"Plasma Cell Hepatitis" in Liver Allografts: Identification and Characterization of an IgG4-Rich Cohort
Identifieur interne : 000468 ( France/Analysis ); précédent : 000467; suivant : 000469"Plasma Cell Hepatitis" in Liver Allografts: Identification and Characterization of an IgG4-Rich Cohort
Auteurs : M. Castillo-Rama [États-Unis] ; M. Sebagh [France] ; E. Sasatomi [États-Unis] ; P. Randhawa [États-Unis] ; K. Isse [États-Unis] ; A. D. Salgarkar [États-Unis] ; K. Ruppert [États-Unis] ; A. Humar [États-Unis] ; A. J. Demetris [États-Unis]Source :
- American journal of transplantation : (Print) [ 1600-6135 ] ; 2013.
Descripteurs français
- Pascal (Inist)
- Wicri :
- topic : Santé publique.
English descriptors
- KwdEn :
Abstract
Plasma cell hepatitis (PCH), also known as "de novo autoimmune" hepatitis, is an increasingly recognized, but suboptimally named and poorly understood, category of late allograft dysfunction strongly resembling autoimmune hepatitis (AIH): They share plasma-cell-rich necro-inflammatory activity on biopsy, auto-antibodies and steroid responsiveness, but overlap with rejection is problematic. A retrospective study of clinical, serological, histopathological and lgG4 immunohistological features of PCH (n = 20) in liver allograft recipients, native liver AIH (n = 19) and plasma-cell-rich renal allograft rejection (n = 20) showed: (1) high frequency (44%) of HLA-DR15; (2) less female predominance (p = 0.03) and (3) n = 9/20 PCH recipients showed >25 IgG4+ plasma cells/high-power field (lgG4+ PCH) versus AIH (n = 1/19, p = 0.008) or plasma-cell-rich kidney rejection (n = 2/20, p = 0.03). The IgG4+ PCH (n = 9) subgroup showed lower alanine transaminase (ALT) (p < 0.01) and aspartate transaminase (AST) (p < 0.05) at index biopsy but (a) higher plasma cell number/percentage, (b) more aggressive-appearing portal/periportal and perivenular necro-inflammatory activity and (c) more severe portal/periportal fibrosis than IgG4- PCH (n = 11). Significant demographic, histopathologic and plasma cell phenotype differences between PCH and AIH suggest distinct pathogenic mechanisms for at least the IgG4+ PCH subgroup likely representing an overlap between allo- and auto-immunity. IgG4+ PCH was associated with fibrosis, but also highly responsive to increased immunosuppression.
Affiliations:
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Pascal:14-0006714Le document en format XML
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<term>Homotransplantation</term>
<term>Identification</term>
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<term>Caractérisation</term>
<term>IgG4</term>
<term>Immunoglobuline</term>
<term>Etude cohorte</term>
<term>Santé publique</term>
<term>Fibrose</term>
<term>Stéroïde</term>
<term>Immunodépresseur</term>
<term>Corticostéroïde</term>
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<front><div type="abstract" xml:lang="en">Plasma cell hepatitis (PCH), also known as "de novo autoimmune" hepatitis, is an increasingly recognized, but suboptimally named and poorly understood, category of late allograft dysfunction strongly resembling autoimmune hepatitis (AIH): They share plasma-cell-rich necro-inflammatory activity on biopsy, auto-antibodies and steroid responsiveness, but overlap with rejection is problematic. A retrospective study of clinical, serological, histopathological and lgG4 immunohistological features of PCH (n = 20) in liver allograft recipients, native liver AIH (n = 19) and plasma-cell-rich renal allograft rejection (n = 20) showed: (1) high frequency (44%) of HLA-DR15; (2) less female predominance (p = 0.03) and (3) n = 9/20 PCH recipients showed >25 IgG4+ plasma cells/high-power field (lgG4+ PCH) versus AIH (n = 1/19, p = 0.008) or plasma-cell-rich kidney rejection (n = 2/20, p = 0.03). The IgG4+ PCH (n = 9) subgroup showed lower alanine transaminase (ALT) (p < 0.01) and aspartate transaminase (AST) (p < 0.05) at index biopsy but (a) higher plasma cell number/percentage, (b) more aggressive-appearing portal/periportal and perivenular necro-inflammatory activity and (c) more severe portal/periportal fibrosis than IgG4- PCH (n = 11). Significant demographic, histopathologic and plasma cell phenotype differences between PCH and AIH suggest distinct pathogenic mechanisms for at least the IgG4+ PCH subgroup likely representing an overlap between allo- and auto-immunity. IgG4+ PCH was associated with fibrosis, but also highly responsive to increased immunosuppression.</div>
</front>
</TEI>
<affiliations><list><country><li>France</li>
<li>États-Unis</li>
</country>
<region><li>Pennsylvanie</li>
</region>
<settlement><li>Pittsburgh</li>
</settlement>
<orgName><li>Université de Pittsburgh</li>
</orgName>
</list>
<tree><country name="États-Unis"><noRegion><name sortKey="Castillo Rama, M" sort="Castillo Rama, M" uniqKey="Castillo Rama M" first="M." last="Castillo-Rama">M. Castillo-Rama</name>
</noRegion>
<name sortKey="Castillo Rama, M" sort="Castillo Rama, M" uniqKey="Castillo Rama M" first="M." last="Castillo-Rama">M. Castillo-Rama</name>
<name sortKey="Demetris, A J" sort="Demetris, A J" uniqKey="Demetris A" first="A. J." last="Demetris">A. J. Demetris</name>
<name sortKey="Demetris, A J" sort="Demetris, A J" uniqKey="Demetris A" first="A. J." last="Demetris">A. J. Demetris</name>
<name sortKey="Humar, A" sort="Humar, A" uniqKey="Humar A" first="A." last="Humar">A. Humar</name>
<name sortKey="Isse, K" sort="Isse, K" uniqKey="Isse K" first="K." last="Isse">K. Isse</name>
<name sortKey="Isse, K" sort="Isse, K" uniqKey="Isse K" first="K." last="Isse">K. Isse</name>
<name sortKey="Randhawa, P" sort="Randhawa, P" uniqKey="Randhawa P" first="P." last="Randhawa">P. Randhawa</name>
<name sortKey="Ruppert, K" sort="Ruppert, K" uniqKey="Ruppert K" first="K." last="Ruppert">K. Ruppert</name>
<name sortKey="Salgarkar, A D" sort="Salgarkar, A D" uniqKey="Salgarkar A" first="A. D." last="Salgarkar">A. D. Salgarkar</name>
<name sortKey="Sasatomi, E" sort="Sasatomi, E" uniqKey="Sasatomi E" first="E." last="Sasatomi">E. Sasatomi</name>
<name sortKey="Sasatomi, E" sort="Sasatomi, E" uniqKey="Sasatomi E" first="E." last="Sasatomi">E. Sasatomi</name>
</country>
<country name="France"><noRegion><name sortKey="Sebagh, M" sort="Sebagh, M" uniqKey="Sebagh M" first="M." last="Sebagh">M. Sebagh</name>
</noRegion>
</country>
</tree>
</affiliations>
</record>
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