Bệnh gan do rượu: Cơ chế phân tử, các dấu ấn sinh học và chiến lược điều trị=Alcoholic liver disease: Molecular mechanism, biomarkers, and therapy strategies

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Tác giả: Nghiêm Luật Nguyễn

Ngôn ngữ: vie

Ký hiệu phân loại:

Thông tin xuất bản: Tạp chí Y học Việt Nam (Tổng hội Y học Việt Nam), 2024

Mô tả vật lý: tr.13-20

Bộ sưu tập: Metadata

ID: 243835

Thêm vào giỏ

Không có mức độ uống rượu nào là an toàn cho sức khỏe. Uống rượu điều độ là uống ít hơn 2 ly mỗi ngày đối với nam và ít hơn 1 ly mỗi ngày đối với nữ. Uống hàng ngày từ 30 đến 50 g rượu trên 5 năm có thể gây bệnh gan do rượu. Sự chuyển hóa ethanol: có nhiều enzyme tham gia vào sự chuyển hóa ethanol thành acetaldehyd rồi thành axetat, gồm alcohol dehydrogenase (ADH), cytochrom P450 2E1 (CYP2E1), catalase (CAT), acetaldehyde dehydrogenase (ALDH), và các enzyme chuyển hóa không oxy hóa như sulfotransferase (SULT), glucuronosyltransferase (UGT) và FAEE synthase (FAEES). Cơ chế phân tử của bệnh gan do rượu (ALD) gồm: (1) các biến đổi về di truyền và biểu sinh
(2) stress oxy hóa
(3) độc tính qua trung gian acetaldehyde và viêm do cytokine và chemokine gây ra
(4) lập trình lại quá trình trao đổi chất
(5) tổn thương miễn dịch
và (6) rối loạn sinh lý của hệ vi sinh đường ruột. Các dấu ấn sinh học của viêm gan do rượu gồm AST >
50 U/L, AST/ALT >
1,5, AST và ALT <
400 U/L, bilirubin toàn phần >
3 mg/dL, giảm albumin và prealbumin huyết thanh, tăng gamma-glutamyltransferase, tăng mức bình thường hóa quốc tế tăng bạch cầu với bạch cầu trung tính chiếm ưu thế, tăng hồng cầu to, thiếu thiamine, giảm tiểu cầu và thiếu vitamin B12 và/hoặc folate. Các chiến lược điều trị bệnh gan do rượu: (1) Phương pháp điều trị chính cho viêm gan do rượu là ngừng uống rượu và kiểm soát hội chứng cai rượu
(2) bổ sung dinh dưỡng
(3) sử dụng các thuốc như corticosteroid và N-acetylcysteine, hoặc pentoxifylline
hoặc ghép gan.No level of alcohol consumption is safe for our health. Moderate drinking is defined as up to 2 drinks per day for men and up to 1 drink per day for women. Daily consumption of 30 to 50 grams of alcohol for over five years can cause alcoholic liver disease. The metabolism of ethanol to metabolites: there are many enzymes that are involved, including alcohol dehydrogenase (ADH), cytochrome P450 2E1 (CYP2E1), catalase (CAT), acetaldehyde dehydrogenase (ALDH), and nonoxidative metabolizing enzymes such as sulfotransferase (SULT), (UDP)- glucuronosyltransferase (UGT), and FAEE synthase (FAEES). The molecular mechanism of alcoholic liver disease (ALD) includes: (1) genetic and epigenetic alterations
(2) oxidative stress
(3) acetaldehyde-mediated toxicity and cytokine and chemokine-induced inflammation
(4) metabolic reprogramming
(5) immune damage
and (6) dysbiosis of the gut microbiota. Biomarkers for alcohol hepatitis include AST >
50 U/L, AST/ALT ratio >
1.5, AST and ALT <
400 U/L, total bilirubin >
3 mg per dL, decreased serum albumin and prealbumin, elevated gamma-glutamyltransferase, elevated international normalized ratio (INR), elevated white blood cell count with neutrophil predominance, macrocytosis, thiamine deficiency, thrombocytopenia, and vitamin B12 and/or folate deficiency. Therapeutic strategies for alcoholic liver disease: (1) The main treatment for alcoholic hepatitis is for a person to stop drinking alcohol and manage alcohol withdrawal syndrome
(2) nutritional supplementation
(3) medications such as corticosteroids and N-acetylcysteine, or pentoxifylline
or liver transplants.

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