الفهرس 
IntroductionOnly 14 pages are availabe for public view
 |  | from | 108 |  |  |
| | | from | 108 | | |
Abstract
Nonalcoholic fatty liver disease (NAFLD) now refers to a spectrum of liver diseases that ranges from steatosis (i.e., fatty infiltration of the liver) to Non-alcoholic steatohepatitis (NASH) ie, steatosis with inflammation and hepatocyte necrosis, to fibrosis and cirrhosis with increased risk of hepatocellular carcinoma. NAFLD is the most common cause of cryptogenic cirrhosis, which is cirrhosis that cannot be explained by hepatitis, alcohol abuse, toxin exposure, autoimmune disease, congenital liver disease, vascular outflow obstruction, or biliary tract disease
Global prevalence of NAFLD is 25.24% with highest prevalence in the Middle East and South America and lowest in Africa. Metabolic comorbidities associated with NAFLD included obesity (51.34%), type 2 diabetes (22.51%), hyperlipidemia (69.16%), hypertension (39.34%), and metabolic syndrome (42.54%). HCC incidence among NAFLD patients was 0.44 per 1,000 person
The mechanism of the liver injury in NAFLD is currently thought to be a “multiple-hit process” where the first “hit” is represented by an increase in liver fat, followed by multiple additional factors that trigger inflammatory activity which leads As a consequence to mitochondrial dysfunction with oxidative stress and production of reactive oxygen species and endoplasmic reticulum (ER) stress-associated mechanisms are activated
NAFLD shares the same etiologic factors with metabolic syndrome, such as obesity, diabetes, and dyslipidemia. These are also major cardiovascular risk factors. Several epidemiological studies indicate that NAFLD, especially in its more severe forms, is linked to an increased risk of cardiovascular disease, and this increased risk is independent from underlying cardio-metabolic risk factors Furthermore, in recent studies, NAFLD itself has been shown as an atherosclerotic risk factor
IL32 was identified as a pro-inflammatory cytokine known to play a role in host defense, inflammatory diseases, and cancer , as a novel factor clearly associated with NAFLD and insulin resistance in patients with obesity. IL32 expression was significantly increased in the liver of patients with NAFLD, and this elevation was more pronounced in patients with NASH.
IL32 was shown also to stimulate the production of several pro-inflammatory cytokines, including TNFα, and to activate typical cytokine signaling pathways of NF-κB. Reversely, TNFα and IFNγ were shown to activate IL32 production in various pathologic contexts, underpinning the presence of an auto perpetuating loop between IL32 and TNFα to sustain inflammation.
The aim is to study serum levels of interleukin 32 in patients with NAFLD to detect its relation to the incidence and severity of NAFLD.
To obtain this aim, we included 80 persons & divided them into 2 groups:
group I: 40 patients with NAFLD as a case group.
group II: 40 healthy subjects as a control group.
We can sum up our results in the following points:
Weight, BMI and Waist circumference were significantly higher among case group when compared with the control group (p<0.001 for all). While there was non statistically significant difference found between two groups regarding Height.
serum levels of AST, ALT, TGS, Total Cholesterol & LDL were significantly higher among patients of case group when compared with patients in the control group (p<0.001 for all). On the other hand, serum levels of Albumin & HDL were significantly lower among patients of case group when compared with patients in the control group (p<0.001 for both). While there was non difference between two groups regarding Total Bilirubin.
Mean Interleukin 32 Concentration in the current study was significantly higher among patients in case group when compared with patients in the control group (76 ng\ml vs 13 ng\ml; p<0.001)
We found a significant statistical negative correlation between Interleukin 32 Concentration & serum Albumin level (r=-0.346; p=0.029). while there was no significant statistical correlation between Interleukin 32 Concentration & each of Age, Weight, Height Height, BMI, Waist, AST, ALT, Total Bilirubin, TGS, T.Cholesterol, HDL & LDL.
We found no significant statistical correlation between Interleukin 32 Concentration & each of FLI score, NAFLD Fibrosis Score and PAUS Size.
The best cut off point of Interleukin 32 Concentration (ng\ml) to detect Cases group was > 22.5 with sensitivity of 100%, specificity of 87.50%, PPV of 88.9%, NPV of 100% and total accuracy of 98.2%.
The best cut off point of Interleukin 32 Concentration (ng\ml) to detect High group was found ≤165 with sensitivity of 90.91%, specificity of 28.57%, PPV of 85.7%, NPV of 40% and total accuracy of 55.8%.
The best cut off point of Interleukin 32 Concentration (ng\ml) to detect Indeterminant group was ≤75 with sensitivity of 48.48%, specificity of 85.71%, PPV of 94.1%, NPV of 26.1% and total accuracy of 62%.
In conclusion: Interleukin 32 can be considered as a prognostic marker for nonalcoholic fatty liver diseases with sensitivity of 100% and total accuracy of 98.2%.
Interleukin 32 Concentration was found to be negatively correlated with serum Albumin level. Although, We found no correlation between Interleukin 32 Concentration & each of Fatty Liver Index score, nonalcoholic fatty liver diseases Fibrosis Score and PAUS Size.
We recommend the use of Interleukin 32 as a diagnostic marker for nonalcoholic fatty liver diseases.
More studies on larger scales are needed to confirm our results.