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

We report on an autopsy case of a 44-year-old woman who died of combined hepatic and renal failure and bacterial infection. Postmortem examination revealed advanced liver cirrhosis and membranoproliferative glomerulonephritis (MPGN), caused by clinically inapparent hepatitis C virus (HCV) infection. The diagnosis was confirmed by reverse transcription polymerase chain reaction (RT-PCR) of HCV RNA in formalin-fixed, paraffin-embedded (FFPE) liver tissue. We conclude that liver cirrhosis and concomitant MPGN should arouse suspicion of HCV infection despite ambiguous or negative results from serological analyses. Specimens of FFPE liver tissue may be used for the diagnosis of HCV infection, even if the tissue was obtained in a postmortem examination.
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PMID:Liver cirrhosis and membranoproliferative glomerulonephritis caused by inapparent hepatitis C virus infection. 1709 58

Endotoxemia and bacterial infection are frequent in patients with cirrhosis. They alter systemic and splanchnic hemodynamics, worsen coagulation disorders, impair liver function and thus may induce variceal bleeding. In variceal bleeding, bacterial infection favours failure to control bleeding, early rebleeding, and death. In patients with cirrhosis and variceal bleeding, antibiotic-prophylaxis decreases bacterial infection and the incidence of early rebleeding, and, more important, significantly decreases the death rate in these patients.
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PMID:[Infection and variceal bleeding in cirrhosis]. 1727 29

Endogenous heparinoids impair coagulation, evidenced by thrombelastography in cirrhotic patients with bacterial infection, but it is not clear which glycosaminoglycans can be detected by native and heparinase-modified thrombelastography. To assess the effects of different glycosaminoglycans on thrombelastography parameters and the reversibility of these effects by heparinase-I-modified thrombelastography. Twenty volunteers were enrolled. Solutions of heparan sulphate, dermatan sulphate, and chondroitin-4-sulphate were prepared at 'equivalent' concentrations, based on the composition and anticoagulant activity of danaparoid. Serial dilutions of each glycosaminoglycan were prepared to achieve 1.0, 0.5, 0.1, and 0.05 U/ml. Native and heparinase-modified thrombelastography, anti-activated factor X activity and heparin cofactor II activity were evaluated at each concentration. A statistically significant heparin-like effect was seen with 1 and 0.5 U/ml heparan sulphate, and 1 and 0.5 U/ml dermatan sulphate, which was completely reversed by heparinase-modified thrombelastography. Anti-activated factor X activity was significantly increased in samples containing heparan and dermatan sulphates. The heparin cofactor II activity decreased with 1.0 and 0.5 U/ml dermatan sulphate and chondroitin-4-sulphate, but not with heparan sulphate. Heparan and dermatan sulphates affect haemostasis when added to whole blood in vitro, detectable by native thrombelastography and completely reversed by heparinase-I-modified thrombelastography. They may therefore be responsible for the heparin-like effect seen by thrombelastography in patients with cirrhosis and bacterial infection.
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PMID:The effects of glycosaminoglycans on coagulation: a thromboelastographic study. 1741 58

Ruptured gastroesophageal varices are the most severe and frequent causes of upper gastrointestinal bleeding in patients suffering from liver cirrhosis, accounting for 80% of all bleeding episodes. Despite recent progress in treatment strategies, variceal bleeding is still considered the most severe type of gastrointestinal bleeding associated with a mortality of 20% at 6 weeks. The most widely accepted explanation for the rupture is the "explosion hypothesis": bleeding is a result of the elevated intravariceal pressure and increased wall-straining due to a rapid increase in the portal pressure gradient. The rupture of the varices and the early rebleeding cannot be attributed solely to mechanical changes. Furthermore, the factors involved in the sudden increase of portal pressure gradient are yet to be discovered. Recently it was postulated that various humoral factors may also play an important role in the pathomechanism of the rupture. The pivotal role of bacterial infection and consequent endotoxaemia must be emphasized. Passage of both viable microbes and microbial products, such as endotoxins from the intestinal lumen to peripheral and portal circulation in cirrhotic patients can be explained by the intestinal bacterial overgrowth, the intestinal dysmotility and the increased intestinal permeability. Endotoxaemia can be a critical factor that triggers a cascade of humoral events, resulting in a further increase of portal pressure, impairment of liver function and worsening of haemostasis, and eventually leads to variceal bleeding. Early administration of prophylactic antibiotics to variceal bleeders recently became an integral and important part of therapeutic strategy. Antibiotics are not only useful in the prevention of early rebleeding but also they are proven to significantly decrease the rate of mortality. The improvement in mortality is equivalent to that seen with terlipressine.
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PMID:[Gastroesophageal variceal haemorrhage--new advances in pathophysiology]. 1748 58

The occurrence of complications marks a turn in the natural history of cirrhosis. The early management, the etiologic treatment of the subjacent disease, the methodological detection of hepatocarcinoma, the prophylaxis of digestive bleeding linked to portal hypertension, the control of ascite and prevention of hepato-renal syndrome allow to improve the prognosis of these patients. Moreover, bacterial infection represents one of the principal factor facilitating the occurrence of another complication. This is why any complication should be considered as secondary to bacterial infection until the refutation.
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PMID:[How to detect the complications of the cirrhosis?]. 1795 21

Acute hemorrhage from esophageal varices due to portal hypertension is a frequent and serious complication of liver cirrhosis. Bacterial infection may be one of the factors influencing such hemorrhage. Endotoxins may increase portal tension and at the same time result in primary hemostasis disorder, thus becoming one of the causes of hemorrhage. The authors of the paper compared the incidence of bacterial infection in 53 patients with varicose hemorrhage due to portal hypertension with 62 patients with liver cirrhosis and portal hypertension without varicose hemorrhage. At least one pathogen was found in considerable 61.1% of the total of patients in the liver cirrhosis group, while the difference between the two groups was but insignificant. No statistically significant difference was found between the group of patients with hemorrhage and those without hemorrhage in terms of presence of bacterial infection in hemoculture, urine, throat, faeces and ascites, nor was there a difference in the etiology of the G+ bacteria, G- bacteria or fungi and yeast infectious agents in the hemoculture, urine, throat, faeces and ascites in either of the groups. No statistically significant difference was found in comparing the patients with a recurrence of hemorrhage (or with mortality) and with infection with those without recurrence of hemorrhage. Bacterial infection was more often found in patients with a recurrence of hemorrhage (75%) as compared with those without any recurrence (52%), and also in patients who died bacterial infection was proven more often than in those who survived (61.9% vs. 58.1%, respectively). There was no difference in morbidity or recurrence of hemorrhage between the patients treated with norfloxacin and ampicilin/sulbactam. No statistically significant difference was recorded between the 1st and 5th day in terms of decrease in bacterial infection. A significant difference was found in the urine etiological agent, where a significant increase in the share of fungal and yeast urine infection (p = 0.011) was recorded after the application of the therapy, as well as a drop in urine infection caused by the G- bacterial agent (p = 0.057).
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PMID:[Bacterial infection and its relation to the genesis and course of varicose hemorrhage]. 1835 59

Liver transplantation with a part of the liver from a healthy living donor can be life saving for selected patients with end-stage liver failure. The experiences with the first 3 adult patients in the Netherlands were as follows. The first patient was a 56-year-old man with primary sclerosing cholangitis, who received half of the liver from his 53-year-old sister. Postoperatively, the donor developed a urinary tract infection, which was treated with antibiotics. The recipient developed fever and paralytic ileus 6 days after transplantation. Relaparotomy revealed minimal bile leakage from the cut surface of the liver, which was corrected with a suture. Three years after donation, both donor and recipient were doing well. The second patient was a 63-year-old man with hepatic cirrhosis due to hepatitis B, recurrent bleeding from varices, and hepatocellular carcinoma. The carcinoma was treated percutaneously with radiofrequency ablation. He was given a liver transplant from his 28-year-old son. The donor later developed transient ileus and mild liver function disorders. The recipient developed a bacterial infection of the ascites, which was treated with antibiotics, and later Candida-oesophagitis and a herpes simplex infection, which were also treated successfully. More than 2 years after donation and transplantation, both donor and recipient were in good condition. The third patient was a 42-year-old man with a chronic hepatitis B virus infection and 2 hepatocellular carcinomas. The donor was his 34-year-old sister-in-law. The recipient developed prolonged jaundice due to stenosis at the site of the bile duct anastomosis, for which a stent was placed. He was discharged in good condition but died 11 months later of cerebral metastases. One year after the procedure, the donor was doing well. The Rotterdam liver transplantation programme with living donors demonstrates that excellent results can be accomplished with minimal risk for the donor.
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PMID:[Liver transplantation with a living donor: the first 3 cases in Rotterdam]. 1849 25

Fever is one of the more common chief complaints of patients who visit emergency departments (ED). Many febrile patients have markedly elevated C-reactive protein (CRP) levels and normal white blood cell (WBC) counts. Most of these patients have bacterial infection and no previous underlying disease of impaired WBC functioning. We reviewed patients who visited our ED between November 2003 and July 2004. The WBC count and CRP level of patients over 18 years of age who visited the ED because of or with fever were recorded. Patients who had normal WBC count (4,000-10,000/L) and high CRP level (> 100 mg/L) were included. The data, including gender, age and length of hospital stay, were reviewed. Underlying diseases, diagnosis of the febrile disease and final condition were recorded according to the chart. Within the study period, 54,078 patients visited our ED. Of 5,628 febrile adults, 214 (3.8%) had elevated CRP level and normal WBC count. The major cause of febrility was infection (82.24%). Most of these patients were admitted (92.99%). There were 32 patients with malignant neoplasm, nine with liver cirrhosis, 66 with diabetes mellitus and 11 with uremia. There were no significant differences in age and gender between patients with and those without neoplasm. However, a higher inhospital mortality rate and other causes of febrility were noted in patients with neoplasm. It was not rare in febrile patients who visited the ED to have a high CRP level but normal WBC count. These patients did not necessarily have an underlying malignant neoplasm or hematologic illness. Factors other than malignant neoplasm or hematologic illness may be associated with the WBC response, and CRP may be a better indicator of infection under such conditions.
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PMID:Characteristics of febrile patients with normal white blood cell counts and high C-reactive protein levels in an emergency department. 1850 22

Pyomyositis is an acute bacterial infection manifesting as pyemic abscess formation in the skeletal muscles. We examined 8 autopsy cases (seven males, one female; age range 21-75 years) of fatal nontropical pyomyositis to better describe individual case characteristics and pathologic features of this rare disease. The pathogen most frequently involved was Staphylococcus aureus. In most cases, there were several abscesses and multiple sites involved. The trunk, shoulder girdle, and thigh muscles were most frequently affected and involvement of multiple sites was a common finding. In 6 cases, a recent trauma had occurred to the anatomic location where the pyemic abscesses were found. Three deceased were known as intravenous drug abusers. Except for the presence of pyomyositis, liver diseases such as cirrhosis in 3 cases, and a fatty liver in 2 cases were the most frequent autopsy findings. Death was due to sepsis in all cases. Because pyomyositis may develop in association with intravenous catheterization in the clinical setting, the question whether pyomyositis was caused by an infected or improperly placed indwelling intravenous catheter may be of forensic importance in the light of alleged medical malpractice. According to our observations, severe underlying illnesses seem not always necessary for fatal outcome of pyomyositis. Because a detailed dissection of superficial as well as deep skeletal muscles during autopsy is a prerequisite for the diagnosis, the disease may be overlooked when this essential step is not performed.
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PMID:Fatal pyomyositis: a report of 8 autopsy cases. 1852 Apr 79

Thrombotic microangiopathy (TMA) has rarely been reported in the setting of liver transplantation. Herein we have reported a successful case of TMA after ABO-incompatible living donor liver transplantation (LDLT) treated with plasma exchange and high-dose intravenous gamma-globulin infusion. A 50-year-old woman was diagnosed with hepatitis C virus-related cirrhosis. We performed an ABO-incompatible LDLT (group B to O) with preoperative plasma exchange to reduce the anti-B hemagglutinin titers to 1:8. The immunosuppressants consisted of tacrolimus, mycophenolate mofetil, and steroid. On postoperative day (POD) 8, her anti-B hemagglutinin titer suddenly increased to 1:64. The serum lactate dehydrogenase (LDH) level was grossly elevated (1518 IU/L). On POD 13, we suspected infection of an intra-abdominal hematoma (Serratia marcescens) which was drained surgically. On day 5 after the reoperation, thrombocytopenia developed with a platelet count of 3 x 10(4)/mm3. A peripheral blood film showed severe red blood cell (RBC) fragmentation. Thus, we made a clinical diagnosis of TMA and reduced the tacrolimus dose. We started intensive daily plasma exchange (4 L/d) with fresh frozen plasma and high-dose intravenous gamma-globulin infusions. One week thereafter, thrombocytopenia improved with reduced transfusion requirements. The peripheral blood film showed normal RBC morphology. The serum LDH returned to baseline levels. Four factors were considered to have caused TMA in this case: the prescription of tacrolimus, ABO-incompatible liver transplantation, bacterial infection, and surgical stress. These factors may have all contributed by causing significant endothelial injury and TMA.
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PMID:Thrombotic microangiopathy after ABO-incompatible living donor liver transplantation: a case report. 1892 97


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