Hyperthyroid liver disease

　　1, The direct effect of thyroid hormones, the liver plays an important role in the metabolism, transformation, excretion of thyroid hormones, and the synthesis of thyroid-binding globulin.

　　2, Hypoxia and ischemia of liver cells caused by hypermetabolic state in hyperthyroidism.

　　3, Disorders in liver energy metabolism.

　　4, Concurrent infections in patients with hyperthyroidism.

　　Firstly, digestive system

　　1, Pancreatic diseases, acute pancreatitis.

　　2, Esophageal and gastrointestinal damage including esophagitis, esophageal ulcer, varices in the lower segment of the esophagus; gastric ulcer, gastric mucosal damage, gastric hemorrhage, etc.

　　3, Fatty liver is commonly seen in the recovery period or after recovery from acute jaundice type hepatitis, as well as chronic hepatitis B or C.

　　4, Primary liver cancer, caused by hepatitis B and C virus infection, is one of the important causes of primary liver cancer.

　　Secondly, complications of endocrine and metabolic systems

　　1, Diabetes.

　　2, Hypoglycemia.

　　3, Endocrine damage.

　　3. Hematological Complications

　　(1) Aplastic Anemia.

　　(2) Leukopenia.

　　(3) Thrombocytopenia.

　　(4) Pure Red Cell Aplastic Anemia.

　　(5) Reactive Lymphocytosis.

　　(6) Hemolytic Anemia.

　　(7) Coagulation Dysfunction.

　　4. Cardiovascular System Complications

　　(1) Cardiovascular Lesions: ① Increased peripheral circulatory resistance. ② Arrhythmia. ③ Myocarditis.

　　(2) Vascular Lesions: ① Necrotizing Multivessel Vasculitis is common in patients with hepatitis B. ② Primary Cold Agglutinin Disease (EMC).

　　5. Urogenital System Complications

　　(1) Hepatitis-Related Glomerulonephritis.

　　(2) Tubular Acidosis.

　　(3) Acute Renal Failure.

　　6. Connective Tissue and Muscle Tissue Complications

　　(1) Skin Lesions: Acute hepatitis can cause urticaria, angioneurotic edema, annular erythema, maculopapular rash; severe hepatitis can present with petechiae, ecchymosis, ulceration, butterfly-shaped erythema on the face, and polymorphic erythema, etc.; cholestatic hepatitis often presents with skin itching; liver cirrhosis patients may have macular hyperpigmentation on the skin of the lower limbs.

　　(2) Joint Lesions: They are usually migratory and symmetrical arthritis.

　　(3) Muscular Lesions: Chronic hepatitis patients commonly experience muscle pain in the extremities, which is generally mild.

　　7. Other Systemic Complications

　　(1) Respiratory System Lesions: ① Viral hepatitis can complicate exudative pleurisy. ② In patients with acute liver failure, various toxic substances in the blood cause changes in alveolar permeability, leading to non-cardiogenic pulmonary edema, which manifests clinically as respiratory distress syndrome.

　　(2) Neurological Lesions: ① Hepatic encephalopathy is a neuro-psychiatric syndrome that occurs during severe hepatitis and liver failure. ② In the early stage of acute hepatitis, some patients may experience transient psychiatric symptoms such as irritability, anger, and insomnia.

　　8. Sjogren's Syndrome.

　　9. Acquired Immune Deficiency Syndrome (AIDS).

　　Liver disease patients must be firm in their confidence to overcome the disease. On one hand, they need to improve their awareness and detection, and achieve early detection and early treatment.

　　Liver function damage caused by hyperthyroidism includes jaundice, elevated liver enzymes, anorexia, aversion to oil, diarrhea, and other gastrointestinal symptoms. Due to the lack of specificity, it should be differentiated from viral hepatitis and antithyroid drug-induced liver damage. Since the mechanisms and treatment methods of these three types of liver damage are different, early and clear diagnosis is particularly important.

　　Firstly, hyperthyroidism with hepatitis and liver damage caused by hyperthyroidism have the following differences:

　　1. Irrelevant to the severity of hyperthyroidism;

　　2. Marked hepatitis symptoms such as anorexia and aversion to oil in the digestive system;

　　3. Positive for hepatitis infection markers;

　　4. Ineffectiveness of antithyroid treatment, etc.

　　Secondly, the diagnosis of antithyroid drug-induced liver damage is usually by exclusion, i.e.,

　　1. Clinical laboratory tests show evidence of liver damage;

　　2. Temporal association between drug use and liver damage, i.e., liver damage occurred after drug use;

　　3. No serological evidence of hepatitis virus infection or autoimmune hepatitis;

　　4. No evidence of chronic liver disease;

　　5. No concurrent use of other known hepatotoxic drugs;

　　6. Liver function improved or recovered after drug discontinuation;

　　7. Pathology shows mononuclear cell and lymphocyte inflammatory infiltration within the hepatic lobules;

　　8. Repeated use of the same drugs can cause liver damage again.

　　It is generally believed that liver damage caused by antithyroid drugs is more common within 3 months after taking medication. The liver damage caused by PTU is mainly characterized by varying degrees of liver cell necrosis, while the liver damage caused by MMI is mainly characterized by intrahepatic cholestasis, that is, cholestasis of liver cells and/or bile ducts. The former is mainly manifested by the elevation of transaminases, and the latter is mainly manifested by the elevation of bilirubin.

　　Prevention first, regular follow-up. It is necessary to check liver function before medication for patients with hyperthyroidism who have a history of hepatitis. Since drug-induced liver damage mostly occurs within 3 months of treatment, regular follow-up of patients within the first 3 months of treatment, monitoring liver function, and informing patients that if they appear symptoms similar to hepatitis, such as anorexia and jaundice, they should seek medical attention immediately.

　　The diagnosis of hyperthyroid liver disease mainly relies on clinical manifestations. Liver function damage caused by hyperthyroidism itself includes jaundice, elevated liver enzymes, loss of appetite, aversion to oil, diarrhea, and other digestive system symptoms. Thyroid ultrasound, abdominal ultrasound.

　　Dietary attention: high energy, high protein, high vitamin diet, limit iodine intake. Increase carbohydrates, appropriately increase minerals and vitamins, especially potassium, calcium, and phosphorus, and limit dietary fiber. Eat less coarse grains, chives, mung bean sprouts, and other fibrous foods.

　　1. The treatment principle for liver damage caused by hyperthyroidism is to control hyperthyroidism primarily. At this time, the daily dose of antithyroid drugs should be appropriately reduced because large doses of drugs are more likely to cause liver damage and cannot improve the remission rate of hyperthyroidism. At the same time, liver function should be strictly monitored. If liver damage continues to progress, medication must be stopped.

　　2. Liver-protecting and jaundice-reducing drugs, such as antipyretic analgesics and estrogens, may cause liver damage after use. These drugs may increase serum thyroid hormone levels, so when hyperthyroid patients take certain drugs, they may promote hepatotoxic effects.

　　3. For patients with mild hyperthyroidism and liver damage, thioamide antithyroid drugs can be used. The author believes that for patients with chronic liver disease or poor liver function after taking medication, radioactive iodine or surgical treatment should be the first choice.