Liver transplantation acute rejection
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mohammed Abdelwahed M.D[2]
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Liver trasnsplantation Microchapters |
Overview
Liver transplantation acute rejection
Early acute cellular rejection mostly occurs within 90 days. [9].
Risk factors for acute rejection [12-16]:
Recipient prothrombin time or bilirubin that remains steadily elevated
Donors older than 50 years
Donor pre-procurement acidosis
Cytomegalovirus genotype gB1 infection
Fewer human leukocyte antigen (HLA)-DR matches
Cold ischemia time greater than 15 hours
For risk of late rejection, low blood concentration of cyclosporine or tacrolimus. [17] [18].
Clinical presentation
- Fever, malaise, abdominal pain, and hepatosplenomegaly.
- None of these is specific for rejection.
- Acute cellular rejection is generally suspected based upon the development of hepatic biochemical test abnormalities: [19-21]
Serum aminotransferases
Alkaline phosphatase
Gamma-glutamyl transpeptidase
Bilirubin level
Hepatocyte derived microRNAs (HDmiRs, mir-122, miR-148a) have been evaluated as markers of acute cellular rejection. [32]
Liver biopsy
- Liver histology is the gold standard for the diagnosis of acute cellular rejection. [33]
- Presence of biliary strictures and biliary anastomosis with mixed inflammatory infiltrate in the portal triad is sign of rejection. [34]
- Nonsuppurative cholangitis is important for the prognosis of rejection. The affected ducts are surrounded by immunocytes, which may also be found between epithelial cells, inside the basement membrane, or even in the lumen.
Histologic rejection activity index for liver transplants
| Category | Criteria | Score |
| Portal inflammation | –– | 1 |
| Expansion of most of all of the triads, by a mixed infiltrate containing lymphocytes with occasional blasts, neutrophils and eosinophils | 2 | |
| Marked expansion of most or all of the triads by a mixed infiltrate containing numerous blasts and eosinophils with inflammatory spillover into the periportal parenchyma | 3 | |
| Bile duct inflammation damage | A minority of the ducts are cuffed and infiltrated by inflammatory cells and show only mild reactive changes such as increased nuclear:cytoplasmic ratio of the epithelial cells | 1 |
| Most or all of the ducts infiltrated by inflammatory cells. More than an occasional duct shows degenerative changes such as nuclear pleomorphism, disordered polarity and cytoplasmic vacuolization of the epithelium | 2 | |
| As above for 2, with most or all of the ducts showing degenerative changes or focal lumenal disruption | 3 | |
| Venous endothelial inflammation | Subendothelial lymphocytic infiltration involving some, but not a majority of the portal and/or hepatic venules | 1 |
| Subendothelial lymphocytic infiltration involving some, but not a majority of the portal and/or hepatic venules | 2 | |
| As above for 2, with moderate or severe perivenular inflammation that extends into the perivenular parenchyma and is associated with perivenular hepatocyte necrosis | 3 |