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PubMed2005

Influence of cumulative number of marginal donor criteria on primary organ dysfunction in liver recipients.

BACKGROUND: The aim of this cohort study was to assess the cumulative effect of marginal donor criteria on initial graft function and patient survival after liver transplantation. METHODS: We included 734 consecutive patients who underwent orthotopic liver transplantation at the Vienna General Hospital between January 1993 and December 2003. We employed the local registry of the Department of Transplant Surgery, where variables of all patients are routinely and prospectively recorded. Primary outcome was initial graft function, secondary outcome was patient survival. RESULTS: Cumulative number of marginal donor criteria was significantly and linearly associated with an increased rate of primary dysfunction (PDF; p = 0.005). In patients with more than three cumulative marginal donor criteria the rate of PDF was 36%. Patient survival was not influenced by the cumulative number of donor criteria (log-rank test, p = 0.81). Independent marginal donor criteria to predict PDF were cold ischemia time >10 h [odds ratio (OR) 0.56; 95% CI 0.32-0.98] and donor peak serum sodium >155 mEq/L (OR 0.44; 95% CI 0.26-0.77), as assessed in a multivariate regression model. CONCLUSIONS: The use of marginal liver donors with more than three marginal donor criteria shows deleterious effects on initial graft function. Noteworthy, patient survival was not associated with marginal donor criteria, which may be explained by early and successful retransplantation of liver recipients with primary non-function.

Cohort Studies↗
PubMed1990

A new method of total parenteral nutrition for surgical neonates: it is possible that cyclic TPN prevents intrahepatic cholestasis.

Cholestasis associated with total parenteral nutrition (TPN) has been reported to be an incidence of 15% to 50% in surgical neonates. This study was designed to prevent the liver dysfunction, especially intrahepatic cholestasis, caused by TPN for surgical neonates. In the last three years, 10 surgical neonates ranged from 1868g to 3500g of birth weight have been treated by cyclic TPN that infuses solutions of TPN and Non-TPN alternately every four hours, because cyclic TPN may reduce an overloading for the liver by the compulsive and continuous TPN. Consequently, no hyperbilirubinemia and abnormal values of the serum transaminases were revealed in these neonates, and good results of nutritional supports were obtained by cyclic TPN. These results suggest that cyclic TPN is useful and safe in nutritional support for neonates, and cyclic TPN is much better than continuous TPN in order to prevent the liver dysfunction.

Alanine Transaminase↗
PubMed2006

Antiviral treatment of chronic hepatitis B with lamivudine in pediatric renal transplantation.

Renal transplantation in patients with chronic hepatitis B virus (HBV) infection is known to be associated with an increased risk for exacerbation of liver dysfunction. Lamivudine has been proven to be a potent inhibitor of hepatitis B virus replication in adults after kidney transplantation. Little is known about its efficacy and safety in pediatric renal transplant recipients. Three cases serve for the discussion to demonstrate the complexity of the clinical course and effective treatment of chronic hepatitis B in pediatric patients awaiting renal transplantation. Two patients on dialysis with a high HBV replication rate were treated with lamivudine before transplantation. After the viral load had decreased below the detection limit, they underwent transplantation successfully. Despite intensified immunosuppression to treat a rejection episode in one and a relapse of the nephrotic syndrome in the other patient, the viral load remained <2.5 pg/mL. Both patients developed a mutation in the YMDD motif of the HBV genome associated with an increase in the HBV replication rate >10,000 pg/mL without deterioration of the liver function. In a third patient with a chronic HBV infection with a low replication rate, lamivudine was started about nine months after kidney transplantation due to an increasing viral load after treatment of an acute rejection episode. Six months later, the HBV DNA was no longer detectable. The patient had no signs of liver dysfunction. Lamivudine in the treatment of chronic HBV infection in pediatric renal recipients seems to be safe and effective in preventing acute liver deterioration. Three clinical cases are discussed with regard to current options in monitoring and antiviral treatment of chronic HBV in pediatric renal transplant recipients.

Adolescent↗
PubMed1998

Population screening for neonatal liver disease: a feasibility study.

BACKGROUND: Extra-hepatic biliary atresia and several other causes of neonatal liver disease carry high mortality and morbidity rates, especially if not treated early in life. Despite professional recommendations, delayed referral of infants with prolonged jaundice continues to be a significant problem. One approach to reducing the age of referral and diagnosis is population screening to detect significant conjugated hyperbilirubinaemia as an index of liver dysfunction. METHODS: To investigate this possibility, and to provide reference data on bilirubin and its conjugated and unconjugated fractions in a normal newborn population, 1157 neonates were anonymously tested (median age 7 days, range 4-28 days) using surplus plasma from routinely collected neonatal screening specimens, using dry slide chemistry. RESULTS: Of 2310 specimens received, 50% were suitable for analysis. The remainder were either haemolysed or insufficient (10% and 40% of the total, respectively). Total bilirubin concentrations ranged from 9 to 428 micromol/l and conjugated bilirubin from 0 to 175 micromol/l, although the latter was rarely increased to more than 30 micromol/l (2.5th-97.5th percentile ranges 15-285 micromol/l and 0-18 micromol/l, respectively). The range of the percentage of conjugated bilirubin was 0-57% (2.5th-97.5th percentile; range 0-20%). CONCLUSION: An increased conjugated bilirubin, expressed as a concentration or as the percentage of the total bilirubin, could be used as a specific marker to screen for liver dysfunction in neonates. This approach has the potential to improve the age of referral and the prognosis of infants with neonatal liver disease.

Bilirubin↗
PubMedDate not supplied

Serum carcinoembryonic antigen in the differential diagnosis of pancreatic cancer: influence of tumour spread, liver impairment, and age.

In order to verify the role of CEA in the differential diagnosis of pancreatic cancer and to evaluate some influencing factors like age, tumor spread and liver dysfunction, this antigen was measured in the sera of 60 control subjects, 45 patients with pancreatic cancer, 37 with chronic pancreatitis, 67 with benign, and 28 with malignant extra-pancreatic diseases. CEA was found to be elevated in 23/45 pancreatic cancers, in 8/37 chronic pancreatitis, in 17/67 benign and in 9/28 malignant extra-pancreatic diseases. Significant correlations were documented between CEA and age in all the subjects; between CEA and immunoglobulins G in liver cirrhosis and between CEA and alkaline phosphatase in gastrointestinal extra-pancreatic malignancies. In pancreatic cancer higher CEA levels were detected in patients with metastases. We can conclude that CEA is of limited value in the differential diagnosis of pancreatic cancer; it does not seem to be able to detect early pancreatic tumors. Age and liver dysfunction may contribute towards elevating this marker in serum.

Adult↗
PubMed1994

Involvement of liver in the decompensation of hemorrhagic shock.

In a hemorrhagic shock model without adequate volume resuscitation we investigated the question whether a biochemical stabilization of liver function by applying 2-mercaptopropionyl-glycine (2MPG) may influence the shock dynamics especially the transition from compensated to decompensated shock and the development of multiple organ failure (MOF). The application of a bolus of 10 mg/kg 2MPG just after hemorrhage had significantly beneficial effects on shock dynamics. All measured blood parameters demonstrate a less severe liver dysfunction. We found a decisive recovery of systemic pH, prolonged high levels of blood glucose, a better ammonia detoxification, arterial ketone ratios (acetoacetate/beta-OH-butyrat) above about 0.25, and a significantly increased survival time from 200 +/- 10 min to more than 240 min after hemorrhage. Decompensation of the 2MPG group started about 60 min after decompensation of the shock group. The transition to decompensation was combined in the shock group as well as in the 2MPG group with a severe liver dysfunction indicated by an arterial ketone ratio below .25. Decreasing levels of blood thiobarbituric reactive material in compensated shock of both groups demonstrate that production of free radicals did not primarily cause decompensation, but increasing levels of thiobarbituric reactive material during decompensation seems to be one of the factors mediating MOF. Our data support the hypothesis of the liver being a barrier against decompensation of shock and MOF.

Acetoacetates↗
PubMed2006

Pegylated interferon alpha-2b for patients with HCV recurrence and graft fibrosis following liver transplantation.

Chronic hepatitis C is a principal indication for liver transplantation. Recurrent viral infection is inevitable and graft disease is common. We report tolerability, safety and efficacy of pegylated interferon alpha 2b (PEG-IFN) monotherapy for patients with hepatitis C virus (HCV) recurrence and fibrosis after liver transplantation. Repeated measurements of serum HCV titer permitted assessment of the kinetics of the antiviral response for all patients. We screened 63 patients transplanted for HCV at our center for antiviral treatment, 14 were eligible and treated, but only 6 completed the proposed 52 weeks of therapy. Eight were withdrawn because of severe/life-threatening side effects/events, including liver dysfunction (4 patients). None of those 8 achieved a sustained virological response (SVR). Five of 6 who completed treatment were HCV RNA negative at the end of treatment, and 2 achieved an SVR. Viral kinetics were similar to published observations for treatment of non-transplanted HCV patients. Patients with genotype non-1 infection displayed a more rapid decline of viral titer than was observed for genotype 1 infection. Post-transplant HCV patients are frequently unsuitable for, or intolerant of PEG-IFN. Liver dysfunction was a major concern.

Adult↗
PubMed1998

Lack of anti-GOR antibody among subjects with GB virus C/hepatitis G virus RNA.

Homologies were sought between the putative amino acid sequences of GB virus C/hepatitis G virus (GBV-C/HGV) and the GOR epitope or the liver/kidney microsome-1 (LKM-1) epitope, which share partial sequence identity with the hepatitis C virus (HCV) polyprotein. Anti-GOR antibody (anti-GOR) was assayed among 100 subjects with GBV-C/HGV RNA. Twenty-one and 25 subjects were coinfected with hepatitis B virus (HBV) or HCV, respectively. Homologies were found between the NS5 or E2 polyproteins of GBV-C/HGV and the GOR epitope or the LKM-1 epitope, respectively. These segments of GBV-C/HGV polyproteins sharing identity with the GOR or the LKM-1 epitope were well conserved among three genotypes of GBV-C/HGV. However, only 1 of 55 subjects (1.8%) with GBV-C/HGV RNA, but not with HBV or HCV, was positive for anti-GOR. The positivity for anti-GOR among the group with GBV-C/HGV RNA alone was significantly lower than that among the groups with HCV RNA (P < 0.01 and P < 0.05, respectively). Only 2 of 55 subjects (3.6%) with GBV-C/HGV RNA alone exhibited elevation of alanine aminotransferase. The incidence of liver dysfunction among the group with GBV-C/HGV RNA alone was significantly lower than the incidence among the groups with GBV-C/HGV RNA and hepatitis B surface antigen (HBsAg) or HCV RNA (P< 0.01 and P< 0.01, respectively). These data indicate that 1) there is no association between GBV-C/HGV infection and the presence of anti-GOR, and 2) GBV-C/HGV infection is not related to chronic liver dysfunction.

Adult↗
PubMed1997

[A case of acute inflammatory demyelinating neuropathy associated with autoimmune-type chronic active hepatitis].

We presented a case of acute inflammatory demyelinating polyneuropathy associated with autoimmune chronic active hepatitis (AI-CAH). This is the third case report of neuropathy in AI-CAH. A 64-year-old male with chronic liver dysfunction was admitted to the hospital because of high fever, distal weakness and sensory disturbance of all extremities, bilateral facial weakness and dysphagia. On neurologic examination, there was bilateral weakness of the upper and lower facial muscles, bulbar palsy and severe distal weakness of all extremities. The deep tendon reflexes were absent and the sensation of touch, pinprick, temperature, and vibration was impaired bilaterally symmetrically in all extremities. Serum biochemistry revealed hyperproteinemia, hypergammaglobulinemia and elevated liver enzymes. Rheumatoid factor, antinuclear antibody anti-smooth muscle antibody were positive. Serological tests for hepatitis B surface antigen and its antibody hepatitis B core antibody, and hepatitis C antibody were all negative. Serum anti-GM1, anti-GD1b, anti-GQ1b and anti-MAG antibodies were negative. Liver biopsy findings were consistent with AI-CAH with marked lymphocytic infiltration in the portal tracts. Albuminocytologic dissociation was noted in CSF. Motorconduction velocity of the median, ulnar and facial nerves were markedly reduced with temporal dispersion. No motor response was evoked in the lower extremities. Needle electromyography revealed denervation and reinnervation potentials in the arm and leg. The sural nerve biopsy showed segmental de- and re-myelination and deposition of IgG components in endoneurium. Neurological symptoms and liver dysfunction improved with corticosteroid treatment. In this case, hypergammaglobulinemia associated with an exacerbation of AI-CAH may be responsible for the acute inflammatory demyelinating neuropathy through an unknown autoimmune mechanism.

Acute Disease↗
PubMed2002

Plasma and urine levels of urinary trypsin inhibitor in patients with acute and fulminant hepatitis.

BACKGROUND AND AIM: Urinary trypsin inhibitor (UTI) is synthesized by hepatocytes and excreted into urine. Plasma and urine UTI levels have been measured to evaluate whether these levels may be useful markers in various pathological conditions. However, there has been no study on plasma and urine UTI levels in patients with acute liver diseases. The aim of the present study was to evaluate plasma and urine UTI levels and their relationship with the severity of hepatic damage in patients with acute liver diseases. METHODS: Plasma and urine UTI levels were measured by newly developed enzyme-linked immunosorbent assay in 15 patients with acute hepatitis (AH), 12 patients with acute severe hepatitis (ASH) and 10 patients with fulminant hepatitis (FH), as assessed on admission. The serial changes in plasma and urine UTI were also observed in some patients with AH and ASH. RESULTS: Plasma UTI levels (U/mL, median [25-75th percentile]) were: 11.0, (9.5-16.1) in patients with AH; 7.8 (5.6-11.5) in those with ASH; 6.5 (4.0-9.5) in patients with FH; and 9.7 (7.3-11.0) in normal controls. Plasma UTI levels in patients with FH were significantly lower than in those with AH. Plasma UTI levels showed significant positive correlations with the levels of prothrombin time (PT), hepaplastin test, antithrombin III, alpha2-plasmin inhibitor, plasminogen (Plg) and fibrinogen. After the recovery of liver dysfunction, increased plasma UTI levels in patients with AH were decreased, whereas previously decreased plasma UTI levels in patients with ASH were increased. Urine UTI levels were significantly increased in patients with AH compared with those of normal controls. In patients with ASH and FH, urine UTI levels were increased but not significantly. Urine UTI levels significantly positively correlated with PT and Plg. After the recovery of liver dysfunction, previously increased urine UTI levels in patients with AH were decreased. The correlation between plasma UTI and urine UTI levels was not significant. CONCLUSIONS: The findings of the present study suggested that the levels of plasma and urine UTI changed in patients with AH and were closely related to the abnormalities of coagulo-fibrinolysis, including PT. Further studies are needed to clarify whether these levels may be useful markers to predict the prognosis of acute hepatitis.

Acute Disease↗
PubMed1993

[Anesthetic management of a patient with HELLP syndrome with bronchial asthma].

We gave anesthesia for cesarean section to 30 year-old female with HELLP syndrome with bronchial asthma. HELLP syndrome is characterized by hemolysis, liver dysfunction and thrombocytopenia, besides syndrome of severe toxemia of pregnancy. After intubation with sevoflurane, diazepam and vecuronium, anesthesia was maintained with nitrous oxide, oxygen, sevoflurane and vecuronium, because she had an attack of bronchial asthma before operation. Though she had no eclampsia nor hypertension during operation, her babies were intubated and were cared in pediatric ward. Though she had improvements of liver dysfunction and thrombocytopenia after operation, it took 2 days to extubated, because she had frequent attacks of bronchial asthma. We conclude that we should perform cesarean section for a patient with HELLP syndrome as soon as possible.

Adult↗
PubMed1998

Retrospective study on the impact of hepatitis C virus infection on kidney transplant patients over 20 years.

BACKGROUND: The majority of chronic hepatitis is ascribable to hepatitis C virus (HCV) infection, whereas the clinical impact has not been understood in kidney transplant recipients. Our current study was carried out to assess the impact of HCV infection on kidney recipients over the long-term, and to investigate the effect and risk of interferon-alpha (IFN-alpha) therapy for chronic active hepatitis C. METHODS: Hepatitis B surface antigen (HBsAg) and antibody to HCV (HCVAb) were examined prospectively and retrospectively in 280 patients, who underwent kidney transplants in the period from 1973 to 1996. The patient survival rate, the graft survival rate, the incidence of liver dysfunction and the cause of mortality among the HCV infected and noninfected groups were analyzed. IFN-alpha therapy was performed on 10 patients with chronic active hepatitis C. RESULTS: Prevalence of the hepatitis virus was quite high at 34.3% (96/280): the frequency of the HBsAg carrier was 3.2% (9/280), that of the HCVAb carrier was 28.6% (80/280) and that of the both carriers was 2.5% (7/280). The other 184 cases (65.7%) were negative for both HBsAg and HCVAb. Liver dysfunction developed at the significantly higher incidence of 55% in HCVAb carriers compared to the 9.2% of the noninfected group (P<0.01). HCVAb carriers had a poor survival rate in the second decade compared to the noninfected group: 83.7% vs. 88.91% for 10-year survival (P=0.44) and 63.9% vs. 87.9% for 20-year survival (P<0.05). The poor survival rate was a result of the mortality from liver disorder. Five patients died of such disease in the infected groups whereas no noninfected patient died in the same period (p<0.01). As the result of IFN-alpha therapy, biochemical activity normalized or improved in eight cases, whereas the HCV-RNA titer was reduced only in three patients. Only one patient maintained normal biochemical markers and undetectable levels of HCV-RNA for 2 years after treatment. The therapy was discontinued for five patients with the adverse effects of acute rejection, deterioration of diabetes, and depression. CONCLUSIONS: HCV infection has a significant impact on kidney transplant recipients over the long term and in particular affects them in the second decade. Our pilot study revealed only partial efficacy of IFN-alpha therapy for HCV-infected recipients, but with the high risk of acute rejection.

Adult↗
PubMedDate not supplied

An evaluation of total parenteral nutrition using Vamin and Aminosyn as protein base in critically ill preterm infants.

A total of 75 preterm infants with gestation less than 32 wk received total parenteral nutrition (TPN) using Vamin and Aminosyn as protein base lasting more than 20 days. They were monitored for signs of liver dysfunction, cholestatic jaundice, and TPN-induced metabolic bone disease (osteopenia of prematurity). It was observed that severity of TPN-induced cholestasis depends on the duration of TPN and quantity of protein infused. When used as a protein base, Vamin seemed to be superior to Aminosyn. TPN-induced metabolic bone disease was strongly correlated to the duration of TPN. We suggest close monitoring of critically ill preterm infants on TPN for quantity of protein infusate, liver dysfunction, cholestatic jaundice, and TPN-induced metabolic bone disease. Intravenous protein intake should be limited to less than 2.5 g/kg/day in preterm infants with gestation less than 32 wk.

Amino Acids↗
PubMed1977

Chronic hepatitis in hemophilia.

The relationship of chronic hepatitis B and/or liver dysfunction to treatment in 113 hemophiliacs was evaluated by the enzyme tests, SGOT and SGPT, and by the presence of circulating hepatis B surface antigen (HbsAg) or antibody (anti-Hbs). The hemophiliacs were divided into three groups according to treatment pattern. Individuals who had received multiple doses of plasma fractions, derived from four or more commercial lots were placed in tgroup I "large Exposure". Group II "Small Exposure" had been treated with fractions from three or fewer lots and Group III "Cryo" had never received commercial fractions, but had been treated with cryoprecipitate. Abnormal liver function tests (LFT's) were found in 87% of Group I and 76% of Group II, but in only 16% of the "Cryo" group. Differences in LFT's were not great between treated VIII and IX deficient patients. All patients treated with 100,000 units or more showed either persistent or intermittent abnormalities. In the high exposure group, this history of past, overt hepatitis had no influence on observed LFT's. The sera of all patients in the high exposure and all, except one, in the low exposure groups were positive for HbsAg or anti-Hbs by RIA. Splenomegaly was found in 13% of fraction-treated patients. We conclude that there is biochemical evidence of liver disease following large exposure to commercial VIII or IX fractions, which should temper the physician's decision to start treatment with these fractions. On the other hand, evidence that their continued use produces mounting liver dysfunction is insufficient to withdraw this very effective and life-changing treatment from these individuals.

Alanine Transaminase↗
PubMed1998

Reduced nitric oxide production by endothelial cells in cirrhotic rat liver: endothelial dysfunction in portal hypertension.

BACKGROUND & AIMS: Intrahepatic vascular resistance is regulated in part by the vasoconstricting and relaxing effects of compounds such as endothelin and nitric oxide (NO). Although the hepatic endothelium is likely to be a prominent source of NO via production by endothelial cell NO synthase (ecNOS), this isoform has not been described in sinusoidal endothelial cells (SECs). The aim of this study was to determine whether ecNOS is produced by SECs, and, if so, to determine whether ecNOS- (mRNA/protein) or SEC-dependent production of NO varies after liver injury. METHODS: A cDNA encoding a 279-bp fragment homologous to bovine ecNOS was isolated and used to detect rat ecNOS mRNA. Liver injury and/or cirrhosis was induced by bile duct ligation or administration of CCl4. NOS activity was quantitated and the presence of NO was detected with highly sensitive nitrite and cGMP assays. RESULTS: ecNOS mRNA and protein (detected by immunoblot) were present only in SECs. Neither ecNOS mRNA abundance nor protein levels varied after liver injury induced by bile duct ligation or repeated CCl4 administration, including in animals with cirrhosis. Because inducible NOS is induced after bile duct ligation but not after CCl4-induced cirrhosis, we examined NOS activity and nitrite- and NO-dependent cGMP production after the latter form of injury. NOS activity and nitrite and cGMP production were significantly reduced in SECs from cirrhotic animals compared with controls (P < 0.05, n = 4-6). CONCLUSIONS: SECs are an important source of ecNOS in the liver; although ecNOS mRNA and protein levels in SECs do not seem to vary with liver injury, ecNOS function is altered, resulting in diminished NO release in SECs from cirrhotic livers. These data have important implications for the pathogenesis of intrahepatic portal hypertension as well as other disorders in which endothelia may be damaged.

Animals↗
PubMed1992

[A case of loxoprofen-induced pulmonary eosinophilia].

A 65-year-old female suffering from lumbago, headache, and hypertension had been treated with nonsteroidal anti-inflammatory drugs (NSAIDs) and antihypertensive drugs. On June 13, 1990, 2 weeks after the commencement of loxoprofen administration, she developed cough and low grade fever. She was treated with antibiotics and NSAIDs without improvement. Laboratory data showed marked eosinophilia (2200/mm3), elevation of IgE (3090 IU/ml), and liver dysfunction. Her chest X-ray revealed no active lesion, but the percentage of eosinophils in BALF was elevated (38%). Because drug-induced eosinophilic pneumonia was suspected, all drugs were discontinued. Her symptoms improved and the abnormalities of laboratory data normalized. The lymphocyte stimulation test was weakly positive with three NSAIDs (loxoprofen, pranoprofen, and alminoprofen). The challenge test by loxoprofen reproduced eosinophilia and liver dysfunction, suggesting that she had loxoprofen-induced eosinophilic pneumonia. To our knowledge, this is the first reported case of loxoprofen-induced lung injury.

Aged↗
PubMedDate not supplied

Ultrastructural study of the remnant liver after extensive hepatectomy in dogs; especially morphological alterations of sinusoidal endothelial cells.

BACKGROUND/AIMS: To investigate the role of sinusoidal endothelial cells in the mechanism of the remnant liver dysfunction after extensive hepatectomy, morphological alteration of sinusoidal endothelial cells and cytoprotective effects of prostaglandin I2 analog were studied by ultrastructural analysis. METHODOLOGY: Mongrel dogs (n = 24) were divided into 3 groups according to the extent of hepatectomy and the use of prostaglandin I2 analog preoperatively. Group 1: 70% hepatectomy (n = 8), Group 2: 84% hepatectomy (n = 8), and Group 3: 84% hepatectomy with administration of prostaglandin I2 analog, preoperatively (n = 8). Morphology of hepatic sinusoidal endothelial cells was examined after hepatectomy in all cases. RESULTS: Group 2: Enlargement of the sinusoidal endothelial fenestrations was transitorily occurred immediately after hepatectomy, but were dramatically decreased in size 24 h after the operation. Most sinusoidal endothelial cells were destroyed and separated from the sinusoidal wall. Fibrin deposits and sludge were found in the Disse's space and sinusoidal lumens, resembling liver failure at 24 h after the operation. Group 1 and 3: sinusoidal endothelial fenestrations remained slightly enlarged at 24 h after the operation, but fibrin deposits or sludge were not observed in sinusoidal lumens. CONCLUSIONS: Our data suggest that extensive hepatectomy changed the morphology of sinusoidal endothelial cells. Administration of prostaglandin I2 analog helped maintain structural integrity of sinusoidal endothelial cells, improved hepatic microcirculation and thus served to reduce remnant liver dysfunction.

Animals↗
PubMed1998

Necrotizing fasciitis caused by Vibrio vulnificus differs from that caused by streptococcal infection.

We reviewed the clinical record of all patients admitted to Saga Medical School Hospital during the most recent 10 years and found that 17 (0.03%) were diagnosed as having necrotizing fasciitis. Bacteriological examination demonstrated that Vibrio vulnificus was the pathogen responsible in five patients (29%). The disease caused by V. vulnificus occurred in the warmer half of the year. All of the patients had underlying chronic liver dysfunction, and three of them had previously consumed raw seafood. In these patients, the predominant skin lesions were oedema and subcutaneous bleeding, such as ecchymosis and purpura, while superficial necrosis was not recognized. Three patients died of systemic complications. By contrast, all of the five patients with necrotizing fasciitis caused by Streptococcus pyogenes had the disorder in winter, and only one of them had chronic liver dysfunction. In skin lesions, subcutaneous bleeding was rare but necrosis was seen often. Despite the high incidence of systemic complications, no patients with streptococcal necrotizing fasciitis died. These findings suggest that the clinical features of necrotizing fasciitis caused by V. vulnificus are different from those of necrotizing fasciitis caused by classical pathogens, and that the two should be differentiated as early as possible to improve the prognosis.

Adolescent↗