Lung transplant outcomes: a review of survival, graft function, physiology, health-related quality of life and cost-effectiveness

Studer, Sean M.

doi:10.1183/09031936.04.00065004

Cited by 162 publications

(117 citation statements)

References 89 publications

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“…The major causes of death following lung transplantation vary with the time following transplantation. Thirty-day mortality is generally related primarily to surgical issues, donor lung preservation, and primary graft dysfunction (PGD) (Studer et al 2004). Infectious causes, malignancy, and chronic lung allograft dysfunction (CLAD) predominate in the subsequent posttransplant period.…”

Section: Discussionmentioning

confidence: 99%

Overview of Clinical Lung Transplantation

Yeung

Keshavjee

2014

Cold Spring Harbor Perspectives in Medicine

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Since the first successful lung transplant 30 years ago, lung transplantation has rapidly become an established standard of care to treat end-stage lung disease in selected patients. Advances in lung preservation, surgical technique, and immunosuppression regimens have resulted in the routine performance of lung transplantation around the world for an increasing number of patients, with wider indications. Despite this, donor shortages and chronic lung allograft dysfunction continue to prevent lung transplantation from reaching its full potential. With research into the underlying mechanisms of acute and chronic lung graft dysfunction and advances in personalized diagnostic and therapeutic approaches to both the donor lung and the lung transplant recipient, there is increasing confidence that we will improve short-and long-term outcomes in the near future.

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Section: Discussionmentioning

confidence: 99%

Overview of Clinical Lung Transplantation

Yeung

Keshavjee

2014

Cold Spring Harbor Perspectives in Medicine

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“…PR further improves exercise and QoL after lung transplantation [78]. According to the International Society for Heart and Lung Transplantation's registry, survival for emphysema is 85.7% at 1 yr and 68.3% at 3 yrs [79], significant complications still impair survival [80]. NPPV NPPV, delivered by nasal or face mask, avoids the risks associated with invasive ventilation.…”

Section: Lung Transplantationmentioning

confidence: 99%

Nonpharmacological treatment and relief of symptoms in COPD

Clini

Ambrosino²

2008

European Respiratory Journal

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Evidence-based guidelines for chronic obstructive pulmonary disease (COPD) have recently been developed.Nonpharmacological treatments have evolved rapidly as an essential part of COPD therapy. They are especially important as complementary interventions in severe or very severe disease, when there is loss in function, a reduction in quality of life and when psychological impairments further complicate the disease.The present article discusses the most used nonpharmacological treatments for severe COPD patients (rehabilitation, long-term oxygen therapy, surgery, noninvasive positive pressure ventilation and supportive nutrition) and their evidence-based usefulness in promoting strategies that relieve symptoms.All of these interventions are used during end-stage disease, to promote self-efficacy, relieve symptoms and prevent further deterioration. These therapeutic options support physicians and allied professionals in improving symptom management for their patients.

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“…autoimmunity; p38 MAPK; focal adhesion kinase; small-airway epithelial cells; RLE-6TN; mouse transplant model; epithelial-mesenchymal transition OBLITERATIVE BRONCHIOLITIS (OB) is characterized by extensive peribronchiolar fibrosis with plugs of granulation tissues (fibroblasts and collagen) that occlude small airways. OB is the key reason that the 5-yr survival of lung transplant recipients is only 50%, the worst of all major solid organ transplants (42,48).Aberrant epithelial repair is a key event in the transplanted lung (1, 9) in which bronchioles lose resident epithelial cells and become occluded by granulation tissue. Abnormal epithelial repair eventually causes an epithelial-to-mesenchymal transition (EMT), a functional and phenotypic change of epithelial cells into spindle-shaped, migratory (43) and matrix-component-secreting mesenchymal cells (10, 41), and a process associated with lung fibrosis (15,27).…”

mentioning

confidence: 99%

IL-17 induces type V collagen overexpression and EMT via TGF-β-dependent pathways in obliterative bronchiolitis

Vittal¹,

Fan²,

Greenspan³

et al. 2013

American Journal of Physiology-Lung Cellular and Molecular Phys

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erative bronchiolitis (OB), a fibrotic airway lesion, is the leading cause of death after lung transplantation. Type V collagen [col(V)] overexpression and IL-17-mediated anti-col(V) immunity are key contributors to OB pathogenesis. Here, we report a previously undefined role of IL-17 in inducing col(V) overexpression, leading to epithelial mesenchymal transition (EMT) and subsequent OB. We observed IL-17-mediated induction of col(V) ␣1 chains [␣1 (V)] in normal airway epithelial cells in vitro and detected ␣1 (V)-specific antibodies in bronchoalveolar lavage fluid of lung transplant patients. Overexpression of IL-17 and col(V) was detected in OB lesions in patient lung biopsies and in a murine OB model. IL-17 is shown to induce EMT, TGF-␤ mRNA expression, and SMAD3 activation, whereas downregulating SMAD7 expression in vitro. Pharmacological inhibition of TGF-␤RI tyrosine kinase, p38 MAPK, or focal adhesion kinase prevented col(V) overexpression and EMT. In murine orthotopic lung transplants, neutralizing IL-17 significantly decreased TGF-␤ mRNA and protein expression and prevented epithelial repair/ OB. Our findings highlight a feed-forward loop between IL-17 and TGF-␤, leading to induction of col(V) and associated epithelial repair, thus providing one possible link between autoimmunity and OB after lung transplantation. autoimmunity; p38 MAPK; focal adhesion kinase; small-airway epithelial cells; RLE-6TN; mouse transplant model; epithelial-mesenchymal transition OBLITERATIVE BRONCHIOLITIS (OB) is characterized by extensive peribronchiolar fibrosis with plugs of granulation tissues (fibroblasts and collagen) that occlude small airways. OB is the key reason that the 5-yr survival of lung transplant recipients is only 50%, the worst of all major solid organ transplants (42,48).Aberrant epithelial repair is a key event in the transplanted lung (1, 9) in which bronchioles lose resident epithelial cells and become occluded by granulation tissue. Abnormal epithelial repair eventually causes an epithelial-to-mesenchymal transition (EMT), a functional and phenotypic change of epithelial cells into spindle-shaped, migratory (43) and matrix-component-secreting mesenchymal cells (10, 41), and a process associated with lung fibrosis (15,27). However, the direct connection between EMT and the in vivo phenomena of fibrosis and fibro-obliterative disease remains controversial.We and others previously reported that OB is associated with dysregulation of two types of collagen: 1) marked increase in type V collagen [col(V)], a quantitatively minor lung collagen (8,14,40), and 2) a decrease in the major lung collagen type I [col(I)] (2, 53). We have shown that prospective monitoring of patients with human lung transplant revealed a critical role of col(V)-specific cellular immunity in OB pathogenesis (14,40). Although overexpression of col(V), an otherwise quantitatively minor collagen, is involved in OB pathology, mechanisms leading to col(V) overexpression are unknown. Thus a mechanistic understanding of the triggers of col(V)...

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Lung transplant outcomes: a review of survival, graft function, physiology, health-related quality of life and cost-effectiveness

Cited by 162 publications

References 89 publications

Overview of Clinical Lung Transplantation

Overview of Clinical Lung Transplantation

Nonpharmacological treatment and relief of symptoms in COPD

IL-17 induces type V collagen overexpression and EMT via TGF-β-dependent pathways in obliterative bronchiolitis

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