Sudan Journal of Medical Sciences (SJMS) | Sudan JMS: Volume 12 (2017), Issue No. 3 | pages: 187-197

DOI: 10.18502/sjms.v12i3.937

Deranged liver among Sudanese Patients with Dengue Virus Infection in Port Sudan Teaching Hospital

Bashir Abdrhman Bashir Mohamed
bashirbashir17@hotmail.com
Port Sudan Ahlia College, Sudan

Abstract

Background Deranged liver is a well-recognized feature of dengue infection, often demonstrated by coagulopathy and mild to moderate increase in transaminase levels although jaundice and fulminant hepatic failure are generally uncommon.

Objective This study aimed to evaluate the hepatic effect of dengue fever amongst Sudanese patients.

Materials and Methods A cross-sectional descriptive study recruited in Port Sudan teaching hospital in the period from February 2013 to June 2014.  334 cases of dengue along with 101 cases of control were enrolled. Rapid immune chromatographic test was used to confirm positive dengue cases and WHO criteria were used for classifying the dengue severity. Prothrombin time (PT), partial thromboplastin time (PTT), fibrinogen level (FB), platelet count (PLT), aspartate aminotransferase (AST), alanine aminotransferase (ALT) and C-reactive protein (CRP) were all measured.

Results PT, PTT, and FB were found to be significantly higher in the infected cohort when compared to the controls (P< 0.0001). PT was prolonged in 9%, PTT was prolonged in 12.6% and shortened by 5.4% of the patients, whereas hypofibrinogenemia in 18.3% and hyperfibrinogenemia in 67.4% of the patients. Bleeding was seen in 10.5% of patients and thrombocytopenia was detected in 83.5% of patients. Out of 334 patients, 101 (30.2%) had abnormal coagulation results. Of 101 patients, 72 were subjected mixing studies for PT and PTT that revealed deficiencies in factors VIII (35%), IX (10%), V (10%), X (19%), and XII (14%). 43.6% patients had elevated AST and 21.8% had elevated ALT.

ConclusionThis study demonstrated that hepatic dysfunction may be attributed to dengue virus infection which evident by prolongation in PT and PTT as well as hypofibrinogenemia and factor deficiencies.   

 

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