الفهرس 
INTRODUCTIONيوجد فقط 14 صفحة متاحة للعرض العام
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المستخلص
Cirrhosis results from different mechanisms of liver injury that lead to necroinflammation and fibrogenesis; histologically it is characterized by diffuse nodular regeneration surrounded by dense fibrotic septa with subsequent parenchymal extinction and collapse of liver structures, together causing pronounced distortion of hepatic vascular architecture. This distortion results in increased resistance to portal blood flow and hence in portal hypertension and in hepatic synthetic dysfunction.
Portal hypertension is hypertension in the hepatic portal system, which is composed of the portal vein and its branches and tributaries. Portal hypertension is defined as elevation of hepatic venous pressure gradient (HVPG). Clinically significant portal hypertension is defined as a hepatic venous pressure gradient of 10 mm Hg or more. This threshold is required for the development of complication of PHT, such as porto-systemic collaterals, varices, ascites and circulatory dysfunction.
EV are Porto-systemic collaterals i.e., vascular channels that link the portal venous and the systemic venous circulation. They form as a consequence of portal hypertension (a progressive complication of cirrhosis), preferentially in the submucosa of the lower esophagus.
Upper endoscopy remains the gold standard for diagnosis of esophageal varices. It is recommended that all patients undergo endoscopy to assess the presence and the size of varices at the time of the diagnosis of cirrhosis. Thereafter, guidelines for the interval of endoscopic screening vary. Currently, the American Association for the Study of the Liver (AASLD) recommends that, if no varices are present at index endoscopy, this should be repeated at 2-3 years in compensated cirrhosis and annually in decompensated cirrhosis. The British Society of Gastroenterology recommends annual screening if grade 1 varices are present at initial screening, and an interval of 3 years if there is no evidence of varices at index endoscopy.
Several studies have evaluated possible non-invasive markers for the predicting the presence of varices in patients with cirrhosis. The conclusion of most of these studies was that a number of clinical, laboratory, and/or radiological variables have been explored as non- invasive alternatives to endoscopy which help in reducing the number of screening endoscopy.
Liver has a key role in glucose metabolism. It maintains normal levels of blood glucose by a combination of glycogenesis, glycolysis, glycogenolysis and gluconeogenesis. These pathways are regulated by a number of hormones including insulin, glucagon, growth hormone and catecholamines. Also liver is the major organ metabolizing insulin. Disturbed homeostasis of glucose and insulin occur more frequently in liver cirrhosis than in general population. More than half of the patients with cirrhosis show abnormal glucose tolerance and about one third show overt diabetes.
Different published clinical studies had suggested that IR was able to independently predict the presence of gastroesophageal varices in cirrhosis. The authors attributed this effect to a possible pathophysiological link between IR and PH.
A low serum zinc concentration is a well-known metabolic disorder in patients with CLD, and previous studies reported the relationship between the progression of liver disease and the decreased zinc values in CLD patients. In patients with CLD, the blood zinc concentrations were lower in patients with liver cirrhosis or hepatocellular carcinoma than in patients with chronic hepatitis, leading to hypothesize that the reduced blood zinc value could be associated with the formation and progression of varices.
The zinc value is not only a parameter indicating an abnormal metal metabolism, but is also a simple parameter associated with various clinical conditions in hepatitis virus related CLD patients, such as the histological stage of liver fibrosis and the severity of varices in the compensated cirrhotic patients.
The study was carried out on 50 cases divided into two groups: group I: 25 splenectomized cirrhotic patients with or without esophageal varices and group II: 25 non splenectomized cirrhotic patients with or without esophageal varices. The extensive exclusion criteria were as follow: presence of diabetes mellitus, hypertension, renal disease, haemochromatosis, history of esophageal bleeding, sclerotherapy or band ligation, and hepatocellular carcinoma.
All patients were subjected to the following after their informed consent: Full history taking, Clinical examination, BMI, Abdominal ultrasound, Upper gastrointestinal endoscopy, Child Pugh classification, Laboratory investigation including: CBC, ALT, AST, serum albumin, prothrombin time and activity, GGT, ALP ,Serum zinc, Homeostasis model assessment of insulin resistance (HOMA-IR).
The main results were:
There was no statistically significant difference between the 2 subgroups of group I and the 2 subgroups of group II according to age and sex.
There was statistically significant relation between BMI, portal vein diameter, child class, low platelet count, low serum albumin and esophageal varices presence in both splenectomized and non splenectomized groups.
The diagnostic performance of HOMA-IR was compared to that of endoscopy which is considered the gold standard in diagnosis of esophageal varices. The receiver operator characteristic (ROC) curve analysis generated a cut off value (COV) of 3.3 that could differentiate between cirrhotic with no EV and cirrhotic with EV with area under the curve of 0.792 with a sensitivity of 73% and a specificity of 71% in splenectomized patients and a cut off value of 3.4 with area under the curve of 0.799 with a sensitivity of 71% and a specificity of 82% in non splenectomized patients.
The diagnostic performance of Zinc was compared to that of endoscopy which is considered the gold standard in diagnosis of esophageal varices. The receiver operator characteristic (ROC) curve analysis generated a cut off value (COV) of 61.5μg/dl that could differentiate between cirrhotic with no EV and cirrhotic with EV with area under the curve of 0.7with a sensitivity of 63% and a specificity of 65% in splenectomized patients and a cut off value of 59.5μg/dl with area under the curve of 0.7 with a sensitivity of 64% and a specificity of 73% in non splenectomized patients.