Objective. To assess the correlation between ultrasound lung comets (ULCs, a recently described echographic sign of interstitial lung fibrosis) and the current undisputed gold-standard high-resolution CT (HRCT) to detect pulmonary fibrosis in patients with SSc. Methods. We enrolled 33 consecutive SSc patients (mean age 54 ± 13 years, 30 females) in the Rheumatology Clinic of the University of Pisa. We assessed ULCs and chest HRCT within 1 week independently in all the patients. ULC score was obtained by summing the number of lung comets on the anterior and posterior chest. Pulmonary fibrosis was quantified by HRCT with a previously described 30-point Warrick score. Results. Presence of ULCs (defined as a total number more than 10) was observed in 17 (51%) SSc patients. Mean ULC score was 37 ± 50, higher in the diffuse than in the limited form (73 ± 66 vs 21 ± 35; P < 0.05). A significant positive linear correlation was found between ULCs and Warrick scores (r = 0.72; P < 0.001). Conclusions. ULCs are often found in SSc, are more frequent in the diffuse than the limited form and are reasonably well correlated with HRCT-derived assessment of lung fibrosis. They represent a simple, bedside, radiation-free hallmark of pulmonary fibrosis of potential diagnostic and prognostic value.

We followed prospectively 834 consecutive patients (70% inpatients), evaluated for suspected pulmonary embolism, for a median time of 2.1 years (range, 0-4.8 yr), and compared the survival rates in patients with proven pulmonary embolism (n = 320) with those without (n = 514). In multivariate analysis, we modeled the probability of surviving in patients with pulmonary embolism as a function of the extent of pulmonary vascular obstruction at baseline. Among patients with pulmonary embolism, a scintigraphic follow-up was pursued to assess the restoration of pulmonary perfusion over a 1-year period. We found that massive pulmonary embolism (vascular obstruction ≥50%) is a risk factor for mortality within the first few days after onset but, subsequently, has no significant effect on survival. The adjusted risk of death in patients with massive pulmonary embolism was 8-fold higher than in patients without embolism within the first day after the incident event. By contrast, the adjusted risk of death for patients with minor or moderate pulmonary embolism (vascular obstruction <50%) was no higher than in patients without embolism at any time after onset. Most of the patients who survived a year after pulmonary embolism showed a nearly complete restoration of pulmonary perfusion with a considerable improvement in arterial oxygenation. Four (1%) of the 320 patients with pulmonary embolism at presentation developed chronic thromboembolic pulmonary hypertension. These patients featured persistent large perfusion defects in sequential lung scans. Pulmonary embolism with vascular obstruction ≥50% is a strong, independent predictor of reduced short-term survival. This underscores the need for a prompt diagnosis of the disease. Monitoring the resolution of pulmonary embolism by lung scanning may prove useful in identifying patients with persistent perfusion abnormalities who may be at risk of chronic thromboembolic pulmonary hypertension.

The lung pathology of severe chronic obstructive pulmonary disease (COPD) has been poorly investigated. We examined surgical specimens obtained from patients with severe (forced expiratory volume in 1 second [FEV₁] = 29 ± 3% predicted, n = 9) or mild/no airflow limitation (FEV₁ = 86 ± 5% predicted, n = 9) and similar smoking history. With histochemical and immunohistochemical methods we quantified the structural changes and the inflammatory cells in small airways and in muscular pulmonary arteries. As compared with smokers with mild/no COPD, smokers with severe COPD had an increased number of leukocytes in the small airways, which showed a positive correlation with the radiologic score of emphysema and with the value of residual volume, and a negative correlation with the values of FEV₁ and carbon monoxide diffusing capacity. The inflammatory process was characterized by an increase in CD8⁺ and CD4⁺ T-lymphocytes in the airway wall and by an increase in macrophages in the airway epithelium. When all smokers were considered together, the smoking history was correlated with both the airway wall and smooth muscle thickness, suggesting that smoking itself may play a role in the development of structural changes. No structural and cellular differences were observed in pulmonary arteries between smokers with severe COPD and smokers with mild/no COPD. In conclusion, in the small airways of smokers with severe COPD, there is an increased number of leukocytes, which is correlated with reduced expiratory flow, lung hyperinflation, carbon monoxide diffusion impairment, and radiologic emphysema, suggesting a role for this inflammatory response in the clinical progression of the disease.

Oxidant/antioxidant imbalance is implicated in the pathogenesis of chronic obstructive pulmonary disease (COPD).The current study examined the expression of antioxidant and pro-oxidant enzymes, haem oxygenases (HO) and inducible nitric oxide synthase (iNOS) respectively, in patients with severe COPD and control smokers without lung function impairment. Immunoreactivity for HO-1, HO-2, iNOS and nitric oxide-derived oxidants expressed as nitrotyrosine (N-Tyr) was quantified in peripheral lung.HO-1+ alveolar macrophages were decreased in severe COPD compared to control smokers, whereas no difference was observed in iNOS+ macrophages. In contrast, severe patients had significantly higher numbers of iNOS+ cells in alveolar walls. These iNOS+ cells were identified as type 2 pneumocytes and their number was inversely related to HO-1+ macrophages. There were no significant differences in N-Tyr immunostaining between the two groups. However, the rate of protein nitration in lungtissue was directly related to iNOS expression and associated with lower valuesofforced expiratory volume in one second/forced vital capacity. HO-2 was constitutively expressed by type 2 pneumocytes and these cells were increased in severe COPD.In conclusion, the results suggest that the enzymes involved in the oxidative stressresponse may have a different role in the lung defence and that imbalance betweenhaemoxygenase-1 and inducible nitric oxide synthase may be associated withthe development of severe impairment in chronic obstructive pulmonary disease patients.