Hepatic Kaposi sarcoma in AIDS: US and CT findings

Abdominal ultrasonography (US) and computed tomography (CT) were performed in two patients with acquired immunodeficiency syndrome (AIDS) and necropsy-proved hepatic Kaposi sarcoma. At US, small (5-12-mm) hyperechoic nodules and dense periportal bands were seen in the liver. These lesions appeared hypoattenuated on baseline and dynamic CT scans and enhanced on delayed scans after a bolus injection of contrast material. Although nonspecific, these features strongly suggest tumor involvement in the liver in patients with AIDS and Kaposi sarcoma

Interleukin-8 expression in bronchoalveolar lavage cells in the evaluation of alveolitis in idiopathic pulmonary fibrosis

AbstractInterleukin-8 (IL-8) is a neutrophilic chemotactic factor which may have a prominent role in the attraction of neutrophils to the lung in idiopathic pulmonary fibrosis (IPF). The objective of this study was to investigate the usefulness of IL-8 expression in bronchoalveolar lavage (BAL) cells in the evaluation of alveolitis in IPF. We analysed the BAL cell expression of IL-8 by immunocytochemistry in 19 patients with IPF (six smokers, three ex-smokers and ten non-smokers) and in a control group composed of 14 individuals (six smokers, eight non-smokers). In IPF, BAL was performed on both the pulmonary lobe with the most extensive involvement and the one less extensively involved on high-resolution computed tomography (HRCT) scans. The percentages and absolute numbers of BAL IL-8+ macrophages from lobes with the most extensive HRCT scan involvement (36 ± 6% and (6 ± 2 × 104 ml−1) (SE) and from those less extensively involved [26% ± 4% and (6 ± 1) × 104 ml−1] were significantly higher with respect to both those from healthy smokers [17% ± 6% and (7 ± 4) × 104 ml−1] and those from non-smokers [2% ± 1% and (1 ± 0·3) × 104 ml−1] (P=0·005 and P=0·001, respectively), without differences between the two lobes. In contrast, both the proportions and the absolute numbers of BAL neutrophils in IPF were significantly higher in lobes with the most extensively involved HRCT scan in comparison with lobes with the least extensive involvement [13% ± 3%, (3 ± 1) × 104 ml−1 vs. 8% ± 2%, (1 ± 0·3) × 104 ml−1, P=0·05]. Moreover, the numbers of BAL neutrophils, but not those of IL-8+ macrophages, correlated with the extent of total pulmonary HRCT scan abnormalities in the most involved lobe (r=0·64, P=0·04). A correlation between neutrophils and IL-8+ cells was not observed. The results of this study suggest that, in IPF, BAL neutrophilia offers a better description of the disease inflammatory process than the expression of IL-8 in BAL cells

A prospective study of lung disease in a cohort of early rheumatoid arthritis patients

Lung disease is common in patients with rheumatoid arthritis (RA). The onset of lung involvement in RA is not well known. The objective is to describe the features and evolution of lung involvement in early RA, its relationship with disease activity parameters, smoking and treatments. Consecutive patients with early RA without respiratory symptoms were included and tracked for 5 years. Lung assessment included clinical, radiological and pulmonary function tests at diagnosis and during follow-up. Peripheral blood parameters (erythrocyte sedimentation rate, C reactive protein, rheumatoid factor and anti-citrullinated peptide autoantibodies) and scales of articular involvement, such as DAS28-CRP, were evaluated. 40 patients were included and 32 completed the 5-year follow up. 13 patients presented lung involvement in the initial 5 years after RA diagnosis, 3 of them interstitial lung disease. Significant decrease of diffusion lung transfer capacity of carbon monoxide over time was observed in six patients, 2 of them developed interstitial lung disease. DLCO decrease was correlated with higher values of CRP and ESR at diagnosis. Methotrexate was not associated with DLCO deterioration or lung disease development. Subclinical progressive lung disease correlates with RA activity parameters. Smoking status and methotrexate were not associated with development or progression of lung disease

Anti-fibrotic Effects Of Pirfenidone And Rapamycin In Primary Ipf Fibroblasts And Human Alveolar Epithelial Cells

Background: Pirfenidone, a pleiotropic anti-fibrotic treatment, has been shown to slow down disease progression of idiopathic pulmonary fibrosis (IPF), a fatal and devastating lung disease. Rapamycin, an inhibitor of fibroblast proliferation could be a potential anti-fibrotic drug to improve the effects of pirfenidone. Methods: Primary lung fibroblasts from IPF patients and human alveolar epithelial cells (A549) were treated in vitro with pirfenidone and rapamycin in the presence or absence of transforming growth factor beta 1 (TGF-beta). Extracellular matrix protein and gene expression of markers involved in lung fibrosis (tenascin-c, fibronectin, collagen I (COM Al], collagen III [COL3A1] and alpha-smooth muscle actin [alpha-SMA]) were analyzed. A cell migration assay in pirfenidone, rapamycin and TGF-beta-containing media was performed. Results: Gene and protein expression of tenascin-c and fibronectin of fibrotic fibroblasts were reduced by pirfenidone or rapamycin treatment Pirfenidone-rapamycin treatment did not revert the epithelial to mesenchymal transition pathway activated by TGF-beta. However, the drug combination significantly abrogated fibroblast to myofibroblast transition. The inhibitory effect of pirfenidone on fibroblast migration in the scratch-wound assay was potentiated by rapamycin combination. Conclusions: These findings indicate that the combination of pirfenidone and rapamycin widen the inhibition range of fibrogenic markers and prevents fibroblast migration. These results would open a new line of research for an anti-fibrotic combination therapeutic approach