الفهرس 
IntroductionOnly 14 pages are availabe for public view
 |  | from | 75 |  |  |
| | | from | 75 | | |
Abstract
Liver cirrhosis is defined pathologically as fibrosis and inflammation of the liver which is caused by chronic HBV, chronic HCV, NASH, NAFLD, chronic alcohol use and auto immune diseases which lead to portal hypertension.
A clinically relevant complication is development of portal hypertension with all its consequences such as ascites, spontaneous bacterial peritonitis and portosystemic collaterals.
Oesophageal varices are defined as portosystemic collaterals developed in cirrhotic patients with portal hypertension.
The presence of red spots, size of varices and severity of cirrhosis are considered to be important predictors of oesophageal varices.
Although the mortality of variceal haemorrhage has declined in the past decades, it is still very high with six-week mortality rate of 37% and a high recurrence rate after the first bleeding incident.
The gold standard method for identifying presence and estimating size of varices is esophagogastroduodenoscopy, (EGD) the disadvantages of which include need for IV sedation and high cost.
Although repeated endoscopic controls in patients with advanced liver fibrosis or cirrhosis are justified, it is an invasive diagnostic procedure with its own risks, therefore non-invasive predictors of portosystemic collaterals are of high interest.
Many non-invasive or minimally invasive methods of screening of oesophageal varices are performed as liver and spleen elastography, imaging methods as CT, MRI and U/S, laboratory tests and capsule endoscopy.
The venous blood is drained from the gall bladder via small vessels directly into the liver with an additional venous blood drain via small veins towards the cystic duct and then with vessels from the common bile duct terminating into the portal venous system.
The gall bladder should be directly affected by portal hypertension causing a thickened gall bladder wall due to impaired venous drainage.
The aim of this study is to evaluate whether non-inflammatory gall bladder wall thickness serve as predictor of oesophageal varices in combination and comparison with other non-invasive clinical and laboratory parameters.
This case-control study was conducted at the Hepatology and Gastroenterology Department, Ain Shams University, Egypt. The study was conducted over a period of one year, from January 2022 until January 2023.
The main results of the study revealed that:
There was no statistically significant difference between both groups as regard age, sex and associated comorbidities
There was no statistically significant difference between both groups as regard the underlying cause of cirrhosis
There was statistically significant higher rate of complaints either gastrointestinal or extra-gastrointestinal in subjects with esophageal varices that those without varices. 60% of subjects with cirrhosis without esophageal varices were referred for screen for CLD.
There was statistically significant higher rate of clinical findings either gastrointestinal or systematic in subjects with esophageal varices that those without varices. 37.78% of subjects with cirrhosis without esophageal varices have normal clinical examination.
There was statistically significant lower Hb level, platelet count, lower albumin level and higher urea, creatinine, higher bilirubin, prolonged PT in subjects with than without esophageal varices.
There were no statistically significant differences in echocardiography in subjects with than without esophageal varices.
There was statistically significant higher GB wall thickness in subjects with than without esophageal varices (9.89±0.71 vs 6.98±0.84). Cirrhosis (100% vs 91.1%), Splenomegaly (57.8% vs 8.9%) and Ascites (97.8%; 60% has moderate and 37.8% massive vs 0%) were statistically significant higher in subjects with than without esophageal varices while hepatomegaly was statistically significant higher in subjects without than with esophageal varices (8.9% vs 05).
Among subjects with cirrhotic with EV, Portal hypertensive gastropathy was detected in most of them that was mild in 33.3%, moderate in 4.4% and severe in 60%. In most of subjects esophageal varices were large sized in 80% and medium sized in 20%. On the other hand, Mild antral gastritis was statistically significant higher in subjects without than with esophageal varices (8.9% vs 05).
Among our studied population all subjects with CTP grade A had Cirrhotic without EV and none of them had EV while 46.7% of subjects with EV were CTP grade and 53.3% were CTP grade C. none of subjects with Cirrhotic without EV were CTP grade B and C.
At cut off point >8.5 mm, GB wall thickness has 95.8% sensitivity and 89% specificity for prediction of EV in subjects with liver cirrhosis