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ABSTRACT: Liver metastases from colorectal cancer are an absolute contraindication for liver transplantation. Aggressive therapy with liver resection and local chemotherapy in selected patients may be able to provide long-term cure. Given the risks of tumor recurrence, whether patients with post chemotherapy complications leading to liver failure should be offered transplantation is a challenging question in an era of limited organ availability. Herein we have presented 2 cases of liver transplantation performed in patients with colorectal cancer metastases treated with liver resection followed by hepatic artery infusion chemotherapy leading to development of sclerosing cholangitis and eventual liver failure. This report demonstrates that liver transplantation may be an option in selected patients with colorectal cancer liver metastases that have been well treated.
Transplantation Proceedings 06/2011; 43(5):2070-4. · 1.00 Impact Factor
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ABSTRACT: A novel frequency analysis algorithm for segmentation of textured cells is presented. The algorithm is developed based on an ideal simulation model and is applicable to real cell images. A simulated cell image is assumed to have an ellipse-like region of textured interior embedded in a relatively flat background. The size of the original image is expanded multiple times by extrapolating it to additional regions with estimated background intensities before a larger sized discrete Fourier transform (DFT) is applied. The idealised model for the cell images shows a direct relationship between the boundaries of the cell regions and the inner zero-crossing lines in the large-sized DFT of the expanded images. The shape, size and orientation of the cell region are determined by the parameters derived from the estimated inner zero-crossing line in the DFT whereas the position of the cell region is determined by searching for the location of the minimum in the moving average with the window shaped the same as the previously acquired cell region. Experimental results of both the simulated and the real microscopic cell images are provided to show the performance of the proposed algorithm.
IET Image Processing 04/2011; · 0.64 Impact Factor
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ABSTRACT: Information about the natural history of small duct primary sclerosing cholangitis (SDPSC) remains scant despite literature suggesting that it constitutes 6-16% of all cases of primary sclerosing cholangitis (PSC). We combined clinical data on SDPSC cases from two tertiary care institutions with liver transplantation programs with the aim of studying the natural history of SDPSC.
Medical records of 25 individuals with SDPSC were reviewed. Diagnosis of SDPSC was based on liver biopsy findings consistent with PSC, a normal cholangiogram, and elimination of known causes of secondary sclerosing cholangitis. Demographic information, symptoms, past medical history, laboratory values, and histologic data were evaluated. Our primary outcome measure was liver transplantation or death. Secondary outcome measures included evidence of end-stage liver disease, development of cholangiocarcinoma, and/or the development of classic PSC on a repeat cholangiogram.
Data on 25 individuals (13 males, 12 females; mean age 40 ± 15 years) diagnosed with SDPSC were analyzed. Upon presentation, 11 patients had symptoms including abdominal pain, fatigue, and pruritus. Inflammatory bowel disease was present in 14 patients (56%) at diagnosis. On initial liver biopsy, 60% had early-stage disease (I or II) and none had cirrhosis. On follow-up (1-168 months, median 17 months), malignancy or progression to classic large duct PSC was not noted. Two (8%) patients had evidence of varices and one of the two also developed ascites; one of these patients underwent liver transplantation and the other one died due to sepsis.
SDPSC, a mild disease at presentation typically runs a benign course and likely is not an early stage of classic PSC. Further studies with a control group of classic PSC and longer follow-up are needed to study the natural history of SDPSC.
Hepatology International 03/2011; 5(3):808-13. · 2.64 Impact Factor
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ABSTRACT: An algorithm is presented for restoration of colour microscopic images with distortions from imperfect microscope lenses having transverse chromatic aberrations, resulting in a magnification that slightly varies with wavelengths or colours. The differential of each colour component image is computed as the difference between the component image and its slightly magnified version. The absolute values in the differential component images are generally higher at the edges where greater discontinuities occur. The two cross-correlation functions of the absolute differentials between red and green colours and between red and blue colours are then computed. The maximum in the two cross-correlation functions were sought, respectively, and the cross-correlation delays were then calculated. The two cross-correlation delays were used to determine dispersions and to realign the three colour components. Results of real microscopic images are provided. The restored image and the original are compared both visually and quantitatively in terms of the estimated entropies measured for the degree of concentrations using vector distributions.
Journal of Microscopy 02/2011; 241(2):125-31. · 1.63 Impact Factor
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ABSTRACT: We describe a case of nevirapine-induced Stevens-Johnson Syndrome (SJS) and fulminant hepatic failure (FHF) requiring liver transplantation. Five weeks prior to admission, a 57-year-old female with HIV infection had been switched to a nevirapine-based regimen of highly active antiretroviral therapy (HAART) with a CD4 cell count of 695/mm(3). Examination of the explanted native liver at initial transplantation revealed massive hepatic necrosis consistent with drug-induced liver injury. Primary graft nonfunction complicated the early postoperative course and liver retransplantation was required. On follow-up 2 years later, she remains in good health with an undetectable viral load on an efavirenz-based regimen of HAART. To our knowledge, this is the first report of successful liver transplantation following SJS and FHF.
American Journal of Transplantation 07/2010; 10(7):1713-6. · 6.39 Impact Factor
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ABSTRACT: Thrombocytopenia typically resolves with resolution of portal hypertension after liver transplantation (LT) but persists in some patients. Identifying risk factors associated with persistent post- LT thrombocytopenia may provide important information about its pathogenesis.
Cirrhotic adults with platelet levels of <150,000 mu/L at the time of LT and followed at least 1 year were studied. A retrospective analysis of lab values, radiologic spleen index (SI), and donor data using nonparametric methods was performed to characterize patients having persistent thrombocytopenia, defined as persistently low platelet levels at 3 and 12 months after LT.
One hundred patients were studied: mean age 55 y (range 23-75 y); platelet count at LT 62,000/microL (range 14,000- 148,000/microL; mean total bilirubin 2.6 mg/dL; mean Mayo end-stage liver disease score 29; SI 1,476 (range 347-4,843 mL; normal 120-480 mL). Platelet count at 3 and 12 months after LT correlated with SI (r = -0.41 and -0.54; P < .001). Fifty-seven patients had persistent thrombocytopenia. Compared with patients whose platelet levels normalized by month 3 or 12, they had higher SI and lower platelet count before LT (P < .001). The SI and platelet levels at the time of LT were independent predictive factors for platelet levels at 3 and 12 months after LT (P < .001).
High SI and low platelet count at the time of LT are associated with persistent thrombocytopenia after LT. They are also independent predictive factors of platelet levels at 3 and 12 months after LT. This suggests that patients may have persistent thrombocytopenia after LT owing to persistence of some degree of hypersplenism and incomplete resolution of splenomegaly.
Transplantation Proceedings 06/2010; 42(5):1769-73. · 1.00 Impact Factor
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ABSTRACT: Perisinusoidal hepatic stellate cells (HSC) are the principal fibrogenic cells in the liver. In animal models, HSC apoptosis is the predominant clearance mechanism of activated HSC, although data evaluating whether the same processes occur in humans are limited. We conducted a cross-sectional study to evaluate the association between HSC apoptosis and fibrosis stage in subjects with chronic hepatitis C virus (HCV) infection (n = 44) and HCV-negative controls with normal liver histology (n = 9). We used immunohistochemical techniques to identify activated (alpha-smooth muscle actin+), proliferative (Ki-67+) and apoptotic (terminal deoxynucleotidyl transferase [TdT]-mediated dUTP nick end-labelling+) HSC in liver biopsy specimens from all subjects. The same pathologist enumerated positive cells per high-power field (HPF, x 200) in 20 periportal/lobular areas. HSC apoptosis was decreased in HCV-positive subjects compared with controls (median 0.4, range 0.0-3.1 vs 1.1, 0.2-3.5 cells/HPF, P = 0.02). Among HCV-positive subjects, HSC apoptosis was decreased in those with moderate to advanced fibrosis (P = 0.04) compared with those with mild fibrosis. By multivariate analysis, HSC apoptosis decreased by an average of 0.14 cells/HPF (95% confidence interval 0.01-0.28 cells/HPF) per increase in fibrosis stage (P = 0.04). While the number of activated and proliferative HSC was significantly increased in HCV-infected subjects compared with that in uninfected controls, the numbers of these cells did not differ between HCV-infected subjects with mild vs moderate/advanced fibrosis. In conclusion, the number of apoptotic HSC was significantly decreased in HCV-infected subjects with advanced fibrosis. In chronic HCV infection, inhibition of HSC apoptosis may be one mechanism by which fibrosis progresses.
Journal of Viral Hepatitis 11/2008; 16(2):141-8. · 4.09 Impact Factor
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ABSTRACT: Infrequently, hepatitis C (HCV) appears to be the cause of hepatic granulomas. Interferon therapy for HCV has been increasingly associated with the development of sarcoidosis.
We sought to determine the incidence of hepatic granulomas in patients with recurrent HCV post liver transplantation (LT).
Between 1994 and 2005, 820 patients were transplanted for HCV at our institution. The pathology database was searched for patients having recurrent HCV and granulomas. At Mount Sinai Medical Center, protocol biopsies have been performed for the last 2 years in patients receiving pegylated interferon-alpha2b and ribavirin (PEG) for recurrent HCV. Review of slides from explanted livers, pre- and post-perfusion biopsies, and all allograft biopsies were evaluated. Lipogranulomas were excluded because of their frequent association with steatosis.
A total of 10,225 liver biopsies were performed on HCV patients, and 25 (0.24%) showed non-caseating epithelioid granulomas. Hepatic granulomas were detected in 14 post-LT HCV patients; 9 patients received PEG. Typically, only 1 lobular granuloma was found. None of these patients had granulomas in the native liver or in any biopsy before interferon therapy; 6/9 patients had undetectable HCV-RNA levels, and 4 had sustained viral response. No other cause for granuloma formation was identified in the 6 patients.
Hepatic granulomas are infrequently found in HCV liver biopsies and rarely found in post-LT biopsies with recurrent HCV. When present, they occur more commonly in patients receiving and virologically responding to PEG therapy. The presence of granulomas in patients with HCV being treated with PEG may not warrant an extensive etiologic work-up for granulomatous hepatitis unless otherwise clinically indicated.
Transplant Infectious Disease 07/2008; 10(3):184-9. · 2.22 Impact Factor
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ABSTRACT: Quantitation of connective tissue versus parenchymal tissue compartments is important in assessment of fibrosis (scarring) and its progression in liver disease. This paper presents a two-step algorithm for quantifying fibrosis in liver biopsies stained with Sirius red. With this staining technique, collagen and cell nuclei appear similarly stained, whereas cytoplasm appears pale. The first step of the algorithm is to separate similarly stained areas occupied by collagen and hepatocyte nuclei. Since the total area of the combined collagen and cell nuclei is usually much smaller than the remaining liver parenchyma, a non-linear intensity mapping is applied to enhance the smaller cluster in order to match the larger one in both intensity and size. The second step is to differentiate the fibrotic areas usually having irregular shapes from hepatocyte nuclei that have relatively uniform size and have circular shape. The proposed algorithm has been applied to quantify the development of progressive fibrosis and its possible regression in liver biopsy specimens from patients with parenteral-induced liver injury undergoing intestinal transplantation.
Journal of Microscopy 07/2008; 231(Pt 1):70-80. · 1.63 Impact Factor
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ABSTRACT: Although epidemiologic studies have documented that hepatitis C virus (HCV)/human immunodeficiency virus (HIV) co-infected patients have accelerated fibrogenesis, especially those with CD4+ cell counts <200 cells/mm(3), the pathogenic mechanisms are poorly understood. We investigated whether severe immunodeficiency in co-infection is associated with changes in intrahepatic inflammatory cytokine mRNA levels. We measured interferon (IFN)-gamma, tumour necrosis factor-alpha, transforming growth factor (TGF)-beta(1), interleukin (IL)-4, IL-10, IL-12p35 and IL-12p40 mRNA levels by real-time PCR performed on liver samples from HCV mono-infected (n = 19) and HCV/HIV co-infected (n = 24) patients. Co-infected patients had decreased intrahepatic mRNA levels of IFN-gamma (P = 0.09), IL-4 (P = 0.05) and IL-12p35 (P = 0.04) compared with mono-infected patients, while IL-10 was increased (P = 0.07). In co-infected patients, IFN-gamma mRNA levels increased linearly with increasing peripheral CD4+ cell counts by 1.23 times relative to the calibrator for every 100 CD4+ cells/mm(3) increase (P = 0.02). No other cytokines were significantly associated with CD4+ cell counts. In conclusion, HIV-induced lymphopenia may result in hepatic inflammatory cytokine suppression in HCV/HIV co-infection. Intrahepatic IFN-gamma levels are significantly reduced in patients with advanced immunodeficiency. Further studies are needed to assess whether decreased IFN-gamma secretion by HCV-specific CD4+ cells may account for accelerated fibrogenesis in these patients.
Journal of Viral Hepatitis 05/2008; 15(5):331-8. · 4.09 Impact Factor
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ABSTRACT: Primary nonfunction (PNF) after liver transplantation is fatal without timely retransplantation. PNF has been associated with many risk factors, but the etiology remains unknown in most cases. Using electron microscopy, we examined the hepatic ultrastructure of donor allografts in patients experiencing PNF and compared the findings with a well-matched group of other donor allografts.
Archival paraffin-embedded pre- and post-reperfusion donor liver biopsies were examined by electron microscopy in 10 patients with PNF and in 10 controls, matched by donor age +/- 5 years, gender, cold ischemic time +/- 1 hour, and donor cause of death. Mitochondria, endoplasmic reticulum, sinusoidal endothelial cells, and the glycogen content of the cells were assessed. The donors' serum peak transaminases, bilirubin and sodium levels, as well as the recipient age and serum creatinine were compared.
There were no significant differences in recipient age at the time of transplantation, peak recipient serum creatinine, donor peak serum transaminase, sodium or bilirubin levels. In all cases, the endoplasmic reticulum and sinusoidal endothelial cells were ultrastructurally normal. Hepatocytes had variable degrees of glycogen pooling. Hepatic steatosis and intramitochondrial inclusions cells were present in 5/10 PNF compared to 0/10 controls patients on preperfusion liver biopsy (P = .17).
Liver allografts from patients suffering from PNF can have mitochondrial ultrastructural changes on preperfusion biopsies.
Transplantation Proceedings 01/2006; 37(10):4339-42. · 1.00 Impact Factor
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ABSTRACT: A 55-year-old Turkish man with a history of chronic hepatitis B for 35 years, presented with incapacitating fatigue and worsening shortness of breath. He was hospitalized several times because of hepatic encephalopathy. He underwent liver transplantation for a clinical diagnosis of Child's C cirrhosis complicated by hepatopulmonary syndrome. The explanted liver, however, was not cirrhotic and demonstrated features of hepatoportal sclerosis. Although treatment for hepatoportal sclerosis is relief of portal hypertension; in rare cases such as in this patient with liver failure, liver transplantation is indicated.
Seminars in Liver Disease 02/2000; 20(3):391-5. · 7.05 Impact Factor
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ABSTRACT: Increased levels of hepatic iron may impair the response of patients with chronic hepatitis C to treatment with interferon-alfa, but combination therapy with ribavirin has demonstrated efficacy in the treatment of hepatitis C. When used alone or with interferon-alfa, ribavirin may cause a dose-dependent reversible hemolytic anemia. We compared the extent and cellular localization of iron deposition in liver tissue from biopsy specimens obtained before and after 36 weeks of therapy with ribavirin or placebo for 59 patients with chronic hepatitis C. Paired slides were available for review from 26 ribavirin and 27 placebo recipients. Iron deposition was assessed using coded slides stained with Perls Prussian blue and was semi-quantitated in hepatocytes, Kupffer cells, and areas of fibrosis. The overall iron score fell by 0.96 in the placebo group and increased 1.69 in the ribavirin recipients. Iron was deposited mainly in hepatocytes; the hepatocyte iron score increased from 2.19 to 3.81 in the ribavirin group. The amount of iron staining in Kupffer cells declined in the placebo group and increased slightly in the ribavirin group. Iron changes in areas of fibrosis were minor and did not differ between groups. Increased total hepatic iron deposition occurred during a 9-month course of ribavirin. Ribavirin-associated hemolysis deposits iron preferentially in hepatocytes. This increased deposition of hepatic iron does not seem to affect the biochemical or histologic response to ribavirin therapy but may have implications for hepatocyte susceptibility to future injury.
American Journal of Clinical Pathology 02/2000; 113(1):35-9. · 2.60 Impact Factor
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ABSTRACT: Recurrent diseases in liver allografts are not uncommon. These occur most frequently in those transplanted for viral hepatitis B and C. We report an unusual case of recurrent process in two consecutive liver allografts received by a 37-year-old woman, who previously had an unremarkable past medical history but developed a rapidly progressive cholestatic liver failure. Histopathologic examination of the native liver showed fibroocclusive lesions of both terminal hepatic venules and portal vein branches. The exuberant fibroobliterative process created dense fibrosis with whorled appearance, and broad fibrous septa connecting adjacent central areas, and sometimes bridging portal to central areas. Dense portal fibrosis resulted in compression atrophy and loss of bile ducts. The first allograft, which failed within 3 months, showed histopathologic findings similar to that of the native liver. A liver biopsy that was performed 20 months after the second liver transplant again showed similar histopathology. The histopathologic features and clinical presentation of this patient suggest an unusual form of recurring progressive fibroobliterative venopathy causing liver failure.
American Journal of Surgical Pathology 07/1999; 23(6):734-7. · 4.35 Impact Factor
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ABSTRACT: Epidemiological studies have detected up to a 9% incidence of hepatitis G (HGV)-RNA in patients with acute and chronic liver disease of unknown etiology. We sought to clarify the role of HGV as a causative agent in cryptogenic cirrhosis by analyzing archival liver tissue for HGV-RNA in patients undergoing orthotopic liver transplantation.
Using a computer database, we identified 54 patients who underwent orthotopic liver transplantation for cryptogenic cirrhosis. After using rigorous serologic and histopathologic screening guidelines, 20 patients were studied, 7 of whom had concurrent hepatocellular carcinoma (HCC). RNA was extracted from archival paraffin-embedded liver tissue; HGV sequences were amplified by nested reverse transcription-polymerase chain reaction using primers designed from the 5' noncoding region.
HGV-RNA was absent from all 20 liver specimens, including those 7 with HCC. Beta-actin RNA, used as a positive control for cellular RNA, was isolated from all 20 liver specimens, including the 7 with HCC.
Utilizing a highly sensitive reverse transcription-polymerase chain reaction assay for HGV-RNA, we were unable to detect HGV-RNA within the livers of patients with cryptogenic cirrhosis or in the HCC arising within them. This lends further evidence to HGV infection not being a cause of cryptogenic cirrhosis and not being associated with the development of HCC in cryptogenic cirrhosis.
Transplantation 05/1999; 67(8):1193-7. · 4.00 Impact Factor
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M I Fiel,
T D Schiano,
H C Bodenheimer,
S N Thung,
T W King,
C R Varma,
C M Miller,
E M Brunt,
S Starnes,
C Prass,
R K Wolff,
B R Bacon
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ABSTRACT: A candidate gene, HFE, was recently described in patients with hereditary hemochromatosis (HH) and found to contain a missense mutation leading to a cysteine to tyrosine substitution (C282Y). A second mutation, H63D, was also found in the gene. This study was undertaken to determine the HFE genotype in liver transplant recipients clinically diagnosed with HH and those incidentally found to have increased iron deposition in their explanted livers and to evaluate whether biochemical or histological hepatic iron indices (HIIs) correlated with homozygosity for the C282Y mutation. We identified 15 patients clinically diagnosed with various liver disorders other than HH who had increased liver iron deposits among 918 adult patients who underwent liver transplantation from 1988 to 1995. Four additional patients were clinically diagnosed as having HH. Archival explant liver tissue was evaluated for the histological HII according to the method of Deugnier et al, in which an index greater than 0.15 suggests homozygosity for HH. The HII was computed according to established methods, with a value greater than 1.9 suggesting homozygosity for HH. A portion of liver tissue was subjected to DNA genotyping using polymerase chain reaction-amplified products. Two of 4 patients with clinically suspected HH were homozygous for C282Y, and 2 patients had neither mutation. One of the 15 patients not suspected to have HH was a C282Y homozygote, 1 was a C282Y heterozygote, 6 were H63D heterozygotes, and 7 had neither mutation. The histological HII was consistent with HH in 13 patients, whereas the HII was consistent with HH in 6 patients. Thus, in patients with end-stage liver disease, despite fulfilling the established clinical criteria for HH using biochemical and histological parameters, only a minority of patients were homozygous for the C282Y mutation. Hepatic iron overload may result from other causes, and in end-stage liver disease, an elevated HII may not accurately predict HH. Other factors that either control or lead to iron absorption may explain iron overload in these patients.
Liver transplantation and surgery: official publication of the American Association for the Study of Liver Diseases and the International Liver Transplantation Society 02/1999; 5(1):50-6.
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ABSTRACT: A case of epithelioid hemangioendothelioma of the liver in a 34-year-old man with clinical and radiologic findings suggestive of Budd-Chiari syndrome is reported. Despite clinical and radiologic findings, percutaneous liver biopsy was suspicious for epithelioid hemangioendothelioma. The patient underwent liver transplantation 2 months later, and histologic examination confirmed this diagnosis. Unusual histopathologic features included extensive areas of capillary-thin vascular structures with open lumina, lack of significant cytologic atypia in the majority of neoplastic cells, and areas with Budd-Chiari-like features in the hepatic parenchyma surrounding the tumor. The neoplastic cells were focally immunopositive for endothelial markers, such as factor VIII-related antigen and CD34 antigen. The unusual clinical presentation may have been due to tumor invasion and fibrous obliteration of terminal hepatic venules and sublobular veins. Epithelioid hemangioendothelioma should be considered when evaluating patients with clinical features of Budd-Chiari syndrome or veno-occlusive disease.
Archives of pathology & laboratory medicine 10/1998; 122(9):846-8. · 2.58 Impact Factor
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ABSTRACT: Recent studies have demonstrated that telomerase, a reverse transcriptase linked to cellular "immortalization," is activated in a variety of malignant human tumors. This study was conducted to determine whether telomerase activity represents a marker of malignant transformation in precancerous (dysplastic) nodules arising in patients with cirrhosis.
Telomerase activity was evaluated in frozen tissue samples of 14 cirrhotic liver specimens and 30 large nodular lesions contained therein, including 13 large regenerative nodules/low grade dysplastic nodules, 10 high grade dysplastic nodules, and 7 hepatocellular carcinomas (HCCs). A modified telomeric repeat amplification protocol was used.
There was a clear-cut difference in telomerase activity levels between HCC (positive or strongly positive) and cirrhotic liver samples (weakly positive or negative). The majority of large noncancerous nodules (86%) exhibited telomerase activity levels similar to HCCs. However, such activity was not limited to dysplastic lesions but also was detected in some large regenerative nodules.
These findings suggest that telomerase activation is an early event in large nodule formation in cirrhosis, which may facilitate the action of other factors in the process of carcinogenesis. Telomerase activity in large hepatic nodules is not always indicative of malignant transformation.
Cancer 06/1998; 82(10):1831-8. · 4.77 Impact Factor
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ABSTRACT: When Caroli's disease, defined as a congenital dilation and ectasia of segmental intrahepatic bile ducts in the absence of other histological abnormalities, is associated with periportal fibrosis, it is termed Caroli's syndrome. We describe the case of a 35-yr-old woman with Caroli's syndrome without clinical manifestation of portal hypertension despite diffuse involvement of the liver who was successfully treated with orthotopic liver transplantation after recurrent nearly fatal episodes of cholangitis.
The American Journal of Gastroenterology 11/1997; 92(10):1938-40. · 7.28 Impact Factor
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ABSTRACT: The safety of transplanting livers with moderate to severe microvesicular steatosis is unknown. Livers that appear fatty are often abandoned at the donor hospital. We have recently used frozen-section biopsy to distinguish between microvesicular and macrovesicular steatosis. We present here our single-center experience with transplantation of 40 allografts with moderate or severe microvesicular steatosis.
We reviewed our data on 426 transplants and identified 40 cases in which the donor liver contained at least 30% microvesicular steatosis. Early graft function, patient and graft survival, and donor risk factors for steatosis were examined, and results in this cohort were compared with results in all other patients who received liver transplants at our center during the same time period. We also analyzed the reliability of donor frozen-section biopsies in quantitating microsteatosis. Persistence of steatosis was assessed on the basis of 1-year follow-up biopsies.
The incidence of primary nonfunction and poor early graft function was 5% and 10%, respectively. One-year patient and graft survival rates were 80% and 72.5%, respectively. Donor obesity and traumatic death were commonly identified risk factors for microvesicular steatosis. Frozen-section biopsy was reliable for pretransplant decision-making about the use of potential grafts, and the steatosis had disappeared from the graft at 1 year in the majority of cases.
Livers with even severe microvesicular steatosis can be reliably used for transplantation without the fear of high rates of primary nonfunction. There was a significant incidence of poor early graft function, but this did not affect outcome. Microsteatosis is usually associated with some underlying risk factor in the donor and is reversible, as demonstrated by follow-up biopsies after transplant.
Transplantation 08/1997; 64(2):248-51. · 4.00 Impact Factor
