Chronic hepatitis B: Clinical, laboratory, and virologic features and response to antiviral therapy at Suez Center for treatment of viral hepatitis (Single center study) | ||||
| Microbes and Infectious Diseases | ||||
| Articles in Press, Accepted Manuscript, Available Online from 24 July 2025 | ||||
| Document Type: Original Article | ||||
| DOI: 10.21608/mid.2025.392732.2875 | ||||
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| Authors | ||||
Mohamed Bayomi Mohammed1; Nashaat Mohamed Soliman2; Bassam Mansour Salama2; Nageh Louis Mahrous   2
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| 1Resident of Endemic and Infectious Diseases, Suez Fever Hospital, Egypt | ||||
| 2Endemic and Infectious Diseases Department, Faculty of Medicine, Suez Canal University, Egypt | ||||
| Abstract | ||||
| Background: Chronic hepatitis B virus remains a significant global health burden, with varied clinical presentations ranging from compensated liver disease to decompensated cirrhosis. Understanding demographic, clinical, biochemical, and imaging profiles over time can guide management and prognosis. Methods: We conducted a 36-month retrospective cohort study of 250 chronic HBV patients to assess demographic characteristics, comorbidities, treatment patterns, clinical status, laboratory markers, and ultrasound findings. Patients were categorized into compensated and decompensated groups (based on presence of signs of liver failure, including ascites, hepatic encephalopathy, variceal bleeding, or jaundice) and monitored for disease progression and viral suppression. Results: The cohort consisted mainly of middle-aged, urban males with common comorbidities such as diabetes and hypertension. Half of infections were detected through screening and half through symptoms. At 36 months, 40.4% were on antiviral therapy, with a shift from Lamivudine to Tenofovir. Decompensated patients showed persistent symptoms like fatigue, jaundice, ascites, and signs of portal hypertension, whereas compensated patients remained largely asymptomatic. Ultrasound findings confirmed advanced cirrhosis and portal hypertension in decompensated patients, with preserved liver structure in compensated cases. Laboratory tests reflected significant liver dysfunction in decompensated patients and milder abnormalities in compensated ones. Viral suppression improved over time, especially in the decompensated group; however this improvement is statistically insignificant between groups. Conclusions: This study delineates clear clinical, biochemical, and imaging distinctions between compensated and decompensated chronic HBV over three years. The findings underscore the importance of early diagnosis, vigilant monitoring, and tailored antiviral strategies to prevent disease progression and improve outcomes. | ||||
| Keywords | ||||
| HBV; Hepatitis; Tenofovir; cirrhosis; HCC | ||||
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