Spontaneous arterial bleeding has been reported rarely. In a patient consuming heavy amounts of alcohol with alcoholic liver cirrhosis, spontaneous bleeding can be evoked by thrombocytopenia, altered platelet function, and shear stress on fully dilated arteries by portal hypertension. Alcohol consumption itself can also predispose a patient to bleeding by influencing the aggregation and activation of platelets, and altering the coagulation and fibrinolysis pathway. All of these mechanisms could cause patients with alcoholic liver cirrhosis to bleed spontaneously; however, conditions inducing peripheral arterial bleeding are very rare. Here, we report three cases of spontaneous arterial bleeding in patients with liver cirrhosis consuming heavy amounts of alcohol. All of the patients bled without any physical trauma, and the involved arteries were the intercostal arteries in two cases and a gastroduodenal artery in the other case. The patients were treated by angiographic embolization. One expired due to recurrence of arterial bleeding despite repeated angiographic embolization and massive transfusion.
Alcohol Drinking ; Arteries ; Blood Platelets ; Embolization, Therapeutic ; Fibrinolysis ; Hemorrhage* ; Humans ; Hypertension, Portal ; Liver Cirrhosis ; Liver Cirrhosis, Alcoholic* ; Recurrence ; Thrombocytopenia

Hepatopulmonary syndrome (HPS) is characterized by a defect in arterial oxygenation that's induced by pulmonary vascular dilatation in the setting of liver disease. Some studies have shown the relationship between the presence of the HPS and the severity of liver disease, but there are only rare cases of HPS inpatient with Child-Pugh class A liver cirrhosis. We report here on a case of a 58 years-old male who suffered from progressive dyspnea for the previous few years. He was diagnosed with alcoholic liver cirrhosis 5 years previously. There was no significant abnormality on the chest radiograph and transthoracic echocardiography, but the arterial blood gas analysis revealed severe hypoxemia. Contrast-enhanced transesophageal echocardiograpy with agitated saline demonstrated a delayed appearance of microbubbles in the left cardiac chambers. Thus, he was finally diagnosed with HPS. This case suggests that we should consider HPS when a patient with compensated liver cirrhosis has unexplained dyspnea.
Anoxia ; Blood Gas Analysis ; Dihydroergotamine ; Dilatation ; Dyspnea ; Echocardiography ; Hepatopulmonary Syndrome ; Humans ; Inpatients ; Liver ; Liver Cirrhosis ; Liver Cirrhosis, Alcoholic ; Liver Diseases ; Liver Transplantation ; Male ; Microbubbles ; Oxygen ; Thorax

We report a very rare case of colonic varix with massive bleeding. A 43-year-old male patient was transferred to our hospital for hematochezia. The patient had a history of chronic liver disease associated with alcohol use. The initial blood pressure was 93/73 mmHg, and the hemoglobin level was 8.4 g/dL. Severe hepatomegaly and periportal fatty infiltration were seen on abdominal computed tomography. Markedly ectatic veins protruded from the luminal side of the proximal ascending colon and drained to the dilated ileocecal and retroperitoneal veins. Emergent colonoscopy failed because of continuous hematochezia and hypovolemic shock, despite massive transfusion. Markedly dilated colonic varices were noticed around the ileocecal and ascending colon on superior mesenteric arteriography. An emergent right hemicolectomy was performed. The presumed bleeding focus was a protruding varix with a red clot on the top of a denuded vein on the anteromedial wall of the proximal ascending colon.
Adult ; Alcoholics ; Angiography ; Blood Pressure ; Colon ; Colon, Ascending ; Colonoscopy ; Gastrointestinal Hemorrhage ; Hemoglobins ; Hemorrhage ; Hepatomegaly ; Humans ; Liver Cirrhosis ; Liver Cirrhosis, Alcoholic ; Liver Diseases ; Male ; Phenobarbital ; Shock ; Varicose Veins ; Veins

Since liver function is changed by chronic liver diseases, chronic liver disease can lead to different hemorheological alterations during the course of the progression. This study aims to compare alterations in whole blood viscosity in patients with chronic liver disease, focusing on the gender effect. Chronic liver diseases were classified into three categories by patient’s history, serologic markers, and radiologic findings: nonalcoholic fatty liver disease (NAFLD) (n = 63), chronic viral hepatitis B and C (n = 50), and liver cirrhosis (LC) (n = 35). Whole blood viscosity was measured by automated scanning capillary tube viscometer, while liver stiffness was measured by transient elastography using FibroScan®. Both systolic and diastolic whole blood viscosities were significantly lower in patients with LC than NAFLD and chronic viral hepatitis (P < 0.001) in male patients, but not in female patients. In correlation analysis, there were inverse relationships between both systolic and diastolic whole blood viscosity and liver stiffness (systolic: r = −0.25, diastolic: r = −0.22). Whole blood viscosity was significantly lower in male patients with LC than NAFLD or chronic viral hepatitis. Our data suggest that whole blood viscosity test can become a useful tool for classifying chronic liver disease and determining the prognosis for different types of chronic liver diseases.
Blood Viscosity ; Capillaries ; Elasticity Imaging Techniques ; Female ; Hemorheology ; Hepatitis ; Hepatitis B ; Humans ; Liver Cirrhosis ; Liver Diseases* ; Liver* ; Male ; Non-alcoholic Fatty Liver Disease ; Prognosis

Humans ; Leptin ; blood ; Liver Cirrhosis ; blood ; etiology ; metabolism ; Liver Diseases, Alcoholic ; complications ; Male ; Transforming Growth Factor beta ; metabolism ; Transforming Growth Factor beta1

OBJECTIVETo study the influence of alcohol on the liver sinusoids endothelial cell (LSEC) fenestrae of rats.

METHODSSetting up the rat model of alcoholic liver disease by orogastric administration of alcohol, then kill the experimental and control groups of rats at the end of 4 weeks, 8 weeks and 12 weeks after alcohol feeding, and also at the end of another 12 weeks after balance foods feeding succeeding with alcohol feeding for 12 weeks. Staining the liver tissue by means of HE method and observing the successive change of LSEC fenestrae by transmission electron microscope.

RESULTSThe normal LSEC was flat with nucleus and organelle arranged regularly. The distal cytoplasm displayed as lamina with many fenestrae, not accompanied by basement membrane (BM) formation under the endothelial cell. At the end of 4 weeks of alcohol feeding, fenestrae decreased at the partial distal LSEC cytoplasm, but no BM developed. At the end of 8 weeks, fenestrae decreased significantly, even disappeared, with the BM developed incompletely under the endothelial cell. Concomitantly, fibroblast with active function developed. At the end of 12 weeks, the changes became more obvious; the complete BM could even be seen. However, this kind of changes was mostly limited in the single or adjoining sinusoids, as well as with little widespread formation of fibrosis. At the end of 12 weeks of stopping alcohol feeding, defenestrae and development of BM attenuated obviously.

CONCLUSIONThe defenestrae and BM of LSEC develop gradually with the chronic alcohol stimulation. Sinusoid capillarization and liver fibrosis even form when significant changes happen. The early change of the limited defenestrae and capillarization may be the basis of alcohol periportal fibrosis formation. This kind of liver fibrosis can be reversible after stopping alcohol feeding.

Animals ; Basement Membrane ; pathology ; Endothelium ; drug effects ; pathology ; Ethanol ; Liver ; blood supply ; pathology ; Liver Cirrhosis, Experimental ; pathology ; Liver Diseases, Alcoholic ; pathology ; Male ; Rats ; Rats, Wistar

Hepatocellular carcinoma (HCC) is one of the leading causes of death in Korea. Chronic hepatitis, alcoholic liver disease and liver cirrhosis are predisposing factor of HCC. Bleeding tendency and hemorrhage resulting from reduced production of coagulation factors or portal hypertension are not uncommon in HCC, moreover spontaneous hemoperitoneum also can occur. Spontaneous hemoperitoneum is a complication of HCC, that is caused by the rupture of HCC mass which abuts on the hepatic capsule. However hemoperitoneum also occurs due to the rupture of vasculature of the mass. Emergency laparotomy is the recommended treatment, however these patients exhibit poor prognosis because of hemodynamic instability followed by combined liver disease. Herein, we report a case of spontaneous hemoperitoneum due to the rupture of subcapsular vessels with invasion of HCC in a 39-years-old man, whose tumor was left undetected.
Blood Coagulation Factors ; Carcinoma, Hepatocellular ; Cause of Death ; Emergencies ; Hemodynamics ; Hemoperitoneum ; Hemorrhage ; Hepatitis, Chronic ; Humans ; Hypertension, Portal ; Korea ; Laparotomy ; Liver Cirrhosis ; Liver Diseases ; Liver Diseases, Alcoholic ; Prognosis ; Rupture

Spontaneous retroperitoneal hemorrhage due to liver cirhosis associated with impaired coagulopathy is very rare disease. Spontaneous retroperitoneal hemorrhage has been recorded as having originated from many retroperitoneal organs and blood vessels, and it may be due to local disease and/or systemic factors. In the majority of patients the bleeding arose from the kidney or adrenal gland. Among the systemic causes of spontaneous retroperitoneal hemorrhage are anticoagulation therapy and chronic hemodialysis during the course of which hemorrhagic complications may occur at many site, including the retroperitoneal space. Blood dyscrasias have been a rare cause of spontaneous retroperitoneal hemorrhage. Conditions reported have been included hemophilia, leukemia, polycythemia and sickle cell trait. Virtually every hemostatic function may be impaired in patients with severe hepatic disease as the result of failure of both the biosynthetic and clearence function of the liver, thrombocytopenia, platelet dysfunction, intravascular coagulation and fibrinogenolysis, and the effects of products of fibrinogen catabolism on the coagulation mechanism. We are reporting a case of spontaneous retroperitoneal hematoma in a patient with alcoholic liver cirrhosis with brief review of literature.
Adrenal Glands ; Blood Platelets ; Blood Vessels ; Fibrinogen ; Hematoma* ; Hemophilia A ; Hemorrhage ; Humans ; Kidney ; Leukemia ; Liver Cirrhosis* ; Liver Cirrhosis, Alcoholic ; Liver* ; Metabolism ; Polycythemia ; Rare Diseases ; Renal Dialysis ; Retroperitoneal Space ; Sickle Cell Trait ; Thrombocytopenia

OBJECTIVES: The objective of this study was to assess the relationship between systolic and diastolic blood pressure (SBP, DBP) and the risk of death from specific causes other than cardiovascular diseases. METHODS: We calculated the risk of specific death by SBP and DBP categories for 506 508 health examinees in 2002-2003 using hazard ratios (HRs) and 95% confidence intervals (CIs) in a Cox proportional hazards model. RESULTS: Compared to normal levels (SBP < 120 or DBP < 90 mmHg), stage I systolic and diastolic hypertension (SBP 140-159, DBP 85- 89 mmHg, respectively) were associated with an increased risk of death from diabetes mellitus, alcoholic liver disease, and renal failure (HR, 1.83; 95% CI, 1.51 to 2.22; HR, 1.24; 95% CI, 1.06 to 1.46; HR, 2.30; 95% CI, 1.64 to 3.21; HR, 1.67; 95% CI, 1.27 to 2.20; HR, 1.99; 95% CI, 1.41 to 2.81; HR, 1.31; 95% CI, 0.99 to 1.73, respectively), but a decreased risk of death from intestinal pneumonia (HR, 0.64; 95% CI, 0.42 to 0.98; HR, 0.59; 95% CI, 0.39 to 0.91). Only stage II systolic hypertension (SBP ≥160 mmHg) was associated with an increased risk of death from pneumonia, liver cirrhosis, and intestinal ischemia (HR, 1.54; 95% CI, 1.19 to 1.98; HR, 1.46; 95% CI, 1.00 to 2.15; HR, 3.77; 95% CI, 1.24 to 11.40, respectively), and stage I and II diastolic hypertension (SBP 140-159 and ≥160 mmHg) were associated with an increased risk of death from intestinal ischemia (HR, 3.07; 95% CI, 1.27 to 7.38; HR, 4.39; 95% CI, 1.62 to 11.88, respectively). CONCLUSIONS: An increase in blood pressure levels may alter the risk of death from certain causes other than cardiovascular diseases, a well-known outcome of hypertension, although the mechanism of these associations is not well documented.
Adult* ; Blood Pressure* ; Cardiovascular Diseases ; Cohort Studies* ; Diabetes Mellitus ; Humans ; Hypertension ; Ischemia ; Liver Cirrhosis ; Liver Diseases, Alcoholic ; Pneumonia ; Proportional Hazards Models ; Renal Insufficiency

Liver fibrosis is a slow, insidious process involving accumulation of extracellular matrix protein in the liver. The stage of liver fibrosis in chronic liver disease (CLD) determines overall morbidity and mortality; the higher the stage, the worse the prognosis. Noninvasive composite scores can be used to determine whether patients with CLD have significant or advanced fibrosis. Patients with low composite scores can be safely followed up in primary care with periodic reassessment. Those with higher scores should be referred to a specialist. As the epidemic of diabetes mellitus, obesity and non-alcoholic fatty liver diseases is rising, CLD is becoming more prevalent. Easy-to-use fibrosis assessment composite scores can identify patients with minimal or advanced fibrosis, and should be an integral part of decision-making. Patients with cirrhosis, high composite scores, chronic hepatitis B with elevated alanine aminotransferase and aspartate aminotransferase, or deranged liver panel of uncertain aetiology should be referred to a specialist.
Alanine Transaminase ; blood ; Aspartate Aminotransferases ; blood ; Decision Making ; End Stage Liver Disease ; complications ; diagnosis ; therapy ; Hepatitis B ; complications ; Humans ; Liver ; pathology ; Liver Cirrhosis ; complications ; diagnosis ; therapy ; Non-alcoholic Fatty Liver Disease ; complications ; diagnosis ; therapy ; Prognosis ; Referral and Consultation ; Treatment Outcome