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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The liver produces almost all the factors involved in coagulation and fibrinolysis. The hepatic reticuloendothelial system also plays an important role in disposing activated coagulation/fibrinolysis-related factors and inhibitors. In liver cirrhosis, the production of coagulation/fibrinolysis-related factors is diminished, as well as its inhibitors. Moreover, the hematological profile is complicated by a decreased rate of clearance, thrombocytopenia induced by hypersplenism, and some qualitative abnormalities of the coagulation factor. Hence, treatment for bleeding tendency observed in cirrhotic patients is diverse.
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PMID:[Disorders of coagulation/fibrinolysis and bleeding tendency]. 811 80

In patients with liver cirrhosis, there were many abnormalities in laboratory tests. Serum GOT, GPT and LDH were elevated due to the liver cell necrosis. The value of ICG tests reflected the decrease of effective hepatic blood flow and the increase of intrahepatic shunt flow. White blood cell counts and the number of platelet were decreased due to the hypersplenism. Serum albumin and cholineesterase levels were decreased more remarkably in patients with alcoholic liver cirrhosis than in patients with viral liver cirrhosis. Raised GOT and GPT levels were lower in aged patients than in young patients. Serial laboratory tests were important for the management of patients with liver cirrhosis.
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PMID:[Blood chemistry, hematology of patients with liver cirrhosis]. 811 9

Hypersplenism is defined as the association of anemia, leukopenia, or thrombocytopenia with bone marrow hyperplasia and splenomegaly. Hypersplenism is common in liver cirrhosis and frequent in patients with portal hypertension. The effects of portacaval shunt are variable; hypersplenism hardly ever improves but rarely develops after surgery. Since the spleen is a major component of the mononuclear phagocyte system, splenectomy reduces antibody synthesis. Although splenectomy abolishes hypersplenism, it may lead to sepsis. Recently, partial splenic embolization, using gelform injected directly into the splenic artery, has been performed in patients with cirrhosis. Partial splenic embolization induces an increase in the number of circulating blood cells. In addition, the levels of albumin, hepaplastintest, cholesterol and cholinesterase are increased significantly after treatment. Partial splenic embolization rarely causes problems and may actually be beneficial.
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PMID:[Hypersplenism in liver cirrhosis]. 811 16

Since April 1985, we have performed a multidisciplinary therapy consisting of partial splenic embolization (PSE), percutaneous transhepatic obliteration (PTO) or transileocolic vein obliteration (TIO), and endoscopic injection sclerotherapy (EIS) for patients with severe gastroesophageal varices and those with a portacaval shunt associated with portal hypertension. In this study, PSE and percutaneous transhepatic portography (PTP) were performed at the same time in seven liver cirrhosis patients with hypersplenism, gastroesophageal varices, or hepatocellular carcinoma. The changes in portal blood flow/pressure and hemodynamics were examined by a thermodilution method. The effects of PSE on blood biochemical parameters such as the platelet count, ICG R15, redox tolerance index (RTI), and oral glucose tolerance test (75 g OGTT) were also evaluated. PSE induced a decrease in the blood flow of the splenic artery and in the splenic vein pressure without decreasing the portal blood flow. The platelet count in the peripheral blood and the RTI increased significantly. These results suggest the possibility that PSE may reduce the potential perioperative risk in hepatocellular carcinoma complicated with liver cirrhosis.
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PMID:Changes in portal hemodynamics and hepatic function after partial splenic embolization (PSE) and percutaneous transhepatic obliteration (PTO). 813 83

Portal hypertension in the presence of chronic hepatitis is generally thought to develop during the progression of the chronic hepatitis to cirrhosis. Before the establishment of assays for diagnosing hepatitis C virus infection, such a case of portal hypertension without liver cirrhosis could be misdiagnosed as idiopathic portal hypertension. It had not fully determined whether portal hypertension might precede the onset of cirrhosis in type C chronic hepatitis. This report presents two cases of women with chronic hepatitis C who developed severe thrombocytopenia; each showed splenomegaly and hypersplenism due to portal hypertension. Angiographic study and histological analysis were conducted to determine the cause of the portal hypertension. Histological evaluation showed an intrahepatic presinusoidal block pattern and fibrotic changes in the periportal area, but no evidence of liver cirrhosis or of other incidental complications such as idiopathic portal hypertension. Both of these patients exhibited normal platelet counts after splenectomy. Thus, type C chronic hepatitis can lead to portal hypertension, as demonstrated in these two patients.
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PMID:Type C chronic hepatitis associated with thrombocytopenia in two patients. 815 75

In patients with bleeding gastric varices from causes other than splenic vein thrombosis, endoscopic sclerotherapy and ablative surgery have yielded poor results. Over a 3-year period starting in June 1989, a total of 30 distal splenorenal shunts were performed prospectively on 19 paediatric and 11 adult patients with bleeding gastric varices and good liver function. The mean (s.d.) age was 17(12) (range 6-50) years; there were 20 male and ten female patients of whom six had cirrhosis, four non-cirrhotic portal fibrosis and 20 portal vein thrombosis. Two patients died and two more had shunt thrombosis; all four were considered failures of treatment. Hypersplenism was present in 15 patients but reverted to normal in 13. In 26 patients the gastric varices disappeared. Concomitant oesophageal varices were present in 22 patients and showed marked regression, with no rebleeding over a mean (s.d.) follow-up of 21(10) (range 7-39) months. A distal splenorenal shunt was effective in controlling gastric variceal haemorrhage in 26 of 30 patients in whom liver function was well preserved.
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PMID:Distal splenorenal shunting for bleeding gastric varices. 815 47

Bacterial peritonitis presents with classic symptoms of fever and abdominal pain. Some patients, however, are completely asymptomatic. Death in the short term is considerable, especially in patients with alcoholic cirrhosis. Cystic fibrosis patients occasionally develop biliary cirrhosis and may have secondary hypersplenism, varices, and ascites. These patients should be at risk for spontaneous bacterial peritonitis. Spontaneous bacterial peritonitis is described in two patients with longstanding hepatic cirrhosis secondary to cystic fibrosis. Both had required splenectomy for complications of portal hypertension. This is a previously unreported, but potentially fatal, complication of cystic fibrosis liver disease. Early diagnostic paracentesis is essential so that appropriate acute management, including antimicrobial treatment can be started. In the long term, these patients deserve immediate paracentesis for any evidence of recurrence. Whether the patient is treated with chronic (continuous) antimicrobial prophylaxis or only receives antimicrobial treatment during periods when bacteraemia is possible (for example, dental work, bronchoscopy), it would seem reasonable in patients with cystic fibrosis to use a wide spectrum antimicrobial agent with activity against Pseudomonas aeruginosa, other common Gram negative organisms, and Staphylococcus aureus.
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PMID:Spontaneous bacterial peritonitis in cystic fibrosis. 820 May 73

We describe a case of spontaneous bacterial peritonitis in a 53 year old man affected by cryptogenic micro-macronodular cirrhosis, portal hypertention, splenomegaly and hypersplenism, who was admitted with hepatic failure and septic shock and successfully treated with antibiotics (combination of clindamycin and netilmycin), surgical abdominal drainage and splenectomy. This case gave reason for a literature review and an update on the therapeutic options in these high risk patients, especially concerning the role of surgery. Spontaneous Bacterial Peritonitis (SBP) is defined as a bacterial infection of ascitic fluid in the absence of any septic focus. It is a typical life-threatening complication of hepatic cirrhosis with ascites. Mortality is very high and ranges from 75% to 97% of patients, due to septic shock and hepatic failure (hepatorenal syndrome, hepatic encephalopathy, gastrointestinal bleeding). Infection with a single organism is found in most cases. Gram negative bacilli are present in about 70% of cases and E. coli (less frequently Klebsiella, Serratia, Pseudomonas) is principally found. Gram positive cocchi comprise an additional 30% of cases. Anaerobic and microaerophilic organisms seem to be rare causes of SBP (2.7-6%); this finding is probably due to the intrinsic bacteriostatic activity of ascites, which contains high oxygen tension (70 mmHg) and is an inhospitable environment for bacteroides and Clostridia. The prevalent isolation of enteric organism suggest that the gut is the most frequent source of infection, even if the pathogenetic mechanism is not yet well known. The right treatment depends on differentiating primary (SBP) from secondary peritonitis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Is the surgical treatment of spontaneous bacterial peritonitis still up-to-date?]. 824 98

Portal vein thrombosis (PVT) is usually a complication of pre-existing cirrhosis, abdominal malignancy (e.g., pancreatic or hepatocellular carcinoma), or abdominal inflammation (e.g., appendicitis, diverticulitis, pancreatitis). Less frequently, PVT can be associated with myeloproliferative or connective tissue disorders or inflammatory bowel disease [1]. PVT can cause or exacerbate portal hypertension; variceal bleeding or hypersplenism may then develop acutely or several years later. PVT also complicates portosystemic shunt surgery or hepatic transplantation. Unfortunately, the signs and symptoms of PVT can be subtle or nonspecific and can be overshadowed by the underlying illness. The radiologist may be the only physician to suggest the preoperative or premortem diagnosis of PVT. Familiarity with the imaging findings of PVT, therefore, is imperative.
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PMID:Portal vein thrombosis: imaging findings. 827 95

Hypersplenism is of great relevance in the management of cirrhosis because of the widespread use of myelodepressant drugs such as interferon or antineoplastic agents. Because no standard therapy exists for this complication, we have evaluated the efficacy and risks of splenic embolization in the treatment of hypersplenism in cirrhosis. Partial splenic embolization was performed in 40 consecutive patients with the following indications: 25 patients with active viral cirrhosis before interferon therapy, 8 patients with unresectable hepatocellular carcinoma before anti-neoplastic chemotherapy and 7 patients with thrombocytopenia associated with spontaneous bleeding events, with high risk of central nervous system hemorrhage or facing major surgery. After selective catheterization of the splenic artery, partial splenic embolization was performed by means of repeated injections of gelatin sponge until a 40% to 60% reduction in the splenic blood flow was achieved. After partial splenic embolization a significant and sustained increase in platelet and white blood cell count was observed during the follow-up period (mean = 13.9 +/- 2.2 mo; range = 1 to 36 mo). The goal of partial splenic embolization was achieved in all but two patients in whom a dose reduction of interferon was needed. Hypersplenism relapsed in only seven patients, and all of them exhibited an embolization of less than 50% of the splenic mass. Postembolization syndrome was the main side effect, but no life-threatening complications were detected. In conclusion, partial splenic embolization is a safe and effective therapy of hypersplenism in cirrhosis.
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PMID:Partial splenic embolization for the treatment of hypersplenism in cirrhosis. 777 40


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