Entity

Time filter

Source Type

Los Angeles, CA, United States

Peng Y.,University of California at Los Angeles | Cai J.,Terasaki Research Institute | Yue C.,University of California at Los Angeles | Qing X.,University of California at Los Angeles
Experimental and Molecular Pathology | Year: 2016

Primary hepatic peripheral T-cell lymphoma (PTCL) is exceedingly rare. We encountered such a case in a 58-year-old Hispanic female with a history of chronic sinusitis and hypothyroidism who presented with 4 weeks of fever and weight loss. Laboratory studies showed altered liver function and mild pancytopenia. Hepatitis and HIV infection were excluded by negative serological tests. A computed tomography (CT) scan showed innumerable small low-density lesions throughout the liver without splenomegaly or lymphadenopathy. CT-guided liver core biopsy showed scattered small lymphoid aggregates located mainly in the portal tracts and periportal regions. Within the lymphoid aggregates, scattered large pleomorphic lymphoma cells were seen, admixed with smaller lymphoid cells and histiocytes. By immunohistochemistry, the lymphoma cells expressed CD2, CD3, CD8, CD30, CD43, CD45, granzyme B, TIA-1, and negative for CD4, CD5, CD7, CD56, βF1, ALK-1, and B-cell markers. In situ hybridization for Epstein-Barr virus-encoded RNA (EBER) was positive in some lymphoma cells. To our knowledge, this is the first reported case of primary hepatic Epstein-Barr virus-associated PTCL with CD30 expression. © 2016. Source


Peng Y.,University of California at Los Angeles | Qing A.C.,Terasaki Research Institute | Cai J.,Terasaki Research Institute | Yue C.,University of California at Los Angeles | And 2 more authors.
Experimental and Molecular Pathology | Year: 2016

Background: Liver is an organ that could either be involved by widespread lymphoma or rarely as a primary site of lymphoma. Although secondary involvement of liver by lymphoma is relatively common, primary hepatic lymphoma (PHL) represents only about 0.016% of all cases of non-Hodgkin lymphoma. Understanding the clinicopathological features of hepatic lymphoma would direct appropriate treatment and patient management. Methods: We did a retrospective cohort study of 19 patients with liver biopsy-proven lymphoma, either as part of a systemic lymphoma or as a primary lesion, who were evaluated and treated at Harbor-UCLA Medical Center between 2004 and 2014. Results: The 19 cases were divided into two groups. Nine of them showing systemic involvement including not only liver but also spleen and/or lymph nodes were grouped together. The other 10 cases which showed confined liver lesions without involvement of other lymphoid structures were grouped in the PHL group. Clinical features of the two groups were compared. Our study demonstrated that PHL most commonly affected middle-aged individuals (median age: 50 years), with a male-to-female ratio of about 2.3 to 1. The most frequent presenting symptom was right upper quadrant pain. In contrast, the group with systemic lymphoma involving liver most commonly affected younger patients (median age: 40 years), with a male-to-female ratio of about 8 to 1, and with abdominal pain as well as fever/chills as the most common presenting symptoms. The tumor burden at the presentation as suggested by serum lactate dehydrogenase (LDH) level was statistically significantly lower in the PHL group compared to the systemic group in this study (p< 0.05). Viral infections were found in both groups, and we did not observe a clear association of any particular viral infection with PHL. Diffuse large B-cell lymphoma was identified as the major type of primary hepatic lymphoma (of 10 cases). Finally, the prognosis in the PHL group demonstrated by the duration of follow-up (average follow up: 50 months) was statistically significantly better than that in the systemic group (average follow up: 5.5 months), p < 0.01. Conclusion: Patients with PHL showed different clinicopathological features from those with widespread lymphoma involving liver. The outcome of the patients with PHL appeared much more favorable than that of the patients with liver involvement by systemic lymphoma in this study. © 2016. Source


Cai J.,Terasaki Research Institute | Terasaki P.I.,Terasaki Research Institute | Zhu D.,Fudan University | Lachmann N.,Charite - Medical University of Berlin | And 3 more authors.
Experimental and Molecular Pathology | Year: 2016

Background: We have found antibodies against denatured HLA class I antigens in the serum of allograft recipients which were not significantly associated with graft failure. It is unknown whether transplant recipients also have denatured HLA class II and MICA antibodies. The effects of denatured HLA class I, class II, and MICA antibodies on long-term graft outcome were further investigated based on their ability to fix complement c1q. Materials and methods: In this 4-year retrospective cohort study, post-transplant sera from 975 kidney transplant recipients were tested for antibodies against denatured HLA/MICA antigens and these antibodies were further classified based on their ability to fix c1q. Results: Thirty percent of patients had antibodies against denatured HLA class I, II, or MICA antigens. Among them, 8.5% and 21.5% of all patients had c1q-fixing and non c1q-fixing antibodies respectively. There was no significant difference on graft survival between patients with or without antibodies against denatured HLA/MICA. However, when these antibodies were further classified according to their ability to fix c1q, patients with c1q-fixing antibodies had a significantly lower graft survival rate than patients without antibodies or patients with non c1q-fixing antibodies (p = 0.008). In 169 patients who lost renal grafts, 44% of them had c1q-fixing antibodies against denatured HLA/MICA antigens, which was significantly higher than that in patients with functioning renal transplants (25%, p < 0.0001). C1q-fixing antibodies were more significantly associated with graft failure caused by AMR (72.73%) or mixed AMR/CMR (61.9%) as compared to failure due to CMR (35.3%) or other causes (39.2%) (p = 0.026). Conclusions: Transplant recipients had antibodies against denatured HLA class I, II, and MICA antigens. However, only c1q-fixing antibodies were associated with graft failure which was related to antibody mediated rejection. © 2015 Elsevier Inc. Source


Dieplinger G.,Terasaki Research Institute | Everly M.J.,Terasaki Research Institute | Briley K.P.,East Carolina University | Haisch C.E.,East Carolina University | And 7 more authors.
Transplant Infectious Disease | Year: 2015

Background: BK polyomavirus (BKPyV) viremia/nephropathy and reduction in immunosuppression following viremia may increase the risk of alloimmune activation and allograft rejection. This study investigates the impact of BKPyV viremia on de novo donor anti-human leukocyte antigen (HLA)-specific antibodies (dnDSA). Patients and methods: All primary renal transplants at East Carolina University from March 1999 to December 2010, with at least 1 post-transplant BKPyV viral load testing, were analyzed. Patients were negative for anti-HLA antibodies to donor antigens (tested via single antigen beads) at transplantation and at first BKPyV testing. Results: Nineteen of 174 patients (11%) tested positive for BKPyV viremia. Within 24 months of BKPyV viremia detection, 79% of BKPyV-viremic patients developed dnDSA. Only 20% of BKPyV viremia-persistent cases, compared to 86% of BKPyV viremia-resolved cases, developed dnDSA (P = 0.03). Poor allograft survival was evident in BKPyV viremia-persistent patients (60% failure by 2 years post BKPyV diagnosis) and in BKPyV viremia-resolved patients with dnDSA (5-year post BKPyV diagnosis allograft survival of 48%). Conclusions: Post-transplant BKPyV viremia and preemptive immunosuppression reduction is associated with high rates of dnDSA. When preemptively treating BKPyV viremia, dnDSA should be monitored to prevent allograft consequences. © 2015 Wiley Periodicals, Inc. Source

Discover hidden collaborations