RAPID DEVELOPMENT OF HEPATOCELLULAR SIDEROSIS AFTER LIVER TRANSPLANTATION FOR NEONATAL HEMOCHROMATOSIS

1996 ◽  
Vol 62 (10) ◽  
pp. 1511-1513 ◽  
Author(s):  
Hiroto Egawa ◽  
William Berquist ◽  
Richard Garcia-Kennedy ◽  
Kenneth Cox ◽  
A. S. Knisely ◽  
...  
Gut ◽  
1998 ◽  
Vol 43 (1) ◽  
pp. 140-145 ◽  
Author(s):  
H Tang ◽  
R Boulton ◽  
B Gunson ◽  
S Hubscher ◽  
J Neuberger

Background—Uncertainty exists about the extent and consequences of a return to alcohol consumption after liver transplantation for alcoholic liver disease (ALD).Aims—To determine the prevalence and consequences of alcohol consumption in patients transplanted for ALD.Methods—A retrospective case controlled study of all patients transplanted for ALD at the Queen Elizabeth Hospital, Birmingham, between 1987 and 1996.Results—Seventy patients with ALD were transplanted, of which 59 survived more than three months; 56 were interviewed. Twenty eight had consumed some alcohol after transplantation; for the nine “heavy drinkers” (HD), the median time to resumption of alcohol intake was six months and for the 19 “moderate drinkers” (MD) it was eight months. There was no significant difference in episodes of acute rejection or compliance with medication between those who were abstinent, MD, or HD. Histological evidence of liver injury was common in ALD patients who had returned to drink. Mild fatty change was found in 1/11 biopsy specimens from abstinent patients but moderate to severe fatty change and ballooned hepatocytes were seen in 3/5 MD and 2/5 HD specimens. Two HD patients had early fibrosis. One HD patient has died of alcohol related complications.Conclusions—Moderate to heavy alcohol consumption occurs in patients transplanted for ALD. Patient recall of abstinence advice is unreliable, and patients return to alcohol mainly within the first year after liver transplantation. Return to alcohol consumption after liver transplantation is associated with rapid development of histological liver injury including fibrosis.


2002 ◽  
Vol 16 (10) ◽  
pp. 672-676 ◽  
Author(s):  
Geneviève Tessier ◽  
Edith Villeneuve ◽  
Jean-Pierre Villeneuve

BACKGROUND: Acute liver failure is a rare condition in which massive liver injury is associated with the rapid development of hepatic encephalopathy. Although viral hepatitis and drug-induced liver injury are the most common causes, no specific etiology is found in a substantial proportion of cases reported from Europe and the United States.AIM: To determine the etiology and outcome of patients with acute liver failure in the authors’ institution.PATIENTS AND METHODS: The charts of 81 consecutive patients admitted to Saint-Luc between 1991 and 1999 were reviewed.RESULTS: The etiology was viral in 27 cases (33.2%), toxic or drug-induced in 22 (27.2%), of unknown origin in 22 (27.2%) and due to various causes in 10 (12.3%) (autoimmune, vascular, cancer). Of the 81 patients, 16% survived without liver transplantation, and 84% died or underwent liver transplantation. Survival without liver transplantation differed according to the mode of presentation: the survival rate was 27% in patients with hyperacute liver failure, 7% in those with acute liver failure and 0% in those with subacute liver failure. Among the 38 patients who underwent liver transplantation, survival one year after transplantation was 71%. In the 30 patients who died without liver transplantation, the main causes of death were cerebral edema and sepsis.CONCLUSIONS: Acute liver failure is associated with a high mortality, and liver transplantation is the treatment of choice. In a significant proportion of cases, the etiology remains undetermined and is probably related to yet unidentified hepatotropic viruses.


2020 ◽  
Author(s):  
Veronica Mugarab Samedi ◽  
Michelle D Ryan ◽  
Essa Al Awad ◽  
Adel Elsharkawy

Abstract Background: Neonatal hemochromatosis (NH) is a rare condition that was the main reason for liver transplantation in infants. With the realization that NH results from the fetal complement-mediated liver injury, intravenous immunoglobulins (IVIG) were successfully introduced for the treatment. Case Presentation: We present two cases of NH from the same family to illustrate the role of antenatal treatment with IVIG in alleviation and possible prevention of this serious morbidity. Conclusion: A prenatal treatment and early postnatal administration of IVIG are effective ways to manage NH that help to reduce the severity of the symptoms, prevent liver failure and avoid the need for liver transplantation Keywords: Neonatal hemochromatosis, Intravenous immunoglobulin, prenatal treatment


1997 ◽  
Vol 112 (4) ◽  
pp. 1372-1375 ◽  
Author(s):  
C Combs ◽  
EM Brunt ◽  
H Solomon ◽  
BR Bacon ◽  
M Brantly ◽  
...  

2016 ◽  
Vol 19 (2) ◽  
pp. 147
Author(s):  
Shin Jie Choi ◽  
Jong Sub Choi ◽  
Peter Chun ◽  
Jung Kyung Yoo ◽  
Jin Soo Moon ◽  
...  

1989 ◽  
Vol 67 (20) ◽  
pp. 1061-1065 ◽  
Author(s):  
H. -U. Lautz ◽  
R. Müller ◽  
C. Wittekind ◽  
S. Mauz ◽  
H. Barg-Hock ◽  
...  

1999 ◽  
Vol 2 (4) ◽  
pp. 360-366 ◽  
Author(s):  
Maria Parizhskaya ◽  
Jorge Reyes ◽  
Ronald Jaffe

Two patients with hemophagocytic lymphohistiocytosis who presented with acute liver failure are reported. Both presented with fever, hepatosplenomegaly, markedly elevated liver function tests, abnormal coagulation profiles, and an increase in serum ferritin. Both infants were diagnosed with neonatal hemochromatosis based on a clinical picture of hepatic insufficiency with hyperferritinemia and were referred for liver transplantation. The first patient died of liver failure and septicemia before transplantation. Review of autopsy material revealed a hepatitis-like pattern and extensive infiltration of liver and other organs including bone marrow by histiocytes, some of which were hemophagocytic. The second patient underwent liver transplantation but died 44 days thereafter from progressive hemophagocytic lymphohistiocytosis. Examination of the resected liver demonstrated a hepatitis-like pattern, proliferation of histiocytes, and hemophagocytosis, and the bone marrow revealed hemophagocytic histiocytosis. Hemophagocytosis recurred in the allograft. Hepatic manifestations are common in hemophagocytic lymphohistiocytosis and overt hepatic failure may occur, but initial presentation as fulminant hepatic failure is not well recognized. Elevated serum ferritin can make the distinction from neonatal hemochromatosis and other forms of neonatal liver failure difficult. Hemophagocytic lymphohistiocytosis should be considered in the differential diagnosis of neonatal liver disease, especially when it is accompanied by cytopenias.


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