The Journal of the Association of Physicians of India · 2021
Coagulation Profile and its Correlation with Severity of Liver Dysfunction and Gastrointestinal Bleed in Alcoholic Liver Disease Patients.
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Bohania Niraj, Agrawal Aparna, Prakash Anupam, Nangia Anita, Kumar Abhishek
Аннотация
INTRODUCTION: The study aimed to determine coagulation factor abnormalities in alcoholic liver disease (ALD) and correlate these with severity of liver dysfunction (Child's class) and gastrointestinal (GI) bleeding.
METHODS: 60 patients of ALD (alcohol intake >10years and clinical, biochemical or radiological evidence of chronic liver disease) were included. Patients with Hepatitis B, Hepatitis C, HIV infection, DIC, low platelet count due to other causes, or on drugs which affect coagulation profile were excluded.
OBSERVATIONS: Age was 44.42 ± 10.26 years (100% males), 53% in Childs class C. Severity of liver dysfunction showed a significant association (p<0.05) with prolongation of prothrombin time (PT), activated partial thromboplastin time (aPTT) and thrombin time (TT), increasing factor VIII and D-Dimer level, low platelet counts, low protein S and factor VII activity; as well as decreasing fibrinogen levels, protein C and antithrombin (AT) III. GI bleed is associated significantly (p<0.05) with PT >20 sec and decreased plasma fibrinogen levels, while normal protein C, normal AT III, normal factor VII, normal factor VIII, normal TT, increased plasma fibrinogen levels, normal PT and normal platelet count appeared to be protective.
CONCLUSIONS: Several coagulation parameters are altered in ALD variably. Alterations in PT, aPTT, TT, factor VIII, D-Dimer, fibrinogen, protein C and AT III levels can be used for grading severity of liver disease. Decreased fibrinogen, protein C activity, AT III activity, factor VII activity, and increased factor VIII activity, are associated with GI bleed.
METHODS: 60 patients of ALD (alcohol intake >10years and clinical, biochemical or radiological evidence of chronic liver disease) were included. Patients with Hepatitis B, Hepatitis C, HIV infection, DIC, low platelet count due to other causes, or on drugs which affect coagulation profile were excluded.
OBSERVATIONS: Age was 44.42 ± 10.26 years (100% males), 53% in Childs class C. Severity of liver dysfunction showed a significant association (p<0.05) with prolongation of prothrombin time (PT), activated partial thromboplastin time (aPTT) and thrombin time (TT), increasing factor VIII and D-Dimer level, low platelet counts, low protein S and factor VII activity; as well as decreasing fibrinogen levels, protein C and antithrombin (AT) III. GI bleed is associated significantly (p<0.05) with PT >20 sec and decreased plasma fibrinogen levels, while normal protein C, normal AT III, normal factor VII, normal factor VIII, normal TT, increased plasma fibrinogen levels, normal PT and normal platelet count appeared to be protective.
CONCLUSIONS: Several coagulation parameters are altered in ALD variably. Alterations in PT, aPTT, TT, factor VIII, D-Dimer, fibrinogen, protein C and AT III levels can be used for grading severity of liver disease. Decreased fibrinogen, protein C activity, AT III activity, factor VII activity, and increased factor VIII activity, are associated with GI bleed.