الفهرس 
HCVOnly 14 pages are availabe for public view
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Abstract
HCV is a leading cause of chronic liver diseases, cirrhosis and hepatocellular carcinoma as well as the most common indication of liver transplantation in many countries.
Hepatic fibrosis is the final event of chronic liver injury, independently from the etiological agent, it is characterized by excessive extracellular matrix (ECM) deposition that distorts the hepatic architecture by forming fibrotic scars, and the subsequent development of nodules of regenerating hepatocytes defines liver cirrhosis.
Liver biopsy is an essential gold standard method for assessing chronic hepatitis and fibrosis and the main goal of the biopsy is to grade and stage liver damage for prognosis and treatment.
There are two main groups of non-invasive methods for evaluation of hepatic fibrosis: the first defined ”serum markers” and the second defined ”radiological group”.
MPV is increased in CHC with advanced fibrosis. Calculation of MPV along with the use of other markers may give further information about severity of liver fibrosis in CHC.
This study was aimed to evaluate the role of mean platelet volume (MPV) as a fibrosis marker in patients with chronic hepatitis C (CHC). This study was carried on 150 patients diagnosed with chronic hepatitis C infection and 20 of healthy volunteers as a control.
They were categorized into 2main groups:
Group 1(patients group): 150 patients with CHC which subdivided according to liver biopsy METAVIR system into 4 subgroups:
F0/F1: no fibrosis /portal fibrosis without septa(17 patients)
F2: portal fibrosis with rare septa (82 patients)
F3: numerous septa without cirrhosis (33 patients)
F4: cirrhosis(18 patients)
Group 2 (control group):20 healthy volunteers as a control group.
Patients of this study were selected from patients attending Tanta Fever Hospital (Interferon Unit), in period from May 2013 to January 2014.
All patients and control were enrolled in this study subjected to:-
1. Full history taking.
2. Complete clinical examinations.
3. Laboratory tests
a. Complete blood count :(HB%- WBCS - platelets)
b. Liver function tests: (ALT, AST, Alkaline Phosphatase, Serum Bilirubin, Prothrombin Time and activity and INR)
c. Renal function tests :( Blood urea and serum creatinine).
d. Schistosomal Ab by ELISA
e. Autoimmune markers (ANA.) f. Alpha-feto- protein
g. TSH
4. Abdominal-pelvic ultrasound.
5. HCV RNA by quantitative PCR.
6. Liver biopsy for histological examination and quantification of liver fibrosis and inflammation.
7. Measuring the mean platelet volume:
Is calculated by the following formula: MPV (FL) = [(platelet (%) / Platelet count (× /L)
Or computerized calculation by complete blood counters (histogram)
The results of this study were tabulated, statistically analyzed and graphically represented.
The present study revealed the following results:
Statistical comparison between the HCV patients GI (Patients group) and G II (Control group) showed no significant differences as regard age and the gender.
Statistical comparison between the HCV patients GI (Patients group) and G II (Control group) showed no significant differences as regard HB%,RBCS and WBCS ,but it showed that significant differences regarding MPV and Platelet count. Statistical comparison between the HCV patients GI (Patients group) and G II (Control group) showed no significant differences as regarding (Total bilirubin, Direct bilirubin ,ALT, AST, Alkaline phosphate and Serum Albumin but it showed significant differences regarding Prothrombin time.
Statistical comparison between the HCV patients GI (Patients group) and G II (Control group) showed no significant differences as regard creatinine and urea.
Statistical comparison between the HCV patients GI (Patients group) and G II (Control group) showed no significant differences as regard Random blood sugar (RBS), Alpha Feto Proteins (AFP), Anti Nuclear Antibody titer (ANA) and Thyroid Stimulating Hormone (TSH).
Statistical comparison between the HCV patients GI (Patients group) and G II (Control group) showed significant differences as regard presence of the schistosomal antibodies.
Statistical comparison between the HCV patients GI (Patients group) and G II (Control group) showed significant differences as regard ultrasonographic findings of the liver. The results of liver biopsy in group I according to activity grades and fibrosis degrees (A1= 52 patients (34.7%), (A2=86 paients (57.3%) and (A3=12 patients (8%).and fibrosis degrees (F1 = 17 patients (11.3%), F2 = 82 patients (54.7%), F3 = 33 patients (22%) and F4 = 18 patients (12%).
Statistical analysis between HCV patients (group I) with different degrees of fibrosis(F0/F1-F2-F3-F4) regarding age ,sex and PCR level of HCV RNA showed no significant differences between them, but showed significant differences with (MPV- Platelets counts- Schistosomiasis -Ultra sounds findings- ALT- AST- Prothrombin time).
Uni-variate Logistic regression analysis showed association between different degrees of the fibrosis (F0/F1-F2-F3) with (MPV- Platelets counts- Schistosomiasis -Ultra sounds findings- ALT- AST- Prothrombin time). Multi-variate Logistic regression analysis shows only 6 variables remained as independent risk factors: (MPV, Schistosomiasis, platelet count, ALT, AST and Prothrombin time).
Statistical comparison between studied groups from aspect of degree of fibrosis and MPV showed significant difference (where p-value < 0.05) where MPV for control versus patients (7.57±0.68 FL vs. 8.95±1.30 FL) and in-between patients of different degree of fibrosis (Mild Fibrosis [F0/F1-F2 [(8.98±0.23 FL) and Sever Fibrosis [F3-F4]: (9.60±1.7 LF). The results of this study suggest that high MPV level especially ≥ 9.22 fl as a cutoff point, may help to predict advanced fibrosis in patients with CHC. However, it should not be forgotten that MPV is not a specific marker for fibrosis where sensitivity (75.7%) and specificity (62%), PPV (40.3 %) and AR (61.8%) and also high NPV (93.4%) seems to be more important in helping to exclude a high fibrosis ratio and fibrosis degree in patients with CHC.