Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0006271 (bronchiolitis)
 5,174 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Transbronchial biopsies (TBBs) are useful to diagnose acute rejection and infection in patients with lung transplants. The value of routine surveillance biopsies (S-TBBs) is not known, and such biopsies with a clinical indication are not without risk and are expensive. One hundred twenty-six 6-mo survivors of heart-lung transplantation (HLT) were studied to determine the effect of stopping S-TBBs on the development of bronchiolitis obliterans syndrome (BOS) and subsequent survival. Fifty-one received transplants while S-TBB was part of routine care (group A), and 75 received transplants after this practice was stopped (group B). There was no difference in patient characteristics. Group A had shorter graft ischemia (p < 0.01) and longer postoperative ventilation (p < 0.01). Maintenance immunosuppression was similar, but group A had more steroid pulses in the second 6 mo after HLT (p < 0.01). The number of patients free from any functional deterioration at 49 to 60 mo after HLT declined to 39% in group A and 64% in group B. The risk of developing BOS grade 1 in group A relative to group B was 1.63 (95% confidence intervals: 0.96-2.79, p = 0.07). Patient survival was similar in the two groups. A total of 86 TBBs were taken in the absence of any signs or symptoms and had low diagnostic yield. In summary, there was no increased incidence of BOS after stopping S-TBBs.
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PMID:Bronchiolitis obliterans syndrome in heart-lung transplantation: surveillance biopsies. 915 80

Lung transplantation is an accepted treatment for a large number of end-stage pulmonary diseases. There are several complications that pertain specifically to lung transplant recipients, including airway ischemia, reperfusion edema, infections, acute rejection, obliterative bronchiolitis, and other postoperative problems relating to surgical technique and immuno-suppressive therapy. Imaging procedures play an important role in the diagnosis and management of these problems.
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PMID:Imaging of lung transplantation. 1058

Despite marked improvements in early survival, long-term outcome after lung transplantation is still threatened by obliterative bronchiolitis (OB). Thought to be a manifestation of chronic allograft rejection, OB affects up to 65% of patients at 5 years after surgery and produces a relentless airflow obstruction. Early and late acute rejection are the primary risk factors for OB, but cytomegalovirus infection and airway ischemia may also play a role. In most patients, OB responds poorly to augmented immunosuppression and eventually leads to infectious complications and terminal respiratory failure. Because early diagnosis is associated with better prognosis, every effort should be made to detect OB in a preclinical stage. This may be best achieved by combining several techniques, such as surveillance transbronchial biopsy and bronchoalveolar lavage, measurements of ventilation distribution and exhaled nitric oxide, and expiratory computed tomography.
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PMID:Obliterative bronchiolitis after lung transplantation. 1074 73

Constrictive bronchiolitis (CB), also termed in lung transplant patients obliterative bronchiolitis, is inflammation and fibrosis occurring predominantly in the walls and contiguous tissues of membranous and respiratory bronchioles with resultant narrowing of their lumens. CB is found in a variety of settings, most often as a complication of lung and heart-lung transplantation (affecting 34% to 39% of patients, usually in the first 2 years after transplantation) and bone marrow transplantation, but also in rheumatoid arthritis, after inhalation of toxic agents such as nitrogen dioxide, after ingestion of certain drugs such as penicillamine and ingestion of the East Asian vegetable Sauropus androgynous, and as a rare complication of adenovirus, influenza type A, measles, and Mycoplasma pneumoniae infections in children. In lung transplants, CB is the single most important factor leading to death thereafter. In one study, the overall mortality rate was 25%. However, at the same time, 87% of patients who were asymptomatic and diagnosed solely by transbronchial biopsy had resolution or stabilization of disease. Decreases in FEV1 from baseline can be used to clinically support CB in transplant patients; the term bronchiolitis obliterans syndrome is used to denote this clinical dysfunction, and a grading system has been established for it that is now widely used in the literature. Significant risk factors for the development of CB in lung transplants include alloantigen-dependent and -independent mechanisms. In the former group are late acute rejection and HLA mismatches at the A loci; in the latter are ischemia/reperfusion injuries to airways that result from the transplantation surgery and cytomegalovirus infection.
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PMID:Constrictive (obliterative) bronchiolitis. 1081 4

Interleukin-10 (IL-10) is a pleiotropic cytokine and its main function is to limit and terminate inflammatory responses. Lung transplantation is a relatively young clinical field compared to the transplantation of other solid organs and long-term survival is still limited. Complications after lung transplantation include ischemia-reperfusion injury immediately after transplantation, acute rejection and infection within the first year after transplantation and chronic allograft dysfunction in form of bronchiolitis obliterans thereafter. In the setting of lung transplantation two key functions of IL-10 might be of interest: (1) the inhibition of inflammatory immune responses; and (2) the inhibition of T-cell mediated immune responses. In animal models, it has been shown that exogenous IL-10 is able to prevent posttransplant ischemia-reperfusion injury as well as to decrease acute rejection. It was also effective in preventing airway obliteration in an animal model of posttransplant bronchiolitis obliterans. Beneficial effects of IL-10 may be found early and late after lung transplantation. Location of IL-10 expression as well as the timing of administration seems to be important for the desired effects.
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PMID:The role of interleukin-10 in lung transplantation. 1218 Aug 18

Pneumonectomy is associated with gross anatomic and physiologic changes of the esophagus. So far, only a few studies have examined the influences of anatomic changes of the esophagus and the resulting physiologic consequences. When pneumonectomy is performed without pulmonary replacement, the esophagus is displaced to the side of pneumonectomy and posteriorly. Indentation of the esophagus by the trachea, bronchus, or aortic arch and dilatation at various levels are present. After pneumonectomy, the peak amplitude of esophageal peristaltic contractions is reduced. This feature is more pronounced in patients who are more than 60 years old and in patients who had their pneumonectomy performed more than 6 years ago. Injury of the vagal nerves, local ischemia, scarring of the esophagus and mediastinum after surgery, and disturbance of the autonomic nervous systems are the major reasons leading to esophageal dysmotility and delayed gastric emptying. Despite the severe morphologic and physiologic changes of the esophagus observed after pneumonectomy, few patients complain of gastrointestinal symptoms after pneumonectomy. Esophageal functional abnormalities may be present in patients with lung cancers before pneumonectomy because of a close anatomic relationship between the esophageal vagal nerve supply and the pulmonary hilum, making the vagal nerves susceptible to disturbances by the tumors or by involved hilar or mediastinal lymph nodes. After pneumonectomy, esophageal dysmotility is exaggerated. After recipient pneumonectomy for thoracic organ transplantation, esophageal dysmotility and delayed gastric emptying are common, but their relationship to gastroesophageal reflux, chronic aspiration, or subsequent development of bronchiectasis and obliterative bronchiolitis is controversial. To reduce the incidence of esophageal dysmotility after pneumonectomy, every effort should be made during surgery to prevent direct injury of the esophagus or the vagal nerves. A prospective study involving a larger patient population is needed to precisely define the problem and its management.
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PMID:Special article: physiologic consequences of pneumonectomy. Consequences on the esophageal function. 1999. 1246 89

Operative mortality in lung transplantation in many centers has decreased to less than 10%. Despite this improvement in early survival, delayed graft failure related to chronic graft rejection continues to limit the survival and function of lung transplant recipients. Chronic lung transplant rejection Bronchiolitis obliterans (BO) is an inflammatory process that leads to fibrous scarring of the terminal and respiratory bronchioles and subsequent total occlusion of the airways. The histological changes are manifest by a progressive obstructive ventilatory defect on spirometric testing. Histologic diagnosis of BO is difficult due to sampling. The term BO syndrome has been developed to allow clinical diagnosis using spirometric criteria. BO is an alloimmune phenomenon, aggravated by airway ischemia, and infection but predicted by frequent and severe acute vascular rejection. It is characterized by increased expression of TGF beta and other cytokines on airway epithelial cells, increased expression of class II antigens in the airways, lymphocytic bronchiolitis, and bronchial epithelial cell proliferation mediated by numerous cytokines. Airway neutrophilia, and activation of neutrophilis with release of their granules into the airway is a precursor of progressive BO. Loss of normal protective mechanisms--leukocyte antiproteases--against this oxidative insult may be an integral part of disease progression. To date treatment of BOS is infrequently successful. Better understanding of the pathophysiology, and earlier recognition of BO may result in improved long term patient and graft survival and function.
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PMID:Bronchiolitis obliterans: the Achilles heel of lung transplantation. 1264 79

Endothelin-1 (ET-1) expression is increased after lung transplantation in association with ischemia reperfusion injury and acute rejection. However, little is known of the role of ET-1 during the development of obliterative bronchiolitis. In this study, we investigated the biological significance of ET-1 in obliterative airway disease development using a rat tracheal allograft model. Immunoreactivity of ET-1 and its receptors ET-RA and ET-RB was increased four-fold in allografts compared with syngrafts and localized to mononuclear cells and smooth muscle cells of the myofibroproliferative lesion and airway wall, indicating that ET-1 may mediate its effects in both a paracrine and autocrine manner in smooth muscle cells. Inhibition of ET-1 action by a nonselective ET-1 receptor antagonist, bosentan, significantly decreased tracheal occlusion, which was linked to delayed epithelial necrosis, suppressed smooth muscle cell proliferation, and a marked reduction in the number of interleukin-1beta and interleukin-2 immunoreactive cells. Our findings show that endogenous ET-1 activation is associated with obliteration of the airway wall, and blocking signaling downstream of ET-1 receptors leads to attenuation of obliterative airway disease. The results suggest that ET-1 has a proproliferative and proinflammatory role in the development of obliterative bronchiolitis.
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PMID:Role of endogenous endothelin-1 in transplant obliterative airway disease in the rat. 1508 65

Although the clinical significance of anti-HLA antibodies in heart and lung transplantation is less well studied than in renal transplantation, several studies have shown that heart and lung recipients transplanted in the presence of donor-specific antibodies are at increased risk for early acute rejection and have a lower graft survival. In an effort to avoid any increase in organ ischemia time, heart and lung candidates with anti-HLA antibodies have to be identified prior to transplantation and crossmatches performed with donor materials obtained prior to organ recovery. Both class I and II antibodies have been found to be associated with chronic rejection, defined in heart transplantation as transplant-related coronary artery disease (TRCAV) and in lung transplantation as obliterative bronchiolitis (OB) or bronchiolitis obliterative syndrome (BOS). Post-transplant de novo development of donor antigen-specific class II antibodies has been found to be especially deleterious, significantly increasing the risk of chronic rejection and poor graft outcome. Based on the review of studies regarding the development of anti-HLA antibodies and thoracic organ allograft rejection several conclusions can be drawn. The presence of class I and II-directed anti-HLA antibodies, detected by any method, are associated with acute and chronic rejection in heart and lung transplantation. Different therapeutic strategies have been used pre-transplantation to decrease the level of anti-HLA antibodies and post-transplantation to maintain low antibody levels or treat rejection, thereby improving graft outcome. Thus, monitoring the presence and the level of anti-HLA antibodies is prognostic of graft outcome and allows for measurement of therapeutic efficacy.
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PMID:Anti-HLA antibody analysis and crossmatching in heart and lung transplantation. 1520 30

Lung transplantation is recognized as the only viable treatment option in a variety of end-stage pulmonary diseases. However, the long-term survival after lung transplantation is limited by the development of obliterative bronchiolitis, and its clinical correlate bronchiolitis obliterans syndrome (BOS), which is considered to represent chronic lung allograft rejection. Histopathologically, BOS is an inflammatory process that leads to fibrous scarring of the terminal and respiratory bronchioles and subsequent total occlusion of the airways. The specific etiology and pathogenesis of BOS are not well understood. The current premise is that BOS represents a common lesion in which different inflammatory insults such as ischemia-reperfusion, rejection, and infection can lead to a similar histological and clinical outcome. However, the low incidence of BOS in non-transplanted individuals and the observation that early development of BOS is predicted by the frequency and severity of acute rejection episodes indicate that alloimmune-dependent mechanisms play a crucial role in the pathogenesis of BOS. The evidence presented in this review indicates that BOS is the result of humoral and cellular immune responses developed against major histocompatibility complex molecules expressed by airway epithelial cells of the lung allograft. This process is aggravated by alloimmune-independent mechanisms such as ischemia-reperfusion and infection. Currently, treatment of BOS is frequently unsuccessful. Therefore, a better understanding of the immunopathogenesis of BOS is of paramount importance toward improving long-term patient and graft survival after lung transplantation.
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PMID:Immune mechanisms in the pathogenesis of bronchiolitis obliterans syndrome after lung transplantation. 1566 18


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