CT scan-measured pulmonary artery to aorta ratio and echocardiography for detecting pulmonary hypertension in severe COPD.

BACKGROUND: COPD is associated with significant morbidity primarily driven by acute exacerbations. Relative pulmonary artery (PA) enlargement, defined as a PA to ascending aorta (A) diameter ratio greater than one (PA:A>1) identifies patients at increased risk for exacerbations. However, little is known about the correlation between PA:A, echocardiography, and invasive hemodynamics in COPD. METHODS: A retrospective observational study of patients with severe COPD being evaluated for lung transplantation at a single center between 2007 and 2011 was conducted. Clinical characteristics, CT scans, echocardiograms, and right-sided heart catheterizations were reviewed. The PA diameter at the bifurcation and A diameter from the same CT image were measured. Linear and logistic regression were used to examine the relationships between PA:A ratio by CT scan and PA systolic pressure (PASP) by echocardiogram with invasive hemodynamics. Receiver operating characteristic analysis assessed the usefulness of the PA:A ratio and PASP in predicting resting pulmonary hypertension (PH) (mean pulmonary artery pressure [mPAP]>25 mm Hg). RESULTS: Sixty patients with a mean predicted FEV1 of 27%±12% were evaluated. CT scan-measured PA:A correlated linearly with mPAP after adjustment for multiple covariates (r=0.30, P=.03), a finding not observed with PASP. In a multivariate logistic model, mPAP was independently associated with PA:A>1 (OR, 1.44; 95% CI, 1.02-2.04; P=.04). PA:A>1 was 73% sensitive and 84% specific for identifying patients with resting PH (area under the curve, 0.83; 95% CI, 0.72-0.93; P<.001), whereas PASP was not useful. CONCLUSIONS: A PA:A ratio>1 on CT scan outperforms echocardiography for diagnosing resting PH in patients with severe COPD.

Disparities in lung transplantation before and after introduction of the lung allocation score.

BACKGROUND: In May 2005, the Lung Allocation Score (LAS) became the primary method for determining allocation of lungs for organ transplantation for those at least 12 years of age in the United States. During the pre-LAS period, black patients were more likely than white patients to become too sick or die while awaiting transplant. The association between gender and lung transplant outcomes has not been widely studied. METHODS: Black and white patients aged ≥ 18 years registered on the United Network for Organ Sharing (UNOS) lung transplantation waiting list from January 1, 2000, to May 3, 2005 (pre-LAS, n = 8,765), and from May 4, 2005, to September 4, 2010 (LAS, n = 8,806), were included. Logistic regression analyses were based on smaller cohorts derived from patients listed in the first 2 years of each era (2,350 pre-LAS, and 2,446 LAS) to allow for follow-up time. Lung transplantation was the primary outcome measure. Multivariable analyses were performed within each interval to determine the odds that a patient would die or receive a lung transplant within 3 years of listing. RESULTS: In the pre-LAS era, black patients were more likely than white patients to become too sick for transplantation or die within 3 years of waiting list registration (43.8% vs 30.8%; odds ratio [OR], 1.84; p < 0.001). Race was not associated with death or becoming too sick while listed for transplantation in the LAS era (14.0% vs 13.3%; OR, 0.93; p = 0.74). Black patients were less likely to undergo transplantation in the pre-LAS era (56.3% vs 69.2%; OR, 0.54; p < 0.001) but not in the LAS era (86.0% vs 86.7%; OR, 1.07; p = 0.74). Women were more likely than men to die or become too sick for transplantation within 3 years of listing in the LAS era (16.1% vs 11.3%; OR, 1.58; p < 0.001) compared with the pre-LAS era (33.4% vs 30.7%; OR, 1.19; p = 0.08). CONCLUSION: Racial disparities in lung transplantation have decreased with the implementation of LAS as the method of organ allocation; however, gender disparities may have actually increased in the LAS era.

Antifungal prophylaxis in solid organ transplant recipients.

Solid organ transplantation is life saving for thousands of patients worldwide with end-stage organ failure, but post-transplantation invasive fungal infections (IFIs) remain a significant cause of morbidity and mortality. To improve patient outcomes, investigators have explored various strategies of prevention, including the use of antifungal prophylaxis with both systemic and topical nonabsorbable agents. Often, the strategy is to identify those patients at highest risk for IFIs who would be expected to derive the most benefit from antifungal prophylaxis. Currently, data support the use of antifungal prophylaxis in liver, lung, small bowel and pancreas transplant recipients. By understanding the epidemiology of post-transplant IFIs and antifungal adverse effects, clinicians may target antifungal prophylaxis more optimally. Herein, we review antifungal prophylaxis with systemic agents among solid organ transplant recipients.

Intracellular Staphylococcus aureus and antibiotic resistance: implications for treatment of staphylococcal osteomyelitis.

UNLABELLED: Staphylococcus aureus is responsible for 80% of human osteomyelitis. It can invade and persist within osteoblasts. Antibiotic resistant strains of S. aureus make successful treatment of osteomyelitis difficult. NULL HYPOTHESIS: antibiotic sensitivities of S. aureus do not change after exposure to the osteoblast intracellular environment. Human and mouse osteoblast cultures were infected and S. aureus cells were allowed to invade. Following times 0, 12, 24, and 48 h ( +/- the addition of erythromycin, clindamycin, and rifampin at times 0 or 12 h), the osteoblasts were lysed and intracellular bacteria enumerated. Transmission electron microscopy was performed on extracellular and intracellular S. aureus cells. In mouse osteoblasts, administration of bacteriostatic antibiotics at time 0 prevented the increase in intracellular S. aureus. If the antibiotics were delayed 12 h, this did not occur. When rifampin (bactericidal) was introduced at time 0 to human and mouse osteoblasts, there was a significant decrease in number of intracellular S. aureus within osteoblasts compared to control. If rifampin was delayed 12 h, this did not occur. Significant time-dependent S. aureus structural changes were observed after exposure to the osteoblast intracellular environment. These studies demonstrate that once S. aureus is established intracellularly for 12 h, the bacteria are less sensitive to antibiotics capable of eukaryotic cell penetration (statistically significant). These antibiotic sensitivity changes could be due in part to the observed structural changes. This leads to the rejection of our null hypotheses that the antibiotic sensitivities of S. aureus are unaltered by their location.