scholarly journals Seronegative fibrosing cholestatic hepatitis С after liver retransplantation for unresectable neuroendocrine tumor liver metastases

Author(s):  
S. E. Voskanyan ◽  
V. E. Syutkin ◽  
M. V. Shabalin ◽  
A. I. Artemyev ◽  
I. Yu. Kolyshev ◽  
...  

We present an uncommon case of liver graft dysfunction caused by seronegative hepatitis C-related fibrosing cholestatic hepatitis after cadaver liver transplantation for unresectable liver metastases of neuroendocrine small intestine cancer followed by living relation donor liver fragment retransplantation for primary graft nonfunction. Early postoperative period was complicated by hepatic artery thrombosis, cerebral hemorrhage, acute cellular rejection, bilateral polysegmental pneumonia, bleeding into neck soft tissues, severe surgical site infection, and sepsis. Anticoagulant therapy, as well as the absence of Hepatitis C Virus antibodies made difficult early diagnostics of fibrosing cholestatic hepatitis. A present-day antiviral therapy produced a complete clinical and virological response. At control examination performed at 240 days after surgery, there were neither signs of cancer progression no graft dysfunction. Liver transplantation in that case was an example of radical and effective treatment method for unresectable liver metastases of neuroendocrine small intestine cancer. Timely diagnosis and proper treatment of fibrosing cholestatic hepatitis made it possible to save the liver graft and patient's life.

2021 ◽  
Vol 14 (5) ◽  
pp. 1491-1495
Author(s):  
Peilin Li ◽  
Masaaki Hidaka ◽  
Yu Huang ◽  
Takanobu Hara ◽  
Kantoku Nagakawa ◽  
...  

AbstractGraft calcification after liver transplantation (LT) has seldom been reported, but almost of all previously reported cases have been attributed to graft dysfunction. We herein report two cases of graft calcification without liver dysfunction after living donor liver transplantation (LDLT). Two patients who underwent LDLT were found to have graft calcification in the early postoperative period (< 1 month). Calcification in the first case was found at the cut edge of the liver at post-operative day (POD) 10, showing a time-dependent increase in calcification severity. The second patient underwent hepatic artery re-anastomosis due to hepatic artery thrombosis on POD4 and received balloon-occluded retrograde transvenous obliteration of the splenic kidney shunt due to decreased portal vein blood flow on POD6. She was found to have diffuse hepatic calcification in the distant hepatic artery area at 1-month post-operation followed by gradual graft calcification at the resection margin at 6-month post-operation. Neither case showed post-operative graft dysfunction. Calcification of the liver graft after LDLT is likely rare, and graft calcification does not seem to affect the short-term liver function in LDLT cases. We recommend strictly controlling the warm/cold ischemia time and reducing the physical damage to the donor specimen as well as monitoring for early calcification by computed tomography.


2015 ◽  
Vol 13 (11) ◽  
pp. 1993-2001.e2 ◽  
Author(s):  
Vincent Leroy ◽  
Jérôme Dumortier ◽  
Audrey Coilly ◽  
Mylène Sebagh ◽  
Claire Fougerou-Leurent ◽  
...  

2000 ◽  
Vol 32 (7) ◽  
pp. 2103 ◽  
Author(s):  
A.R.N Rao ◽  
A.K.K Chui ◽  
L.W Shi ◽  
L Tsai ◽  
C.D Leon ◽  
...  

2012 ◽  
Vol 2012 ◽  
pp. 1-6 ◽  
Author(s):  
Consolato Sergi ◽  
Reem Abdualmjid ◽  
Yasser Abuetabh

Liver transplantation has been a successful therapy for liver failure. However, a significant number of recipients suffer from graft dysfunction. Considerably, ischemia and reperfusion (I/R) injury is the most important factor leading to organ dysfunction, although the pathogenesis has not been fully described. I/R injury have several established features that are accompanied by and/or linked to bile duct loss or ductopenia, cholestasis, and biliary ductular proliferations in the posttransplant liver biopsy. However, biliary marker levels increase usually only 5–7 days after transplantation. Intermediate filaments are one of the three cytoskeletal proteins that have a major role in liver protection and maintaining both cellular structure and integrity of eukaryotic cells. We reviewed the canine liver transplantation model as I/R injury model to delineate the intermediate filaments of the cytoskeleton that are probably the determinants in changing the phenotype of hepatocytes to cholangiocytes. Remarkably, this interesting feature seems to occur earlier than frank cholestasis. We speculate that I/R liver injury through a phenotypical switch of the hepatocytes may contribute to the poor outcome of the liver graft.


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