Gene/Protein Disease Symptom Drug Enzyme Compound
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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)

Serum levels of interleukin-6 (IL-6), interleukin-8 (IL-8) and tumor necrosis factor (TNF)-alpha were frequently measured during the first 30 days after allogeneic bone marrow transplantation (BMT) in 84 consecutive adult patients. Major transplant-related complications (MTCs) occurred in 33% of cases and included veno-occlusive liver disease, idiopathic pneumonia syndrome, severe endothelial leakage syndrome and >grade II acute graft-versus-host disease. Compared with patients having minor complications, those with MTCs developed higher levels at times of maximal clinical signs (all cytokines, P<0.001), between days 0-5 post-BMT (IL-6 and IL-8, P<0.05) and days 6-10 (L-6, P<0.001; IL-8 and TNF, P<0.01) post-BMT. We could not discriminate patterns of cytokine release that were specific for any subtype of MTC. Higher levels of IL-8 during days 0-5 were associated (P=0.044) with early (<40 days) death. Multivariate analysis including patient and transplant characteristics as well as post-BMT levels of C-reactive protein showed that high average levels of one or more of the cytokines within the first 10 days post-BMT were independently associated with MTC (Odd's ratio: 2.3 [1.2-4.5], P=0.011). This study shows that systemic release of proinflammatory cytokines contributes to the development of MTC and provides a rationale for pre-emptive anti-inflammatory treatment in selected patients.
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PMID:Proinflammatory cytokines and their role in the development of major transplant-related complications in the early phase after allogeneic bone marrow transplantation. 1276 83

Antithymocyte globulin (ATG) is increasingly used in pre-allogeneic stem cell transplantation (allo-SCT) conditioning regimens to prevent graft rejection and graft-versus-host disease. However, ATG was also found to be associated with increased incidence of thrombosis during organ transplantation. In the present study, we tested the coagulation status of 21 patients with hematologic malignancies undergoing allo-SCT who received ATG-based (11 patients) or non-ATG-based (10) conditioning treatment. We assessed several thrombophilia markers as well as circulating total and endothelial microparticles (TMP/EMP) and soluble CD40 ligand (CD40L). No significant difference in the mean values of prothrombin time, partial thromboplastin time, fibrinogen, antithrombin, protein C, protein S, thrombin-antithrombin III complex, homocysteine levels, prevalence of genetic thrombophilia markers and levels of EMP, TMP or CD40L was observed between the ATG-treated and ATG-untreated patients, as well as before and after conditioning in each group separately. Platelet counts decreased significantly in ATG-treated patients; however, this decrease was not associated with clinical or laboratory evidence of disseminated intravascular coagulation. No patient developed thromboembolic event or veno-occlusive liver disease. Our results suggest that allo-SCT is not associated with increased hypercoagulability and addition of ATG to conditioning regimen has no significant procoagulant effect.
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PMID:Assessment of the coagulation profile in hemato-oncological patients receiving ATG-based conditioning treatment for allogeneic stem cell transplantation. 1524 31

We studied 228 consecutive stem cell transplant recipients, screened for reactivation of human herpesvirus-6 (HHV-6) in peripheral blood and other specimens as clinically indicated by means of qualitative polymerase chain reaction. Among them, 197 received an allograft and 31 autograft. Ninety-six of 228 patients (42.1%) showed HHV-6 reactivation in peripheral blood and 129 of 228 (56.6%) demonstrated HHV-6 in at least one of the specimens tested. 41.9% of patients were asymptomatic when HHV-6 was identified. Clinical features, noted when HHV-6 was detected, included interstitial or alveolar pneumonia, gastroduodenal and colorectal disease, bone marrow suppression and liver disease. However, based on clinical and histopathological criteria, HHV-6 was considered a causal agent in only a minority of patients, in particular, those suffering from bone marrow suppression (n = 11), gastroduodenitis (five), colitis (three), interstitial/alveolar pneumonia (five), skin rash (one), pericarditis (two) and encephalitis (one). HHV-6 reactivation was significantly associated with the occurrence of graft-versus-host disease [odds ratio (OR) 5.31], Epstein-Barr virus coinfection (OR 8.89) and unrelated donor transplantation (OR 5.67) indicating an increased stage of immunosuppression.
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PMID:Impact of human herpesvirus-6 after haematopoietic stem cell transplantation. 1560 51

Lymphocytic destructive cholangitis is a histological pattern associating bile duct intraepithelial lymphocytic infiltration and bile duct epithelial damage. Lymphocytic destructive cholangitis is an important diagnostic feature of primary biliary cirrhosis, but it can also be seen in primary sclerosing cholangitis, autoimmune hepatitis, the so-called overlap syndrome, acute or chronic viral hepatitis C, drug-induced hepatitis, and acute rejection or graft-versus-host disease in liver or bone marrow transplantation. In the present paper we report a case of acute hepatitis with lymphocytic destructive cholangitis on liver biopsy. Clinical and biological examinations showed that the patient had hepatitis E with no other cause of liver disease. Therefore, hepatitis E should be considered as a diagnostic possibility when liver biopsy shows acute hepatitis and lymphocytic destructive cholangitis. The mechanism of bile duct damage in hepatitis E remains unknown.
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PMID:Acute hepatitis E: a cause of lymphocytic destructive cholangitis. 1589 7

Therapy of acute graft-versus-host disease (GVHD) aims to selectively alter the graft- host interactions to foster antitumor effect and minimize antihost effects. The immunosuppression produced by the various therapies ranges from broad, nonselective effects to relatively narrow targeted impact. Despite advances in understanding the pathophysiology of GVHD, newer agents with more selective effects have not yet produced therapeutic advances. The newer targeted agents continue to produce a degree of immunosuppression in which infection and relapse of malignancy are all too common. High-dose systemic steroids remain, as they have for two decades, the initial treatment of choice. Patients failing to respond to steroids continue to represent a challenge, as no second-line therapy is clearly superior to the others. However, some of the new agents appear to be particularly effective in certain organs involved with acute GVHD. For those patients with steroid-refractory GVHD involving primarily the gut, we favor infliximab with concomitant antifungal therapy. For those with primarily skin or liver disease, we favor extracorporeal photochemotherapy.
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PMID:Treatment of Gastrointestinal Acute Graft-Versus-Host Disease. 1591 14

Liver disease is a well-known cause of early morbidity and mortality affecting 80% of patients receiving allogeneic bone-marrow transplantation (BMT). Drug toxicity, veno-occlusive disease (VOD), acute graft-versus-host disease (GVHD), and fungal, bacterial, and viral infections are the most frequent hepatic complications during this period. The aim of this retrospective study was to determine the prevalence and etiology of liver disease and its impact on mortality as well as to assess the predictive value of pre BMT hepatic biochemical tests on the subsequent occurrence of acute and/or chronic GVHD and patient mortality. Of a total of 236 patients who underwent allogeneic BMT, 82 were analysed. Liver dysfunction was found in 88%. The causes of liver disease were: acute GVHD, 40.2%; chronic GVHD, 15.9%; unknown, 9.8%; sepsis, 7.3%; hepatotoxicity, 6.1%; VOD, 3.7%; acute hepatitis and disease recurrence, 2.4%. The mortality rate was 37%. We found acute liver failure (ALF) in 10% of the deaths (8 patients). The causes of ALF in these cases were acute GVHD progression in 5, herpetic hepatitis in 1, disease recurrence in 1, and VOD in 1. The correlation coefficients indicating positive predictive values of pre BMT hepatic biochemical tests for the subsequent occurrence of acute GVHD, chronic GVHD, and mortality were 0.27, 0.14, and 0.43, respectively. There was no significant difference between patients with abnormal or normal pre BMT liver function tests in the frequency of acute and chronic GVHD or mortality.
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PMID:[Liver dysfunction in recipients of hematopoietic stem cells. Impact on mortality]. 1607 3

Chimerism and graft-versus-host disease (GVHD) pose significant risks to liver transplant patients. The risk of chimerism and GVHD is higher among cases of living-related liver transplant (LRLT). Donors homozygous at all HLA loci carry a higher risk for GVHD. Herein we present a case of LRLT. The recipient suffered from end-stage liver disease and received a right lobe graft from his son. After 8 months posttransplant, the patient developed profound bone marrow depression. The patient was negative for CMV, Brucella, HHV6, HHV8, HBV, HCV, and parvovirus. No skin or GI signs of GVHD were noted. The patient and donor were HLA typed by SSP. The donor was homozygous for all HLA loci while the patient shared the class II homozygosity and was class I heterozygous. Chimerism studies were prompted after noting that the neutrophil compartment of the patient was homozygous for all HLA loci. This initiated further studies of the PMN and lymphocytes by microsatellite analysis. A total 15 microsatellites were analyzed. The results suggest that the majority (75%) of the PMNs and 45% of the lymphocytes were of donor origin. The patient was treated with G-CSF; his WBC counts returned to normal. At 2.5 years posttransplant the patient had not developed GVHD, despite the large number of donor lymphocytes circulating in his bloodstream. The only complaint he had was severe arthritis, which was treated with steroids. It must be investigated whether this was the result of GVHD.
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PMID:Neutrophils and lymphoid chimerism after adult living-related liver transplantation from a homozygous donor. 1638 27

Viral hepatitis is the third most common cause of liver disease in allogeneic transplant recipients and causes significant morbidity and mortality. When treating patients with hematological malignancies, an emphasis should be placed on identification of patients at risk for viral hepatitis with appropriate screening. Initial screening serology should include anti-HCV, HBsAg, anti-HBs, and anti-HBc testing. When hepatitis B exposure has been documented, prophylaxis of viral reactivation for all HBsAg-positive patients with a nucleoside analogue should be implemented. HCV infection appears to have little short-term impact on survival after bone marrow transplantation, but is a risk factor for veno-occlusive disease (VOD) and graft-versus-host disease (GVHD). In the long-term survivor, HCV infection can lead to significant morbidity and mortality due to the development of cirrhosis, decompensation, and liver cancer. Since effective antiviral therapies are available for both hepatitis B and C, routine screening and selected intervention is recommended once reactivation and disease recurrence is documented. In this chapter we will highlight the mechanisms of virus reactivation, clinical manifestations, and management strategies to minimize acute and chronic morbidity in this population.
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PMID:Viral hepatitis: manifestations and management strategy. 1712 86

Liver injury is a common complication in allogeneic hematopoietic stem cell transplantation. Its major causes comprise graft-versus-host disease (GVHD), infection, and toxicities of preparative regimens and immunosuppressants; however, we have little information on liver injuries after reduced intensity cord blood transplantation (RICBT). We reviewed medical records of 104 recipients who underwent RICBT between March 2002 and May 2004 at Toranomon Hospital. Preparative regimen and GVHD prophylaxis comprised fludarabine/melphalan/total body irradiation and cyclosporine or tacrolimus. We assessed the etiology of liver injuries based on the clinical presentation, laboratory results, comorbid events, and imaging studies in 85 patients who achieved primary engraftment. The severity of liver dysfunction was assessed according to the National Cancer Institute Common Toxicity Criteria version 2.0. Hyperbilirubinemia was graded according to a report by Hogan et al (Blood. 2004;103:78-84). Moderate to very severe liver injuries were observed in 36 patients. Their causes included cholestatic liver disease (CLD) related to GVHD or sepsis (n = 15), GVHD (n = 7), cholangitis lenta (n = 5), and others (n = 9). Median onsets of CLD, GVHD, and cholangitis lenta were days 37, 40, and 22, respectively. Frequencies of grade 3-4 alanine aminotransferase elevation were comparable across the 3 types of hepatic injuries. Serum gamma-glutamil transpeptidase was not elevated in any patients with cholangitis lenta, whereas 27% and 40% of patients with CLD and GVHD, respectively, developed grade 3-4 gamma-glutamil transpeptidase elevation. Multivariate analysis identified 2 risk factors for hyperbilirubinemia; grade II-IV acute GVHD (relative risk, 2.23; 95% confidential interval, 1.11-4.47; P = .024) and blood stream infection (relative risk, 3.77; 95% confidential interval, 1.91-7.44; P = .00013). In conclusion, the present study has demonstrated that the hepatic injuries are significant problems after RICBT, and that GVHD and blood stream infection contribute to their pathogenesis.
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PMID:Hepatic injury following reduced intensity unrelated cord blood transplantation for adult patients with hematological diseases. 1716 12

Acute and chronic liver disease contributes significantly to morbidity and mortality following hematopoietic cell transplantation (HCT). The best prognostic indicator for the development of severe liver dysfunction is an early rise in liver function test results after HCT. The leading causes soon after HCT are acute graft-versus-host disease (GVHD), sinusoidal obstruction syndrome, drug and total parenteral nutrition hepatotoxicity, sepsis, and viral infection. Hepatic herpesvirus and fungal infections after HCT, though uncommon, can be life-threatening and warrant immediate diagnosis and treatment. Hepatitis B, hepatitis C virus, iron overload, and chronic GVHD are among the most common causes for chronic liver disease after HCT. Because treatments are directed at the underlying etiology of liver disease, prompt diagnosis by means of laboratory tests, hepatic imaging, and often liver biopsy is required after HCT.
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PMID:Hepatic complications of hematopoietic cell transplantation. 1733 79


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