληλη θεραπεία, όπως η αιμορραγία του άνω γαστρεντερίτιδα, ascites, ηπατική εγκεφαλοπάθεια κ.λπ., ανάλογα με τα αποτελέσματα της εξέτασης και τα κλινικά συμπτώματα να εκτελείται αντιδραστική υποστήριξη της θεραπείας.