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PubMed1983

Histiocytosis X in children: patterns of disease and results of treatment.

The pathologic materials and clinical courses of 36 children aged 1 month-22 years, with histiocytosis X (H-X) seen at the Philadelphia Children's Cancer Research Center from 1970 to 1979 were reviewed. The pathologic subtype of H-X was favorable (type II) in 31 patients, unfavorable (type I) in one patient, and unclassified in four patients whose specimens were limited to a skin biopsy. Sixteen patients had localized H-X involving bone (14 patients), soft tissue (1 patient), or skin only (1 patient); all are alive and well after treatment with surgery alone (12 patients), radiation therapy (RT) (3 patients), or observation (1 patient); only 1 of the 16 developed recurrent H-X. The other 20 patients presented with multifocal H-X involving the skeleton alone (3 patients); the skeleton and soft tissues other than liver (7 patients); soft tissue exclusive of the liver (3 patients); soft tissue including the liver (4 patients); or soft tissues, skeleton, and liver (3 patients). These 20 patients were treated with surgery alone (1 patient), RT (4 patients), or multiple drugs +/- RT (15 patients). Seven of the 20 patients are alive and well without recurrence at a median of 4 years after diagnosis. Nine of the 20 patients, including 3 with liver dysfunction, responded completely to initial therapy but developed recurrence; each was retreated with drugs and is alive and well at a median of 4 years. The remaining 4 patients had widespread disease with dysfunction of the liver and/or hematopoietic system at diagnosis, failed to respond, and died. We conclude that (1) patients with multiple bony lesions with or without associated soft tissue disease or skin involvement have a favorable outlook and do not require systemic chemotherapy; (2) systemic treatment also is unnecessary for patients with localized H-X since recurrence is rare; (3) drugs can benefit patients with multifocal H-X, although the optimal duration of therapy is unclear; and (4) favorable response to treatment indicates high probability of disease-free survival. However, organ dysfunction at diagnosis is ominous: four of seven patients with liver dysfunction are dead, as are all three patients who presented with peripheral blood count depression.

Adolescent↗
PubMed2004

Mitochondrial dysfunction in liver disease and organ transplantation.

The mitochondria play a crucial role in maintaining hepatocyte integrity and functions. Mitochondrial defects are either inherited or acquired. Mitochondria dysfunction occurs when the hepatocyte experience excessive physiologic stress. Its clinical presentation depends on the severity of the stress. It varies from mild abnormalities in liver biochemical tests to manifestations of acute or chronic liver failure. Mitochondria dysfunction is implicated in most liver disease and in early graft dysfunction after liver transplantation. This review will address the role of mitochondria in liver disease.

Journal Article↗
PubMed1993

[Liver impairment in kidney transplant recipients. 1. Prevalence and clinical significance of hepatitis C].

The prevalence and the clinical significance of hepatitis C (HCV) infection in recipients of kidney transplantation was assessed using second generation anti-HCV antibody (anti-HCV-2). Out of 88 patients whose preoperative sera were available for anti-HCV-2 determination, 27 patients (30.7%) were positive. Transfusion units were significantly larger and the duration of hemodialysis was significantly longer in the patients with anti-HCV-2 than those without. In 10 patients whose preoperative sera were negative for anti-HCV-2, seroconversion was documented after the operation, so that the postoperative positive rate of anti-HCV-2 increased to 42.9% (39/91). Seroconversion from positive to negative was observed in only one patient. Out of 91 patients who were followed-up at least 3 months after operation, 66 patients (72.5%) developed liver dysfunction. According to the criteria of non-A, non-B post-transfusion hepatitis established by the Japanese Society of Digestive Disease, 31 of 66 patients (34.1%) were diagnosed as "definite", 21 patients (23.1%) as "suspicious". The anti-HCV-2 positive rate was 90.3% in the "definite" group, which was significantly higher than the other groups. Liver dysfunction in the patients with anti-HCV-2 had a tendency for a chronic or prolonged course. Out of 20 patients in whom liver dysfunction continued for more than 1 year, 18 patients were positive for anti-HCV-2. It is concluded from this study that the prevalence of hepatitis C is very high in kidney transplant recipients with HCV as the main and most important etiologic factor of liver dysfunction, especially in chronic liver impairment.

Adolescent↗
PubMed2003

Hepatocyte growth factor prevents chronic allograft dysfunction in liver-transplanted rats.

BACKGROUND: Hepatocyte growth factor (HGF) is a growth factor with multiple biologic properties, including mitogenic, morphogenic, anti-apoptotic, and antifibrogenic activities. Long-term administration of the deletion variant of HGF (dHGF) might contribute to the prevention of chronic liver allograft dysfunction, which is attributed to immunologic and nonimmunologic reactions. METHODS: Low-dose tacrolimus was administered to rat-liver recipients after transplantation. Effects of dHGF on transplanted livers treated with low-dose tacrolimus were investigated. RESULTS: Rats receiving liver transplants treated with only low-dose tacrolimus administration showed chronic allograft dysfunction. Treatment with dHGF prolonged the survival time of rats that received liver allografts and suppressed fibrosis of liver allograft. Treatment with dHGF also suppressed the expression levels of interleukin (IL)-1beta, caspase-1, and transforming growth factor (TGF)-beta mRNAs in liver allografts. CONCLUSIONS: The findings indicate that dHGF may prevent chronic liver-allograft dysfunction and thus may become a novel treatment for chronic liver-allograft dysfunction.

Animals↗
PubMed2000

A comparison of the pattern of liver involvement in dengue hemorrhagic fever with classic dengue fever.

The impact of dengue on liver function was studied on fifty serologically confirmed dengue cases admitted to Hospital Universiti Kebangsaan Malaysia (HUKM). Twenty-five of these patients had classic dengue fever (DF) and 25 had grade 1 or 2 dengue hemorrhagic fever (DHF). There were more (60%) DHF patients with hepatomegaly compared to DF (40%) but the difference was not statistically significant. Analysis of the liver profile showed that liver dysfunction was commoner in DHF compared to DF, indicating that the degree of liver impairment may be related to the severity of DHF. Hyperbilirubinemia was noted in 3 (12%) DHF and 2 (8%) DF patients. The mean (range) serum bilirubin was higher in DHF [14.2(5-50) micromol/l] compared to DF [10.9(5-30) micromol/l)] (p > 0.05). Elevated levels of serum alanine aminotransferase (ALT) and alkaline phosphatase (ALP) were observed more frequently in DHF (20 and 12 patients respectively) compared to DF (16 and 8 patients respectively). Nine (36%) DHF and 6 (24%) DF patients had concomitant elevation of ALT and ALP levels. The mean (range) serum ALT levels were 109.3(23-325) U/l in DHF and 90.8(13-352) U/l in DF (p > 0.05). The mean (range) serum ALP levels were 102.2(15-319) U/l in DHF and 93.3(34-258) U/l in DF (p > 0.05). The ALT and ALP levels were significantly higher in DHF patients with spontaneous bleeding than those without bleeding (p < 0.05) None of the patients developed fulminant hepatitis. The immunoregulatory cells, which include the T (CD3), B (CD 19), CD4, CD8, CD5 and natural killer (NK) cells were significantly lower in DHF compared to DF patients (p < 0.05). However, the reduction in these cell counts did not correlate with the liver dysfunction seen in DHF patients. In conclusion, hepatomegaly and liver dysfunction were commoner in DHF compared to DF.

Adolescent↗
PubMed2005

The 'small for size' liver syndrome.

PURPOSE OF REVIEW: Small-for-size syndrome (SFSS) is a clinical syndrome described following liver transplantation (LT) and extended hepatectomy. New evidence has emerged documenting the importance of preoperative evaluation of functional liver mass, liver quality, influence of portal hypertension, and variations in surgical technique to improve outcome. RECENT FINDINGS: SFSS is characterized by postoperative coagulopathy and liver dysfunction due to insufficient functional liver mass. Recent radiologic advances allow accurate preoperative estimation of total, graft, and remnant liver volume (RLV). In adult-to-adult living donor liver transplantation (LDLT), a graft-to-recipient body weight ratio > or = 0.8% or graft weight ratio > or = 30% are important to avoid SFSS. Minimal functional RLV following extended hepatectomy is > or = 25% in a normal liver, and > or = 40% with preoperative liver dysfunction. Preoperative portal vein or hepatic artery embolization to increase RLV and function after extended hepatectomy, and the increasing use of parenchymal-sparing segmental resections have improved outcome. In LT, the evolving use of split livers, LDLT and marginal grafts has resulted in increased recognition of SFSS. This has led to a renewed interest in defining the pathophysiology, and the development of new surgical techniques to reduce its incidence. SUMMARY: Current radiologic imaging techniques can be used to evaluate liver volume and the risk of SFSS following LT and extended hepatectomy. Intraoperative techniques to predict postoperative dysfunction are emerging, and may be helpful in directing the use of pre-emptive surgical interventions. The future lies in the development of perioperative liver protection and support in predicted SFSS, and enhancement of healthy liver regeneration.

Adult↗
PubMed1984

Clinical manifestations of congenital syphilitic hepatitis: implications for pathogenesis.

To study the clinical course and biochemical features of congenital syphilitic hepatitis, the records of all 22 pediatric patients admitted to North Carolina Memorial Hospital between 1969 and 1979 with a positive maternal, cord blood, or serum VDRL were reviewed. Of the seven infants identified with symptomatic congenital syphilis, five had clinical and biochemical evidence of liver dysfunction. All five were jaundiced (peak bilirubin ranged from 8.4 to 29.8 mg/dl, in each case greater than 40% conjugated). Peak transaminase elevation ranged from seven to 150 times normal. Serum glutamic-oxaloacetic transaminase exceeded serum glutamic-pyruvic transaminase in each infant, the difference ranging to 7,400 U. The onset of illness did not occur until after treatment had been initiated in two of these five cases. Liver dysfunction increased with treatment in all four infants with serial enzyme determinations. Liver dysfunction also persisted for more than 6 weeks after adequate treatment in two cases. Liver biopsy 5 weeks after treatment in another infant showed giant cell hepatitis. These observations suggest that treatment can potentiate liver dysfunction in congenital syphilis and that viable treponemes are not necessarily essential in the pathogenesis of the hepatitis.

Alanine Transaminase↗
PubMedDate not supplied

Liver failure is uncommon in adults receiving long-term parenteral nutrition.

BACKGROUND: Abnormal liver enzymes and endstage liver disease are reported to occur in 25%-100% and 15%-40% of adult patients receiving long-term parenteral nutrition (PN), respectively. The purpose of this historic cohort study was to investigate the incidence of and possible factors leading to the development of liver disease in our large home PN population. METHODS: All patients on home PN for at least 6 months from July 1991 through June 2002 were eligible. Patients were excluded if they had active malignancy, underlying liver disease, or exposure to a hepatotoxin. The presence of PN-associated liver disease was only considered if test results were elevated on more than 1 occasion over at least 6 or more months. The severity of liver-associated enzymes was based on the degree of elevation and was stratified as mild (<2 times normal), moderate (2-5 times normal), and severe (>5 times normal). Severe liver dysfunction was defined as having all of the following criteria: total bilirubin >3 mg/dL; albumin <3.2 g/dL; and prothrombin time >3 seconds prolonged. A cumulative logit model was used to compare age, gender, underlying disease, PN indication, and PN formulas in patients with normal vs abnormal laboratory test results. RESULTS: Two hundred eight patients received PN for more than 6 months, 36 had exclusion criteria, and 10 could not be analyzed, because of incomplete laboratory test results, leaving 162 in the study group. The average PN duration was 2.14 +/- 2.19 years (maximum, 10.28 years). Abnormal liver tests occurred in 154 patients, with most having a moderate elevation of alkaline phosphatase or aspartate aminotransferase; severe liver dysfunction occurred in 7 patients; 1 patient had completely normal liver enzymes. On average, patients received a PN formula that was high in amino acids (1.45 +/- 0.65 g/kg/d), modest in energy (24.7 +/- 13.4 kcal/kg/d), and in most cases with enough lipid emulsion to meet essential fatty acid requirements (0.28 +/- 0.25 g/kg/d). Only female gender was found to be associated with a greater likelihood of liver failure (p = .02). There was a trend toward a greater amount of total calories, dextrose calories, and duration of PN exposure leading to the development of severe liver dysfunction. CONCLUSIONS: When long-term PN is given with a modest amount of total energy and a minimal amount of lipid emulsion, abnormal liver enzymes are common, but severe liver dysfunction is unusual.

Alkaline Phosphatase↗
PubMed2003

Association between ABCB1 (multidrug resistance transporter) genotype and post-liver transplantation renal dysfunction in patients receiving calcineurin inhibitors.

OBJECTIVE: Renal dysfunction is a common and costly adverse outcome of long-term treatment with calcineurin inhibitors (CNIs). We conducted a retrospective, case-control study to test whether the risk of renal dysfunction in liver transplantation patients receiving CNIs is associated with the 2677G>T transversion in exon-21 of the gene (ABCB1) encoding P-glycoprotein. A total of 120 non-Hispanic white patients were evaluated. RESULTS: The overall incidence of renal dysfunction by year 3 post-transplantation was 40%. The frequency of renal dysfunction was reduced among patients with an ABCB1 2677TT genotype, as compared to those with a 2677GG genotype. Subjects with a heterozygote genotype behaved phenotypically like the 2677GG group. Comparing those subjects with a 2677TT genotype to the combined group of subjects with a 2677GG, TG, AT, or AG genotype resulted in an odds ratio of 0.26 (0.09-0.77). When subjects were stratified by gender, the frequency of renal dysfunction was reduced among men with an ABCB1 2677TT genotype, relative to men with different genotypes. A similar odds ratio was obtained for women, but it did not achieve significance. When 18 subjects with an elevated SCr concentration just prior to surgery were excluded from the year 3 analysis, the association between the 2677TT genotype and chronic renal dysfunction in the remaining cohort was strengthened comparing genotype groups. CONCLUSIONS: Based on these results, we conclude that homozygosity for the ABCB1 2677T (S893) allele is associated with reduced risk of chronic renal dysfunction among liver transplantation patients receiving an immunosuppressive regimen containing CNIs.

Calcineurin Inhibitors↗
PubMed2004

[Case of NASH exacerbated after testectomy due to seminoma].

A 41-year-old Japanese male was admitted to our hospital because of the increased levels of serum AST, ALT, and gamma-GTP on December 18, 2002. He was diagnosed with right testis seminoma in 1994 and had received right high orchiectomy and radiation therapy. At that time, liver dysfunction was not pointed out. As weight was increased in 2001, liver dysfunction was pointed out. He was diagnosed as left testis seminoma in June, 2002, left high orchiectomy and chemotherapy was performed. Abdominal ultrasonography showed the moderate fatty liver, and hepatic histopathology revealed a typical and remarkable steatohepatitis with lymphocyte infiltration. He had no life history of alcohol-consumption, and he was diagnosed as non-alcoholic steatohepatitis (NASH). He was treated with a low-calorie diet, which showed favorable effects on his serum levels of AST, ALT, gamma-GTP, and LDH. This case suggests that the altered sex hormone balance might exacerbate NASH because liver dysfunction was particularly worsened after bilateral high orchiectomy.

Adult↗
PubMed1992

Sulfur amino acid metabolism in hepatobiliary disorders.

Sulfur amino acid metabolism was studied in patients with mild to severe forms of liver dysfunction and compared with that of healthy controls. Patients with mild liver dysfunction (for example, Gilbert's syndrome) had a normal sulfur amino acid metabolism. With increased inflammatory activity and cirrhosis (for example, chronic active hepatitis, alcohol-induced cirrhosis, and hepatic coma) a decreased ability to metabolize methionine (to cysteine, with cystathionine accumulation) and cysteine (to inorganic sulfate, with thiosulfate and N-acetylcysteine accumulation) was found. In contrast, transaminative metabolism of sulfur amino acids was preserved in patients with advanced forms of liver dysfunction, suggesting that transamination of sulfur amino acids is performed not only in the liver but also in extrahepatic tissues. Some implications of these findings are discussed.

Adolescent↗
PubMedDate not supplied

Central bisegmentectomy of the liver: experience in 16 patients.

Fourteen patients with hepatocellular carcinoma and mild to moderate liver dysfunction and 2 with metachronous liver metastases from rectal cancers underwent central bisegmentectomy of the liver, i.e., en bloc removal of the left medial and right anterior segments. One patient who had undergone preoperative liver artery embolization died in the hospital. Four patients survived without relapse 60-135 months postoperatively. Eleven patients had recurrent tumors, all in the liver remnant, and 2 also had recurrent tumors in the lungs. Six patients who relapsed died 28-93 months postoperatively. Four were alive with disease at 7-89 months, 1 after a second liver resection 54 months after central bisegmentectomy. Six of the 16 patients survived for 5 years or more. The results are favorable for these advanced tumors, often in the presence of liver dysfunction. The indications, technique, and results are discussed.

Aged↗
PubMed2002

Pharmacokinetics of omeprazole given by continuous intravenous infusion to patients with varying degrees of hepatic dysfunction.

OBJECTIVE: To examine the pharmacokinetics of omeprazole during intravenous infusion in patients with varying degrees of liver dysfunction (Child-Pugh categories A to C). DESIGN: Nonblinded single-period study. PATIENTS: Thirteen patients, five males and eight females with a mean age of 59 years and proven hepatic cirrhosis, classified according to Child-Pugh criteria as A (n = 5), B (n = 4) or C (n = 4). METHODS: Each patient received an 80mg bolus of omeprazole over 30 minutes followed by a continuous infusion of 8 mg/h for 47.5 hours. Blood samples were taken frequently throughout the infusion and during the subsequent 24-hour washout period for determination of omeprazole and its metabolites. Laboratory screening was also performed at the start of the study, after 72 hours and at the 14 day follow-up visit. RESULTS: Data were evaluable for 12 patients. For omeprazole, the mean total area under the plasma concentration-time curve (AUC) was 286.5 micromol x h/L, peak plasma concentration was 14.9 micromol/L and terminal elimination half-life was 4.1 hours; these values were higher than those observed historically in control patient populations. Concentrations of the metabolite omeprazole sulphone were also increased, but there was a decrease in concentrations of hydroxy-omeprazole. Deviations from normal values increased with increasing disease severity for all parameters. For example, in patients with liver dysfunction of Child-Pugh categories A, B and C, AUC(48 )was 240.8, 280.4 and 323.3 micromol x h/L compared with 151.3 micromol x h/L in the historical control population. Despite its altered pharmacokinetics, omeprazole was not associated with any serious or untoward effects. CONCLUSION: Exposure to omeprazole following intravenous administration was higher in patients with liver dysfunction than in the normal population. However, even in patients with severely impaired liver function, the omeprazole plasma concentration did not change by more than 100% and the drug was well tolerated.

Adult↗
PubMed1999

Soluble fas ligand in natural killer cell lymphoma.

We measured serum soluble Fas ligand (sFasL) in a patient with natural killer cell lymphoma, and investigated relationship between sFasL and liver dysfunction. An elevated level of sFasL was decreased after local radiation therapy, and liver function improved. When lymphoma relapsed, liver dysfunction reappeared and the level of sFasL increased parallelly. Lymphoma cells expressed mRNA of FasL. This suggested that this liver dysfunction was induced by some remote effectors, and sFasL was one of candidates of these effectors.

Adult↗
PubMed2004

Cytochrome P450 1A2 is a major determinant of lidocaine metabolism in vivo: effects of liver function.

OBJECTIVES: This study was designed (1) to evaluate the effect of a cytochrome P450 (CYP) 1A2 inhibitor, fluvoxamine, on the pharmacokinetics of intravenous lidocaine and its 2 pharmacologically active metabolites, monoethylglycinexylidide (MEGX) and glycinexylidide (GX), to confirm recent in vitro results indicating that CYP1A2 is the main isoform responsible for lidocaine biotransformation and (2) to assess whether liver function has any influence on the fluvoxamine-lidocaine interaction. METHODS: The study was carried out in 10 healthy volunteers and 20 patients with cirrhosis, 10 with mild (Child grade A) and 10 with severe (Child grade C) liver dysfunction, according to a randomized, double-blind, 2-phase, crossover design. In one phase all participants received placebo for 6 days; in the other phase they received 50 mg fluvoxamine for 2 days and 100 mg fluvoxamine for the next 4 days. On day 6, a 1-mg/kg lidocaine dose was administered intravenously 2 hours after the last dose of fluvoxamine or placebo. Plasma concentrations of lidocaine, MEGX, GX, and fluvoxamine were measured up to 12 hours after lidocaine injection. RESULTS: The effects of fluvoxamine coadministration were dependent on liver function. Lidocaine clearance was decreased on average by 60% (from 12.1 mL/min.kg to 4.85 mL/min.kg, P <.001) in healthy subjects and by 44% (from 9.83 mL/min.kg to 5.06 mL/min.kg, P <.001) in patients with mild liver dysfunction, with proportional increases in terminal half-lives, whereas virtually no effect was produced in patients with severe liver dysfunction (4.21 mL/min.kg versus 3.65 mL/min.kg, P >.05). Analogous effects were observed on MEGX and GX formation kinetics, which were drastically impaired in healthy subjects and patients with mild liver cirrhosis but virtually unaffected in patients with severe cirrhosis. CONCLUSION: CYP1A2 is the enzyme principally responsible for the metabolic disposition of lidocaine in subjects with normal liver function. The extent of fluvoxamine-lidocaine interaction decreases as liver function worsens, most likely because of the concomitant decrease in the hepatic level of CYP1A2. These observations indicate that results obtained in healthy subjects cannot be extended a priori to patients with liver dysfunction, but the clinical consequences of inhibition of drug metabolism must also be assessed in such patients.

Anti-Arrhythmia Agents↗
PubMed2003

Isolated intestinal transplantation: proof of clinical efficacy.

BACKGROUND AND AIMS: Isolated intestinal transplantation has been limited by poor patient and graft survival. If high survival could be achieved and if parenteral nutrition-associated liver disease were reversible, this procedure could be more widely applied, with early liver dysfunction indicating the need for transplant evaluation. METHODS: Twenty-six patients who had failed parenteral nutrition received 28 isolated intestinal transplants. We analyzed patient and graft survival, the effect of sirolimus on the severity and frequency of rejection, and the reversibility of liver dysfunction after transplant. RESULTS: Three-year actuarial patient and primary graft survival were 88% and 71%, respectively. Two patients underwent successful retransplants. Twenty-two patients are alive at a mean of 21+/-15 (median 18; range 3-51) months. Actuarial survival with freedom from parenteral support is 81% at 3 years (21 of 26 patients). Actuarial freedom from parenteral support among survivors is 95.5% at 3 years (21 of 22 patients). Early rejection was less frequent with sirolimus (34% vs. 70% without sirolimus) (P=0.007). Moderate and severe rejection was less frequent with sirolimus (1/11 episodes vs. 9/17 episodes without sirolimus) (P=0.05). No grafts were lost after introduction of sirolimus. In all four patients with advanced liver dysfunction, fibrosis and cholestasis regressed within 1 year. CONCLUSIONS: High patient survival and parenteral nutrition-free survival can be achieved after isolated intestinal transplantation. Sirolimus treatment has eliminated graft loss. Parenteral nutrition-associated liver disease is reversible with intestinal transplantation. Refractory liver dysfunction in patients receiving parenteral nutrition should prompt consideration for isolated intestinal transplantation.

Adult↗
PubMed1998

Hepatic resection in the elderly.

From 1986 to 1995 a total of 97 patients > 65 years of age underwent hepatic resections at the Department of General Surgery, Hospital Lainz, Vienna, Austria. The population consisted of 39 men and 58 women with a mean age of 74.0 +/- 5.5 years. Primary neoplasia of the liver was the cause of resection in 35 patients, gallbladder cancer in 16 patients, and metastatic disease to the liver (due to colorectal cancer in 70%) in 40 patients. The rate of major resections (> or = 3 liver segments) was 96% for primary neoplasia of the liver, 70% for metastatic disease to the liver, and 50% for gallbladder cancer; the associated mortality rates were 23%, 2.5%, and 25%, respectively. The magnitude of the resection had a significant influence on survival for gallbladder cancer (p = 0.02) and for primary neoplasia of the liver (p = 0.002) but not for metastatic disease to the liver. This reflects the high rate of cirrhosis in hepatocellular and cholangiocellular carcinoma (88%) and gallbladder cancer (37.5%). Both pre- and postoperative severe liver dysfunction had a significantly higher risk for postoperative mortality and morbidity, which showed an incremental risk with age. Another organ system able to predict outcome at the beginning of treatment by its moderate severe dysfunction were the lungs. Overall, only right and extended right lobectomies carried a significantly higher risk for postoperative mortality and morbidity. Postoperative complications were recorded in 43% of our patients, with infection the most frequent problem in nearly all of these patients (95%). Pneumonia was the leading complication associated patient survival. All patients who developed pneumonia as a late complication during a complicated postoperative course died postoperatively. The postoperative Goris score of the patients who died was 6.9 +/- 2.9 (range 3-11), whereas the surviving patients' score averaged 2.2 +/- 1.9 (range 0-9), which was significantly different (p = 0.0003). None of the 54 patients with a GORIS score < or = 2 died postoperatively, whereas 5 of 6 patients with a score > or = 9 died (p = 0.0001). Severe liver dysfunction rather than the extent of resection influences clinical mortality. Patients > 80 years of age with a preoperative severe liver dysfunction showed a postoperative mortality of 57%, and all of these patients developed postoperative complications. Therefore resection cannot be recommended for those patients. Cirrhosis led to an unacceptable mortality of 44% after hepatic resection of > or = 5 liver segments for primary neoplasia of the liver. Major resections cannot be recommended in the aged with gallbladder cancer because 50% of the patients died after such operations. Overall, only resection of > or = 5 liver segments with segments I to III or less remaining were found to pose a major risk for clinical mortality and morbidity, but the cause of death was preexisting liver dysfunction and cirrhosis in all of these patients. Major resections of large neoplasia of the liver can be recommended even in the aged, but a preoperative preselection of patients with respect to liver function and pulmonary function preoperatively may help lower the postoperative morbidity and mortality, especially in patients who will undergo resection of > or = 5 liver segments. Major hepatic resection for metastatic disease to the liver in the elderly carries no additional survival risk. Patients > 65 years of age and especially those > 80 years of age are more liable to succumb to postoperative organ failure and complications, especially infections.

Aged↗
PubMed2003

Impact of donor, recipient, and graft features on the development of primary dysfunction in liver transplants.

OBJECTIVES: To establish the utility of eight anatomic/pathologic suboptimal and 9 others graft features, versus in 20 donor versus 14 recipient characteristics to predict primary transplant dysfunction. PATIENTS AND METHODS: We reviewed 248 consecutive liver transplants performed at the Hospital Ramón y Cajal, Madrid, in 206 patients over a 79-month period. At least one biopsy specimen was obtained from 169 grafts (68.1%). Recipients were classified as showing primary function or dysfunction, the latter group being subdivided into primary failure and inadequate initial function. The primary function and inadequate initial function groups were defined in terms of transaminases less or more than 2000 IU and prothrombin activity over or under 50%, respectively during posttransplant days 2 to 7. RESULTS: The following graft-related rates were recorded: arteriopathy 6.5%, steatosis 29.4% (macrovesicular 26.4%, microvesicular 4.7%, or both 1.7%), hepatocyte vacuolization 14.2%, sinusoidal ectasia 12.4%, hepatocellular necrosis 44.7%, and neutrophilic infiltration 24.4%. The only significant factors in the multivariate analysis were cause of donor death other than cranioencephalic trauma (P=.032) and moderate steatosis (30%-60% affected hepatocytes); (P=.012). CONCLUSIONS: The only factors that seem to influence the development of primary liver dysfunction were a moderate degree of graft steatosis and a cause of brain death other than cranioencephalic trauma.

Blood Pressure↗