Lung cancer in chronic obstructive pulmonary disease: enhancing surgical options and outcomes.

Patients with chronic obstructive pulmonary disease (COPD) are at increased risk for both the development of primary lung cancer, as well as poor outcome after lung cancer diagnosis and treatment. Because of existing impairments in lung function, patients with COPD often do not meet traditional criteria for tolerance of definitive surgical lung cancer therapy. Emerging information regarding the physiology of lung resection in COPD indicates that postoperative decrements in lung function may be less than anticipated by traditional prediction tools. In patients with COPD, more inclusive consideration for surgical resection with curative intent may be appropriate as limited surgical resections or nonsurgical therapeutic options provide inferior survival. Furthermore, optimizing perioperative COPD medical care according to clinical practice guidelines including smoking cessation can potentially minimize morbidity and improve functional status in this often severely impaired patient population.

Effect of obesity on asthma phenotype is dependent upon asthma severity.

BACKGROUND: We recently reported that obese and non-obese patients with asthma have similar airflow limitation and bronchodilator responsiveness, but obese patients have more symptoms overall. There is limited information on the effect of obesity on asthmatics of varying severity measured by objective physiological parameters. Understanding how obesity affects asthmatics of differing severity can provide insights into the pathogenesis of asthma in the obese and a rationale for the therapeutic approach to such patients. METHODS: Participants with asthma from two American Lung Association--Asthma Clinical Research Center (ALA-ACRC) studies were grouped by tertiles of airflow obstruction (forced expiratory volume in one second (FEV(1)%) predicted, FEV(1)/forced vital capacity (FVC)) and methacholine reactivity (PC(20)FEV(1)). Within each tertile, we examined the independent effect of body mass index (BMI), divided into normal weight, overweight, and obese categories, on lung function, airway reactivity, and symptoms. RESULTS: Overall, both FEV(1) and FVC decreased and symptoms worsened with increasing BMI; airway reactivity was unchanged. When stratified by the degree of airflow obstruction, higher BMI was not associated with greater airway reactivity to methacholine. Higher BMI was associated with more asthma symptoms only in the least obstructed FEV(1)/FVC tertile. When stratified by degree of airway reactivity, BMI was inversely associated with FVC in all PC(20)FEV(1) tertiles. BMI was directly associated with asthma symptoms only in those with the least airway reactivity. CONCLUSIONS: Obesity does not influence airway reactivity in patients with asthma and it is associated with more symptoms only in those with less severe disease.

Diet and asthma.

PURPOSE OF REVIEW: The goal of this review is to assess recent additions to the medical literature that contribute to the clinical question: 'How might diet act as a disease modifier in patients with asthma?' In vitro, animal, and epidemiologic data are presented as justification for interventional studies, which form the basis of clinical recommendations and decision-making. RECENT FINDINGS: A number of studies suggest roles for n-3 fatty acids, soy isoflavones, vitamin D, and antioxidants as modifiers of asthma severity. However, these studies are generally complicated by small sample sizes and either negative results or findings that are of questionable clinical significance. SUMMARY: The available literature regarding dietary manipulation as asthma therapy is largely unconvincing. Although mechanistic and epidemiologic studies provide a rationale for diet therapies, there are few interventional studies with positive, clinically relevant endpoints. Future studies must include sufficient numbers of well selected patients and measure effects on exacerbations, symptoms, lung function, and medication use.

Alveolar epithelium and Na,K-ATPase in acute lung injury.

Active transport of sodium across the alveolar epithelium, undertaken in part by the Na,K-adenosine triphosphatase (Na,K-ATPase), is critical for clearance of pulmonary edema fluid and thus the outcome of patients with acute lung injury. Acute lung injury results in disruption of the alveolar epithelial barrier and leads to impaired clearance of edema fluid and altered Na,K-ATPase function. There has been significant progress in the understanding of mechanisms regulating alveolar edema clearance and signaling pathways modulating Na,K-ATPase function during lung injury. The accompanying review by Morty et al. focuses on intact organ and animal models as well as clinical studies assessing alveolar fluid reabsorption in alveolar epithelial injury. Elucidation of the mechanisms underlying regulation of active Na+ transport, as well as the pathways by which the Na,K-ATPase regulates epithelial barrier function and edema clearance, are of significance to identify interventional targets to improve outcomes of patients with acute lung injury.

Long-term survival after "drop metastases" of renal cell carcinoma to the bladder.

Renal cell carcinoma can metastasize to virtually any organ, yet isolated bladder metastases are exceedingly rare, and most of these patients die within 1 year of diagnosis. Proposed mechanisms of renal cell carcinoma metastases to the bladder include hematogenous spread, lymphatic dissemination, and "drop metastases" by way of the urinary tract. We present the longest reported survival after isolated "drop metastases" of renal cell carcinoma to the bladder.