Augmentation of Graft-Versus-Host Reaction by Cytomegalovirus Infection Resulting in Interstitial Pneumonitis

Grundy, Jane E.; Shanley, John D.; Shearer, Gene M.

doi:10.1097/00007890-198505000-00018

Cited by 98 publications

(44 citation statements)

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“…The mouse model shows that a host immune response is required for CMVinduced pneumonitis (Shanley, Pesante & Nugent, 1982;Grundy, Shanley & Shearer, 1985) and that the syndrome can be prevented by continued immunosuppression. All of the clinical findings in human allograft patients are consistent with these data so we have hypothesized elsewhere that CMV pneumonitis in allograft patients is an immunopathological condition while in AIDS patients lung infection may be asymptomatic or may cause disease through extensive cell lysis (Grundy, Shanley & Griffiths, 1987).…”

Section: Pneumonitismentioning

confidence: 99%

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The status of CMV as a human pathogen

Griffiths

Grundy

1988

Epidemiol. Infect.

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Cytomegalovirus (CMV) is a common infectious agent which is well adapted to its host. Following primary infection, which is almost always asymptomatic in people with normal immunity, the virus establishes latency at sites which are unknown. The virus is probably maintained in this latent state by immune surveillance mechanisms since immunosuppression frequently leads to reactivation of virus.Cytomegalovirus has been identified in most anatomical areas of the human body. The aim of this article is to define criteria for pathogenicity so that clinical and experimental data can be reviewed to determine if CMV is likely to cause disease at these various clinical sites. Thus, patients have been shown to die frequentlywithCMV but do they diefromit?

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Section: Pneumonitismentioning

confidence: 99%

“…However, it is not clear whether CMV triggers GVHD or whether the profoundly immunosuppressive effect of GVHD (and that of its treatment) are responsible for CMV reactivation. In the mouse model, CMV has been shown to accentuate the GVH reaction (Grundy, Shanley & Shearer, 1985).…”

Section: Allograft Effectsmentioning

confidence: 99%

The status of CMV as a human pathogen

Griffiths

Grundy

1988

Epidemiol. Infect.

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“…Radiation injury may also predispose to the development of a local graft-i;erj«5-host reaction which might be responsible for the high mortahty seen with pulmonary infections in BMT patients. This is supported by experiments in the mouse which demonstrated that animals with GVHD infected with CMV develop a fatal infection, whereas CMV-infected, non-GVHD mice do not (Grundy et al, 1985). An excess of CD8+ cells has previously been demonstrated in the skin of patients with GVHD and a prolonged CD4+CD8+ imbalance in the pedpheral blood of patients who receive non-T-depleted marrow (Favrot et al, 1983).…”

Section: Discussionmentioning

confidence: 82%

Pneumonitis in bone marrow transplant recipients results from a local immune response

Milburn

Bois

Prentice

et al. 1990

Clinical and Experimental Immunology

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SUMMARYEighteen recipients of allogeneic T cell-depleted bone marrow who developed 22 episodes of interstitial pneumonitis were investigated by bronchoalveolar lavage for the cause of pneumonitis. The cells obtained were examined using a panel of monoclonal antibodies with immunocytochemical techniques to identify lymphocyte subsets and the presence of surface molecules indicative of lymphocyte activation. The majority of patients had an excess of lymphocytes in lavage and most of these cells were positively stained with the McAb recognizing the CD8 antigen (suppressor/cytotoxic type T cells). Although the proportions of CD4+ (helper type) T cells were below nonnal, the absolute numbers were within normal limits, thus the CD4:CD8 ratio was consistently 1:1 or less. A large proportion of the CD8+ cells displayed HLA-DR molecules (RFDRl+), interleukin-2 (IL-2) receptors (CD25+) and high concentration of CD7 antigen (RFT2+). Further analysis revealed that most CD8+ cells were CD5+ (RFTl +) yet a large proportion (20-40%) were CD5-. A majority of CD8+ cells was also CD38+ (RFT10+) and Leu7+. No clear correlation between the emergence ofa raised proportion ofaetivated CD8+ cells and diagnosed cytomegaiovirus infection was found. These results demonstrate, however, that cells with the phenotype of the resident T cells of the bronchial epithelium (CD8+CD5") emerge to the air spaces and express activation markers. This raises the intriguing paradox of an aggressive local immune response occurring in an otherwise immunosuppressed group of patients.

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“…HLAmismatch, increasing recipient age, female donors for male patients, type of GVHD prevention, CMV positivity and others are established risk factors for the development of GVHD. 8 With the exception of interferon-␣, 9 drugs have never been described as triggering substances in the development of GVHD.…”

Section: Resultsmentioning

confidence: 99%

Contrast media triggering cutaneous graft-versus-host disease

Vavricka

Furrer

Wolfensberger

et al. 2002

Bone Marrow Transplant

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Summary:Adverse reactions to iodinated contrast media are varied and known to develop in patients with asthma and a history of allergy. We describe three successful allogeneic bone marrow transplantation (BMT) patients, who all developed dermal graft-versus-host disease (GVHD) after receiving contrast media. Cutaneous GVHD triggered by contrast media has not been reported to date and has implications for the assessment, monitoring and treatment of patients during the post-transplant period. Bone Marrow Transplantation (2002) 29, 899-901. DOI: 10.1038/sj/bmt/1703564 Keywords: bone marrow transplantation; graft-versushost disease; contrast media Graft-versus-host disease (GVHD) is a singularly important threat to the successful outcome of allogeneic stem cell transplantation and prevention and treatment of GVHD are of critical importance for transplant physicians and patients. Prophylactic use of cyclosporin A (CsA) and methotrexate (Mtx) successfully reduces the incidence of acute GVHD. Some studies suggest a reduction in chronic GVHD with prolonged CsA prophylaxis. [1][2][3] Additional studies have shown, that random red cell transfusions given shortly before transplantation may be associated with a decreased risk of chronic GVHD, whereas unirradiated donor buffy coat or marrow reinfusions are associated with an increased risk for development of chronic GVHD. 4,5 Splenectomy appeared to increase the risk for development of chronic GVHD, possibly due to increased rates of infection in splenectomized patients. 6 As another possibility, which could be of prophylactic importance, we report three allogeneic BMT patients who experienced contrast mediainduced cutaneous GVHD. Case reports Case 1A 49-year-old patient underwent allogeneic BMT from his HLA-identical brother for AML M4 in first CR. He received GVHD prophylaxis with CsA beginning with 10 mg/kg/day, adjusted to provide serum levels of 150-250 g/l, Mtx (15 mg/m 2 on day 1 and 10 mg/m 2 on days 3, 6 and 11), and IvIgG (0.5 g/kg/week). No serious complications occurred and rapid engraftment was achieved. Pre-existing pulmonary aspergillosis was treated with intravenous amphotericin B. Acute GVHD occurred on day +43 (grade 2, skin) without other organ involvement. The skin rash settled after 4 months. Six months after BMT the patient was still receiving CsA (5 mg/kg/day p.o.). Computed thoracoabdominal tomography was performed for evaluation of the aspergillosis infection. As contrast medium, 120 ml of iodixanolum 550 mg (Visapaque 270) was used. Six hours after application of the contrast medium, the patient developed generalized erythroderma with a pruritic and painful skin rash. Therapy with prednisone 50 mg p.o. and cetirizin 10 mg p.o. was begun. The initial changes were limited to the more superficial skin layers, with formation of new lichen planus-like papules and scaling erythematous plaques involving facial skin, palms and soles. These findings were associated with dryness of mouth and conjunctivae. A skin biopsy showed chronic GVHD with typical epide...

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Augmentation of Graft-Versus-Host Reaction by Cytomegalovirus Infection Resulting in Interstitial Pneumonitis

Cited by 98 publications

References 0 publications

The status of CMV as a human pathogen

The status of CMV as a human pathogen

Pneumonitis in bone marrow transplant recipients results from a local immune response

Contrast media triggering cutaneous graft-versus-host disease

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