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2.
Lung ; 188(5): 381-5, 2010 Oct.
Article in English | MEDLINE | ID: mdl-20607268

ABSTRACT

Lung transplantation (LTX) requires continual systemic immunosuppression, which can result in infections that may compromise recipient survival. A recent outbreak of Acinetobacter baumannii at our institution resulted in infections experienced in both LTX recipients and nontransplant patients. A retrospective review was conducted of patients who had A. baumannii recovered from blood, other normally sterile body fluids, and/or respiratory secretions and who had clinical follow-up extending to 1 year postinfection. A. baumannii was considered "multidrug-resistant" when its growth was not inhibited by minimum inhibitory concentrations of multiple antibiotics. Despite the resistance profile, patients were treated with a combination of antibiotics, which included tigecycline, colistimethate, and when susceptible, imipenem. Once infection was diagnosed, immunosuppression was reduced in all LTX recipients. Six LTX recipients became infected with A. baumannii and were contrasted to infections identified in 14 non-LTX, nonimmunosuppressed patients. A. baumannii was persistently recovered in 4 of 6 LTX recipients (66.7%) compared with only 1 of 14 (7.1%) non-LTX patients (χ(2) = 9.9, p = 0.005). LTX recipients received antibiotic therapy for an average of 76 ± 18.4 days compared with 16.0 ± 6.8 days for the non-LTX patients (p = 0.025, Mann-Whitney U test). All 4 of the 6 (66.7%) LTX recipients died as a consequence of their infection compared with 1 of 14 (7.1%) of the non-LTX patients (χ(2) = 9.9, p = 0.005). Despite receiving more antibiotic therapy, LTX recipients who were infected with multidrug-resistant A. baumannii were less likely to clear their infection and experienced greater mortality compared with non-LTX patients.


Subject(s)
Acinetobacter Infections/etiology , Acinetobacter Infections/mortality , Acinetobacter baumannii/isolation & purification , Lung Transplantation/adverse effects , Pneumonia, Bacterial/etiology , Pneumonia, Bacterial/mortality , Acinetobacter Infections/diagnostic imaging , Anti-Bacterial Agents/therapeutic use , Colistin/analogs & derivatives , Colistin/therapeutic use , Humans , Imipenem/therapeutic use , Immunosuppressive Agents/therapeutic use , Minocycline/analogs & derivatives , Minocycline/therapeutic use , Pneumonia, Bacterial/diagnostic imaging , Radiography , Retrospective Studies , Tigecycline
4.
Radiology ; 203(3): 715-9, 1997 Jun.
Article in English | MEDLINE | ID: mdl-9169693

ABSTRACT

PURPOSE: To determine the radiographic and computed tomographic (CT) characteristics of acute eosinophilic pneumonia. MATERIALS AND METHODS: Twelve consecutive patients with acute eosinophilic pneumonia were included in the study. The diagnosis was based on clinical symptoms and results of bronchoalveolar lavage. Plain chest radiographs were obtained in all patients; CT scans were obtained in three patients. Two thoracic radiologists reviewed the radiographs and CT scans. RESULTS: Ten patients had bilateral areas of air-space opacity on images obtained at presentation; in seven of these patients, interstitial areas of opacity were also present. Two patients had bilateral interstitial areas of opacity and no areas of air-space opacity. Interlobular septal thickening and ground-glass attenuation were present on CT scans in two patients; patchy bilateral consolidation was present on CT scans in one patient. Pleural effusion was present on radiographs in seven patients (58%) and was bilateral in five. Pleural effusion was present at some point during the course of disease in all patients. In all patients, air-space disease markedly improved within 3 days of initiation of treatment with corticosteroids. CONCLUSION: Acute eosinophilic pneumonia should be considered as a possible diagnosis when a previously healthy person presents with acute respiratory failure of unknown origin.


Subject(s)
Pulmonary Eosinophilia/diagnostic imaging , Tomography, X-Ray Computed , Acute Disease , Administration, Oral , Adolescent , Adult , Aged , Anti-Inflammatory Agents/administration & dosage , Anti-Inflammatory Agents/therapeutic use , Bronchoalveolar Lavage , Bronchoscopy , Female , Glucocorticoids/administration & dosage , Glucocorticoids/therapeutic use , Humans , Injections, Intravenous , Male , Methylprednisolone/administration & dosage , Methylprednisolone/therapeutic use , Middle Aged , Pleural Effusion/diagnostic imaging , Pleural Effusion/pathology , Prednisone/administration & dosage , Prednisone/therapeutic use , Pulmonary Alveoli/diagnostic imaging , Pulmonary Alveoli/pathology , Pulmonary Eosinophilia/drug therapy , Pulmonary Eosinophilia/pathology , Radiography, Thoracic , Respiratory Insufficiency/diagnostic imaging , Respiratory Insufficiency/pathology
5.
Medicine (Baltimore) ; 75(6): 334-42, 1996 Nov.
Article in English | MEDLINE | ID: mdl-8982150

ABSTRACT

Idiopathic acute eosinophilic pneumonia (AEP) is an acute febrile illness that may be mistaken for an infectious pneumonia. Patients are often young and otherwise healthy. Clues to considering this disorder in a differential diagnosis include the acuity and severity of the clinical presentation and an initial chest X-ray with diffuse infiltrates, often interstitial, and the presence of Kerley B lines and/or evidence of pleural fluid. The diagnosis can be made through examination of bronchoalveolar lavage fluid in most cases, with careful exclusion of other similar eosinophilic lung disease. Although it can lead to life-threatening respiratory failure, AEP is easily treatable with corticosteroids. This disease has not been reported to recur in any patients to this point.


Subject(s)
Pulmonary Eosinophilia , Acute Disease , Adolescent , Adult , Aged , Female , Humans , Male , Middle Aged , Pulmonary Eosinophilia/diagnosis , Pulmonary Eosinophilia/therapy
6.
J Lab Clin Med ; 125(3): 356-69, 1995 Mar.
Article in English | MEDLINE | ID: mdl-7897303

ABSTRACT

Alveolar macrophages have been shown to be major producers of the potent proinflammatory cytokines interleukin-1 beta and tumor necrosis factor-alpha, and of the antiinflammatory cytokine interleukin-1 receptor antagonist. During the adult respiratory distress syndrome the normally surfactant-coated alveolus becomes flooded with plasma proteins, altering the milieu of alveolar cells such as alveolar macrophages. To understand alveolar macrophage function during the adult respiratory distress syndrome, the individual and combined effects of surfactant and plasma on alveolar macrophage cytokine production was examined. A synthetic surfactant (Exosurf) and a bovine-derived surfactant (Survanta) both inhibited production of interleukin-1 beta, pro-interleukin-1 beta, tumor necrosis factor-alpha, and interleukin-1 receptor antagonist in a dose-dependent manner. This inhibition was noted when both endotoxin and heat-killed Staphylococcus aureus were used as stimuli. Autologous plasma also inhibited interleukin-1 beta and tumor necrosis factor-alpha release in a dose-dependent manner, but, unlike surfactant, plasma did not inhibit interleukin-1 receptor antagonist release. Similarly, the combination of plasma and surfactant inhibited interleukin-1 beta and tumor necrosis factor-alpha release but not interleukin-1 receptor antagonist release. In support of these data, interleukin-1 receptor antagonist was detectable in five of six bronchoalveolar lavage fluid samples from patients with adult respiratory distress syndrome at a mean concentration of 465 pg/ml; on the other hand, interleukin-1 beta was not detectable in any of these samples. These results indicate that the relative production of interleukin-1 beta, tumor necrosis factor-alpha, and interleukin-1 receptor antagonist can be altered depending on the local concentration of both surfactant and plasma.


Subject(s)
Biological Products , Immune Tolerance , Macrophages, Alveolar/physiology , Phosphorylcholine , Plasma/physiology , Pulmonary Surfactants/physiology , Bronchoalveolar Lavage Fluid/chemistry , Drug Combinations , Enzyme-Linked Immunosorbent Assay , Fatty Alcohols/pharmacology , Female , Humans , Interleukin-1/antagonists & inhibitors , Interleukin-1/biosynthesis , Lipopolysaccharides/pharmacology , Male , Polyethylene Glycols/pharmacology , Protein Precursors/antagonists & inhibitors , Pulmonary Surfactants/pharmacology , Receptors, Interleukin-1/antagonists & inhibitors , Respiratory Distress Syndrome/metabolism , Tumor Necrosis Factor-alpha/antagonists & inhibitors , Tumor Necrosis Factor-alpha/biosynthesis
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