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The article presents a case of an unusual cause of patchy ground-glass opacity. It involves a 33-year old man who was admitted with acute respiratory distress following a suicide attempt. It states that an axial thin-section computed tomographic (CT) scan revealed multiple patchy ground-glass opacities with accentuated interlobular septal thickening in both upper lung fields. Related topics are discussed.

Cannabis is widely smoked in Europe and its increasing use is becoming a major public health problem. Adulterating cannabis with glass beads or sand is a new trick used by dealers to increase the weight and boost profits. These recent practices are not without danger. We report two cases of respiratory symptoms related to the use of this kind of adulterated cannabis. The first case is a 33 year-old patient admitted for an acute inhalation pneumonitis secondary to smoking cannabis adulterated with grit sand. The CT scan showed patchy ground-glass opacities, mainly in the upper lobes. A broncho-alveolar lavage, examined under polarized light, revealed birefringent intracellular particles, identified as silica, in alveolar macrophages. Spontaneously clinical and radiological improvements were observed after stopping the use of contaminated cannabis. The second patient, who smoked cannabis mixed with glass beads, described epistaxis, mouth ulcers, sore throats and cough. CT scan and BAL were normal. Adulteration of cannabis with microscopic glass beads, alone or mixed with sand, is a recent and widespread practice in Europe. These anecdotal reports prompted the French Department of Health to advise cannabis smokers of the harmfulness of these contaminants.

Introduction: Necrotising sarcoid granulomatosis is a rare clinical entity, characterised by the development of nodular pulmonary opacities, the diagnosis if which is based on the identification of characteristic pathological lesions., Case Report: A 44-years-old male smoker presented with cough and fever. With the exception of a few basal crepitations clinical examination was normal. The chest x-ray showed multiple areas of alveolar consolidation scattered throughout both lung fields, some of which were cavitated. The thoracic CT scan confirmed the presence of cavitating nodules and hilar and mediastinal lymphadenopathy. Samples for mycobacteria were negative. A search for anti-neutrophil cytoplasmic antibodies was negative. Fibreoptic bronchoscopy was normal but transbronchial biopsies revealed giant cells. Lung biopsies taken by video thoracoscopy showed non-caseating granulomata with areas of fibrinoid necrosis and perivascular infiltration with lymphocytes, histology characteristic of necrotising sarcoid granulomatosis. Resolution occurred without treatment. The parenchymal lesions regressed leaving residual cavities. Four years later, following an episode of haemoptysis, the patient was found to have a squamous cell carcinoma (T1N0M0) and aspergillomas in the pulmonary cavities., Conclusions: Our observation demonstrates that the cavities of necrotising sarcoid granulomatosis may be complicated by aspergillomas.

The first step in the diagnosis of a pleural effusion is to determine the exudative or transudative nature of the fluid. The purpose of this work was to compare different biological criteria commonly used in clinical practice. Among 118 pleural effusion fluids studied, 24.6% were exudates and 75.6% were transudates. The different parameters studied were Light criteria, Costa criteria, protein content, cholesterol content, and lactate dehydrogenase activity in the pleural fluid. The results showed that the Light criteria enabled classing all the fluids as exudates or transudates. We were also able to demonstrate that simple assay of lactate dehydrogenase activity in the pleural fluid gave comparable results, avoiding the need for further blood samples.

The authors present the case of three young female patients, of the same family, with all quickly fatal Primary Pulmonary Hypertension (PPH). Their clinical signs and paraclinical investigations were suggestive of a PPH and excluded all others causes of Pulmonary Hypertension. These observations recall the possible familial cases of this rare and very severe disease. It emphasizes as well the possible revelation of the disease during or after a pregnancy. So the members of this family, essentially first the young women who wish to have children, need a medical detection.

Pulmonary alveolar proteinosis (PAP) is a rare disease characterized by the accumulation of lipoproteinaceous material within the alveoli. Though many studies addressed biochemical data in bronchoalveolar lavage (BAL) effluent, poor attention was payed to cell profile in PAP. We report the case of a 40 year old woman, presenting with progressive respiratory failure and bilateral pulmonary infiltrates. BAL and transbronchial biopsy confirmed PAP. Therapeutic whole lung lavage led to full clinical and radiological remission. Sequential BAL follow-up was started over a 4-year period. As previously reported, lymphocytes were increased prior to whole lung lavage. This pattern subsequently remained, whereas recurrence or superinfections did not occur. The mechanism of this disorder is unclear and deserves further investigation.

In 19 patients suffering from lobar pneumonia and treated with antibiotics, bronchoalveolar lavages were performed in attempt to follow the course of the biological disorders caused by the pulmonary bacterial infection. The cytologic study of the fluid harvested from 14 patients with normal immune reactivity showed, firstly, a polymorphonuclear leucocytosis and, after about ten days, a lymphocytosis, reaching 30 to 70% of the alveolar cell population. These cell disorders existed only in the lobe affected by the pneumonia process. In five alcoholics (one of them also splenectomized), the polymorphonuclear leucocytosis lasted 15 to 25 days and the lymphocytosis was delayed and moderate. We also searched for the pneumococcal antigen by counter-current immunoelectrophoresis using a polyvalent antiserum. We found it in 13 patients, 7 with a positive hemoculture for pneumococcus and 6 negatives. Clearance of this antigen was slow, non modified by alcoholism. We found this antigen in two patients later, between the 90th and 110th days, in the lavage fluid concentrated fifty times. The quantitative and qualitative study of the immunoglobulins revealed considerable individual variations, owing to the variable intensity of the local inflammation phenomenons and to the technical difficulties of their dosage in the lavage fluid.

Among 189 patients treated for massive or repeated hemoptysis by transcatheter techniques between 1973 and 1983, a prospective study was attempted between 1979 and 1983 (72 patients) to search for bleeding of pulmonary arterial origin. Among these 72 patients, six were treated by surgical (one) or angiographic (five) occlusion of segmental pulmonary arteries. Pulmonary erosive pseudoaneurysms were seen in five cases (one with intracavitary aspergilloma, two with cavitary tuberculosis, and two with pyogenic abscesses). Among these six cases, one patient died from massive hemoptysis, one from unknown causes, and four are still alive. They are compared with five other patients who died from massive hemoptysis among 117 patients treated only by embolization of their systemic arteries between 1973 and 1979 (one with cavitary tuberculosis, two with intracavitary aspergillomas, one with an abscess of the lung, and one with a necrotic hilar cancer). A pulmonary arterial source of bleeding should be considered in addition to systemic arterial sources in the setting of destructive lung disease.

The cell populations in the alveoli are exposed to the environment and react differently to each type of challenge (mineral particles, toxic gases, infections, antigenic substances. . .). Amongst the best studied of these irritant factors is tobacco smoke which in the long term leads to a number of changes both in the distribution of alveolar cells and also their function and morphology. Amongst acute and sub-acute pathogens, bacterial infections produce a rapid poly-morpho-nuclear neutrophilia and then a lymphocytosis; oxygen and oxidising agents in general lead to a neutrophilia which amplifies the pulmonary parenchymal changes related to the release of toxic metabolites of oxygen. The inhalation of antigenic substances also disturbs the behaviour of alveolar cells: activation of macrophages in the presence of allergy in those sensitized to IgE and immediate attraction of neutrophils preceding a T lymphocyte alveolitis in hypersensitivity pneumonia. It is possible to categorise several patterns of reaction in intra-pulmonary cells when challenged by some insult, a direct cytotoxic action, the accumulation of inflammatory cells and immunological competence corresponding to the concept of "a neutrophil alveolitis" or a "T cell alveolitis" with the development of emphysematous lesions. An understanding of the cellular make-up present in the alveoli when reacting to an external pathogen enables a better approach to the pathophysiological mechanisms in question.