Pathology of Liver Transplantation

Porter, K. A.

doi:10.1111/j.1600-065x.1969.tb00209.x

Cited by 40 publications

(28 citation statements)

References 23 publications

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“…Early in the history of liver transplantation, the main goal was to prolong survival by recognizing and preventing ACR. In 1969, Porter20 was the first to describe centrilobular necro‐inflammation in liver allografts as a manifestation of ACR in untreated animal models and in humans who were treated with azathioprine. Cyclosporine, a calcineurin inhibitor, became available in the early 1980s and revolutionized immunosuppressive therapy.…”

Section: Discussionmentioning

confidence: 99%

“…In 1991, Demetris et al27 showed in a rat model that the terminal hepatic venular region is a site of primary sensitization in rejection, in part because of its rich content of antigen presenting cells. To date, several groups have supported CP as an immune‐mediated process, and many have associated CP with adverse outcomes, such as graft loss and the development of ductopenic rejection 2–4, 11, 15, 16, 20, 23, 24, 28, 29. Although the Banff criteria for acute rejection19 considers CP to be a feature of severe ACR, many studies1–6 have shown that even isolated CP can be a manifestation of ACR in the early posttransplant period (assuming that other etiologies, such as a vascular insult, have been excluded).…”

Section: Discussionmentioning

confidence: 99%

“…Interestingly, in addition to being a component of ACR, CP has been found to be an important component of late allograft injury and dysfunction. Even though Porter20 first described centrilobular hepatocyte atrophy and centrilobular reticulin condensation and collapse as a repair mechanism following acute rejection, it has taken 3 decades to incorporate these findings into a classification scheme of chronic rejection 7. However, it is now generally accepted that isolated CP is also a characteristic feature of late‐onset ACR and/or early chronic rejection 6–9.…”

Section: Discussionmentioning

confidence: 99%

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The prevalence and natural history of untreated isolated central perivenulitis in adult allograft livers

et al. 2008

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Central perivenulitis (CP) in the allograft liver can be associated with portal-based acute cellular rejection and autoimmune hepatitis or can occur in isolation (isolated CP). Although several studies have demonstrated the significance of CP, the prevalence and natural history of untreated isolated CP have not been well studied. We examined 100 adult allograft liver recipients who had long-term follow-up, had routine protocol biopsies, and received no treatment for isolated CP. Isolated CP was identified in 28 (28%) patients. It occurred late at a mean of 658 days. Interestingly, patients with late isolated CP (defined as Ͼ3 months posttransplant) usually manifested only mildly to modestly elevated liver function tests. However, late isolated CP was associated with prior and subsequent allograft complications. Nearly all (94%) cases of late isolated CP occurred in patients who had early episodes of CP and/or acute cellular rejection. Of 13 patients who developed adverse outcomes in their allografts (zone 3 fibrosis in 10, de novo autoimmune hepatitis in 3, and ductopenia in 3), all experienced episodes of prior CP, and 12 (92%) had late CP; 1 patient required retransplant for chronic rejection, but all were alive within the last year. In summary, "transplant-associated" isolated CP occurs in 28% of adult patients, early CP is predictive of late CP, and late CP (often present as isolated CP) is associated with long-term liver injury in some patients.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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The prevalence and natural history of untreated isolated central perivenulitis in adult allograft livers

et al. 2008

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“…Early studies of liver allograft rejection were focused mainly on inflammatory changes occurring in portal tracts but also recognized the presence of inflammation involving hepatic venous endothelium and the surrounding liver parenchyma 18–22. The susceptibility of perivenular regions to immune‐mediated injury probably is related to these areas containing potent donor antigen‐presenting cells, which can trigger an alloimmune response 23.…”

Section: Possible Causes Of Perivenular Necrosis In the Liver Allograftmentioning

confidence: 99%

Questionable necessity to remove the submandibular gland in neck dissection

et al. 2011

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Saliva is of major importance in taste, speech, swallowing, and protection against dental caries. Neck dissection surgery and/or radiotherapy may impair the function of the submandibular glands. Over the years, there has been a trend toward more conservative approaches to neck dissection. Metastasis to the submandibular gland itself is extremely rare and if removal of the lymph nodes of sublevel IB is imperative, it seems feasible to preserve the submandibular gland, unless it is involved by direct tumor extension of the primary tumor or the adjacent metastatic lymph nodes. Clinical studies to validate this concept are needed.

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“…CPV (zone 3 inflammation surrounding the hepatic vein) with or without associated zone 3 necrosis is usually immunologically mediated, and mostly represents rejection in the context of liver transplantation 207 208 209 210 211. Besides AIH, other causes of perivenular necrosis and inflammation are much less likely 212…”

Section: De Novo Hepatitismentioning

confidence: 99%

Liver allograft pathology: approach to interpretation of needle biopsies with clinicopathological correlation

2009

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The spectrum of diseases encountered in post-transplant liver pathology biopsies is broad. In this review, these have been divided as belonging to one of three categories: (1) new-onset/de novo post-transplant abnormalities (early and late), (2) rejection, and (3) recurrence of original disease. The clinical and pathological features of the entities making up each category, with the relevant differential diagnosis and overlaps between and within these groups, are discussed and illustrated. Recurrent or de novo neoplasms make up a fourth category not included in this review. Early new-onset conditions are mostly related to surgical complications, donor factors and ischaemia to the graft. These include reperfusion/preservation injury, lipopeliosis, small-for-size-syndrome, biliary sludge syndrome and hepatic artery thrombosis. The various forms of rejection (cellular, chronic, antibody-mediated, and late atypical rejection) are detailed. Most chronic liver diseases can and do recur in the graft. They may display features that overlap with de novo conditions (eg, primary sclerosing cholangitis versus chronic rejection). As with most cases of allograft biopsy interpretation, accurate diagnosis rests with careful correlation of histological features with clinical, imaging and laboratory findings, and often comparison with previous sequential and follow-up biopsies. Late-onset new diseases include biliary strictures, idiopathic chronic hepatitis and de novo autoimmune hepatitis, among others. This review provides a practical approach to the interpretation of these challenging biopsies. Selected difficult scenarios or conundrums are identified and discussed in the relevant sections.

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Pathology of Liver Transplantation

Cited by 40 publications

References 23 publications

The prevalence and natural history of untreated isolated central perivenulitis in adult allograft livers

The prevalence and natural history of untreated isolated central perivenulitis in adult allograft livers

Questionable necessity to remove the submandibular gland in neck dissection

Liver allograft pathology: approach to interpretation of needle biopsies with clinicopathological correlation

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