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)

'Spontaneous' blood mononuclear cell DNA synthesis was studied in 83 bone marrow transplantation (BMT) recipients and 58 controls. Prior to BMT, patients with chronic myeloid leukemia had increased DNA synthesis, which decreased dramatically after conditioning and transplantation. After engraftment, patients with syngeneic marrow or allogeneic marrow without graft-versus-host disease (GVHD) had increased DNA synthesis compared to healthy controls. However, patients with acute GVHD (AGVHD) had a significantly increased DNA synthesis compared to patients without GVHD (p less than 0.001). DNA synthesis increased with increasing grade of AGVHD. Among patients with severe AGVHD, recipients of HLA-mismatched marrow had higher lymphocyte DNA synthesis at diagnosis of GVHD and maximum values compared to HLA-matched siblings (p less than 0.05). At diagnosis of GVHD, patients who developed grades II-IV GVHD with progressive disease had higher DNA synthesis, 23.9 +/- 4.0 x 10(3) c.p.m. (mean +/- SE) compared to 11.1 +/- 2.7 x 10(3) c.p.m. in patients in whom GVHD resolved (p less than 0.02). DNA synthesis during GVHD was lower in sheep erythrocyte rosette-forming cells (E-RFC) compared to enriched non-E-RFC. Herpes simplex virus, cytomegalovirus, bacterial septicemia and chronic GVHD had no major effect on lymphocyte DNA synthesis in these patients.
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PMID:DNA synthesis in human blood mononuclear cells correlates with severity of acute graft-versus-host disease. 284 39

Logistic regression was used to analyze the influence of pretransplant herpesvirus antibodies, in both patients and donors, on the development of acute graft-versus-host disease in 111 consecutive HLA-identical bone marrow recipients. In bivariate analysis, recipient seropositivity for cytomegalovirus (P = 0.01), donor seropositivity for herpes simplex virus (P = 0.02), and low bone marrow cell dosage (P less than 0.05) were associated with a high incidence of grade II-IV acute GVHD. In multivariate analysis the P values were P less than 0.05 for a positive recipient CMV serology and P = 0.07 for a positive donor HSV serology. Positive serology for 1-2 herpes-viruses among recipients or donors both resulted in a 12% incidence of grade II-IV acute GVHD. Positive serology for 3-4 herpesviruses among patients or donors resulted in an incidence of 32% and 38% of acute GVHD, respectively (P less than 0.05). It is concluded that recipient and donor pretransplant herpesvirus immunity can be used to calculate the risk of moderate-to-severe acute GVHD.
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PMID:Pretransplant herpesvirus serology and acute graft-versus-host disease. 284 12

The influence of pretransplant herpes-virus antibodies in 126 marrow-graft recipients and their HLA-identical (A, B, C, DR) sibling donors on the incidence of grades II-IV acute graft-versus-host disease (GVHD) was studied in relation to previously reported risk factors for GVHD. Logistic regression procedures were used to control for confounding factors. Increasing donor age (odds ratio 3.7 per decade; p = 0.02) and donor seronegativity for Epstein-Barr virus (EBV; odds ratio 10.1; p = 0.005) were associated with a high incidence of GVHD. Total rather than selective gastrointestinal decontamination (odds ratio 0.1; p = 0.004), donor seronegativity for herpes simplex virus (HSV; odds ratio 0.1; p = 0.003), and recipient EBV-seronegativity (odds ratio 0.05; p = 0.002) were associated with a low incidence of GVHD. Pretransplant EBV and HSV serology may thus contribute substantially to the estimation of the risk for GVHD.
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PMID:Herpes-virus immunity and acute graft-versus-host disease. 288 Oct 39

This investigation uses different polyclonal activators of in vitro immunoglobulin production to elicit immunoregulatory profiles of B cells, T cells, T4 cells, and T8 cells from 25 recipients (13 with and 12 without chronic graft-v-host disease [GVHD] ) after HLA-identical marrow transplantation for aplastic anemia or hematologic malignancy. Pokeweed mitogen, Epstein-Barr virus, herpes simplex type 1 virus, and tetanus toxoid were used to induce immunoglobulin production as measured by a plaque assay. Multiple defects in the various lymphoid subsets were found in both groups of patients. There was defective b cell function, lack of T cell or T4 cell subset helper activity, and increased T cell, T4 cell, or T8 cell suppressor activity after stimulation with the various activators. Inconsistent B, T, T4, and T8 cell functions in the marrow graft recipients provide evidence for (a) different functional groups of cells within each subset responsive to different polyclonal activators; (b) a spectrum of immune capabilities within each phenotype lineage; (c) different patterns of immune reconstitution for each lymphocyte subset after marrow grafting; and (d) chronic GVHD altering recovery of in vitro functional responses to the different polyclonal activators.
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PMID:The regulation of immunoglobulin synthesis after HLA-identical bone marrow transplantation: VI. Differential rates of maturation of distinct functional groups within lymphoid subpopulations in patients after human marrow grafting. 298 45

Forty-two patients undergoing bone marrow transplantation were included in a randomised, double-blind and placebo controlled trial of prolonged acyclovir prophylaxis against infections with viruses of the herpes group. Twenty patients were allocated to receive acyclovir and 22 to receive placebo. Acyclovir or placebo was administered i.v. at a dose of 250 mg/m2 twice daily, starting 5 days before transplantation. At 5 weeks after transplantation, administration was changed to tablets, 400 mg three times daily (children less than 6 years, 200 mg three times daily) and continued until 6 months after transplantation. In the placebo group, 10 acute herpes simplex virus (HSV) infections occurred in 7 patients (5 HSV-1 and 2 HSV-2), and another patient repeatedly shed HSV in throat washings. Five patients developed herpes zoster. Among patients receiving acyclovir only one episode of HSV infection occurred and no herpes zoster. The difference in the number of infection episodes and the number of infected patients was strongly significant (p = 0.0002 and 0.0017, respectively). The only acyclovir patient who reactivated HSV was terminally ill, and it is highly likely that she did not absorb a sufficient amount of the orally administered drug to control infection. All HSV and varicella zoster virus (VZV) infections were reactivations, and 9 of 10 patients who developed HSV infections or shed virus had a pre-transplantation HSV IgG titer of greater than 10 000 (ELISA). Acyclovir had no effect on cytomegalovirus (CMV), time of engraftment, or graft versus host disease (GVHD). Apart from a possible allergic reaction (skin rash) to acyclovir tablets, no adverse reactions were seen during this long prophylaxis with acyclovir.
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PMID:Acyclovir prophylaxis in bone marrow transplant recipients. 300 28

The cases of 13 allogeneic marrow transplant recipients who had undergone laparotomy for manifestations of severe enteritis were reviewed to determine the causes of the severe intestinal disease and to assess the relation between clinical, histologic, and microbiologic findings. Laparotomies were performed a median of 63 days (range, 11 to 273 days) after transplantation for suspected peritonitis, intestinal obstruction, or bleeding. Intestinal tissue was available from small bowel resections in nine patients, intraoperative biopsies in one, and from autopsies in three patients who died shortly after laparotomy. Widespread small bowel ulceration was present in all 13 cases. Four causes of ulceration were identified: chemoradiation toxicity (n = 2), acute graft-versus-host disease (GVHD) (n = 5), opportunistic infections superimposed on either GVHD or toxicity from chemotherapy (n = 4), and Epstein-Barr virus-associated lymphoproliferative disorder (n = 2). Intestinal infections, unrecognized before laparotomy, were due to cytomegalovirus (CMV), herpes simplex virus (HSV), adenovirus, and Torulopsis glabrata. CMV- and HSV-infected cells, often lacking diagnostic inclusions, were identified in the intestine by in situ hybridization with biotinylated DNA probes. Eleven patients died in the perioperative period, and two died 452 and 558 days after surgery of complications of chronic GVHD. Poor outcomes were related to extensive intestinal involvement, which was commonly underestimated before surgery, failure to diagnose intestinal infections early, poor marrow function, impaired immunity, and refractoriness of severe GVHD.
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PMID:Diffuse intestinal ulceration after marrow transplantation: a clinicopathologic study of 13 patients. 301 41

The cellular immune response to herpesviruses was studied in 46 recipients of marrow grafts (23 autologous, 23 allogeneic). That study was performed in vitro by evaluating the degree of lymphocyte proliferative responses to herpes simplex virus (HSV), cytomegalovirus (CMV), and varicella zoster virus (VZV). No primary infections with any of those viruses were noted after bone marrow transplantation (BMT). The incidence of active infection in seropositive patients was significantly lower after autologous BMT than after allogeneic BMT (HSV, 2/22 vs. 11/22 patients, respectively, P = 0.007; CMV, 4/12 vs. 9/10 patients, respectively, P = 0.02; VZV, 3/23 vs. 11/23 patients, respectively, P = 0.02). After autologous BMT, the restoration of cellular immunity to the three viruses occurred at a clearly faster rate than after allogeneic BMT. That pattern may have contributed to the low incidence of active infections with those viruses after autologous BMT. Recipients of allogeneic marrow from donors with a positive lymphocyte proliferation test to HSV had a significantly increased incidence of active HSV infection post-BMT (8/9 patients) than those who received marrow from donors with a negative test (3/13 patients; P = 0.008). Acute or chronic graft-versus-host disease (GVHD) decreased the cellular immune response to the three herpes viruses, but not significantly. Our program of vaccinations with diphtheria and tetanus toxoids started in the fourth month post BMT. Chronic GVHD patients who were vaccinated had a clearly impaired cellular immune response to both toxoids as compared with those without chronic GVHD.
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PMID:Cellular immunity to vaccinations and herpesvirus infections after bone marrow transplantation. 301 33

We prospectively studied patients with enigmatic nausea and vomiting after allogeneic marrow transplantation to define the causes of this syndrome. Fifty consecutive episodes of persistent vomiting were investigated using physical examination and laboratory tests, endoscopic biopsies and brushings, and clinical follow-up for four weeks. Potential causes of vomiting were identified in 39 of the 50 cases (78%). Fifteen cases had gastrointestinal infections (mainly herpesviruses), 13 had unsuspected acute intestinal graft-versus-host disease (GVHD), 8 had intestinal infection plus acute GVHD, and 3 had other causes (subdural hematomas, bacteremia, and encephalitis). In the remaining 11 cases, no cause of vomiting was found. Endoscopy was necessary for diagnosis in 36 cases and required a combination of methods: routine histology, cytology, viral culture, and immunohistology using monoclonal antibodies to cytomegalovirus (CMV) and herpes simplex virus type 1. Patients with unexplained vomiting or intestinal GVHD had significant improvement of nausea and vomiting over the four-week observation period, but those with CMV did not (P = .01). We conclude that most allogeneic marrow transplant patients with enigmatic nausea and vomiting have gastrointestinal herpesvirus infections, acute GVHD, or both. Untreated CMV infections and persistent GVHD are associated with protracted vomiting in these patients.
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PMID:A prospective study of unexplained nausea and vomiting after marrow transplantation. 302 71

The interactions between humoral and cellular immunity to herpes simplex virus (HSV) in bone marrow donors, the occurrence of active HSV infections, and the development of grades II-IV acute graft-versus-host disease (GVHD) in their HLA-A,B,C,DR-identical sibling recipients were studied. The absence of IgG-class HSV antibodies in the marrow donors was associated with a low incidence of GVHD: 38 of 53 recipients (72%) of marrow from HSV-seropositive donors developed GVHD versus only two of 15 recipients (13%) with HSV-seronegative donors (p = 0.0004). The cellular immunity to HSV was studied in vitro by evaluating the degree of lymphocyte proliferative responses to that virus and was also significantly associated with GVHD: 30 of 43 recipients (70%) of marrow from donors with a positive test developed GVHD versus 10 of 25 recipients (40%) of marrow from donors with a negative test (p = 0.03). The previously reported risk for GVHD attributed to donor CMV antibodies increased the risk of GVHD due to donor HSV antibodies. Of 31 recipients of marrow from donors who were both HSV- and CMV-seropositive, 27 (85%) developed GVHD versus 11 of 22 recipients (50%) of marrow from HSV-seropositive but CMV-seronegative donors (p = 0.008).
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PMID:Marrow donor immunity to herpes simplex virus: association with acute graft-versus-host disease. 303 83

Bone marrow transplants experience severe immuno-deficiency as a consequence of pretransplant radiation and chemotherapy, transient granulocytopenia before marrow engraftment, and post-transplant prevention and treatment of graft-versus-host disease with immuno-suppressive agents. During periods of granulocytopenia, chemoprophylaxis with the oral fluorinated quinolones can prevent colonization and infection with gram-negative bacilli, is better tolerated than oral non-absorbable antibiotics or trimethoprim-sulfamethoxazole and is more cost-effective than laminar-air-flow isolation or prophylactic granulocyte transfusions. Antifungal prophylaxis with oral nystatin, ketoconazole or amphotericin B, however, has not been consistently effective; empiric intravenous amphotericin B therapy is still the most reliable way to prevent fatal fungal infections. Following marrow engraftment, cytomegalovirus infection and interstitial pneumonia can be prevented in cytomegalovirus-seronegative patients by the use of cytomegalovirus-seronegative blood products and cytomegalovirus immune globulin. In cytomegalovirus-seropositive patients, prophylactic DHPG (ganciclovir) is currently being evaluated in a controlled clinical trial. Herpes simplex and varicella-zoster infections can be treated effectively with intravenous acyclovir, but routine acyclovir prophylaxis is not cost-effective. Trimethoprim-sulfamethoxazole is used for prophylaxis of Pneumocystis carinii pneumonia and may be continued in patients with chronic graft-versus-host disease for prevention of late post-transplant bacterial infections.
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PMID:Prophylaxis of infection in bone marrow transplants. 312 17


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