Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The mortality and morbidity of hepatic resection for hepatocellular carcinoma (HCC) have decreased in recent years because of the various advances in hepatic resection. Various improvements are evident in dissecting apparatus, liver hepatic inflow clamp, cold hepatic perfusion technique, intraoperative ultrasonography, accurate assessment of hepatic function, autologous blood transfusion, and so on. Five-year survival after hepatic resection for HCC was reported at 26-59% in Eastern as well as Western series. The prognostic factors were portal invasion, multiplicity, serum alpha-fetoprotein level, tumor size, associated cirrhosis, age, alcohol abuse, histologic classification, DNA ploidy, and surgical margin. Segmental or lobar hepatic resection brought about better survival, especially in stage I and II patients. Effective adjuvant therapy should improve the diagnosis.
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PMID:Advances in hepatic resection and results for hepatocellular carcinoma. 872 8

We investigated the viability of rat cirrhotic livers preserved cold using an isolated rat liver perfusion model. Cirrhosis was induced by intravenous thioacetamide injection. Normal and cirrhotic livers were reperfused immediately or following 6 h of preservation through the portal vein with Krebs-Henseleit buffer and hyaluronic acid added. Cirrhotic livers with short cold ischemia showed higher portal venous resistance than their normal counterparts (p < 0.05), while cirrhotic livers preserved for 6 h exhibited marked elevation of the portal venous resistance as compared with their fresh counterparts or normal liver preserved cold for 6 h (p < 0.05). Similarly, the oxygen consumption of cirrhotic livers with short cold preservation was lower than that of normal livers (p < 0.05), which was further reduced by 6 h of cold preservation (p < 0.05). The bile output was not different between normal and cirrhotic livers. The sinusoidal endothelial cell function of cirrhotic livers as assessed by the clearance of hyaluronic acid was impaired even after a short period of cold ischemia. Histologically, cirrhotic livers showed severe sinusoidal endothelial cell damage, hepatocellular swelling, and marked septal edema which became more prominent by cold preservation. We conclude that the viability of the cirrhotic liver is impaired even by a short cold exposure, and that the prolongation of cold ischemia of the cirrhotic liver leads to further deterioration of the viability.
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PMID:Tolerance of the cirrhotic liver to cold ischemia: ex vivo analysis in rats. 883 68

We analyzed the long-term clinical course of 71 patients with RNA-positive hepatitis C virus (HCV) infection after liver transplantation. Patients with reinfection after transplantation for HCV-related liver disease, or de novo infection at transplantation were followed for up to 12 years. Cumulative survival for patients with HCV infection at 2, 5, and 10 years after transplantation was 67%, 62%, and 62%, respectively. It was not significantly different from that in patients transplanted for other nonmalignant diseases without HCV infection. The main factor determining long-term survival was the presence or absence of hepatocellular carcinoma (HCC) at transplantation. The 5-year survival rate for HCV patients with or without HCC was 35% versus 73%, respectively (P < .05). No deaths because of viral hepatitis of the graft were observed. Deaths in the first year after transplantation were caused by infectious complications, cardiovascular problems, or rejection; deaths after more than 12 months were exclusively because of recurrence of HCC. Biochemical and histological evidence of hepatitis was found in the majority of the patients, only 16% had normal alanine aminotransferase (ALT) values throughout. Twenty-two percent of patients complained of symptoms, with hepatitis C being the cause in 82% of these. Two patients lost their HCV-RNA for prolonged, ongoing periods of time. The severity of the posttransplantation hepatitis was unrelated to age, sex, severity of liver disease before transplantation, cold ischemic time of the graft, duration of the operation, transfusions, the number of rejection episodes, or the long-term immunosuppressive regime. Only initial short-term therapy with interleukin 2 (IL2) receptor antibodies adversely influenced inflammatory activity. Viral genotype did not influence the course of the graft hepatitis in our series. Histology showed inflammation in 88% of the biopsies and signs of fibrosis in 24%. Mean ALT values correlated with inflammation but not with fibrosis in the biopsies. Porto-portal bridging was observed in six patients, one patient developed cirrhosis within 2 years after orthotopic liver transplantation (OLT). We conclude that chronic hepatitis develops in the majority of patients with HCV infection after liver transplantation. Carrier states without significant laboratory abnormalities are observed in approximately 16%, biochemical abnormalities without symptoms are seen in 60%, and symptomatic disease develops in a quarter of the patients. The disease course closely resembles that seen in nontransplanted hepatitis C patients. It is generally mild but little over 10% of patients develop signs of fibrosis of the graft during the first decade.
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PMID:Long-term outcome of hepatitis C virus infection after liver transplantation. 898 91

We report on the successful regrafting of a transplanted liver. The donor liver was first grafted into a patient suffering from cryptogenic cirrhosis; the patient died 1 day after the elective transplantation of cerebral bleeding. The well-functioning graft was harvested again and transferred to our institution. After another 12 h of cold ischemia, the liver was reperfused in an urgently registered patient with recurrence of hepatitis B in his first graft. The transplantation was successfully performed and the patient is now doing well, more than 5 months after regrafting with the reused liver.
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PMID:Successful regrafting of a transplanted liver. 916 69

The strong association of HCV infection with MC-II and the selective concentration of the virus with the WA mRF in the cryoglobulins are compelling suggestions that the virus is directly involved in production of the mRF and the pathophysiology of MC-II. There is, however, only limited data on HCV involvement in both processes. In cutaneous vasculitis, which is the most prevalent clinical feature of the disease, there is evidence that complexes of HCV, mRF and IgG are formed in situ from components of the cryoglobulins that are present in the blood in a dissociated state. It is postulated that local factors, cooling and stasis predispose to formation of these lesions in the lower limbs. However, since cutaneous vasculitis does not correlate with cryoglobulin levels and may not be induced by cold challenge, other factors may be involved. In particular, the conditions which activate the vascular endothelial cells, leading to the leukocytoclastic vasculitis, require delineation. In contrast to cutaneous vasculitis, HCV RNA has not been prominently detected in immune complexes in MPGN lesions and has not been detected at all in the peripheral neuropathy lesions. These preliminary observations suggest that different pathophysiological processes are involved in for these lesions than in cutaneous vasculitis. From the correlation of remission of disease with decreased cryoglobulinemia and viremia in treated patients with MC-II, and from immunohistological data on the hepatitic lymphoid follicles in MC-II (see chapter 7), it appears that an antigen-driven benign proliferation of B cells is responsible for production off mRF and cryoglobulinemia. New findings have suggested that one mechanism for developing mixed cryoglobulinemia may be that HCV-VLDL complexes that contain apo E2 are poorly endocytosed by the LDLR, which may be a major route of entry of the virus to the cell; persistence of the complexes in the circulation may then stimulate mRF production. This new hypothesis is based only on initial in vitro observations and require independent confirmation and validation in vivo. From indirect clinical evidence it has also been postulated that mRF in some patients may limit the cytopathology in MC-II, resulting in a lower prevalence of cirrhosis in these patients. These findings suggested another hypothesis, which is that the mRF prevents spread of infection to hepatocytes and other permissive and nonpermissive cells by blocking endocytosis of HCV-VLDL complexes by the LDLR. Furthermore, data on the composition of cryoglobulins, the molecular composition of WA mRF and the characterization of monoclonal B cells in the liver of patients with MC-II (see chapter 7) suggest that a specific population of B cells may be involved in the host response to HCV infection. These are B cells that proliferate with little or no somatic mutations of the immunoglobulin genes, are self-replicating, are stimulated by self antigens in a T cell-independent manner and bear the CD5 marker. The proliferation of this B cell population may be the host's response to the attempt by the virus to circumvent the immune response by complexing with host lipoproteins. It is proposed that HCV complexed to VLDL is the antigen that directly stimulates the proliferation of these primordial type B cells. Testing of these hypotheses may produce insights not only into the etiology of mixed cryoglobulinemia but possibly into the mechanisms by which HCV circumvents the immune response and established chronic infection.
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PMID:The etiology and pathophysiology of mixed cryoglobulinemia secondary to hepatitis C virus infection. 926 35

A high positivity of cold activation of complement has been reported in Japanese patients having hepatitis B virus-negative chronic hepatitis. Although the cause of cold activation of complement is unknown, the involvement of hepatitis C virus (HCV) has been suspected. We studied the positivity of cold activation of complement in 253 patients, including 93 patients with chronic hepatitis C infection who received 6MU natural interferon-alpha per day for 24 continuous weeks. Cold activation was positive in 38% of patients with chronic hepatitis C and in 46% of patients with liver cirrhosis C. We did not detect cold activation in asymptomatic HCV carriers; patients with chronic hepatitis B, liver cirrhosis B, or alcohol-related liver damage; or in the controls. Cold activation was also negative in HCV-RNA-negative patients who responded completely to interferon-alpha, and in HCV-RNA-positive patients who responded partially whose serum alanine transaminase levels were normalized after interferon treatment. In the patients who had a relapse of hepatitis C after interferon treatment, positivity of cold activation increased sharply. We conclude that HCV-associated liver damage is related to the development of cold activation of complement. Cold activation is useful for monitoring the response to interferon in patients with chronic hepatitis C infection.
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PMID:Hepatitis C virus-related liver damage is related to cold activation of complement. 941 71

Ex situ partial liver resection was performed in 2 patients with hepatocellular carcinoma (HCC) with Child A-liver cirrhosis that was untreatable by conventional liver resection techniques. In both cases, an extended left lobectomy was first performed, and then the autologous lateral segment was transplanted after removing segment 4 (or + a part of segment 5, 8) together with the tumor by the bench procedure. Although there might have been no difference in preoperative liver function in these cases, the postoperative course was quite different. The first case was successful with an uneventful postoperative course, but, the second case went into postoperative liver failure and the patient died of multiple organ failure on the 20th postoperative day. The cause of liver failure in the second case might be attributable to: 1) prolongation of cold preservation time for the bench procedure (196 min); or 2) over reduction of the native remnant liver (right lobe) due to resection of the huge tumor. In conclusion, the technique using ex situ partial liver resection and transplantation of the remnant section of the liver might be a useful method to extend surgical treatment for some cases of HCC untreatable by conventional liver resection. However, the indications should be carefully considered in each case, since graft damage can occur rapidly during the bench procedure due to combined liver cirrhosis.
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PMID:[Surgical treatment for hepatocellular carcinoma: liver resection using transplantation techniques]. 964 87

We have investigated the clinical characteristics of renal damage and associated complications of 79 patients with accidental hypothermia whom we encountered over the last 5 years. All patients were male, with an average age of 58.9 +/- 9.2 years. Most of these patients were homeless. Body temperature on admission was 29.3 +/- 3.0 degrees C. The most common clinical manifestations on admission were consciousness disturbance and severe hypotension. Complications, including increase in serum transaminase, alcoholism, pneumonia, liver cirrhosis, sepsis, diabetes mellitus, hypoglycemia, acidosis, and an increased level of serum CPK and amylase were found frequently on admission. Death within 48 hours after admission occurred in 23 cases (the death rate; 23/79 = 29%). Renal damage was found in 36 cases (36/79 = 46%), consisting of acute renal failure (ARF) in 27, and acute on chronic in 6. Urinary diagnostic indices suggested that the etiological factor for ARF was pre-renal, which responded well to passive rewarming and an appropriate fluid replacement therapy, resulting in full recovery in most of the cases (the recovery rate; 25/27 = 93%). Among patients with renal damage, there were no cases requiring dialysis. The present data suggest that accidental hypothermia is a fatal condition with an extremely high death rate. It also is associated with multiple complications including ARF. The main cause for ARF is pre-renal, possibly caused by cold diuresis or dehydration superimposed on the underlying diseases such as alcoholism, diabetes mellitus, liver cirrhosis. Such complications, independent of renal damage, determine the patient's prognosis.
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PMID:[Clinical characteristics of renal damage in patients with accidental hypothermia]. 1050 43

The majority of patients undergoing orthotopic liver transplantation (OLT) have end-stage liver disease secondary to hepatitis C virus (HCV) infection. Although OLT does not cure the disease and recurrent virus is present in all patients, relatively few patients with recurrent viremia develop clinical disease. When the disease recurs, however, the results can be devastating. Factors associated with increased risk for recurrent HCV disease remain controversial. We hypothesized that preservation injury may predispose to the severity of HCV disease after OLT. We reviewed our series of OLTs performed for HCV cirrhosis between January 1994 and December 1998 (n = 56; 62 transplants). Patients were grouped according to the severity of recurrent hepatitis C. Group 1 had no or mild HCV disease (n = 36), and group 2 had moderate to severe HCV disease (n = 20). The duration of ischemic rewarming during graft implantation was significantly associated with the severity of recurrent hepatitis C (P <.04). The estimated chances of severe disease within the first year post-OLT after 30, 60, or 90 minutes of ischemic rewarming time were 19%, 40%, and 65%, respectively. Cold ischemia time, transaminase levels, and prothrombin time did not correlate with the severity of hepatitis C. In conclusion, our data suggest that the duration of ischemic rewarming predisposes to severe recurrent hepatitis C. This finding warrants the investigation of the pathogenesis of recurrent HCV disease after ischemic injury. Reduction of rewarming time should be stressed in OLT, particularly in patients with HCV cirrhosis.
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PMID:Prolonged rewarming time during allograft implantation predisposes to recurrent hepatitis C infection after liver transplantation. 1091 61

Transplants and centers Between 1988 and 1998 the number of liver transplants performed in the US more than doubled from 1,713 to 4,487; the number of centers increased from 59 to 116. The number of living donor, segmental, and multiple organ transplants also increased over time. The rate of increase in the number of centers has slowed over the last few years. Outcomes. Survival among pediatric recipients. The one- and 7-year graft survival rates for pediatric recipients were 72% and 62%, respectively. The one- and 7-year patient survival rates were 85% and 79%. Patient survival did not decrease much after the first 2 years and graft survival stabilized after 4 years posttransplant. Some of the factors associated with increased odds of graft failure and patient death at 6 months posttransplant included having a previous transplant; being hospitalized, in the ICU, or on life support at the time of transplant; creatinine > 2 mg/dl; donor age and race/ethnicity; and transplant type. Factors associated with decreased odds of graft failure or patient death were recipient gender, recipient race/ethnicity, having a metabolic disease and receiving a living donor liver. Among grafts/recipients surviving the first 6 months after transplantation, recipient race/ethnicity, primary liver disease, having a previous transplant, donor age and race/ethnicity, and transplant type were associated with a greater relative risk of graft failure and mortality. Survival among adult recipients. The one- and 7-year graft survival rates among adult recipients were 77% and 57%, respectively. The one- and 7-year patient survival rates were 85% and 67%. Survival rates decreased steadily at all time points following transplantation. Some of the factors associated with increased odds of graft failure and mortality at 6 months after transplantation were recipient age and race/ethnicity; primary liver disease; having a previous transplant; being hospitalized, in the ICU, or on life support at the time of transplant; longer cold ischemia time; older donor age, race/ethnicity, or gender; and having a non-identical recipient/donor blood type match. Having cholestatic liver disease/cirrhosis and shorter cold ischemia times were associated with decreased odds of graft failure and mortality. Many of these characteristics also affected grafts and patients surviving the first 6 months, including recipient race/ethnicity, primary liver disease, previous transplant, and donor age.
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PMID:Liver transplantation in the United States: a report from the UNOS Liver Transplant Registry. 1103 23


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