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العنوان
A Study the Association between Glycometabolism and Nonalcoholic Fatty Liver Disease in Obstructive Sleep Apnea patients /
المؤلف
Sharaf, Fatma El-Sayed.
هيئة الاعداد
باحث / فاطمة السيد شرف
مشرف / غادة عاطف عطية
مشرف / يوسف محمد منصور
مشرف / السياجي علي عبد العزيز
الموضوع
Chest Diseases.
تاريخ النشر
2023.
عدد الصفحات
96 p. :
اللغة
الإنجليزية
الدرجة
ماجستير
التخصص
الطب الرئوي والالتهاب الرئوى
تاريخ الإجازة
22/11/2023
مكان الإجازة
جامعة طنطا - كلية الطب - الامراض الصدرية
الفهرس
Only 14 pages are availabe for public view

from 144

from 144

Abstract

The condition known as non-alcoholic fatty liver disease, which encompasses illnesses such as non-alcoholic fatty liver, hepatic fibrosis, cirrhosis, non-alcoholic steatohepatitis, as well as hepatocellular carcinoma, has emerged as one of the most frequent causes of chronic liver disease around the world. This is due to the fact that diets high in saturated fats are associated with an increased risk of developing liver disease. It has a considerable influence on the rates of morbidity also death connected to liver-related conditions. Although the mechanisms underlying the pathogenesis of non-alcoholic fatty liver disease are still unknown, the ”two-hit hypothesis” is the prevalent thought for the progression of non-alcoholic fatty liver disease. This is despite the fact that the ”two-hit hypothesis” is the prevalent idea. The information that is available at this time points toward a ’’multiple hit’’ hypothesis, which takes into account oxidative stress, lipotoxicity, gut microbiota, insulin resistance, malfunctioning mitochondrion, as well as genetic & epigenetic variables. It is possible that obstructive sleep apnea & intermittent nocturnal hypoxia, both of which can lead to oxidative stress, lipid peroxidation, and systemic inflammation, are a part of the ”second hit” and are responsible for the progression of non-alcoholic fatty liver disease from the early stage to the stage of non-alcoholic steatohepatitis. In the meantime, new research suggests that obstructive sleep apnea has a strong connection to the evolution of non-alcoholic fatty liver disease in either children or adults. Aim of the work The major goal of the trial was to evaluate the link among the glycometabolism of individuals with obstructive sleep apnea in addition to the existence of non-alcoholic fatty liver disease. Patients and methods: This was a study that was carried out in the chest Department of Tanta University at Tanta University Hospital. It was a cross-sectional study. Forty individuals who exhibited symptoms of OSA, such as increased daytime sleepiness, snoring, as well as witnessed apnea, participated in the study. Inclusion criteria: Patients that suspect OSA for example excessive snoring, daytime sleepiness and witnessed apnea.their age was over 18 years old . Non of these individuals had ever been diagnosis as OSA. Exclusion criteria: • Patients with hyperparathyroidism • Persons with hepatitis B and C • Chronic kidney disease • Those with acute inflammatory disease or have condition affect bon metabolism • Persons taking medication affecting on endocrine system • Persons have alcohol consumption • The following parameters were done for all patients: • Full history taking and complete clinical examination • Rotuine blood examination as cbc • BMI, neck and waist circumference • Overnight polysomnography • Biochemical investigation as FBG,TC(LDLc-HDLc) andTri . • Abdominal ultrasound to evaluate the liver. The main results of the study revealed that: • The mean ESS score was 12, which pointed to excessive daytime sleepiness; moreover, the mean STOP-Bang score was 5 that, further classifying the risk of OSA into a mild, moderate and high-risk category, later presented in 82.5% of cases. Additionally, the mean AHI was 40( SD 28), which classified the patients into normal cases (7.5%), mild OSA (15%) moderate OSA (20%) and severe groups; the last represented 57.5% of cases. • The majority of the studied patients (82.5%) were at high risk to have OSA. • The mean PLT count was within the normal range; however, the mean serum level of AST, ALT, and FBS was within the upper average value, while the lipid profile means value exceeded the normal reference range. • The frequency of mild and moderate hepatomegaly exceeded 70% of cases, as well as the frequency of non-alcoholic fatty liver, which based on HSI classification, was higher (85%); of them, the frequency of liver fibrosis based on the FIB-4 index classification was 42.5%. • Patients with NAFL had significantly higher BMI, NC, WC, SBP, and DBP, p<0.001, 0.01, 0.003, 0.05, and 0.05, respectively. However, age, sex, and smoking habits had no significant association with NAFL, p>0.05. • Patients with NAFL had a significantly increased ESS score and higher risk of having OSA, p=0.05; however insignificant difference regarding SB score, p= 0.11. Additionally, AHI was significantly raised in persons with NAFL, plus the frequency of severe degree of OSA was significantly higher, p=0.001 and 0.02, respectively. Moreover, RDI, and ODI, showed significantly higher levels in patients with NAFL, p< 0.001 for all of them, also TS90% was significantly higher in NAFL ,p=0.001; however, La SO2 % was significantly lower in NAFL, p=0.008. • AST and ALT were significantly higher in cases with NAFL, p=0.05 and <0.001; in addition, FBG was substantially higher, too, p=0.001. Regarding the lipid profile, only HDLc and Tc were significantly higher in NAFL patients, p=0.05 and <0.001. • FBG and TC were significantly higher in patients with OSA with NAFL, p=0.0110 & 0.0004. • FBG, HDL-c and TC had significant difference in patients according to OSA severity, p=0.0001, 0.0114 and 0.0007. • Incidence of fatty liver had significant difference in patients with and without OSA, p= 0.002. • Incidence of fatty liver had significant difference in OSA patients according to the severity, p=0.0001. • Independent predictor of NFLD were BMI >30 [OR: 7.714 (95%CI: 1.165-51.064); p-value=0.034] and severe OSA [OR: 29 (95%CI: 2.773-303.306); p-value=0.005]. Other confounders included Smoking [OR: 1.778 (95% CI: 0.286-11.039); p-value 0.537], Male sex [OR: 5.625 (95%CI: 0.593-53.377);p-value0.132] and Age > 50years [OR: 1.000 (95%CI:0.176-5.673); p-value 0.999]. • Uivaridate logistic regression analysis show that independent predictor of NFLD were BMI >30 [OR: 1.862 (95%CI: 0.379-3.174); p-value=0.001] and severe OSA [OR: 6.8 (95%CI: 3.379-3.174); p-value=0.001]. Other confounders included Smoking [OR: 1.259 (95% CI: 0.658-2.409); p-value 0.533], Male sex [OR: 1.771 (95%CI: 1.069-2.935); p-value0.101] and Age > 50years [OR: 1.417 (95%CI: 0.726-2.765); p-value 0.376].