Susceptibility of pseudomonas aeruginosa to cefepime versus ceftazidime in patients with cystic fibrosis.

STUDY OBJECTIVES: To compare the susceptibility of respiratory cultures of Pseudomonas aeruginosa obtained from patients with cystic fibrosis to cefepime versus ceftazidime. The pattern of cumulative resistance of P aeruginosa to cefepime in patients who had received at least one treatment course of cefepime between two sputum cultures was also characterized. DESIGN: Prospective consecutive data collection. SETTING: University-affiliated cystic fibrosis clinic and medical center. PATIENTS: Eighty patients with cystic fibrosis who had at least one sputum culture positive for P aeruginosa with reported microbiologic susceptibilities to cefepime and ceftazidime. INTERVENTION: Patient data was collected and analyzed. Measurements and Main Results. Two hundred and thirty-one P aeruginosa isolates were collected over 6 months. A total of 16.4% and 8.7% of the isolates were nonsusceptible to cefepime and ceftazidime, respectively (p=0.01). In eight patients who had not received cefepime before the study period, nonsusceptibility was 11.8% and 27.2% before and after exposure to cefepime, respectively. CONCLUSIONS: Susceptibility of P. aeruginosa isolates in patients with cystic fibrosis was lower with cefepime than with ceftazidime. Follow-up surveillance to determine changes in susceptibility of P aeruginosa isolates to cefepime is warranted.

Effects of therapeutic doses of albuterol on beta2-adrenergic receptor density and metabolic changes.

Beta2-agonist drugs at inhaled supratherapeutic doses or when given orally or parenterally alter peripheral lymphocyte beta2-adrenoceptor density (betaAR) and have demonstrable metabolic effects. However, it is not known whether these changes occur at therapeutic inhaled doses. We therefore studied the effects of therapeutic doses of inhaled albuterol in five asthmatic subjects (mean age 23.0+/-2.4 years) and six normal subjects (mean age 28.3+/-3.3 years). Subjects were studied in a randomized, double-blind protocol in which each subject received either inhaled albuterol (270 microg four times daily) for 2 weeks followed by placebo or vice versa in two sequential 2-week periods separated by a 2-week washout period. In the asthmatics, baseline FEV1 increased significantly (p < 0.05) after 2 weeks of inhaled albuterol treatment compared to the initial visit and after 2 weeks of placebo (mean FEV1: 3.2 L+/-0.7 L, 2.9 L+/-0.5 L, and 3.0 L+/-0. 7 L, respectively). Baseline peripheral lymphocyte betaAR was not significantly different (p > 0.05) between the asthmatic (mean: 757+/-176) and normal subjects (mean: 732+/-251). However, in neither group was there any significant change (p > 0.05) in betaAR or plasma potassium, insulin, or glucose, either acutely or after 2 weeks of albuterol therapy. The present study confirms that there is no difference in peripheral lymphocyte betaAR between asthmatic and normal subjects and also shows that at therapeutic doses of inhaled albuterol, there are no significant changes in betaAR or metabolic effects.

Monitoring sleep and breathing: methodology. Part I: Monitoring breathing.

There is considerable variation in monitoring techniques and definitions of sleep-disordered breathing. Work underway in the Sleep Heart Health Study may help to clarify these issues. Home and portable monitoring have the potential to improve cost and convenience of diagnosis and treatment of sleep disorders but are currently indicated only in specific instances. Detection and monitoring of pediatric sleep-disoriented breathing varies considerably from that of adults.

Variability of peripheral blood lymphocyte beta-2-adrenergic receptor density in humans.

Beta2-adrenergic receptor (betaAR) density on peripheral blood lymphocytes has been used as an index to reflect the betaAR state of the body. Lymphocytes betaARs are unequally distributed among lymphocyte subpopulations, with the highest density on CD8+ cells and the lowest on CD4+ cells. Thus, the measurement of peripheral blood lymphocyte betaAR density could vary with changes in CD4+ and CD8+ cell concentrations. We examined the individual and intersubject variance of betaAR density and lymphocyte subpopulations over time in 10 normal subjects, studied on 3 to 5 different d always at approximately 9:00 A.M. over a 4- to 12-wk period. Peripheral blood lymphocytes were isolated and beta2-adrenergic receptor density was determined by specific binding of [125I]-(-)iodopindolol, and lymphocyte subpopulations were measured by flow cytometry. Average receptors per lymphocyte were 776 +/- 183. Whereas the absolute values of CD4+% and CD8+% cell concentrations varied little in individual subjects (coefficient of variation 9.5% and 11.1%, respectively), the individual betaAR variance was greater (coefficient of variation 22.4%). However there was a significant correlation between betaAR and CD4+% and CD8+% cell concentration (correlation coefficients: -0.58, p < 0.001; +0.51, p < 0.001, respectively). This information is relevant to interpretations of changes in peripheral betaAR in humans.

Pralidoxime continuous infusion in the treatment of organophosphate poisoning.

OBJECTIVE: To report a case of organophosphate poisoning treated with a continuous infusion of pralidoxime chloride. CASE SUMMARY: A 27-year-old white man presented with extreme agitation, muscle weakness and fasciculations, and respiratory failure after ingesting an organophosphate pesticide (Dursban, active ingredients chlorpyrifos and xylene) as a suicide attempt. Atropine sulfate and pralidoxime chloride were administered intermittently, but the patient continued to be extremely agitated and have muscle fasciculations. Subsequently, a continuous intravenous infusion of pralidoxime (8 mg/mL concentration) at 500 mg/h was initiated to help control breakthrough nicotinic symptoms. Therapy with atropine and pralidoxime was continued for approximately 72 hours. Therapy was discontinued due to the predominance of anticholinergic symptoms and the patient's increased awareness. DISCUSSION: Severe organophosphate poisoning with nicotinic and/or central manifestations should be treated with pralidoxime in addition to atropine. The rationale supporting the use of pralidoxime as a continuous infusion in this case includes: (1) slow absorption of organophosphate compounds following exposure to large quantities, (2) unknown quantity ingested, (3) delayed nicotinic effects from redistribution of lipid-soluble organophosphate and metabolic activation of phosphorothioates such as chlorpyrifos, and (4) intensive care monitoring. There is limited documentation in the literature of continuous infusions of pralidoxime used to treat organophosphate poisoning and the stability of the admixture is unknown. CONCLUSIONS: A continuous pralidoxime infusion successfully managed the prolonged nicotinic symptoms seen after ingestion of an organophosphate. A continuous infusion of pralidoxime may be particularly useful in cases of organophosphate poisoning when the extent of chemical exposure or quantity of chemical ingested is unknown but potentially toxic and the therapy must be symptomatically managed.