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Query: UMLS:C0341503 (bacterial peritonitis)
 1,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patients with advanced hepatitis C virus (HCV) are at risk of death and are candidates for liver transplantation. After transplantation, HCV recurs and may rapidly progress to cirrhosis and graft loss. Treatment is needed to prevent progression of disease and minimize recurrence after liver transplantation. We evaluated the effectiveness, tolerability, and outcome of a low accelerating dose regimen (LADR) of antiviral therapy in the treatment of patients with advanced HCV. One hundred twenty-four patients (male/female ratio 81:43; age range 37-71 years; 70% genotype 1) were treated with LADR. Sixty-three percent had clinical complications of cirrhosis (ascites, spontaneous bacterial peritonitis, varices, variceal hemorrhage, encephalopathy). The mean Child-Turcotte-Pugh (CTP) score was 7.4 +/- 2.3, and the mean MELD score was 11.0 +/- 3.7. Fifty-six patients were CTP class A, 45 were class B, and 23 were class C. Forty-six percent were HCV RNA-negative at end of treatment, and 24% were HCV RNA-negative at last follow-up. Sustained virological response (SVR) was 13% in patients infected with genotype 1 HCV and 50% in patients infected with non-1 genotypes (P < .0001). Non-1 genotype, CTP class A (genotype 1 only), and ability to tolerate full dose and duration of treatment (P < .0001) were predictors of SVR. Twelve of 15 patients who were HCV RNA-negative before transplantation remained HCV RNA-negative 6 months or more after transplantation. In conclusion, in a sizeable proportion of patients with advanced HCV, LADR may render blood free of HCV RNA, stabilize clinical course, and prevent posttransplantation recurrence.
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PMID:Treatment of advanced hepatitis C with a low accelerating dosage regimen of antiviral therapy. 1602 97

Portal hypertension is one of the main consequences of cirrhosis. It results from a combination of increased intrahepatic vascular resistance and increased blood flow through the portal venous system. The condition leads to the formation of portosystemic collateral veins. Esophagogastric varices have the greatest clinical impact, with a risk of bleeding as high as 30% within 2 years of medium or large varices developing. Ascites, another important complication of advanced cirrhosis and severe portal hypertension, is sometimes refractory to treatment and is complicated by spontaneous bacterial peritonitis and hepatorenal syndrome. We describe the pathophysiology of portal hypertension and the current management of its complications, with emphasis on the prophylaxis and treatment of variceal bleeding and ascites.
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PMID:Current management of the complications of portal hypertension: variceal bleeding and ascites. 1668 12

Cirrhosis is the 12th leading cause of death in the United States. Individuals with cirrhosis are at risk for many potential complications. Complications can be managed or detected early with proper outpatient management. The most lethal of these complications is bleeding esophageal varices. All patients with cirrhosis should be screened for the presence of varices and treated when indicated. The most common complication seen in these patients is ascites. Ascites can be treated with dietary modifications and a diuretic regimen. Other potential complications include spontaneous bacterial peritonitis, hepatocellular carcinoma, hepatic encephalopathy, hepatorenal syndrome, and hepatopulmonary syndrome. The outpatient management of these complications will be discussed in this paper, along with the use of vaccinations, educating patients about the avoidance of hepatotoxic drugs, and when to refer a patient for liver transplant.
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PMID:Outpatient management of cirrhosis: a narrative review. 1680 Apr 15

Major complications of cirrhosis include ascites, spontaneous bacterial peritonitis, hepatic encephalopathy, portal hypertension, variceal bleeding, and hepatorenal syndrome. Diagnostic studies on ascitic fluid should include a differential leukocyte count, total protein level, a serum-ascites albumin gradient, and fluid cultures. Therapy consists of sodium restriction, diuretics, and complete abstention from alcohol. Patients with ascitic fluid polymorphonuclear leukocyte counts of 250 cells per mm3 or greater should receive empiric prophylaxis against spontaneous bacterial peritonitis with cefotaxime and albumin. Patients who survive an episode of spontaneous bacterial peritonitis should receive long-term prophylaxis with norfloxacin or trimethoprim/sulfamethoxazole. Patients with gastrointestinal hemorrhage and cirrhosis should receive norfloxacin or trimethoprim/sulfamethoxazole twice daily for seven days. Treatment of hepatic encephalopathy is directed toward improving mental status levels with lactulose; protein restriction is no longer recommended. Patients with cirrhosis and evidence of gastrointestinal bleeding should undergo upper endoscopy to evaluate for varices. Endoscopic banding is the standard treatment, but sclerotherapy with vasoconstrictors (e.g., octreotide) also may be used. Prophylaxis with propranolol is recommended in patients with cirrhosis once varices have been identified. Transjugular intrahepatic portosystemic shunt has been effective in reducing portal hypertension and improving symptoms of hepatorenal syndrome, and can reduce gastrointestinal bleeding in patients with refractory variceal hemorrhage. When medical therapy for treatment of cirrhosis has failed, liver transplantation should be considered. Survival rates in transplant recipients have improved as a result of advances in immunosuppression and proper risk stratification using the Model for End-Stage Liver Disease and Child-Turcotte-Pugh scoring systems.
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PMID:Cirrhosis and chronic liver failure: part II. Complications and treatment. 1697 21

Intestinal microflora plays an important role in the pathogenesis of hepatic cirrhosis (HC) complications. These patients are at a high risk of bacterial infections, mainly spontaneous ascitis infection or spontaneous bacterial peritonitis, pneumonia, or pleural empyema. Other HC complications, such as varicose vein hemorrhage, gastropathy, hepatorenal and hepatopulmonary syndromes, and portopulmonary hypertension, develop mainly due to portal hypertension. Portal hypertension is primarily caused by increased intrahepatic resistance, while after the forming of collateral circulation high portal pressure is maintained by increased splanchnic blood inflow secondary to vasodilatation. Itraorganic vasodilatation initiates hyperdynamic circulatory status, which exacerbates HC complications. Intestinal microflora plays a role in the development of both infectious complications and hyperdynamic circulatory status in HC. The article contains evidence of the influence of intestinal microflora on the development of HC complications.
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PMID:[The role of intestinal microflora in the development of complications of hepatic cirrhosis-associated portal hypertension]. 1792 83

Cirrhosis is the terminal phase of hepatic fibrosis, that leads to impaired hepatic function and blood flow. Liver cirrhosis is the final stage of many hepatic diseases characterized by chronic cellular destruction. The complications of liver cirrosis are the result of the hepatocellular lesion and portal hypertension. The most frequent complications are ascites, spontaneous bacterial peritonitis, hepatic encephalopathy, gastroesophageal varices, portal hypertensive gastropathy, hypersplenism, hepatocellular carcinoma, methabolic disorders, hepatorenal syndrome and hepatopulmonary syndrome. We review the current approach of cirrhosis and its complications in order to improve the prevention and therapeutics of this frequent disease.
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PMID:[Chronic viral hepatitis: protocol proposal for the management of cirrhosis]. 1862 97

Timely surveillance for varices and hepatocellular carcinoma, prophylaxis against spontaneous bacterial peritonitis (SBP) improve survival in patients awaiting transplantation. Early diagnosis of minimal or overt hepatic encephalopathy can delay life threatening complications, reduce need for hospitalization, and potentially improve survival pending liver transplantation.
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PMID:Care of the cirrhotic patient. 1944 22

Liver cirrhosis represents the final common pathway of virtually all chronic liver diseases, and is characterized by an accumulation of extracellular matrix rich in fibrillar collagens. Patients with cirrhosis are at risk of developing many potential complications. The most common complication seen in patients with liver cirrhosis is ascites, and the most lethal one is bleeding varices. Other intermediate and late stage complications include spontaneous bacterial peritonitis, hepatic encephalopathy, and hepatorenal syndrome. The mortality and morbidity attributable to liver disease in Korea have decreased continuously over the past decades, probably due to the implementation of universal vaccination and potent antiviral therapies. In addition, recent advances in the understanding of the pathophysiology of cirrhosis and in various management approaches to cirrhosis complications will contribute to the steady improvement in patient outcomes in this country. This review article outlines recent changes in etiologies and prognosis, and the advances in management of cirrhosis in Korea.
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PMID:Current status of liver diseases in Korea: liver cirrhosis. 2003 79

Liver cirrhosis is associated with a wide range of cardiovascular abnormalities including hyperdynamic circulation, cirrhotic cardiomyopathy, and pulmonary vascular abnormalities. The pathogenic mechanisms of these cardiovascular changes are multifactorial and include neurohumoral and vascular dysregulations. Accumulating evidence suggests that cirrhosis-related cardiovascular abnormalities play a major role in the pathogenesis of multiple life-threatening complications including hepatorenal syndrome, ascites, spontaneous bacterial peritonitis, gastroesophageal varices, and hepatopulmonary syndrome. Treatment targeting the circulatory dysfunction in these patients may improve the short-term prognosis while awaiting liver transplantation. Careful fluid management in the immediate post-transplant period is extremely important to avoid cardiac-related complications. Liver transplantation results in correction of portal hypertension and reversal of all the pathophysiological mechanisms that lead to the cardiovascular abnormalities, resulting in restoration of a normal circulation. The following is a review of the pathogenesis and clinical implications of the cardiovascular changes in cirrhosis.
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PMID:Cardiovascular changes in cirrhosis: pathogenesis and clinical implications. 2061 8

A 75-year-old man with general malaise and appetite loss was transferred to our hospital for assessment and treatment of liver failure. Laboratory findings on admission showed anemia, and gastroduodenoscopy (GDS) revealed linear esophageal varices and tensive duodenal varices (DV) in the second portion of the duodenum. Systemic examinations did not reveal any significant lesion capable of explaining his anemia, except for DV. Balloon-occluded retrograde transvenous obliteration was carried out to prevent DV bleeding. Good pooling of sclerosant was observed using two balloon catheters. However, contrast-enhanced computed tomography after the procedure revealed no thrombosis in DV, and the patient complained of tarry stools before additional therapy. Emergent GDS revealed ruptured DV with fresh blood and erosions on the surface. Emergent endoscopic obliteration using the tissue adhesive N-butyl-2-cyanoacrylate was carried out and complete hemostasis was achieved. Although no rebleeding episodes were observed after emergent obliteration, the patient died of sepsis following spontaneous bacterial peritonitis 53 days after admission. Autopsy revealed that DV dropped out, and the deep vein was replaced by granulation tissue. No signs of thrombi were detected, except varices. This autopsy case revealed the difficulty in DV management.
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PMID:Successful endoscopic hemostasis for ruptured duodenal varices after balloon-occluded retrograde transvenous obliteration. 2117 90


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