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Query: UMLS:C0018133 (graft-versus-host disease)
 18,032 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report a patient with fatal hepatitis B virus (HBV) reactivation after treatment for chronic graft-versus-host disease (GVHD) following allogeneic peripheral blood stem cell transplantation to treat chronic myelogenous leukemia. The presence of antibodies to hepatitis B surface antigen (HBsAb) prior to transplantation indicated previous HBV infection. Liver damage first developed 8 months after transplantation with the disappearance of HBsAb. Hepatitis B antigen was first noted during an examination of liver damage that occurred 22 months after transplantation. Retrospective examination of serum by real-time detection polymerase chain reaction (RTD-PCR) revealed HBV in both the first and second episodes of liver damage (89 copies/mL and 2 x 10(6) copies/mL, respectively). HBV may have been reactivated, leading to fatal liver damage in this HBsAb-positive patient. We propose that RTD-PCR-based analysis should be performed to diagnose liver dysfunction after hematopoietic stem cell transplantation.
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PMID:Hepatitis B virus reactivation in a patient with chronic GVHD after allogeneic peripheral blood stem cell transplantation. 1172 74

We performed a retrospective survey in 62 hematopoietic cell transplantation (HCT) centers in Japan in which all HCTs performed between 1986 and 1998 were reviewed, and those involving hepatitis B virus surface antigen (HBsAg)-positive donors were identified. One hundred and thirty-five patients who underwent allogeneic HCT (alloHCT) were studied for complications related to hepatitis B virus (HBV) or hepatitis C virus (HCV). The median follow-up period was 24 months. Positivity for HBsAg was observed in 32 patients (24%) throughout the study. Twenty-six of the 32 patients were HBsAg carriers before alloHCT, whereas the remaining 6 became HBsAg(+) after alloHCT. Forty-two recipients were anti-HBs antibody (HBsAb)-positive, and 58 recipients (43%) were HCV Ab(+). Eleven of 26 (42%) HBsAg(+) recipients survived between >4 and >119 months. Six of 26 cases received transplants from HBsAg(+) donors, and, although they had not developed acute graft-versus-host disease, 4 of 6 died of hepatic and renal failure within 10 months after HCT. After transplantation, 5 patients showed serologic evidence of HBV reactivation, whereas 4 patients showed evidence of an immune response to HBV. Viral reactivation occurred during the tapering of the immunosuppressive agent. However, 3 of 5 were alive at the time of this report, suggesting that reactivation is not directly correlated with severe liver dysfunction. Seventeen patients (13%) of 135 recipients developed hepatic failure. Eight (47%) of 17 were diagnosed with fulminant hepatitis and 5 (29%) with veno-occlusive disease (VOD). VOD was observed in 12% of both HBsAg(+) and HCVAb(+) patients. In this study, the relatively high incidence of HBV events occurred after alloHCT, and, therefore, we should consider a protocol for active immunization of donors and recipients against HBV. Moreover, although the presence of HBV or HCV is not a contraindication for alloHCT, we recommend a careful follow-up of recipients after transplantation, especially during immunosuppression tapering.
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PMID:Retrospective study on the impact of hepatitis B and hepatitis C virus infection on hematopoietic stem cell transplantation in Japan. 1199 65

We conducted a retrospective study with the aim of identifying risk factors and clinical characteristics associated with HBV reactivation and clinical flare after allogeneic stem cell transplantation (aSCT). We reviewed the King Faisal Specialist Hospital and Research Center International Bone Marrow Transplant Registry database from January 1998 to June 2000. Complete serological screening for HBV was available in 128 of 131 patients transplanted during that period. Fifty-four (42%) had evidence of prior infection and recovery from HBV before transplant (hepatitis B core antibody positive, B surface antigen negative). Forty-two were evaluable for HBV reactivation and clinical flare. Six (14%) reactivated with clinical flare as documented by seroconversion and/or positive HBV DNA in the serum with biochemical hepatitis at 5.5, 18, 18, 19, 21 and 23 months post-transplant. Five of fifteen patients with chronic graft-versus-host disease (cGVHD) reactivated with clinical flare in contrast to 1/27 without cGVHD (RR: 9.0, 95% CI: 1.2-70.1 P < 0.02). HBV reactivation with clinical flare occurred during immunosuppressive therapy tapering or withdrawal in all patients. In conclusion, hepatitis B core antibody positive allogeneic stem cell recipients with cGVHD are at significant risk of HBV reactivation with clinical flare.
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PMID:Hepatitis B virus reactivation with clinical flare in allogeneic stem cell transplants with chronic graft-versus-host disease. 1218 38

We observed a 45-year-old man with acute hepatitis B while receiving treatment of chronic graft-versus-host disease (GVHD) of the liver. When he developed a sudden elevation of serum aminotransferases 17 months after bone marrow transplantation, he was under immunosuppressive therapy consisting of cyclosporin A against chronic GVHD of the liver. Serologic tests for hepatitis B virus (HBV) showed no reactivation but de novo acute infection. The serum levels of aminotransferases after elevation of biliary tract enzymes increased mildly. However, icterus was not observed in his sequential course. A liver biopsy specimen revealed mild acute liver injury accompanied by slight degeneration of bile ducts. It is presumed that owing to immunosuppressive therapy, his liver dysfunction was relatively mild, and the hepatitis became quiescent without becoming serious. On the other hand, the serum of the patient remained hepatitis B surface antigen positive for more than 1 year after the onset of the hepatitis, which suggested chronicity of HBV infection.
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PMID:Chronic graft-versus-host disease complicated by acute hepatitis B. 1254 5

Aging of T cells is characterized by a series of alterations in surface antigen expression and a concomitant decline in functional activity in many assays. We have extended this analysis by comparing the ability of T cells from mice of different ages to cause graft-versus-host disease (GVHD) by using a parent into F(1) model (C57BL/6 T cells into C57BL/6 x C3H host animals). Young (3-5 months), adult (12-14 months), or old (19-24 months) T cells were introduced into irradiated F(1) hosts. Animals that had undergone transplantation were assessed for clinical and pathologic evidence of GVHD and for survival. At a given T-cell dose (2 x 10(6) cells), there was a T-cell (donor) age-dependent decline in severity of GVHD, with all recipients of young T cells succumbing to lethal GVHD, 75% of recipients of adult T cells succumbing, and no deaths occurring among recipients of old T cells. In vivo CD4 T-cell expansion was greater for young than old T-cell groups after transplantation, whereas old CD8 cells showed enhanced in vivo expansion compared with young cells. Among CD4 and CD8 cells, the T-cell receptor repertoire, surface antigen expression on activated cells, and homing receptor function were similar for all ages after expansion in vivo. The progeny of old T cells reisolated after transplantation expressed type 1 cytokines (interferon-gamma and tumor necrosis factor-alpha) at a lower frequency than young cells and had decreased cytolytic function against H-2(k)-bearing target cells. This provides a partial explanation for the decreased GVHD. Carboxyfluorescein diacetate succinimidyl ester labeling of transplanted cells showed comparable rates of proliferation when comparing GVHD-competent (12 months) and GVHD-incompetent (19 months) T cells in both syngeneic and F(1) host animals. We suggest that the lack of effector activity demonstrated by old T cells in vivo is a reflection of a cell-autonomous defect downstream of signals required for antigen-driven proliferation.
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PMID:Increasing T-cell age reduces effector activity but preserves proliferative capacity in a murine allogeneic major histocompatibility complex-mismatched bone marrow transplant model. 1520 66

The appearance of hepatitis B surface antigen (HBsAg) in patients previously positive for antibody to this antigen (HBsAb) is called reverse seroconversion, a rare complication after hematopoietic stem cell transplantation (HSCT), which occurs almost exclusively after HSCT from an HBsAb-negative donor and the development of chronic graft-versus-host disease (CGVHD). However, we experienced a patient who developed reverse seroconversion 23 months after unrelated HSCT even in the absence of immunosuppressants use or CGVHD. Serum immunoglobulin level was persistently normal. Therefore, all HBsAb-positive recipients should be considered to be at risk for HBV reactivation, even in patients without any risk factors.
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PMID:Reverse seroconversion of hepatitis B virus after allogeneic hematopoietic stem cell transplantation in the absence of chronic graft-versus-host disease. 1929 17

Impact of hepatitis B virus (HBV) infection on haematopoietic stem cell transplantation (HSCT) was reported earlier since late 1980s. It was shown that changing patterns of HBV serological markers was accompanied by variable severity of hepatitis after transplantation. Recipient's hepatitis B virus surface antigen (HBsAg) positivity was not considered an absolute contra-indication to allogeneic HSCT. However, HBsAg positivity was an important risk factor of reactivation hepatitis after transplantation, especially in allogeneic setting. Managing HBV reactivation in HSCT recipients was not successful till the availability of lamivudine since mid-1990s. For HBsAg-positive recipients, prophylactic lamivudine has been shown to significantly reduce reactivation hepatitis. As for HBsAg-negative recipients, there have been a small number of patients who develop so-called reverse seroconversion, that is, appearance of HBsAg after transplantation. In addition to chronic graft-versus-host disease, the risk was also high in allogeneic HSCT recipients who received fludarabine-antithymocyte globulin-containing conditioning regimens. The HBV is harboured earlier in the recipients before transplantation rather than transmitted via transfusion. At present, the optimal duration of lamivudine prophylaxis is not well-defined, and there are several fatal cases associated with early withdrawal and resistant HBV mutants. In conclusion, in HBV-endemic areas, the war between HBV and HSCT recipients continued even though several anti-HBV agents and molecular detection techniques are available. It deserves additional effort to overcome and also presents a chance to elucidate underlying mechanisms of HBV immunity, which are not easily studied in non-HSCT setting.
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PMID:Hepatitis B infection in haematopoietic stem cell transplantation: still unresolved. 1949 97

We investigated the serological changes in hepatitis B virus (HBV)-related markers in 55 and 26 hepatitis B surface antigen (HBsAg)-negative patients undergoing allogeneic and autologous stem cell transplantation, respectively, over the past 4 yr. Five of the 17 allogeneic and one of the five autologous patients with pretransplant anti-hepatitis B core antigen antibodies (anti-HBc) were HBsAg-positive after transplantation, whereas none of the patients negative for anti-HBc were HBsAg-positive in both groups. All patients who became HBsAg-positive received steroid-containing immunosuppressive therapy for chronic graft versus host disease (GVHD) or myeloma. Four of the six patients developed flare of HBV hepatitis, and two patients did not. One patient developed fulminant hepatitis treated with lamivudine and plasma exchange. Other five patients received entecavir from the detection of HBsAg. Although HBV-DNA levels became below the limit of detection in all patients, HBsAg positivity remained in three patients after 6 months of treatment. We concluded that anti-HBc positivity is a risk factor for reactivation of HBV after both autologous and allogeneic transplantation, and HBV-related markers should be monitored regularly in these patients. We also stress the efficacy of pre-emptive use of antiviral agents in controlling HBV replication and limiting hepatic injury due to reactivation of HBV in these patients.
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PMID:High risk of hepatitis B-virus reactivation after hematopoietic cell transplantation in hepatitis B core antibody-positive patients. 1950 85

Reactivation of resolved hepatitis B virus (HBV) infection has been reported in allogeneic hematopoetic stem cell transplantation (HSCT) recipients, but its epidemiology is not well characterized. We performed a retrospective assessment of the timing and risk factors of HBV reactivation among patients with resolved HBV infection undergoing allogeneic HSCT between January 2000 and March 2008. HBV reactivation was defined as development of positive hepatitis B surface antigen after transplant. Among the 61 patients with resolved HBV infection before transplant (hepatitis B core antibody-positive, hepatitis B surface antigen-negative), 12 (19.7%) developed HBV reactivation. The cumulative probability of HBV reactivation 1, 2, and 4 years after transplant was 9.0%, 21.7%, and 42.9%, respectively. In a time-dependent Cox model, the adjusted hazard ratio (HR) of HBV reactivation for patients with pretransplant hepatitis B surface antibody levels <10 milli-international units per milliliter (mIU/mL) was 4.56 (95% confidence interval [CI] 1.23-16.9) compared to those with levels > or =10 mIU/mL; the adjusted HR among patients who developed extensive chronic graft-versus-host disease (cGVHD) was 7.21 (95% CI 1.25-41.5) compared to those who did not. HBV reactivation is a common late complication among allogeneic HSCT recipients with pretransplant resolved infection. Screening for HBV reactivation should be considered for at-risk HSCT recipients. In this cohort, HBV reactivation often developed in patients with cGVHD. Liver biopsy was useful in those patients with both to delineate the contribution of each to liver dysfunction.
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PMID:Hepatitis B virus reactivation following allogeneic hematopoietic stem cell transplantation. 1966 Jul 17

After transfusion, the presence of contaminating white blood cells (WBC) in blood components may result in either deleterious or positive immunological responses. We have previously reported that photodynamic treatment (PDT) with meso-substituted mono-phenyl-tri-(N-methyl-4-pyridyl)-porphyrin (Tri-P(4)) and red light can inactivate pathogens in red blood cell (RBC) products. The present study explored the effect of PDT on contaminating WBC in RBC products with varying hematocrit (Hct). After PDT, we evaluated adaptive and innate immunomodulation through allogeneic and mitogenic stimulation. PDT resulted in decreased T-cell proliferation which was more pronounced with lower Hct. Dark effect of porphyrin Tri-P(4) was remarkable on antigen-presenting cells affecting expression of co-stimulatory molecules CD80/CD86. Finally, cytokine profile after PDT revealed a mixed Th1/Th2 type response while surface antigen expression supported the development of alternatively activated macrophages (AAM phi or Type 2 macrophages) instead of dendritic cells. In conclusion, PDT with Tri-P(4) altered proliferation, allo-stimulation, cell surface antigen expression and cytokine profiles of the cells. These results suggest that PDT may be potentially useful in preventing transfusion-associated graft-versus-host disease and alloimmunization. It seems worthwhile to further explore PDT-induced immunomodulation to optimize conditions which may result in allo-tolerance by AAM phi.
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PMID:Impact of photodynamic treatment with meso-substituted porphyrin on the immunomodulatory capacity of white blood cell-containing red blood cell products. 1984 42


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