ABSTRACT
Amoebic liver abscess is a complication of amoebiasis that needs early diagnosis and proper treatment before further complications occur. We report a-35 year old female presented by fever and dyspnea due to huge liver abscess complicated by massive right side empyema. The patient was effectively treated by percutaneous drainage for both the right lobe abscess and empyema together with pharmacologic agents
ABSTRACT
Patients with liver cirrhosis are frequently prone to dyspeptic symptoms. The exact cause of these symptoms is unknown. GIT hormones were suggested to have a role in dyspepsia in these patients. The aim of this study was to evaluate the role of vasoactive intestinal polypeptides [VIP] and gastrin in dyspeptic symptoms in cirrhotic patients, and their impaction on the occurrence of esophageal motility disorders and GERD in such patients. Three groups of patients were included in this study, group I includes 20 cirrhotic dyspeptic patients, group 11 includes 10 cirrhotic asymptomatic patients and group III includes 10 non-cirrhotic patients with dyspepsia. Upper GIT endoscopy, 24 hour ambulatory esophageal PH monitoring, esophageal manometric study, and estimation of gastrin and VIP serum levels were done to all patient groups. GERD [acid score > 22] was found in 16[80%], 5 [50%] and 3 [30%] in groups I, I1 and III, respectively with a statistically significant difference between the groups. Serum gastrin and VIP were found to be elevated in group I [175.4 +/- 41.9 and 15,l +/- 3.8] compared with groups II and III [150.7 +/- 35.1 , 9.2 +/- 3.2 and 101.7 +/- 33.3 , 533 +/- 2.5, respectively] with a statistically significant increase in symptomatic cirrhotic patients compared with asymptomatic cirrhotic and symptomatic non-cirrhotic patients. Non-specific esophageal motility disorders [NEMD] was found in 7 [35%], 2 [20%] and 3 [30%] in groups I, II and XII respectively. There are positive correlation between VIP and gastrin and negative correlation between pH and both VIP and gastrin. In conclusion, dyspepsia in cirrhotic patients may ba attributed to elevated GIT hormones as these hormones are elevated in cirrhotic symptomatic patients co~nparcd to, asy~nptomntic cirrhotic paticnts and symptomatic non-cirrhotic patients with dyspepsia. These symptoms are due to increased incidence of GERD, NEMD in cirrhotic symptomatic patients and increased gastric acid production due to elevated serum gastrin. The increased VIP s e m level has an inhibitory effect on GIT motility sharing in dyspeptic symptoms