Relapsing bronchiolitis obliterans organising pneumonia and chronic sarcoidosis in an atopic asthmatic patient.

Asthma is thought to be a Th2 disease while sarcoidosis is considered a Th1 granulomatous disorder. Organising pneumonia is a histologic pattern of lung injury. When it has no recognisable cause it is defined as cryptogenic organising pneumonia. We herein report the case of a patient with recurrent and steroid sensitive organising pneumonia associated with chronic sarcoidosis in an atopic, moderate persistent asthmatic patient. Each disease has been documented with transbronchial biopsies and recurrence of organising pneumonia was suggested by clinical features and by follow up HRCT which shows distinctive signs even in associated disease. Steroids are the mainstay of therapy for these disorders and especially for the consolidated processes typical of organising pneumonia but prognostic indices for relapse and progression are lacking.

Sarcoidosis of the thyroid gland associated with hyperthyroidism: review of the literature and report of two peculiar cases.

Sarcoidosis is a systemic disease characterized by non-caseating granulomas that rarely involve the thyroid gland. Thyroid sarcoidosis has seldom been documented, and few cases have so far been described in association with hyperthyroidism. Here, we review the literature on this association, report two patients presenting with hyperthyroidism and histologically-proven sarcoidosis, and discuss related clinical, biochemical, pathological and genetic findings.

Haemorrhagic pericardial effusion in an asbestos worker.

BACKGROUND: Occupational exposure to asbestos may cause pleural and lung disorders and, less frequently, diseases of the peritoneum and pericardium. An exceedingly small number of cases of benign pericardial effusion have been described so far in the medical literature. OBJECTIVES: To report a rare case of haemorrhagic pericardial effusion caused by occupational asbestos exposure in a patient with pre-existent aortic regurgitation, bilateral pleural plaques and no signs of interstitial lung involvement due to asbestosis. METHODS: A thorough clinical and instrumental evaluation (laboratory tests, tuberculin skin test, chest X-rays, transthoracic and transesophageal echocardiography, contrast coronary and aortic angiography, a histological examination of pericardial and pleural surgical specimens) was performed to examine all the known causes of pericardial effusion. RESULTS: The tests performed did not demonstrate any specific cause of pericardial effusion. Surgical assessment three months later, during an aortic valve replacement, showed no signs of aortic dissection or intraparietal hematoma. A nine-year follow up did not reveal any reoccurrence of pericardial effusion. CONCLUSIONS: Asbestos related pericardial effusion is rarely described in the medical literature but must be considered in patients with previous occupational asbestos exposure. There are no specific clinical or pathological aspects indicative of this etiology and the diagnosis remains one of exclusion. A thorough occupational history should be obtained in patients with pericardial effusion of unknown etiology.

The influence of hay-packing techniques on the presence of saccharopolyspora rectivirgula.

Environmental factors influencing the growth, distribution and viability of thermophilic actinomycetes, especially Saccharopolyspora rectivirgula as an agent of extrinsic allergic alveolitis in farms workers, were studied. Total microbial count, eumycetes and thermophilic actinomycetes were determined on 96 hay samples, randomly collected, from small prismatic and large cylindrical bales, 30 air samples before and after animal feeding, and various surfaces in two farms located in the province of Reggio Emilia, Italy. The number of thermophilic actinomycetes (potentially responsible for hypersensitivity pneumonitis) was higher in hay samples from large cylindrical bales than in those from small prismatic bales. The structural characteristics of the buildings (barns with stalls, poor ventilation) and the feeding practices (manual handling of hay, constant presence of hay in feedings corridors) contributed to the dispersion of high levels of thermophilic actinomycetes spores (potentially responsible for extrinsic allergic alveolitis). The ventilation system proved to be inadequate in reducing the number of microorganisms present.

Human health and air conditioning systems.

In air-conditioned buildings indoor air quality is closely dependent on the efficiency of air-conditioning and humidifier systems since these systems provide a suitable environment for the proliferation of microorganisms. Pollutants released by microorganisms are termed 'bioaerosols' and may be spread in the indoor environment through the air-conditioning system. Moreover, the tightening of the buildings in which central air-conditioning systems are usually located increases the levels of indoor pollutants. Both hypersensitivity and infectious diseases are associated with bioaerosol exposure, whereas the sick building syndrome (a complex of symptoms described among workers in modern office buildings which are hermetically sealed and mechanically ventilated) is very unlikely to have a bioaerosol component.

Primary malignant non-Hodgkin's lymphoma of the lung arising in mucosa-associated lymphoid tissue (MALT).

We describe a 10 yr follow-up of a patient with a primary malignant non-Hodgkin's lymphoma of the lung, arising in mucosa-associated lymphoid tissue (MALT). Although the patient was not treated with chemotherapy or radiotherapy, no peripheral spread occurred, confirming that MALT-associated lymphomas apparently remain localized until late in the course of the disease.

[Round atelectasis of the lung: clinicopathological study of 6 cases and review of the literature]. / Atelettasia rotonda del polmone: studio clinicopatologico di 6 casi e revisione della letteratura.

OBJECTIVE: To report about 6 new patients with round atelectasis of the lung, 1 of them professionally exposed to asbestos and another to silicates. RESULTS: The patients, 5 males and 1 female, presented with a peripheral, rounded pulmonary opacity, simulating a neoplasm. The examination of the surgical specimen revealed a pleuritis, with multiple pleural folding: the underlying lung parenchima was compressed, but otherwise unremarkable. CONCLUSIONS: Round atelectasis is relatively unusual for the pathologist. However, the correct diagnosis is potentially important, because the lesion can be the sign of a significant asbestos exposure.

Comparison of leukocyte counts in sputum, bronchial biopsies, and bronchoalveolar lavage.

To determine the relationship between inflammatory cells in sputum, bronchoalveolar lavage (BAL), and bronchial mucosa, we counted the number of leukocytes in sputum, BAL, and bronchial biopsies obtained from subjects with asthma and with chronic bronchitis in stable condition or during exacerbations. Sputum was induced by inhalation of hypertonic saline in the asthma group. Spontaneous sputum was collected in the chronic bronchitis groups. Differential counts of leukocytes were performed on cytospin preparations of sputum and BAL. Eosinophils, macrophages, neutrophils, and lymphocytes were quantified in the submucosa of the bronchial biopsies. In asthma and in stable chronic bronchitis, the percentages of neutrophils were significantly higher in sputum than in BAL, whereas the opposite was true of the percentages of macrophages and lymphocytes. The lymphocyte was the predominant cell infiltrating the bronchial submucosa in all groups. BAL eosinophils correlated with submucosal and sputum eosinophils in the asthma and exacerbated chronic bronchitis groups. A similar trend was observed between submucosal and sputum eosinophils. In conclusion, the relative proportion of inflammatory cells was different in sputum, BAL, and bronchial mucosa. However, there was a fairly good agreement between the number of eosinophils counted with the three techniques in asthmatics and in exacerbated chronic bronchitics, suggesting that sputum cell analysis may be used for a noninvasive assessment of airway eosinophilia.

Airflow limitation in chronic bronchitis is associated with T-lymphocyte and macrophage infiltration of the bronchial mucosa.

To investigate whether the airway inflammatory process is different in patients with chronic bronchitis with airflow limitation and those with chronic bronchitis without airflow limitation, we obtained bronchial biopsies from 14 subjects with chronic sputum production and fixed airway obstruction, and from 10 subjects with chronic sputum production and normal FEV1, all with a history of cigarette smoking. Paraffin-embedded and frozen bronchial biopsies were examined by immunohistochemistry to identify the number of neutrophils (neutrophil-elastase), eosinophils (antieosinophil cationic protein [EG-2]), mast cells (tryptase), T-lymphocytes (CD3), T-lymphocyte subpopulations (CD4 and CD8), B-lymphocytes, and macrophages (CD68) in the submucosa. Subjects with chronic bronchitis with airflow limitation had a greater number of T-lymphocytes (p < 0.01) and macrophages (p < 0.05) than subjects with chronic bronchitis without airflow limitation, whereas the T-lymphocyte subpopulations and the numbers of B-lymphocytes, neutrophils, eosinophils, and mast cells were similar in the two groups. When all the subjects were considered together, the number of T-lymphocytes correlated inversely with the values of FEV1 (r = 0.46, p < 0.02). In conclusion, airflow limitation in subjects with chronic bronchitis is associated with an increased number of T-lymphocytes and macrophages in the bronchial mucosa.

Airway eosinophilia in chronic bronchitis during exacerbations.

To examine the nature and the degree of airway inflammation in chronic bronchitis during exacerbations, bronchial biopsies and sputum were obtained in 11 subjects with chronic bronchitis examined during an exacerbation, and in 12 subjects with chronic bronchitis examined under baseline conditions. All subjects were nonatopic. Lobar bronchial biopsies were assessed using histochemical and immunohistochemical techniques, and sputum was examined for differential cell counts of leukocytes. Subjects with bronchitis during exacerbations had, on average, 30-fold more eosinophils in their bronchial biopsies than did those examined under baseline conditions (p < 0.001). Although to a lesser extent, the numbers of neutrophils (p < 0.01), T-lymphocytes (CD3) (p < 0.05), VLA-1-positive cells (p < 0.01), and TNF-alpha positive cells (p < 0.05) were also increased during exacerbations. By contrast, the T-lymphocyte subpopulations (CD4 and CD8) and the numbers of macrophages, mast cells, IL-2R-positive cells, and IL-1 beta-positive cells were similar in the two groups of subjects, as well as the percentages of ICAM-1- and E-selectin-positive vessels. Eosinophils were also increased in sputum of subjects with exacerbations when compared with those examined under baseline conditions (p < 0.05). In conclusion, exacerbations of chronic bronchitis are associated with a marked airway eosinophilia and with a milder increase in the number of neutrophils, activated T-lymphocytes, and TNF-alpha-positive cells in the bronchial mucosa.

Upregulation of adhesion molecules in the bronchial mucosa of subjects with chronic obstructive bronchitis.

To determine whether adhesion molecules and cytokines are upregulated in the bronchial mucosa of chronic bronchitics, we obtained bronchial biopsies in 16 chronic bronchitics, in eight asymptomatic smokers, and in seven normal nonsmoking subjects. Bronchial biopsies were examined by immunohistochemistry to identify the expression of E-selectin and intercellular adhesion molecular-1 (ICAM-1) on vessels and on bronchial epithelium, and the expression of interleukin-1 beta (IL-1 beta), tumor necrosis factor-alpha (TNF-alpha), neutrophil elastase, and eosinophil cationic protein (EG-2) on cells in the submucosa. Chronic bronchitics had an increased number of E-selectin-positive vessels when compared with both asymptomatic smokers (p < 0.05) and normal subjects (p < 0.01). The numbers of ICAM-1-positive vessels, neutrophils, and IL-1 beta, TNF-alpha-, and EG-2-positive cells were not significantly different in the three groups of subjects examined. When the bronchitic group was divided according to the presence or absence of airway obstruction, the increased number of E-selectin-positive vessels persisted only in bronchitics with airway obstruction, who also had an increased expression of ICAM-1 on basal epithelial cells. We concluded that in the bronchial mucosa of chronic bronchitics with airway obstruction, there is an increased expression of E-selectin on vessels and of ICAM-1 on basal epithelial cells, suggesting the involvement of these adhesion molecules in the pathogenesis of the disease.

Effect of smoking cessation on airway inflammation in chronic bronchitis.

To investigate the effect of smoking cessation on the airway inflammatory process present in nonatopic subjects with chronic bronchitis, we obtained bronchial biopsies from nine current smokers and seven exsmokers, all with symptoms of chronic bronchitis at the time of the study, and from seven healthy nonsmoking subjects. The exsmokers had stopped smoking on average 13 yr before the study, yet cough and production of sputum had persisted. Bronchial biopsies were assessed using immunohistochemical techniques to investigate the number of inflammatory cells, the markers of mononuclear cell activation, and the expression of endothelial adhesion molecules and cytokines in the subepithelium. Current smokers and exsmokers had an increased number of macrophages, IL-2R-positive cells, VLA-1-positive cells, ICAM-1-positive vessels, and E-selectin-positive vessels compared with normal nonsmoking subjects, but the number of cells positive for neutrophils, EG-2, CD3, CD4, CD8, TNF-alpha and IL-1 beta were similar among the three groups. No differences were observed between current smokers and exsmokers for any parameter examined. In conclusion, the inflammatory process present in the airway mucosa of current smokers may persist after smoking cessation in subjects who continue to have symptoms of chronic bronchitis.