Diffuse alveolar hemorrhage in autologous bone marrow transplant recipients☆

Robbins, Richard; Linder, James; Stahl, Marlin G.; Thompson, Austin B.; Haire, William D.; Kessinger, Anne; Armitage, Jamés O.; Arneson, Mark; Woods, Gail L.; Vaughan, William P.

doi:10.1016/0002-9343(89)90690-6

Cited by 56 publications

(98 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…28,29 Early after transplant, IPS has a mortality rate of 60-75%. [30][31][32] Thus, late IPS may have a somewhat better outcome than those developing earlier post transplant. Strategies to prevent late pneumonia can be developed based on the patient risk factors and infectious etiologies.…”

Section: Discussionmentioning

confidence: 99%

Incidence, risk factors, and mortality from pneumonia developing late after hematopoietic stem cell transplantation

Chen

Boeckh

Seidel

et al. 2003

Bone Marrow Transplant

View full text Add to dashboard Cite

Summary:The incidence, etiology, outcome, and risk factors for developing pneumonia late after hematopoietic stem cell transplantation (SCT) were investigated in 1359 patients transplanted in Seattle. A total of 341 patients (25% of the cohort) developed at least one pneumonic episode. No microbial or tissue diagnosis (ie clinical pneumonia) was established in 197 patients (58% of first pneumonia cases). Among the remaining 144 patients, established etiologies included 33 viral (10%), 31 bacterial (9%), 25 idiopathic pneumonia syndrome (IPS, 7%), 20 multiple organisms (6%), 19 fungal (6%), and 16 Pneumocystis carinii pneumonia (PCP) (5%). The overall cumulative incidence of first pneumonia at 4 years after discharge home was 31%. The cumulative incidences of pneumonia according to donor type at 1 and 4 years after discharge home were 13 and 18% (autologous/syngeneic), 22 and 34% (HLA-matched related), and 26 and 39% (mismatched related/unrelated), respectively. Multivariate analysis of factors associated with development of late pneumonia after allografting were increasing patient age (RR 0.5 for o20 years, 1.2 for 440 years, P ¼ 0.009), donor HLA-mismatch (RR 1.6 for unrelated/mismatched related, P ¼ 0.01), and chronic graft-versus-host disease (GVHD; RR 1.5, P ¼ 0.007). Our data suggest that extension of PCP prophylaxis may be beneficial in high-risk autograft recipients. Further study of long-term anti-infective prophylaxis based on patient risk factors after SCT appear warranted.

show abstract

Section: Discussionmentioning

confidence: 99%

Incidence, risk factors, and mortality from pneumonia developing late after hematopoietic stem cell transplantation

Chen

Boeckh

Seidel

et al. 2003

Bone Marrow Transplant

View full text Add to dashboard Cite

show abstract

“…25 Certain drugs (alkylating agents) 26 and total body irradiation 27 may be toxic to pulmonary endothelium, thus predisposing to subsequent pulmonary edema and in some cases, hemorrhage. [27][28][29] During neutrophil recovery, following cytotoxic chemotherapy or stem cell transplantation, a spiraling production and release of cytokines and products of neutrophil degranulation and oxydative metabolism occurs leading to local (such as in the lung where the neutrophils may be initially sequestered) and systemic (eg fever and a diffuse increase in capillary permeability) tissue injury. Multiple cytokines have been implicated in the pathogenesis of ES, including those predictive of GVHD and multi-organ failure, 25 those which are likely mediators of CLS (IL-2, TNF-␣, INF-gamma) 30,31 and IL-8, which is integral to neutrophil regeneration and function.…”

Section: Pathophysiologic Mechanisms Of Esmentioning

confidence: 99%

Engraftment syndrome following hematopoietic stem cell transplantation

Spitzer

2001

Bone Marrow Transplant

362

386

View full text Add to dashboard Cite

Summary:During neutrophil recovery following hematopoietic stem cell transplantation, a constellation of symptoms and signs including fever, erythrodermatous skin rash, and noncardiogenic pulmonary edema often occur. These clinical findings have usually been referred to as engraftment syndrome, or, reflecting the manifestations of increased capillary permeability, capillary leak syndrome. While described most often following autologous stem cell transplantation, a similar clinical syndrome has been observed followed allogeneic stem cell transplantation. Distinction from graft-versus-host disease in the allogeneic setting however, has been difficult. Recent experience with non-myeloablative conditioning for stem cell transplantation, however, reveals that an engraftment syndrome independent of GVHD may occur. In some cases, this engraftment syndrome may be a manifestation of a host-versus-graft reaction (graft rejection). While cellular and cytokine interactions are believed to be responsible for these clinical findings, a distinct effector cell population and cytokine profile have not been defined. Engraftment syndromes are likely associated with an increased transplant-related mortality, mostly from pulmonary and associated multiorgan failure. Corticosteroid therapy is often dramatically effective for engraftment syndrome, particularly for the treatment of the pulmonary manifestations. A proposal for a more uniform definition of engraftment syndrome has been developed in order to allow for a reproducible method of reporting of this complication and for evaluating prophylactic and therapeutic strategies. Bone Marrow Transplantation (2001) 27, 893-898.

show abstract

“…In addition, a patient should have progressively bloodier return on bronchoalveolar lavage (BAL) from three separate subsegmental bronchi or the presence of X20% hemosiderinladen macrophages in the absence of a clear cardiac or infective etiology for hemorrhage. [11][12][13][14][15]25 The BAL appearance and iron stain are complementary. Soon after the onset of hemorrhage, BAL may be bloody and the iron stain may be negative.…”

Section: Introductionmentioning

confidence: 99%