Esophageal and Gastric Varices ; diagnosis ; etiology ; pathology ; Hemorrhage ; Humans ; Liver Cirrhosis ; complications ; pathology

No abstract availble.
Duodenoscopy ; Esophageal and Gastric Varices/*diagnosis/etiology/pathology ; Gastrointestinal Hemorrhage/*diagnosis/etiology/pathology ; Humans ; Male ; Middle Aged ; Pancreatic Neoplasms/*complications ; Tomography, X-Ray Computed

Portal hypertensive gastropathy (PHG) is a term used to define the endoscopic findings of gastric mucosa with a characteristic mosaic-like pattern with or without red spots, and a common finding in patients with portal hypertension. These endoscopic findings correspond to dilated mucosal capillaries without inflammation. The pathogenesis of PHG in not well known, but portal hypertension and some humoral factors seem to be crucial factors for its development. Pharmacological (e.g. propranolol), or interventional radiological (such as transjugular intrahepatic portosystemic shunt) procedures may be useful in preventing re-bleeding from PHG. The classic features of gastric antral vascular ectasia (GAVE) syndrome include red, often haemorrhagic lesions predominantly located in the gastric antrum which can result in significant blood loss. Although the pathogenesis of GAVE is not clearly defined, it seems to be a separate disease entity from PHG, because GAVE generally does not respond to a reduction of portal pressures. Endoscopic ablation (such as argon plasma coagulation) is the first-line treatment of choice. This review will focus on the incidence, clinical importance, etiology, pathophysiology, and treatment of PHG and GAVE syndrome in the setting of portal hypertension.
Esophageal and Gastric Varices/*diagnosis/etiology/therapy ; Gastric Antral Vascular Ectasia/*diagnosis/etiology/therapy ; Gastric Mucosa/metabolism/pathology ; Humans ; Hypertension, Portal/*complications ; Portasystemic Shunt, Transjugular Intrahepatic ; Vasodilator Agents/therapeutic use

An infarction of regenerative nodules in liver cirrhosis is a rare abnormality characterized by their coagulative necrosis. We presume that ischemic necrosis is induced by a sudden reduction in the portal and arterial blood flows after blood loss or shock. Most patients with infarcted regenerative nodules have experienced previous episodes of gastrointestinal hemorrhage. Awareness of the entity of infarcted regenerative nodules and its inclusion in the differential diagnosis of multiple hepatic nodules in liver cirrhosis is important, particularly in patients with an episode of gastrointestinal bleeding. The possible difficulty of differentiating infarcted regenerative nodules in liver cirrhosis from hypovascular hepatocellular carcinoma by initial imaging findings alone means that a liver biopsy and serial imaging might be helpful in the differential diagnosis. We report three cases of multiple infarcted regenerative nodules in liver cirrhosis after gastrointestinal hemorrhage.
Adult ; Diagnosis, Differential ; Esophageal and Gastric Varices/*complications/diagnosis ; Gastrointestinal Hemorrhage/*complications/diagnosis/etiology ; Hepatic Artery ; Humans ; Infarction/*diagnosis/etiology ; Liver/*blood supply/pathology ; Liver Cirrhosis/etiology/*radiography ; Liver Regeneration/physiology ; Male ; Middle Aged ; Tomography, X-Ray Computed

Systemic sclerosis (SSc) is a chronic systemic disease that affects the skin, lungs, heart, gastrointestinal tract, kidneys, and musculoskeletal system. Although up to 90% of patients with scleroderma have been estimated to have gastrointestinal involvement, liver disease has been reported only rarely. A 51-year-old woman was hospitalized due to esophageal variceal bleeding. Her serum was positive for anti-nuclear antibody and anti-centromere antibody. Sclerodactyly was noted on both hands, and she had recently developed Raynaud's syndrome. Punch biopsy of the hand showed hyperkeratosis, regular acanthosis, and increased basal pigmentation in the epidermis, and thick pale collagenous bundles in the dermis. Liver biopsy showed chronic active hepatitis with bridging fibrosis. Consequently, she was diagnosed with liver cirrhosis due to autoimmune hepatitis (AIH) combined with SSc. AIH had subsided after administration of prednisolone at 40 mg per day. She received 5-10 mg/day of prednisolone as an outpatient, and her condition has remained stable. Patients with either AIH or SSc should be monitored for further development of concurrent autoimmune diseases. The early diagnosis of AIH combined with SSc will be helpful in achieving optimal management.
Anti-Inflammatory Agents/therapeutic use ; Antibodies, Antinuclear/blood ; Esophageal and Gastric Varices ; Female ; Gastrointestinal Hemorrhage ; Hepatitis, Autoimmune/complications/*diagnosis/drug therapy ; Humans ; Liver Cirrhosis/*diagnosis/etiology/pathology ; Middle Aged ; Prednisolone/therapeutic use ; Raynaud Disease/diagnosis ; Scleroderma, Systemic/complications/*diagnosis ; Skin/pathology