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Viral Infection in Acute Exacerbation of Idiopathic Pulmonary Fibrosis.

Idiopathic pulmonary fibrosis is a progressive, uniformly fatal interstitial lung disease. An acute exacerbation of idiopathic pulmonary fibrosis is an episode of acute respiratory worsening without an identifiable etiology. Occult viral infection has been proposed as a possible cause of acute exacerbation.

OBJECTIVES: To use unbiased genomics-based discovery methods to define the role of viruses in acute exacerbation of idiopathic pulmonary fibrosis.

METHODS: Bronchoalveolar lavage and serum from patients with acute exacerbation of idiopathic pulmonary fibrosis, stable disease, and acute lung injury were tested for viral nucleic acid using multiplex polymerase chain reaction, pan-viral microarray, and high-throughput cDNA sequencing.

RESULTS: Four of forty-three acute exacerbation of idiopathic pulmonary fibrosis patients had evidence of common respiratory viral infection (Parainfluenza (n=1), Rhinovirus (n=2), Coronavirus (n=1)); no viruses were detected in the bronchoalveolar lavage from stable patients. Pan-viral microarrays revealed additional evidence of viral infection (herpes simplex virus (n=1), Epstein-Barr virus (n=2), and torque teno virus (TTV) (n=12)) in acute exacerbation patients. TTV infection was significantly more common in acute exacerbation patients than stable controls (p=0.0003), but present in a similar percentage of acute lung injury controls. Deep sequencing of a subset of acute exacerbation cases confirmed the presence of TTV but did not identify additional viruses.

CONCLUSIONS: Viral infection was not detected in the majority of acute exacerbation of idiopathic pulmonary fibrosis cases. TTV was present in a significant minority of cases, as well as cases of acute lung injury; the clinical significance of this finding remains to be determined.

The Th17 Pathway in Cystic Fibrosis Lung Disease.

Rationale Cystic fibrosis (CF) is characterized by bronchoalveolar neutrophilia, but submucosal lymphocytosis. We hypothesized that Th17 lymphocytes are part of this submucosal infiltrate.

Objectives Quantification and phenotyping of the lymphocytic infiltrate in the bronchial submucosa of patients with CF (n=53, of which 20 were newly diagnosed), non-CF bronchiectasis (n=17) and healthy controls (n=13).

Methods We measured IL-17 levels in bronchoalveolar lavage and CD4+, CD8+ and IL-17+ cell counts in endobronchial biopsies. Correlations were made with infection status and other inflammatory markers. Potential cellular sources of IL-17 were determined by double staining.

Measurements and main results IL-17+ cell counts (median[interquartile range]cells/mm(2)) were significantly higher in established CF (205[115-551]) and non-CF bronchiectasis (245[183-436]) than controls (53[12-82]) (p<0.01 for both). Newly diagnosed CF patients had intermediate counts (171[91-252]). IL-17 positive CD4+ T cells, γδT-cells, NKT cells and neutrophils were identified. Bronchoalveolar lavage IL-17 levels(pg/ml) were highest in established CF (14.6[2.2-38.4]), low in newly diagnosed CF patients and controls (1.7[1.7-1.74]; 1.7[1.7-3]) and intermediate in non-CF bronchiectasis (9.1[1.7-34]pg/ml) (KW p=0.001). There was a significant correlation between IL-17 and neutrophil counts (p<0.001, R=0.6) as well as IL-4 (p<0.001, R=0.84).

Conclusions Th17 lymphocytes are present in the airway submucosa in CF, even in a young, newly diagnosed group. Other IL-17+ cells include neutrophils, γδ T cells and NKT cells.

Update on the diagnosis and treatment of Pneumocystis pneumonia.

Pneumocystis is an opportunistic fungal pathogen that causes an often-lethal pneumonia in immunocompromised hosts. Although the organism was discovered in the early 1900s, the first cases of Pneumocystis pneumonia in humans were initially recognized in Central Europe after the Second World War in premature and malnourished infants. This unusual lung infection was known as plasma cellular interstitial pneumonitis of the newborn, and was characterized by severe respiratory distress and cyanosis with little or no fever and no pathognomic physical signs. At that time, only anecdotal cases were reported in adults and usually these patients had a baseline malignancy that led to a malnourished state.

In the 1960-1970s additional cases were described in adults and children with hematological malignancies, but Pneumocystis pneumonia was still considered a rare disease. However, in the 1980s, with the onset of the HIV epidemic, Pneumocystis prevalence increased dramatically and became widely recognized as an opportunistic infection that caused potentially life-treating pneumonia in patients with impaired immunity. During this time period, prophylaxis against this organism was more generally instituted in high-risk patients. In the 1990s, with widespread use of prophylaxis and the initiation of highly active antiretroviral therapy (HAART) in the treatment of HIV-infected patients, the number of cases in this specific population decreased. However, Pneumocystis pneumonia still remains an important cause of severe pneumonia in patients with HIV infection and is still considered a principal AIDS-defining illness. Despite the decreased number of cases among HIV-infected patients over the past decade, Pneumocystis pneumonia continues to be a serious problem in immunodeficient patients with other immunosuppressive conditions. This is mostly due to increased use of immunosuppressive medications to treat patients with autoimmune diseases, following bone marrow and solid organ transplantation, and in patients with hematological and solid malignancies.

Patients with hematologic disorders and solid organ and hematopoietic stem cell transplantation are currently the most vulnerable groups at risk for developing this infection. However, any patient with an impaired immunity, such as those receiving moderate doses of oral steroids for greater than 4 weeks or those receiving other immunosuppressive medications are at also at significant risk.

Transtracheal oxygen therapy.

Transtracheal oxygen therapy (TTO) has been used for long-term oxygen therapy for nearly 30 years. Numerous investigators have explored the potential benefits of TTO. Those results are reviewed in this article. TTO is best viewed not as a catheter but as a program for care.

This article discusses patient selection for TTO. Publications evaluating complications are reviewed. In the past, a modified Seldinger technique (MST) was used for the creation of the tracheocutaneous fistula. The rather long program required for tract maturation with MST was labor-intensive and required substantial patient education and monitoring, particularly during the immature tract phase. Minor complications were not infrequent. More recently, the Lipkin method has been used to create a surgical tract under conscious sedation with topical anesthesia. The procedure is safe and well tolerated. Transtracheal oxygen is initiated the day following the procedure. Similarly, the tract matures in 7 to 10 days rather than the 6 to 8 weeks with MST. More rapid healing time and superior tract characteristics substantially reduce complications. The TTO program tailored for the Lipkin procedure is shortened, streamlined, and much less labor-intensive. Optimal outcomes with the TTO program require a committed pulmonologist, respiratory therapist, nurse, and surgeon (for the Lipkin procedure).

This article discusses new directions in the use of transtracheal gas delivery, including the management of obstructive sleep apnea. Preliminary investigations regarding transtracheal augmented ventilation are presented. These include nocturnal use in severe chronic lung disease and liberation from prolonged mechanical ventilation.

Functional disability 5 years after acute respiratory distress syndrome.

There have been few detailed, in-person interviews and examinations to obtain follow-up data on 5-year outcomes among survivors of the acute respiratory distress syndrome (ARDS).

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