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Percutaneous fine-needle aspiration is a well established method for the diagnosis of peripheral lung lesion. In order to compare different methods of aspiration, we analyze retrospectively two different series: 267 fine needle aspirations (FNA) compared with the histological diagnosis on surgical specimens and 292 lung biopsies using a coaxial technique with comparison between cytological diagnosis--smears and imprints--and histological diagnosis simultaneously obtained on the same specimen. The sensitivity (91%), the specificity (90%) and the overall typing accuracy related to the histological types obtained by FNAB are equivalent to those of the literature. The low rate of pneumothorax in the series (6%) is related to the use of immediate interpretation of the specimen. Automated biopsy with a coaxial cutting needle provide cytological specimens--smears and imprint--with a high rate of sensibility (95.3%) and of sensibility (98%). The overall sensitivity of the cytological methods alone is better than biopsy (95.3% vs. 92.9%), but the typing accuracy is not as good as biopsy alone (98% vs. 100%). False-positive and false-negative diagnoses are the same in both series. In conclusion the percutaneous aspiration method choose to establish a morphological diagnosis in lung lesion depends now on the habits of the radiologist and the pathologist.

A 47 year old woman developed idiopathic bronchiolitis obliterans organizing pneumonia (BOOP) presenting with haemoptysis and diffuse multiple cavitary nodules. The disease was histologically confirmed by open lung biopsy after other entities had been excluded. The patient responded to a course of corticosteroids. This BOOP should be added to the list of diseases with multiple cavitary nodules.

The anatomical lesions of three subjects suffering from pulmonary histiocytosis X and treated with lung transplantation were studied in order to detail the changes occurring in late stages of the disease; the early stages are known on account of lung biopsies done with a diagnostic aim. All the subjects were, at the time of transplantation, in a precarious clinical state and were practically bed-bound as a result of their dyspnoea with a history of histiocytosis X which had been known for 9, 7 and 3 years respectively; one patient had a cardiopulmonary bypass and two unilateral lung transplant. The results of the histological study produced data which was slightly discordant from the communly held ideas; the de Langerhans cells persist in large numbers and after many years of the evolution of the disease, even though other elements of the granuloma have practically disappeared. Fibrosis is absent playing no role in the genesis of the respiratory failure. The lesions are destructive, leading to a disappearance of the alveolar capillary bed which is the source of the dyspnea. The honeycomb cavities to the destroyed lung are varied in nature: most correspond to the disappearance of the dividing walls of the alveoli or the pulmonary acinus, some others related to dilated terminal bronchioles and finally others to hollowed out granulomas which have become cavities. The peculiar characteristic of the lung allows for destructive cavities to be produced by the airflow, submitted to a process of auto-aggravation by the elastic forces and the tension of the pulmonary parenchyma.

The clinician confronted to the diagnosis of infiltrative lung disease has to consider a wide spectrum of aetiologies. Among them, diffuse fibrosing interstitial lung disease is characterized by the deposition of collagen within alveolar structures. Either acute alveolar injury or chronic inflammatory alveolitis can induce pulmonary fibrosis. Basic research investigates the cells, the cytokines, and the extracellular matrix involved in the perpetuation of the fibropoliferative process.

We studied 77 patients with biopsy-proven WG and pulmonary manifestations, to characterize the nature and frequency of the clinical, imaging and endoscopic features of this condition. Pulmonary symptoms were cough, mild dyspnea, hemoptysis and chest pain. Five patients had no pulmonary symptoms. Imaging features consisted of nodules, infiltrates and pleural opacities. A CT scan proved useful by disclosing cavities in opacities or opacities which were not seen on an x-ray film. Fiberoptic bronchoscopy was performed in 74 patients, and it was macroscopically abnormal in 55 percent (showing bronchial inflammation or stenosis or both or isolated hemorrhage). Six patients presented with alveolar hemorrhagic syndrome. Four patients had a pleural exudate rich in polymorphonuclear leukocytes. The WG was limited to the lung in seven patients. Sixteen patients died because of active disease or iatrogenic complications (two). An improved knowledge of clinical and imaging features of WG could help the clinician reach an earlier diagnosis.

We report four cases of primary pulmonary pseudolymphoma and lymphoma with the usual features of these disorders: lack of symptoms, radiological opacities sometimes multiple with soft wooly contours and air bronchograms, and slowly evolving pattern. The distinction between pseudolymphoma and lymphoma, prior to histological diagnosis is currently controversial. Immunological studies aim at defining whether the lymphoid proliferation is polyclonal or monoclonal (the benign process being considered polyclonal and the malign monoclonal). This distinction works in some cases, as in one of our cases of lymphoplasmacytic lymphoma with a monoclonal IgM gammopathy, a predominance of cells containing IgM on immunofluorescence, and an illness evolving over 9 years. Other cases raise discussion points such as one of our patients with classical histological characteristics of pseudolymphoma, an absence of monoclonal markers on immunofluorescence, but having a monoclonal gammopathy in the serum. This example raises the question as to the possible coexistence of, or a switch over from, a polyclonal to a monoclonal process. In this way the primary pulmonary lymphoproliferative process ought to be considered as one element in a large spectrum ranging from benign to malign disorders and not as distinct illnesses with definitive patterns.

Diffuse pulmonary hemorrhages may occur in pulmonary vasculites, including Wegener disease, systemic lupus erythematosus, Behçet disease, and other systemic vasculites. The pulmonary bleeding is often the first manifestation of the disease and frequently denotes a severe form. The etiologic diagnosis can be established only by performing a surgical lung biopsy, which is often a difficult decision. Leukoclastic capillaritis of the alveolar septa is the common features shared by all the vasculites responsible for pulmonary hemorrhage.

A patient, 37 years old in 1966, presented hemoptysis and an excavated lesion of left upper lobe; there were no acid-fast bacilli in the sputum, but he was considered as having tuberculosis. After one year of treatment, the lesion had progressed and was removed surgically; pathologic diagnosis was silicosis. During the following years, three excavated lesions developed in the controlateral lung. When seen in 1979, the patient had consolidation of the whole right upper lobe and an excavated mass of right lower lobe. Amyloidosis was suggested; the pathologic sections of 1967 were reviewed and confirmed amyloidosis.

The authors report on six cases of pulmonary xanthogranuloma. They stress the latent character of these dense, round isolated parenchymatous tumors. The tumors have an homogeneous aspect without calcifications and regional adenopathies. The radio-clinical diagnosis is difficult to assess because the para-clinical examinations are regularly negative. The differential diagnosis is made either clinically, especially with hamartochondroma and peripheral cancer, or histologically according to the predominance of various types of cells, especially with a solitary plasmocytoma, a lymphoma or a sclerosant hemangioma. Histology is the only key to diagnosis. For these reasons, the decision for surgical intervention presents a problem as the patients, often young, present no visible signs and the lesions evolve but very slowly.

We report a case of lipoid pneumonia complicated by supra-infection with Mycobacterium fortuitum. The diagnosis of a lipoid pneumonia was suggested by the CT Scanner which showed a negative density in the pneumonic tissue. The supra-infection by the mycobacterium dit not change the radiological opacities which stayed the same following a cure of the mycobacterial infection. A histo-pathological study showed evidence of macrophages with voluminous lipid inclusions but equally the atypical mycobacteria were associated with a giant cell-epithelioid reaction. In patients with a lipoid pneumonia the possibility of an infection should be considered and a supra-infection with an atypical mycobacterium should be looked for. At the same time, when a bacteriological study of sputum or fibreoptic aspiration of a rapidly growing mycobacterium is obtained this should raise the possibility of oil inhalations. Alveolar lavage seems to be a technique which seems to be entirely appropriate to obtain the diagnosis of the two concomitant disorders.

Twenty one cases of amyloidosis of the lower respiratory tract were seen at a single center. In three patients, multifocal bronchial amyloid plaques led to stenosis and atelectasis, and in two, small pseudotumor masses were an incidental bronchoscopic finding. Two patients had nodular parenchymal amyloidosis, in one of whom the lesions were progressive and in the other static. Fifteen patients had diffuse parenchymal amyloidosis. Two of these had severe interstitial involvement and died in respiratory failure; eight had congestive cardiac failure, and parenchymal amyloidosis was a post-mortem finding; two had senile cardiorespiratory amyloidosis, also found at autopsy; and in three, the amyloidosis was associated with malignancy. The degree of respiratory embarrassment seemed to be related to the amount of amyloid in the gas diffusion zones, irrespective of the etiology of amyloidosis.