الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
CMV affects the liver and overall immunological status of the
host body. Specifically in HCV patients, co-infection with CMV can
suppress the host immune system, affects the IFN-mediated antiviral
pathway and thus becomes an additional threat to the host and may
contribute to the complexity of disease outcome in HCV infection.
This study was conducted on 40 patients with chronic HCV
infection aimed to study the impact of HCMV infection in response
rates of patients with chronic HCV infection to interferon-ribavirin
combination therapy.They were selected from Shebin El Kome Fever
Hospital in the period between June 2014 to January 2015. They were
21(52.5% males) and 19 (47.5% females), their ages ranged between
21and 55 years.They were classified into the following groups
according to response to (Peg – INF) and (RBV) combination therapy:
- group I (non responders): Included 20 chronic HCV patients
with any form of non response to therapy{complete non
response (10 patients ) & breakthrough at week 24 (7 patients)
and at week 48(3 patients)}.They were 12 males (60%) and 8
females (40%),Their ages ranged between 22 and 55 years with
mean value 39.80±8.60.
- group II (responders): Included 20 chronic HCV patients
with adequate response to therapy at the end of treatment (48
weeks).They were 9 males (45 %) and 11 females (55 %), Their
ages ranged between 21and 48 years with mean value
34.75±8.04.
For this purpose, all patients and controls were subjected to
thorough history taking, complete clinical examination, laboratory investigations {including - CBC, Liver function tests, Kidney function
tests, Blood sugar level (Fasting & postprandial) and HbA1c, TSH,
Serum Alpha fetoprotein, ANA, latex for RF, anti CCP as indicated,
serology for schistosomiasis, HBS Ag, Pregnancy test in females in
child bearing period, Imaging study (abdominal ultrasound), ECG,
Liver Biopsy, PCR studies(Quantitative PCR for HCV RNA &
Qualitative PCR for HCMV DNA)}.
Statistical analysis revealed:
No significant difference between studied groups as regard age
& sex distributions.
No significant difference between studied groups as regard
pretreatment CBC findings and liver function tests.
Non of studied patients had clinical evidences of hepatic
decompensation or manifestation of hepatocelluar faluire.Also,
non of the studied groups patients had imaging evidences of
portal hypertention, ascites, hepatic focal lesions or portal vien
thrombosis.
No significant difference between studied groups as regard
mean values of quatitative PCR for HCV RNA and levels of
viremia.
Significant difference between studied groups as regard stages
of fibrosis (40% of non responders were F3 versus 15% of
responders, 55% of non responders were F2 versus 40% of
responders while 5% of non responders was F1 versus 45% of
responders). On the other hand there was no significant
difference between studied groups as regard grades of
necroinflammations.
Significant increase in the mean values of serum αFP in non
responders when compared with responders, while there was no
significant difference between studied groups as regard BMI.
Non of studied patients had obesity.
Significant increases in the number of patients with positive
PCR - HCMV DNA in non responders when compared with
responders (14 out of 20 patients versus 5 out of 20 patients
respectively).
Rising of serum αFP (≥5 ng/ml),higher stages of fibrosis or
positive serum qualitative HCMV-DNA were independant risk
factors of non responses of chronic HCV patients to (Peg –
INF) and (RBV) combination therapy. Combination of 2 or all
of the above factors as a risk for non response could not be
statistically assessed due to small number of patients.