Nine parameters define decompensation of hepatic disease induced by the Delta virus
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ŢURCANU, Adela, TCACIUC, Eugen, TOFAN-SCUTARU, Liudmila, DRANGOI, Irina, ANDRIESH, Lucia P., DUMBRAVA, Vlada-Tatiana, PINEAU, Pascal. Nine parameters define decompensation of hepatic disease induced by the Delta virus. In: Journal of Gastrointestinal and Liver Diseases, 2019, nr. S2(28), p. 88. ISSN 1841-8724.
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Journal of Gastrointestinal and Liver Diseases
Numărul S2(28) / 2019 / ISSN 1841-8724 /ISSNe 1842-1121

Nine parameters define decompensation of hepatic disease induced by the Delta virus


Pag. 88-88

Ţurcanu Adela1, Tcaciuc Eugen1, Tofan-Scutaru Liudmila1, Drangoi Irina1, Andriesh Lucia P.1, Dumbrava Vlada-Tatiana1, Pineau Pascal2
 
1 ”Nicolae Testemițanu” State University of Medicine and Pharmacy,
2 Institut Pasteur
 
 
Disponibil în IBN: 24 august 2022


Rezumat

Objectives. Worldwide, approximately 15-20 million people have hepatitis delta virus. The virus can only replicate within the context of chronic hepatitis B virus (HBV) infection. However, hepatitis delta virus causes the most severe form of viral hepatitis, including rapid progression of liver cirrhosis, decompensated liver disease and an increased risk of liver cancer. The Republic of Moldova is a country were Hepatitis Delta is responsible for an important burden of diseases. Aim of the study: to investigate the clinical evolution of HDV infection and evaluate the incidence of complications of cirrhosis, HCC and mortality in a cohort of 300 Moldovan patients for a median period of 5.2 years Materials and methods. In the present cross-sectional study, we described demographic, clinical and biological features of 300 HDV-infected patients attending care in three Moldovan centers. Results. TThe mean age of the patients was 49±9years with a slight excess of women (118 vs 106). All were anti-HBe negative but hepatitis B virus (HBV) DNA was detectable in 28.1% of cases. The mean HDV RNA load was 5.6±1.7 log10 IU/mL. The principal risk factor of HDV was intrafamilial transmission (39.8%). A large subset of the patients was already affected by liver cirrhosis (55.5%) and among these 52% were presenting signs of decompensation. The time distance from the diagnosis of cirrhotic disease was correlated with the length of HDV infection (Pearson r=0.470, P<0.0001) but not with that of HBV infection. A set of nine biochemical parameters was significantly different between cirrhotic and non-cirrhotic HDV-infected patients. The most significant factors (<1.0) were hemoglobin (122 ±15g/L vs 133 ±16g/L, 1.7), platelets count (111±65G/L vs 159±47G/L, 5.3), albumin concentrations (31.8 ±6.9g/L vs 37.4±3.9g/L, 3.3) and index Normalized ratio (INR, 1.41±0.25 vs 1.18±0.16, 1.5). Conclusions. The most important characteristic of chronic delta hepatitis appears to be its propensity to progress rapidly to cirrhosis, and our study showed that the relative risk for individuals with chronic HDV infection of developing progressive liver disease and HCC varies greatly, based largely on disease activity and level of viral HBV/HDV replication.

Cuvinte-cheie
hepatitis D, HDV, liver cirrhosis