Graft-versus-host disease in lung transplantation: 4 case reports and literature review

Luckraz, Heyman; Zagolin, Mónica; McNeil, Keith; Wallwork, J.

doi:10.1016/s1053-2498(02)00811-2

Cited by 27 publications

(18 citation statements)

References 24 publications

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“…Recently, the documentation of GvHD by FISH and HLA typing has been reported [4,15,16]. In our case, chimerism analysis was based on amplification of the different STR loci and the gender marker amelogenin, whereas initial interphase FISH analysis of retained BM biopsy was, interestingly, not able to confirm the existence of donor cells.…”

Section: Discussionmentioning

confidence: 75%

Catastrophic graft-versus-host disease after lung transplantation proven by PCR-based chimerism analysis

Worel

Bojic

Binder

et al. 2008

Transplant International

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Summary Acute graft‐versus‐host disease (GvHD) is a rare complication after solid organ transplantation. We describe a 52‐year‐old female developing neutropenia and fever 48 days after single lung transplantation for chronic obstructive pulmonary disease. Bone marrow (BM) biopsy suggested drug‐induced marrow failure, so immunosuppression was reduced. Five days later a maculopapular skin rash was observed, progressing to a generalized erythema with desquamation. Skin biopsy was suspectable for GvHD, so immunosuppression was re‐initiated. PCR‐based chimerism analysis of BM revealed 78% donor cells. Intensified immunosuppression resulted in temporary improvement, but BM aplasia recurred and the patient experienced severe GvHD of gut and liver. Despite extensive immunosuppression the patient died from multi‐organ failure 99 days after transplantation. This report describes the occurrence of neutropenia as an early presenting sign of acute GvHD after lung transplantation. We therefore recommend incorporating GvHD in the differential diagnosis of neutropenia after solid organ transplantation, calling for early chimerism analyses.

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Section: Discussionmentioning

confidence: 75%

Catastrophic graft-versus-host disease after lung transplantation proven by PCR-based chimerism analysis

Worel

Bojic

Binder

et al. 2008

Transplant International

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“…A diagnosis of GVHD was favored over the suspicion of incidental, concomitant aplastic anemia because of the typical multiorgan stigmata of the former (fever, skin rash, liver dysfunction) and the demonstration of significant donor macrochimerism. Cases such as this are rarely reported [14][15][16][17][18] as acute GVHD tends to occur more commonly following transplantation of liver, small bowel, or marrow. The incidence of GVHD after liver transplantation is approximately 1 percent 19 whereas it may reach 50 percent with bone marrow transplantation (BMT).…”

Section: Discussionmentioning

confidence: 99%

Lung transplantation complicated by graft‐versus‐host disease and confounded by incidental transfusion‐associated macrochimerism

et al. 2008

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This case demonstrates SOT-GVHD, with the unusual feature of concomitant macrochimerism from transfusions. SOT-GVHD likely predisposed this patient to the observed transfusion-associated macrochimerism. However, the dissociation between transfusion-attributable macrochimerism and attributable pathology is intriguing. Furthermore, the risk spectrum of transfusion-associated macrochimerism and TA-GVHD in solid organ transplant recipients with and without the complication of SOT-GVHD is unknown and warrants further study.

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“…After blood perfusion has been re-established in the transplanted lung, immune cells from the recipient colonise the graft and start to replace the donor immune cells. Although a few cases of graft versus host disease have been described in association with lung transplantation [23], in the majority of transplanted patients, the donor lymphocytes disappear from the BAL fluid within three months, and the donor alveolar macrophages disappear from the BAL fluid within 6 months of transplantation [24]. This is either due to apoptosis or due to the deleterious effect of the recipient immune response to the allograft.…”

Section: Discussionmentioning

confidence: 99%

Recurrent sarcoid granulomas in a transplanted lung derive from recipient immune cells: Fig. 1—

Milman¹,

Andersen²,

Burton³

et al. 2005

Eur Respir J

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From 1992From -2004, single lung transplantation has been performed in seven patients with end-stage pulmonary sarcoidosis at the Danish National Centre for Lung Transplantation. The objective was to assess whether recurrent sarcoid granulomas in the lung graft are derived from recipient or donor immune cells.Three patients had sarcoid recurrence in the lung graft, but none had clinically overt extrathoracic sarcoidosis. Graft sex-mismatch was present in one patient, a 52-yr-old female having a lung graft from a male donor. In order to discriminate between recipient and donor cells fluorescence in situ hybridisation (FISH), using probes for both X-and Y-chromosomes, was applied on transbronchial lung biopsies (TBB) from the lung graft containing sarcoid granulomas.The recipient's explanted lung contained multiple active sarcoid granulomas. TBB from the implanted donor lung 5 months after transplantation showed sarcoid granulomas. FISH showed that the immune cells in the granulomas were X-chromosome positive and Y-chromosome negative and, therefore, were derived from the recipient.In conclusion, the results indicate that recurrent sarcoid granulomas in the transplanted lung are derived from recipient's immune cells, having colonised the lung allograft.

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Graft-versus-host disease in lung transplantation: 4 case reports and literature review

Cited by 27 publications

References 24 publications

Catastrophic graft-versus-host disease after lung transplantation proven by PCR-based chimerism analysis

Catastrophic graft-versus-host disease after lung transplantation proven by PCR-based chimerism analysis

Lung transplantation complicated by graft‐versus‐host disease and confounded by incidental transfusion‐associated macrochimerism

Recurrent sarcoid granulomas in a transplanted lung derive from recipient immune cells: Fig. 1—

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