Alcohol dependence is a chronic and relapsing disease that causes mental and organ damage due to long-term heavy drinking, which has serious adverse effects on individuals and society. Previous studies have shown that even after inpatient treatment, the relapse rate of alcohol-dependent patients can be as high as 60% – 70% within 3 months after discharge. Currently, the mechanisms associated with relapse to drinking in alcohol-dependent patients are still unclear. And most of the studies reported in the past have been about the relationship between psychosocial factors and relapse to drinking, while few studies have examined the relationship between biological indicators and relapse to drinking. Therefore, in this paper, we summarize the recent literature to explore the biological markers related to alcohol dependence relapse and discuss the progress of research on relapse prediction, in order to provide reference and help to reduce the relapse rate and improve the quality of life of patients.

Alcohol withdrawal syndrome (AWS) is a serious disorder affecting alcohol-dependent patients who abruptly stop or reduce their drinking. Mild or moderate AWS usually appears within 6 to 24 h after the last drink, and symptoms may include increased blood pressure and rapid pulse, tremors, high fever, irritability, anxiety, headache, nausea, and vomiting. These symptoms may progress to a more severe AWS characterized by delirium tremens, seizures, coma, cardiac arrest, and death. This article will analyze the phenobarbital (PB) treatment of AWS and make a brief review.

Alcohol withdrawal syndrome (AWS) refers to a series of symptoms and signs that chronic alcoholics experience when they suddenly stop drinking or reduce their drinking, usually 12 to 24 h later. These include tremors, fatigue, sweating, hyperreflexia, and gastrointestinal symptoms. This article will analyze the drug treatment of this disease and make a brief review.

Objective: rupture of liver metastases with disturbance of consciousness accompanied by aggravation of hemiplegia is very rare. We describe the clinical features of a case of spontaneous rupture of liver metastasis tumors with disturbance of consciousness and progression of right limb hemiplegia. Methods: collect the patient’s medical history, conduct a detailed physical examination, timely improve the relevant laboratory and imaging examination, formulate a comprehensive treatment plan, and track the changes of the disease and the treatment effect. Results: the patient presented with blurred consciousness, hemiplegia of the right limb, and epigastric tenderness when admitted to the hospital. No evident new lesions were found on cranial computed tomography (CT). Blood routine examination showed that hemoglobin decreased significantly compared with before. Abdominal CT showed tumor rupture and bleeding. The patient in critical condition did not have operation conditions, but improved after conservative treatment. Conclusion: when patients with liver metastasis tumors suddenly have a disturbance of consciousness and progress of hemiplegia, they should not only be considered to have acute cerebrovascular diseases, but also the possibility of rupture of liver metastasis tumors. If only treated according to acute stroke, it will endanger their lives. For the liver metastasis tumor rupture, if there is no opportunity for embolotherapy, timely conservative treatment with drugs can also achieve good results.