Anastassios V. Koutsopoulos

Decreased Small Airway and Alveolar CD83+ Dendritic Cells in COPD

BACKGROUND Dendritic cells (DCs) have been reported to be increased in the small airways of patients with COPD, but the maturity status of these cells is unclear. We have quantified the numbers of cells expressing markers associated with DC maturation. METHODS Lung tissue was obtained at resection for lung cancer from 41 patients with COPD (30 current smokers and 11 ex-smokers; 32 steroid-treated patients and 9 steroid-naïve patients), 19 ex-smokers without COPD and 9 never-smokers without COPD. Tissue sections were immunostained for CD1a to mark immature DCs, and for CD83, fascin, and DC-lysosome-associated membrane protein (DC-LAMP) to delineate mature DCs. RESULTS The volume density (ie, the volume of DCs as the percentage volume of the airway wall) comprising CD83+ DCs was significantly reduced in patients with COPD (median, 0; range, 0 to 5.1%) vs smokers (median, 2.8%; range, 0 to 10.2%) and never-smokers (median, 1.9%; range, 0.8 to 5.1%) without COPD (p = 0.000 and 0.012, respectively). Using a semiquantitative score for the alveolar wall, CD83+ DCs also were decreased in patients with COPD (median, 0; range, 0 to 2%) vs smokers (median, 1%; range, 0 to 2%) and never-smokers (median, 1%; range, 0.7 to 2%) without COPD (p = 0.004 and 0.04, respectively). No differences were detected in CD83+ DCs between current smokers and ex-smokers with COPD or between steroid-treated and steroid-naive patients. No differences were detected in CD1a+ DCs. Fascin and DC-LAMP were found to have poor specificity for mature DCs. CONCLUSIONS COPD is associated with decreased numbers of (mature) CD83+ DCs in small airways and alveoli. The relevance of such a reduction on pulmonary immune responses requires further investigation.

Altered Surfactant Protein-A Expression in Type II Pneumocytes in COPD

BACKGROUND Pulmonary surfactant protein A (SP-A) is a lectin, with multiple functions that contribute to innate host defense and the regulation of the inflammatory process in the lung. In normal conditions, SP-A seems to protect against the effects of smoking. However, studies in smokers with or without COPD are limited. METHODS Western blots on lung tissue specimens from 60 male subjects (32 patients with COPD, 18 smokers without COPD, and 10 control nonsmokers) for SP-A and the housekeeping protein actin were carried out. Additionally, the SP-A expression pattern was evaluated by immunohistochemistry in formalin-fixed, paraffin-embedded lung tissue sections from the same subjects. RESULTS Western blots revealed significantly higher SP-A levels in control nonsmokers (4.8 +/- 0.05) when compared with patients with COPD (0.6 +/- 0.7) and smokers without COPD (2.4 +/- 0.9), (P < .05). However, differences that were not statistically significant were observed in SP-A levels among the patients with COPD and the smokers without COPD (P = .12). The immunohistochemical examinations showed an increase in the overall number of type II pneumocytes per high-power field in patients with COPD, but a decreased ratio of SP-A positive type II pneumocytes to total type II pneumocytes, compared with smokers without COPD (P = .001). This ratio was also correlated with FEV(1) (percent predicted [% pred]), (r = 0.490, P = .001). The overall number of alveolar macrophages per high-power field was significantly higher in patients with COPD compared with smokers without COPD (P = .001). The ratio of SP-A positive alveolar macrophages was increased in patients with COPD when compared with smokers without COPD (P = .002), while this was correlated with airway obstruction (FEV(1), % pred) (r = 0.281, P = .04). CONCLUSIONS Our results indicate that altered SP-A expression could be another link to COPD pathogenesis and highlights the need for further studies on surfactant markers in COPD.

A novel combination of multiple primary carcinomas: Urinary bladder transitional cell carcinoma, prostate adenocarcinoma and small cell lung carcinoma- report of a case and review of the literature

BackgroundThe incidence of multiple primary malignant neoplasms increases with age and they are encountered more frequently nowadays than before, the phenomenon is still considered to be rare.Case presentationWe report a case of a man in whom urinary bladder transitional cell carcinoma, metachronous prostate adenocarcinoma and small cell lung carcinoma were diagnosed within an eighteen-month period. The only known predisposing factor was that he was heavy smoker (90–100 packets per year). The literature on the phenomenon of multiple primary malignancies in a single patient is reviewed and the data is summarized.ConclusionIt is important for the clinicians to keep in mind the possibility of a metachronous (successive) or a synchronous (simultaneous) malignancy in a cancer patient. It is worthy mentioning this case because clustering of three primary malignancies (synchronous and metachronous) is of rare occurrence in a single patient, and, to our knowledge, this is the first report this combination of three carcinomas appearing in the same patient.

Active Remodeling in Idiopathic Interstitial Pneumonias: Evaluation of Collagen Types XII and XIV

Fibril-associated collagens with interrupted triple helices (FACITs) XII and XIV act as fibril organizers and assist in the maintenance of uniform fibril size. We investigated the spatial expression patterns of collagens XII and XIV in cryptogenic organizing pneumonia (COP)/organizing pneumonia (OP) and in idiopathic pulmonary fibrosis (IPF)/usual interstitial pneumonia (UIP) and compared them to normal human lung. Study subjects included 10 patients with COP/OP, 10 patients with IPF/UIP, and 8 control subjects. Immunostaining for collagens XII and XIV was carried out in paraffin-embedded human lung tissue sections. Picrosirius red histochemical staining for collagen I expression and electron microcopy to evaluate fibril diameter were also performed. In normal lung, collagens XII and XIV were expressed in perivascular and subpleural connective tissue. In COP/OP, both collagens showed intense staining in perivascular connective tissue, thickened alveolar septae, and subpleural areas. In IPF/UIP, XII and XIV were expressed in perivascular connective tissue, in areas of established fibrosis, and in areas of subpleural thickening. Only collagen XII was expressed in granulation tissue plugs in COP/OP and in fibroblastic foci in IPF/UIP. Collagen type I was overexpressed in fibrotic areas. Electron micrographs revealed obvious fibril diameter alteration and fusion in the same areas. FACITs XII and XIV are expressed in normal and fibrotic lung. Unlike collagen XIV, collagen XII was expressed in granulation tissue plugs in COP/OP and in fibroblast foci in IPF/UIP. This may suggest a possible distinct role for both collagens in the modulation of the extracellular matrix during the onset of fibrotic process.

Meningioangiomatosis with predominantly cellular pattern.

A case of meningioangiomatosis (MA), in a 10‐year‐old‐girl with refractory complex partial and secondary generalized seizures, starting at the age of 8 years, is presented. MRI evaluation revealed a lesion located at the left frontal lobe; the patient underwent surgical lesionectomy. Histology revealed the lesion to have the features of MA. The patient is symptom‐free a year postoperation. We report the histological, immunohistochemical and imaging findings in view of previous pertinent reports.

Is a miliary chest pattern always indicative of tuberculosis or malignancy

Case Report A 36-year-old Caucasian woman presented with a 10-month history of increased dyspnea on exertion that pro-gressed to marked shortness of breath at rest a few days prior to hospital admission. Her past medical history in-cluded a hysterectomy 24 months previously, secondary to the enucleation of a leiomyoma, which was compli-cated by uncontrolled bleeding. Physical examination was remarkable for labored respirations with a rate of 28 breaths/min and inspiratory crackles at both lungs. PaO