PubMed · 7659658
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J Dickson. 1995. Corticosteroid joint injection: how to avoid the risks.. https://pubmed.ncbi.nlm.nih.gov/7659658/
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OBJECTIVE: To define the incidence of complications of endotracheal intubation and the factors associated with these complications. STUDY DESIGN: During a 22-month period, 227 intubated infants weighing <1,501 g were followed prospectively in a neonatal intensive care unit. Detailed records of events associated with airway management were kept after every intubation, in addition to clinical data. RESULTS: Eleven infants (4.8%) developed respiratory stridor after extubation which was treated with either systemic corticosteroids, racemic epinephrine and/or reintubation for respiratory failure. Four infants were submitted for bronchoscopy, mild subglottic stenosis with tracheal edema was found in 1 patient, granulation tissue and airway edema were noted in 3 infants. Traumatic intubation, prolonged ventilation, multiple intubations and bacterial colonization of the endotracheal tube were the factors associated with postextubation stridor. CONCLUSIONS: Subglottic stenosis is an infrequent complication of endotracheal intubation with current airway management of very-low-birth-weight infants. Less severe complications are still common, but they are usually amenable to clinical treatment. Bronchoscopy should be performed selectively only in infants with clinical evidence of airway obstruction after extubation.
Unstimulated peripheral blood mononuclear cells (PBMCs) from corticosteroid-resistant (CR) but not corticosteroid-sensitive (CS) asthmatics demonstrate increased activating peptide-1 (AP-1)- and decreased glucocorticoid receptor (GR)-DNA binding. We test whether these abnormalities are associated with excessive generation of c-fos, the inducible component of AP-1. The c-fos transcription rate, mRNA and protein levels, and GR-DNA binding were quantitated in PBMCs, T cells, and monocytes from CS, CR, and nonasthmatic subjects. There was a 1.7-, 4.2-, and 2.3-fold greater increase in the baseline c-fos transcription rate, mRNA expression, and protein levels, respectively, in PBMCs derived from CR compared with CS patients. At optimal stimulation with PMA, there was a 5.7-, 3.4-, and 2-fold greater increase in the c-fos transcription rate, mRNA accumulation, and protein levels, respectively, in CR compared with CS PBMCs. These abnormalities were detected in both the T cell and monocyte subpopulations. PMA stimulation converted PBMCs from a CS to a CR phenotype and was associated with direct interaction between c-Fos and the GR. Pretreatment of PBMCs from CR patients with c-fos antisense oligonucleotides enhanced GR-DNA binding activity in CR PBMCs stimulated with dexamethasone. We suggest that increased c-fos synthesis provides a major mechanism for the increased AP-1- and decreased GR- DNA binding seen in CR asthma.
Corticosteroids containing a C21 primary hydroxyl group were derivatised with 9-anthroyl cyanide. The reagent was prepared as a solution in acetonitrile, containing 0.1% triethylamine, at a concentration of 2 mg/ml. Approximately 1 microg of corticosteroid was reacted with 100 microl of this reagent, at 45 degrees C for 2 h. The fluorescent derivatives were separated by HPLC on a silica column, 250x4.6 mm I.D., by stepwise elution, with a mobile phase of 2-propanol-hexane (2:98) for 20 min, followed by 2-propanol-hexane (7:93) from 20 to 40 min. The fluorescence detector was set to 370-nm excitation and 470-nm emission. The relatively low temperature for derivatisation avoided reaction with secondary hydroxyl groups and also prevented thermal degradation of the corticosteroids.