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Antiviral Therapy and Outcomes of Patients with Pneumonia Caused by Influenza A Pandemic (H1N1) Virus.

Antiviral Therapy and Outcomes of Patients with Pneumonia Caused by Influenza A Pandemic (H1N1) Virus.

PLoS One. 2012;7(1):e29652

Authors: Yang SG, Cao B, Liang LR, Li XL, Xiao YH, Cao ZX, Jia HY, Yu HJ, Xu Z, Gu L, Yang YD, Chen Y, Du WB, Yan XX, Liang ZA, Zhang W, Zhang CL, Chen W, Guo CP, Jiang XL, Yang M, Deng GM, Yu KJ, Hu K, Zou Q, Li LJ, Wang C,

Abstract
BACKGROUND: There is limited data on the clinical outcome of patients with pandemic H1N1 (pH1N1) pneumonia who received oseltamivir treatment, especially when the treatment was administered more than 48 hours after symptom onset. METHODS: During the pandemic in 2009, a cohort of pH1N1 influenza pneumonia was built in China, and their clinical information was collected systematically, and analyzed with Cox models. RESULTS: 920 adults and 541 children with pneumonia who didn't receive corticosteroids were analyzed. In-hospital mortality was higher in adults who did not receive antiviral therapy (18.2%) than those with who received oseltamivir ≤ 2days (2.9%), between 2-5 days (4.6%) and >5 days after illness onset (4.9%), p<0.01. A similar trend was observed in pediatric patients. Cox regression showed that at 60 days after symptoms onset, 11 patients (10.8%) who did not receive antivirals died versus 4 (1.8%), 18 (3.3%), and 23 (3.7%) patients whose oseltamivir treatment was started ≤ 2days, between 2-5days, and >5 days, respectively. For males patients, aged ≥ 14 years and baseline PaO(2)/FiO(2)<200, oseltamivir administration reduced the mortality risk by 92.1%, 88% and 83.5%, respectively. Higher doses of oseltamivir (>3.8 mg/kg/d) did not improve clinical outcome (mortality, higher dose 2.5% vs standard dose 2.8%, p>0.05). CONCLUSIONS: Antiviral therapy might reduce mortality of patients with pH1N1 pneumonia, even when initiated more than 48 hours after onset of illness. Greater protective effects might be in males, patients aged 14-60 years, and patients with PaO(2)/FiO(2)<200.

PMID: 22276122 [PubMed - as supplied by publisher]

Factors associated with the initiation of proton pump inhibitors in corticosteroid users.

Proton pump inhibitors (PPIs) and corticosteroids are commonly prescribed drugs; however, each has been associated with fracture and community-acquired pneumonia. How physicians select patients for co-therapy may have implications for potential additive or synergistic toxicities.

METHODS: We conducted a retrospective cohort study of 13 749 incident corticosteroid users with no prior PPI exposure using the HealthCore Integrated Research Database(SM) . We used logistic regression to evaluate the association between PPI initiation in the first 30 days of steroid therapy and corticosteroid dose, clinical risk factors including comorbid diseases, and medication use including prescription nonsteroidal anti-inflammatory drugs (NSAIDs).

RESULTS: A new PPI prescription within 30 days of starting corticosteroids was filled by 1050 patients (7.6%). PPI use was associated with the number of baseline comorbid conditions (OR = 1.21 for each additional condition, 95%CI = 1.13-1.28), recent hospitalization (OR = 4.71, 95%CI = 4.02-5.52), prednisone dose higher than 40 mg/day (OR = 1.87, 95%CI = 1.45-2.41), history of gastroesophageal reflux or gastric ulcer disease (OR = 1.54, 95%CI = 1.24-1.91), renal insufficiency (OR = 2.06, 95%CI = 1.73-2.46), and liver disease (OR = 1.82, 95%CI = 1.45-2.28). The concomitant use of prescription NSAIDs was also associated with PPI use (OR = 1.89, 95%CI = 1.32-2.70); however, the total use of PPIs in this group was low (6.3%, 95%CI = 4.4-8.2%).

CONCLUSIONS: Overall, PPI therapy among corticosteroid users was uncommon, even among those with risk factors for gastrointestinal toxicity. PPI use was significantly more common among patients who had recently been hospitalized, had a greater burden of comorbid illness, or were receiving high daily doses of corticosteroids. Copyright © 2012 John Wiley & Sons, Ltd.

Inhaled antibiotics for nosocomial pneumonia.

Pneumonia, especially the more severe forms, is associated with considerable morbidity and mortality. Systemic use of antibiotics is the cornerstone of the management of pneumonia in all patients, including critical care patients.

Several adjunctive strategies have been suggested to improve management. Notably, localized treatment in the lungs via the instillation or inhalation or nebulization of antibiotics may offer the theoretical advantage of a therapy which targets the lung while it has no systematic effects. However, the use of inhaled antibiotics is controversial. Methods of antibiotic delivery and microbiology vary between available studies and despite the favorable profile of this strategy, concerns have been raised by early data that this therapeutic approach may increase the appearance of resistant bacteria.

In this report, we reviewed available evidence from animal and human clinical studies in respect of the role of inhaled antibiotic therapy in pneumonia. In most studies, pneumonia cure rates were found to be comparable to that of systemic antibiotic only therapy and occasionally better.

Inhaled antibiotic therapy was found to have an acceptable safety profile by avoiding systemic toxicity; despite previous concerns regarding the emergence of antimicrobial resistance, recent studies did not support such concerns. However, in respect of the sparity of data larger randomized trial are needed to shed more light in this promising form of treatment.

Chlamydophila pneumonia inhibits the corticosteroid-induced suppressions of metalloproteinase-9 and tissue inhibitor metalloproteinase-1 secretion by human peripheral blood mononuclear cells.

Chlamydophila pneumoniae infection has been suggested to be associated with severe asthma characterized by persistent airway limitation, which may be related to airway remodeling.

We investigated whether C. pneumoniae infection affected the secretion of metalloproteinase-9 (MMP9) and tissue inhibitor metalloproteinase-1 (TIMP1), and altered the responsiveness of inflammatory cells to corticosteroids. Human peripheral blood mononuclear cells (PBMC) were cultured in vitro in the presence or absence of C. pneumoniae.

Secretion of both MMP9 and TIMP1 was strongly suppressed by dexamethasone treatment in uninfected cells. MMP9 secretion was also significantly inhibited by dexamethasone in C. pneumoniae-infected cells, but TIMP1 secretion was not; hence the MMP9 to TIMP1 ratio decreased. Interestingly, expression of human glucocorticoid receptor (GR)β, which is believed to confer resistance to corticosteroids, was enhanced by dexamethasone treatment in C. pneumoniae-infected PBMC.

We conclude that C. pneumoniae infection may promote airway remodeling by decreasing the ratio of MMP9 to TIMP1 secreted by inflammatory cells, and by altering cellular responsiveness to corticosteroids.

An Association Between Neutrophils and Immunoglobulin Free Light Chains in the Pathogenesis of COPD.

CONCLUSION: This study describes for the first time an association between neutrophils and IgLC in the pathophysiology of COPD, which could open new avenues to targeted treatment of this chronic disease. PMID: 22227380 [PubMed - as supplied by publisher] (Source: American Journal of Respiratory and Critical Care Medicine)

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