Patients who obtaining hepatitis D infection either as co-infection or super-infection, become chronic hepatitis B infected, which then they can undergoes as active chronic hepatitis B infected or inactive carriers, but hepatitis D infection, remains active and dominates the further deterioration and hepatic injury. Most of the patients having progressively deteriorating of liver function and increased susceptibility having a liver cirrhosis and even end-stage liver failure .

1. State Medical and Pharmaceutical University
“Nicolae Testemitanu“
Faculty OF Medicine Nr.2
Department of Hepatology and Gastroenterology
DIPLOMA THESIS
CHRONIC HEPATITIS D: CLINICAL AND PARACLINICAL
PECULIARITIES
Author:
Jaber Samer
Group: 1648
Conductor:
Dr. Berliba Elina
Associate Professor

2. The magnitude of the problem
 Five percent of chronic HBV carriers, (15 million to 20)
million individuals worldwide, are also infected with HDV,
In combination with hepatitis B virus, hepatitis D has the
highest mortality rate of all the hepatitis infections (20%).
 Two epidemiologic patterns of hepatitis D infections exist: in
Mediterranean countries infection is endemic among HBV
carriers, and the virus is transmitted by close personal
contact. In Western Europe and North America, HDV is
confined to persons exposed to blood or blood products, like
e.g. intravenous drug addicts sharing unsterilized injection
needles.
 The incidence of HDV is increasing in Russia, eastern
Europe, Japan, and India.

3. The magnitude of the problem

4. Introduction
 Patients who obtaining hepatitis D infection either as co-
infection or super-infection, become chronic hepatitis B
infected, which then they can undergoes as active chronic
hepatitis B infected or inactive carriers, but hepatitis D
infection, remains active and dominates the further
deterioration and hepatic injury.
 Most of the patients having progressively deteriorating of
liver function and increased susceptibility having a liver
cirrhosis and even end-stage liver failure .

5. Delta Virus and Its Infection
 HDV, the only member of the genus Deltavirus, is a defective
RNA virus that co-infects with and requires the helper
function of HBV for its replication and expression .
 Incubation periods for hepatitis B and D ranges from 30–180
days (mean, 8–12 weeks) .
 Hepatitis D viral infection can occur either as a co-infection
with HBV or as a superinfection in an HBsAg-positive,
chronic carriers of HBV patient.

6. Delta Virus and Its Infection
 Consequences Of HDV infection

7. Delta Virus and Its Infection
Consequences Of HDV infection :
 Acute Hepatic Failure
 Acute Hepatic Failure  Incubation  Chronic HDV
 Chronic HDV  Cirrhosis

8. Purpose and aims
To evaluate the clinical symptoms and the para-clinical
results, that is presented in patients with Chronic
hepatitis Delta, in comparison with patients who
presented chronic hepatitis B alone.

9. Purpose and aims
Objectives:
 Assessment of clinical features in patients with chronic hepatitis D.
 Evaluation of para-clinical results (echography, Fibroscan, liver
scintigraphy) in patients with chronic hepatitis D and B.
 Estimation of CBC and laboratory liver syndromes (cytolytic, cholestatic,
hepatodepressive, immuno-inflammatory) in patients with chronic
hepatitis D.
 Research serological markers of viral hepatitis and viremia in patients
included in the study.
 Evaluation of fibrosis stage in patients with chronic hepatitis B and D
according to the results of FibroScan.

10. Material and research methods
Patients :
Thirty-six patients, twenty with chronic HDV infection, 10 males and 10
females, with median age of 40.2, and other 16 with chronic HBV infection, 15
males and 1 female, with median age of 43.3, were observed, evaluated and
investigated consecutively in the period of their hospitalization .
The control group (III) consisted of 20 practically healthy persons, 55% (11)
males and 45% (9) women without exacerbated hereditary history in the
absence of liver and gastrointestinal pathology.

11. Material and research methods
Protocol :
 I have evaluated the levels of serum HBV-DNA,HDV-RNA,
and all serological markers of HBV, HDV, HCV , in patients
with chronic HDV infection and in patients with chronic HBV
infection .
 In addition , all clinical complains and feature , and para-
clinical investigations of general blood , and biochemical
analysis was evaluated too .
 All patient that has been evaluated and investigated were
obtained from the department of hepatology and
gastroenterology from the republican hospital .

12. Material and research methods
Patients :
 Risk factor for acquiring HDV and HBV infection

13. Results and discussion
Physical and clinical examination
 Right upper quadrant (RUQ) pain

14. Results and discussion
Physical and clinical examination
 Fatigue and Weakness

15. Results and discussion
Physical and clinical examination
 Jaundice

16. Results and discussion
Physical and clinical examination
 Abdominal distention and Bloating

17. Results and discussion
Biochemical Analysis
Chronic HDV
Infection –I
Chronic HBV
Infection -II
Control group - III p I - II
ALT (U/l) 97,55+8,5 58,6±9,8 24,76±1,34 p<0,05
AST (U/l) 78,83+6,2 44,5+10,7 19,42±1,26 p<0,05
 Cytolytic syndrome was estimated to be increased , (ALT and AST values ) increased in
patients with chronic HDV , versus the patients with chronic HBV and the control
healthy group.
Bilirubin (mcmol/l) 18,8+3,3 17,25+2,2 11,48±1,04 p>0,05
Alkaline
Phosphatase (U/l)
79,9+7,9 69,2+5,24 62,0±7,68 p>0,05
GGT (U/l) 59,4+14,24 36,6+7,6 29,16±2,45 p>0,05
 Cholestatic syndrome was detected to be increased too in the level of bilirubin and its
conjugated fraction, γ –GT, alkaline phosphates , in patients with chronic HDV , versus
the patients with chronic HBV and the control healthy group.

18. Results and discussion
Biochemical Analysis
 hepatodepressive syndrome was detected to be decreased in
serum protein, serum albumin, prothrombin index (in HDV
versus HBV patients).
Prothrombin (%) 72,6%+2.6 86%+0,2 86,6±0,76 p>0,05
Serum Albumin (g/l) 33,5±1,2 42,1±1,9 50,9±1,58 p>0,05
Leukocytes x 109/l 3,6+0,57 5,4+0,41 5,68±0,16 p<0,05
Thrombocytes x
109/l
156,8+10,2 185,4+12,5 258±9,8 p<0,05
Lymphocytes (%) 41%+0,23 38+0,24 24,68±1,2 p>0,05
ESR (mm/h) 8,83+1,84 4,92+0,95 10,62±0,9 p>0,05
 Investigation of immuno-inflammatory syndrome was detected that , white blood cell
and platelet counts decreased in HDV versus the control group, as well as to patients
with HBV.

19. Results and discussion
Physical And Para-Clinical Investigations
 Clinical And Para-clinical Investigations in Chronic HDV
And HBV patients

20. Results and discussion
Fibroscan – Elastography
According to the median results that obtained during
the Fibroscan , patients with Chronic HDV infection
have median of 8.2±0,99 kilopascal that correspond to
Metavir Fibrosis stage F1-F2 in average , versus
patients with Chronic HBV infection have median of
6.1±0,36 kilopascal that correspond to Metavir Fibrosis
stage F0-F1 .
Patients with Chronic HDV Patients with Chronic HBV
8.2±0,99 kilopascal 6.1±0,36 kilopascal
Metavir Fibrosis stage F1-F2 Metavir Fibrosis stage F0-F1

21. Results and discussion
Serological Markers
 Serological Markers in patients with Chronic HDV And HBV
infection

22. Results and discussion
Viral Count
 Detected HDV RNA - on Chronic HDV

23. General conclusions
 The clinical presentation of patients with chronic hepatitis D
shows the predominance of astheno-vegetative syndrome
(100%), moderate and severe pain in right right upper
quadrant (75%), hepatomegaly (60%) and splenomegaly
(33%) versus patients with chronic hepatitis B, which these
events have a smaller share. Clinical disturbances are more
severe in chronic hepatitis D versus chronic hepatitis B.
 In patients with HDV was found veridical pronounced
cytolytic syndrome, manifested by increase of ALT and AST
compared with control group (p<0,001) and patients with
HBV (p<0,05), also was determined tendency towards
reduction of prothrombin and albumin compared with
chronic hepatitis B.

24. General conclusions
 Research blood count have revealed a decreased of white blood cell
(p<0,01) and platelet counts (p<0,001) in HDV versus the control group, as
well as to patients with HBV (p<0,05 for white blood cell and platelet
counts).
 After evaluating the viral markers in HDV patients we have detected the
presence of HBsAg, anti-HBcor and anti-HDV in all patients (100%),
HBeAg (positive) – in 25% of patients, anti-HBe – in 75%.
 The HDV RNA was found present in all investigated patients with chronic
hepatitis D, the a low titre of HBV DNA was detected in 5 (24%) patients.
 Patients with chronic hepatitis D were with more pronounced degree of
fibrosis (median of 8.2±0,99 kP that correspond to Metavir Fibrosis stage
F1-F2) determined by FibroScan versus patients with HBV infection
(6.1±0,36 kP that correspond to Metavir Fibrosis stage F0-F1).