الفهرس 
Non-Alcoholic Fatty Liver DiseaseOnly 14 pages are availabe for public view
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Abstract
Nonalcoholic fatty liver disease (NAFLD) is a disease gaining
increasing interest worldwide. It ranges from simple nonalcoholic
steatosis to nonalcoholic steatohepatitis (NASH), is characterized by
steatosis, inflammation and fibrosis, and may lead to liver cirrhosis and
hepatocellular carcinoma. Nonalcoholic fatty liver disease shares
common pathogenetic mechanisms with other components of the insulin
resistance or metabolic syndrome, with adipokines playing a crucial role.
The prevalence of Nonalcoholic fatty liver disease increases in
parallel with the epidemics of obesity and type 2 diabetes mellitus. nonalcoholic steatohepatitis diagnosis requires liver biopsy, an invasive
method, thereby developing noninvasive markers for Nonalcoholic fatty
liver disease represents a field of extensive research, targeting to replace
liver biopsy or identify candidates for liver biopsy. Furthermore, despite
the high prevalence of the disease, Nonalcoholic fatty liver disease
treatment remains an unmet medical need.
Activin A is a member of the tumor growth factor (TGF)-β
superfamily and is regarded as a multifunctional cytokine expressed in a
wide range of tissues and cells, where it regulates cellular differentiation,
homeostasis of cell number and tissue architecture, inflammation, cell
proliferation and apoptosis.
In hepatocytes, a complex role has been attributed to activin A; it is
reported to be beneficial against lipid accumulation, but it may promote
hepatic inflammation and fibrosis. It enhances the expression of collagen
and TGF-β1, induces mitochondrial β-oxidation, down-regulates fatty
acid synthase activity, promotes decreased weight percentage of saturated
fatty acids, alters the composition of polyunsaturated fatty acids and promotes matrix metalloproteinase activity. Its expression is elevated in
the fibrotic liver and it has been proposed to contribute to liver fibrosis
through induction of matricellular proteins, including connective tissue
growth factor, in hepatocytes and hepatic stellate cells. Moreover, it
inhibits the proliferation and induces apoptosis of hepatocytes,
contributing to the termination of liver regeneration; the proliferation of
liver progenitor cells and their mediated liver regeneration are controlled
by activin A.
Activin A is a member of the transforming growth factor (TGF)-
superfamily along with TGF- and the bone morphogenetic proteins.
Originally described as an inducer of follicle-stimulating hormone
release, activin A has more recently been recognized as a multifunctional
cytokine expressed in a wide range of cells and tissues with roles in the
regulation of wound repair, cell differentiation, apoptosis, and
inflammation, and growing evidence implicates activin A in the
pathogenesis of various inflammatory disorders, such as rheumatoid
arthritis, inflammatory bowel disease, and atherosclerosis.
Recent studies suggest that activin A, a member of the transforming
growth factor (TGF) superfamily, is involved in the pathogenesis of liver
disorders. We sought to explore its possible role in non-alcoholic fatty
liver disease (NAFLD).
The main results of the study revealed that:
In the Steatosis group there were 10 (28.6%) males and 72 (72%)
females, with mean age of 35.89 (±9.10 SD) with range (20-55)
years.
In the NASH group there were 18 (51.4%) males and 17 (48.6%)
females, with mean age of 35.17 (±10.10 SD) with range (21-54)
years. In the Control group there were 8 (40%) males and 12 (60%) females, with mean age of 37.15 (±10.18 SD) with range (24-55)
years. There was no statistically significant difference between the
three studied groups as regard demographic data.
There was high statistically significant difference between the
studied groups as regard weight and BMI.
In the Steatosis group the mean Liver size was 13.97 (±1.29 SD)
with range (12-16) cm, all the patients (100%) had enlargedechogenic liver.
In the NASH group the mean Liver size was 13.71 (±1.36 SD) with
range (12-16) cm, all the patients (100%) had enlarged-echogenic
liver.
In the control group the mean Liver size was 9.85 (±1.5 SD) with
range (8-12) cm, all the patients (100%) had Normal liver.
There was high statistically significant difference between the
studied groups as regard liver size.
There was high statistically significant difference between the
studied groups as regard ALT, AST, total and direct bilirubin, plts
count and activin A, significant difference between the studied
groups as regard Albumin.
there was high statistically significant difference between the
studied groups as regard APRI score, FIB-4.
there was high correlation between Activin A and BMI, APRI
score, FIB-4 and liver size with high significance (p<0.001).
Using Activin A. it was shown that above 858.5, it can
discriminate between NAFLD and non-NAFLD with level of
sensitivity 100% and specificity 100%.
Based on our findings, we recommend for further studies on larger
sample size to emphasize our conclusion.