Greatly increased prevalence of esophageal dysmotility observed in persons with spinal cord injury.

The effects of spinal cord injury (SCI) on esophageal motility are largely unknown. Furthermore, due to the complete or partial loss of sensory innervation to the upper gastrointestinal tract, a symptom-based diagnosis of esophageal dysmotility is problematic in the SCI population. To determine the prevalence and characterize the type of motility disorders observed in persons with chronic SCI compared with that of able-bodied (AB) controls based on esophageal pressure topography isometrics acquired by high-resolution manometry and categorized by application of the Chicago Classification. High-resolution manometry of the esophagus was performed in 39 individuals: 14 AB, 12 with paraplegia (level of injury between T4-T12) and 13 with tetraplegia (level of injury between C5-C7). A catheter containing multiple pressure sensors arranged at 360° was introduced into the esophagi of subjects at a distance that allowed visualization of both the upper esophageal sphincters (UES) and lower esophageal sphincters (LES). After a period to acquire pressures at baseline, subjects were asked to perform 10 wet swallows with 5-mL boluses of isotonic saline while esophageal pressure and impedance were being recorded. No significant differences were noted for gender, age, or body mass index between AB and SCI groups. Twenty-one of 25 (84%) subjects with SCI had at least one motility abnormality: 12% with Type II achalasia, 4% with Type III achalasia, 20% with esophagogastric junction outflow obstruction, 4% with the hypercontractile esophagus, and 48% with peristaltic abnormalities (weak peristalsis with small or large defects or frequent failed peristalsis). In contrast, only 7% (1 out of 14) of the AB subjects had any type of esophageal motility disorder. Despite the lack of subjective complaints and clinical awareness, esophageal dysmotility appears to be a highly prevalent condition in persons with SCI. The use of new and improved techniques, as well as a more stringent classification system, permitted the identification of the presence of nonspecific motility disorders in almost all SCI subjects, including four individuals who were previously undiagnosed with achalasia. Future work in persons with SCI is required to clarify the clinical impact of this observation and to study potential associations between esophageal dysmotility, gastroesophageal reflux disease, and pulmonary function. An increased awareness of esophageal dysfunction in the SCI population may lead to the development of new clinical guidelines for the diagnosis, prevention, and treatment of these largely unrecognized disorders.

International spinal cord injury pulmonary function basic data set.

OBJECTIVES: To develop the International Spinal Cord Injury (SCI) Pulmonary Function Basic Data Set within the framework of the International SCI Data Sets in order to facilitate consistent collection and reporting of basic bronchopulmonary findings in the SCI population. SETTING: International. METHODS: The SCI Pulmonary Function Data Set was developed by an international working group. The initial data set document was revised on the basis of suggestions from members of the Executive Committee of the International SCI Standards and Data Sets, the International Spinal Cord Society (ISCoS) Executive and Scientific Committees, American Spinal Injury Association (ASIA) Board, other interested organizations and societies and individual reviewers. In addition, the data set was posted for 2 months on ISCoS and ASIA websites for comments. RESULTS: The final International SCI Pulmonary Function Data Set contains questions on the pulmonary conditions diagnosed before spinal cord lesion,if available, to be obtained only once; smoking history; pulmonary complications and conditions after the spinal cord lesion, which may be collected at any time. These data include information on pneumonia, asthma, chronic obstructive pulmonary disease and sleep apnea. Current utilization of ventilator assistance including mechanical ventilation, diaphragmatic pacing, phrenic nerve stimulation and Bi-level positive airway pressure can be reported, as well as results from pulmonary function testing includes: forced vital capacity, forced expiratory volume in one second and peak expiratory flow. The complete instructions for data collection and the data sheet itself are freely available on the website of ISCoS (http://www.iscos.org.uk).

Pulmonary complications in cardiac transplant recipients.

BACKGROUND: The incidence of pulmonary complications in heart transplant recipients has not been extensively studied. We report pulmonary complications in 159 consecutive adult orthotopic heart transplantations (OHTs) performed in 157 patients. MATERIALS AND METHODS: Retrospective review of medical records. RESULTS: Forty-seven of 159 recipients (29.9%) had 81 pulmonary complications. Pneumonia was the most common (n = 27), followed by bronchitis (n = 15), pleural effusion (n = 10), pneumothorax (n = 7), prolonged respiratory failure requiring tracheotomy (n = 7), and obstructive sleep apnea syndrome (n = 6). All patients with late-onset (> 6 months after transplantation) community-acquired bacterial pneumonia presented with fever, cough, and a new lobar consolidation on the chest radiograph, and responded promptly to empiric antibiotics without undergoing an invasive diagnostic procedure. In contrast, early-onset nosocomial bacterial pneumonias carried a 33.3% mortality rate. A positive tuberculin skin test result was associated with a significantly higher rate of pulmonary complications (62.5% vs 26.8%, p = 0.007). Lung cancer and posttransplant lymphoproliferative disorder (PTLD) developed exclusively in 6 of the 61 patients (8.1%) who received induction immunosuppression with murine monoclonal antibody (OKT3). CONCLUSION: Pulmonary complications are common following heart transplantation, occurring in 29.9% of recipients, and are attributed to pneumonia of primarily bacterial origin in one half of cases. Late-onset community-acquired pneumonia carried an excellent prognosis following empiric antibiotic therapy, suggesting that in the appropriate clinical setting invasive diagnostic procedures are unnecessary. Analogous to reports in other solid-organ transplant recipients, induction therapy with OKT3 was associated with an increased incidence of lung cancer and PTLD. Overall, the development of pulmonary complications after OHT has prognostic significance given the higher mortality in this subset of patients.

Sarcoidosis and transplantation.

BACKGROUND AND AIM OF WORK: Organ transplantation is an accepted treatment for patients with end-stage organ failure. There is limited information about transplantation in patients with sarcoidosis. While there has been no systematic study of transplantation in sarcoidosis, there have been several reports of patients with sarcoidosis undergoing organ transplantation. The purpose of this review is to analyze the available literature. METHODS: We reviewed the literature regarding transplantation of kidney, liver, heart, heart-lung and lung in patients with sarcoidosis with attention to survival, complications and the incidence of recurrence of sarcoidosis in the transplanted organ and at distant sites. RESULTS: Survival and complication rates are similar to those of patients undergoing transplantation for other indications. Recurrence of pulmonary sarcoidosis has been estimated to be 47% following lung transplantation. The published cases represent a fraction of the patients reported to the International Registry maintained by the United Network of Organ Sharing (UNOS). CONCLUSIONS: Transplantation can be carried out safely in patients with sarcoidosis. Recurrence is frequent, often asymptomatic, and does not compromise graft function or patient survival. Radiographic abnormalities or symptoms associated with recurrence are responsive to increased adrenocorticosteroid therapy. Exacerbation of sarcoidosis in transplant recipients occurs in the setting of intense immunosuppression.

Sarcoidosis mythology.

BACKGROUND: Sarcoidosis continues to be shrouded by anecdotal misinformation which has gained credence by repetition. These myths have been developing for the past 50 years and continue to accumulate, despite remedial data. Among the most egregious myths are that sarcoidosis is a disease of Blacks, that the chest radiography is diagnostic of sarcoidosis, and has chronologic significance, that serum angiotensin converting enzyme and bronchoalveolar lavage are diagnostic of sarcoidosis and serve as guides to therapy, that the Kveim-Siltzbach test is not a reliable diagnostic test for sarcoidosis, that sarcoidosis is difficult to diagnose, and that sarcoidosis is tuberculosis. METHODS AND RESULTS: The literature regarding these myths has been reviewed and supported by the experience with more than 10,000 patients with sarcoidosis who have been treated at Mount Sinai Medical Center, New York. CONCLUSIONS: Sarcoidosis occurs with varying frequency among all races. The chest radiograph typical of sarcoidosis can be mimicked by other granulomatous and neoplastic diseases. The classic radiographic stages, from 0 to 111, do not reflect the time course of sarcoidosis can be made relatively easily in most patients, but its etiology is still unknown.

Peptidase inhibitors potentiate lysylbradykinin-induced bronchoconstriction in the rat.

To determine whether lysylbradykinin (LBK, kallidin) causes bronchoconstriction in animals and if peptidase inhibitors modulate the response, we studied the effects of LBK administered by aerosol in rats and assessed whether pretreatment with aerosolized solutions of enalaprilat, an inhibitor of angiotensin converting enzyme (ACE), or phosphoramidon, an inhibitor of endopeptidase 24.11 (EP 24.11, neutral endopeptidase), altered the response. Accordingly, LBK-induced bronchoconstriction was measured in anesthetized, mechanically ventilated, specific pathogen-free, Sprague-Dawley rats by body plethysmography and followed by continuous determination of lung resistance (RL) and maximal expiratory flow (MEF). Incremental doses of aerosolized LBK were administered by nebulization to obtain a concentration that caused a 5-15% increase in RL, which was designated the BC10 dose. We found that pretreatment with aerosolized enalaprilat (1 mM) 3 min prior to a BC10 dose of LBK significantly increased RL as compared to the BC10 dose alone (129 +/- 4.1% vs. 105 +/- 2.4%, P < 0.002, n = 4) and significantly decreased MEF (83 +/- 1.5% vs. 97 +/- 1.4%, P < 0.008, n = 4). Following pretreatment with aerosolized phosphoramidon (1 mM), significant increases in RL (113 +/- 1.4% vs. 106 +/- 1.6%, P < 0.019, n = 7) and decreases in MEF (92 +/- 0.9% vs. 95 +/- 0.9%, P < 0.035, n = 7) were observed (paired Student's t-test). The above findings demonstrate the effects of LBK on airway caliber for the first time in an animal model, and suggest that ACE and EP 24.11 contribute to degradation of the peptide in the airway.

Impairment in gas exchange after granulocyte colony stimulating factor (G-CSF) in a patient with the adult respiratory distress syndrome.

We describe the previously unreported finding of reproducible arterial d desaturation after successive injections of granulocyte colony stimulating factor in a orthotopic liver transplant recipient with the adult respiratory distress syndrome and antibiotic-induced neutropenia.

Effects of peptidase inhibitors on bradykinin-induced bronchoconstriction in the rat.

Objectives of this study were to determine if aerosolized bradykinin causes bronchoconstriction in anesthetized, mechanically ventilated rats, and if pretreatment with enalaprilat, an inhibitor of angiotensin-converting enzyme (ACE), or phosphoramidon, an inhibitor of endopeptidase 24.11 (EP 24.11), alters the response. We found that aerosolized bradykinin elicited a reproducible bronchoconstrictor response that was significantly amplified by pretreatment with aerosolized enalaprilat or phosphoramidon. Neither inhibitor alone affected airway tone or caused nonspecific airway hyperreactivity. These findings indicate that both ACE and EP 24.11 contribute to bradykinin degradation in rat airways.