Inflammatory response to acute hypoxia in humans.

BACKGROUND: In animal studies hypoxia is known to cause an inflammatory response, inducing multiple transcription factors and activating molecular processes at the cellular level. However, it is not known whether acute hypoxia causes similar inflammatory effects in humans, although such an assumption is commonly made. METHODS: The effects of acute hypoxic exposure were studied in 12 healthy adults: Each subject was studied on 2 different days. Group 1 (mean age 33 ± 5.5 years; 2 females, 4 males) was exposed either to a hypoxic gas mixture or room air for 30 min and Group 2 (mean age 26.5 ± 7.5 years; 3 females, 3 males) for 60 min. Measurements of circulating adhesion molecules (AMs), Clara cell secretory protein (CC16), hypoxia inducible factor 1α (HIF-1α), vascular endothelial growth factor (VEGF), interleukin-6 (IL-6), tumor necrosis factor (TNF-α), and C reactive protein (hsCRP) were made at baseline and at intervals following exposure for 240 min. RESULTS: No significant changes were seen in circulating AMs, CC16, TNF-α, IL-6 or hsCRP, although both HIF-1α and VEGF levels increased significantly (p < 0.05) after hypoxic exposure. CONCLUSIONS: Acute hypoxic exposure in normal man does not induce a measurable change in inflammatory or epithelial biomarkers, in contrast to studies at the cellular level in animals. However, acute hypoxic exposure does induce the expression of HIF-1α and VEGF. These results indicate that in humans acute hypoxic exposure for up to 60 min does not induce a generalized inflammatory response, indicating that the human response to hypoxia is more complex than inferred from animal/cellular studies.

Tracheal aspirate Gram stain has limited sensitivity and specificity for detecting Staphylococcus aureus.

BACKGROUND AND OBJECTIVE: The increasing incidence of respiratory infections due to methicillin resistant Staphylococcus aureus has resulted in increased empirical use of antibiotics active against this pathogen. There are limited data available as to whether the Gram stain of respiratory tract secretions accurately predicts growth of S. aureus. We theorized that the distinctive morphology of S. aureus would allow rapid, accurate identification of the organism in respiratory secretions. METHODS: The authors reviewed all available Gram stains of tracheal aspirates sent to our hospital's microbiology laboratory between 1 April 2008 and 31 October 2008, while blinded to the culture result, and recorded the presence or absence of organisms with a morphology consistent with S. aureus. These results were correlated with the semiquantitative culture result. RESULTS: Among 136 tracheal aspirates studied, 50 (37%) grew S. aureus. The Gram stain was read as positive for organisms consistent with S. aureus in 34 of these. Among 86 samples that did not grow S. aureus, the Gram stain was read as negative in 62. Therefore, the Gram stain had a sensitivity of 68%, a specificity of 72%, a negative predictive value of 80% and a positive predictive value of 59% for culture of S. aureus. False negative Gram stains were more likely when the culture revealed only rare or small growth of S. aureus (P = 0.01). CONCLUSIONS: In this study, the tracheal aspirate Gram stain read by an experienced clinician who was not a microbiologist, was not accurate enough to reliably predict the growth of S. aureus.

Pulmonary artery agenesis and Kommerell's diverticulum presenting with hemoptysis.

Unilateral pulmonary artery agenesis is a rare congenital anomaly that is commonly associated with additional cardiovascular abnormalities. We report a case of intrapulmonary hemorrhage and hemoptysis in a patient with left-sided pulmonary artery agenesis as well as the first description of this anomaly in a patient with a diverticulum of Kommerell. The patient was successfully treated by performing a left pneumonectomy.

Two faces of MAC-induced lung disease.

Lung disease due to mycobacterium avium complex (MAC) is being increasingly recognized. The clinical and radiological manifestations are varied and treatment is complex. We present two cases of MAC-induced lung disease to illustrate this disease.