Biomedical subjects
Publications and source records attributed to M Brauner.
Diagnosis of pleural plaques depends on adequate knowledge of the normal anatomy of the pleura and intercostals spaces which is indispensable for understanding the normal computed tomographic images of the thorax and anatomic variants.
Malignant tumors of the pleura are most often diffuse, nethertheless they are sometimes localized. There is an overlap of the radiologic features of the benign and malignant pleural lesions. The differential diagnosis may be difficult, even on histological sample. Imaging allows the diagnosis of pleural involvement, suggests the malignity, guides percutaneous or thoracoscopic biopsies of the pleura, defines extent of the tumor and follows the course of the disease. We will describe the malignant pleural tumors: pleural metastases, pleural involvement of broncho-pulmonary cancer, of lymphoma and leukaemia. Then the rare pleural tumors will be described: malignant pleural fibroma, sarcoma, histiocytoma and hemangiopericytoma.
BACKGROUND: Pulmonary hypertension (PH) is a rare complication of sarcoidosis, although it is not uncommon in advanced disease. METHODS: A retrospective series of 22 sarcoidosis patients (16 men) of mean (SD) age 46 (13) years with PH was divided into two groups depending on the absence (stage 0: n = 2, stage II: n = 4, stage III: n = 1) or presence (n = 15) of radiographic pulmonary fibrosis at the time of PH diagnosis. RESULTS: In both groups PH was moderate to severe and there was no response to acute vasodilator challenge. In non-fibrotic cases no other cause of PH was found, suggesting a specific sarcoidosis vasculopathy, although no histological specimens were available. In cases with fibrosis there was no correlation between haemodynamics and lung volumes or arterial oxygen tensions, suggesting other mechanisms for PH in addition to pulmonary destruction and hypoxaemia. These included extrinsic arterial compression by lymphadenopathies in three cases and histologically proven pulmonary veno-occlusive disease in the five patients who underwent lung transplantation. Ten patients received high doses of oral prednisone for PH (stage 0: n = 1, stage II: n = 4 and stage IV: n = 5); three patients without pulmonary fibrosis experienced a sustained haemodynamic response. Survival of the overall population was poor (59% at 5 years). Mortality was associated with NYHA functional class IV but not with haemodynamic parameters or with lung function. CONCLUSION: Two very different phenotypes of sarcoidosis combined with PH are observed depending on the presence or absence of pulmonary fibrosis. PH is a severe complication of sarcoidosis.
INTRODUCTION: Chronic beryllium disease (CBD) is an occupational lung disease caused by the inhalation of beryllium dust, fumes or metallic salts. CURRENT DATA: Beryllium affects the lungs via particles deposited in the pulmonary alveoli. These are ingested by alveolar macrophages which act as antigen presenting cells to CD4+ T lymphocytes. T lymphocytes proliferate in response to beryllium antigens and combined with macrophages produce numerous epithelioid granulomas with the release of inflammatory cytokines (IFNgamma, IL-2, TNFalpha and IL6) and growth factors. Beryllium induces macrophage apoptosis which reduces its clearance from the lung which in turn contributes to the host's continual re-exposure and thus a chronic granulomatous disorder. Pulmonary granulomatous inflammation is the primary manifestation of CBD, but the disease occasionally involves other organs such as the liver, spleen, lymph nodes and bone marrow. The clinical, radiological, and histopathological features of CBD can be difficult to distinguish from sarcoidosis. The Beryllium lymphocyte proliferation test (BeLPT) demonstrates a beryllium specific immune response, confirms the diagnosis of CBD, and excludes sarcoidosis. CONCLUSIONS AND PERSPECTIVES: CBD provides a human model of pulmonary granulomatous disease produced by an occupational exposure, occurring more frequently in those with a genetic pre-disposition. It can be differentiated from sarcoidosis by specific immunological testing.
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Explore the source record for details and available documents.
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Imaging plays an important role in identifying thoracic, abdominal and neurological localizations of sarcoidosis as well as ENT and bone localizations. It contributes to disease detection and is helpful for diagnostic, prognostic and therapeutic decision making and useful for therapeutic monitoring. The chest x-ray is particularly important in the initial work-up and to follow well-tolerated disease. Other investigations, depending on the localization, are helpful to follow the course of severe or chronic sarcoidosis.
Mediastinal and pulmonary localizations are found in 90% of al patients with sarcoidosis. In half the cases, the disease is not severe and is reversible without treatment. In the other half of cases, early or late respiratory complications can be seen. Early complications include subacute respiratory insufficiency by interstitial lung disease or by bronchial airway obstruction. Among late complications, the most frequent is pulmonary fibrosis. Four computed tomography patterns are found with variable functional impairments and course. Chronic obstructive respiratory insufficiency can be the consequence of specific bronchial lesions or pulmonary fibrosis surrounding proximal bronchi. Cor pulmonale is seen in 5% of cases. Aspergilloma seen in fibroemphysematous lesions can be the cause of major hempoptysis. Respiratory complications account for half of the 5% of deaths due to sarcoidosis. Respiratory complications are most often seen in radiographic stage III and IV disease. Treatments, mainly corticosteroids, only exert a suspensive effect but reduce the incidence and severity of respiratory manifestations. The gain obtained by treatment depends on the choice of the best time of institution and on the quality of monitoring. Lung transplantation is useful in most severe cases unresponsive to medical treatment.
False-positive or over-calling of findings at chest radiography may have important consequences by generating numerous and unnecessary examinations. The advances made in thoracic imaging have currently decreased the number of technical errors. However, we are frequently confronted with visual illusions or with failure to recognize anatomical variants, either congenital, age-related or physiological in nature. Other difficulties are due to functional variations. Over-calling depends on the clinical context, which may inadequately suggest an interstitial lung process, abnormalities of the vascularization or of the hila. In this article, several examples of false positives will be illustrated. An explanation for these appearances, based on the underlying etiology, will be provided.
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Infiltrative lung diseases (ILD) include more than 130 diseases. Chronic and acute forms of ILD must be differentiated. In each group, cases with a known cause or with an unknown cause have to be individualized. For the physician, the distinctive sign of ILD is the evidence of diffuse pulmonary opacities on chest X rays or a suggestive pattern on pulmonary function tests. The diagnosis of chronic ILD depends on epidemiologic data ("a priori" probabilities), anamnestic informations, clinical and radiological (radiography and tomodensitometry) findings which make possible to consider a diagnosis of high probability in at least 60% of cases and reduce the gamut of hypothesis in the others. Other investigations (blood, endoscopy, broncho-alveolar lavage and sometimes surgical lung biopsy) lead to the final diagnosis. Most frequent chronic ILD are sarcoidosis, idiopathic pulmonary fibrosis and connective disease associated ILD. In case of acute ILD, diagnostic procedures depend on the severity of the disease and symptomatic treatment is urgent. The main lung lesion is either oedema or alveolitis. Main acute ILD are respectively cardiogenic oedema, lesional oedema, intra-alveolar hemorrhage, infectious ILD and acute eosinophilic pneumonia. The diagnostic approach depends on the presence of an initial orientation. Sometimes, several causes are associated.
Tuberculosis (TB) remains a common disease in the World. Its incidence has risen steadily since 1985, despite a preexisting continuous decreasing of its frequency due to an effective chemotherapy. Nonwhite people, socioeconomically disadvantaged, chronically debilitated groups and AIDS patients are the most concerned. Chest radiography remains the first imaging modality to evaluate TB. Widely radiographic appearances can be encountered, including normal chest X-ray. CT can be useful in all stages of the disease, particularly when clinical and radiological findings are in disagreement and/or when imaging findings are equivocal. CT should be proposed at the end of an effective antituberculous treatment to better subsequently detect fine lesions suggestive of reactivation TB.
PURPOSE: To document the changes observed at sequential magnetic resonance (MR) imaging of sarcoidosis lesions of the central nervous system (CNS) during treatment with corticosteroids. MATERIALS AND METHODS: The abnormalities detected in 24 patients (mean follow-up, 36 months) were compared before and after therapeutic periods (n = 75) that were divided into attack (high-dose), upkeep (decreased-dose), and minimal (low-dose) periods. Parenchymal lesions were classified as type 1 (enhanced with gadolinium), type 2 (demyelinating), or type 3 (lacunar) and were assessed as regressing, stable, or progressing. RESULTS: Seven of the 24 patients had several types of lesions. Isolated type 3 lesions (six patients) were the only lesions not associated with neurologic deficit. Type 1 lesions (13 patients) regressed in 22 of 22 attack periods and progressed in nine of 27 upkeep and minimal periods. MR imaging depicted relapses in patients with multifocal CNS involvement or long-standing CNS impairment or in those who had previously received steroid therapy. Type 2 (seven patients) and type 3 (13 patients) lesions remained stable in 68 of 68 therapeutic periods. Type 1 lesions appeared in three patients with type 2 and type 3 lesions during two upkeep and three minimal periods. Findings at follow-up MR imaging contributed to the reintroduction of high-dose corticosteroid therapy in eight patients. CONCLUSION: MR imaging can be used to differentiate between reversible and irreversible lesions in CNS sarcoidosis. MR imaging can be a useful tool for adjusting treatment to prevent irreversible CNS damage.
High-resolution computed tomography (HRCT) has proved to be very useful in the diagnosis and follow-up of pulmonary Langerhans cell histiocytosis (PLCH), but the precise relationships between nodules and thin-wall cysts observed by HRCT, and granulomatous or cystic lesions present in lung tissue, remain to be established. The aim of this study was to compare quantitative data obtained by HRCT and those obtained by histopathological examination of corresponding lung tissue specimens in patients with biopsy-proven PLCH. The results demonstrated that the extent of nodular abnormalities was strongly correlated with the density of florid granulomatous lesions in lung tissue. A strong correlation was also found between the extent of cystic abnormalities and the density of cavitary lesions, but the latter included both still inflammatory cavitary granulomas and cicatricial fibrous cysts. Interestingly, small isolated florid granulomas were found in lung tissue from most patients with a predominant cystic CT scan pattern. Taken together, these results demonstrate that HRCT has to be considered with caution to evaluate the histopathological activity of PLCH. Patients presenting with predominant HRCT cystic abnormalities should benefit from a long-term follow-up. Because these patients are susceptible to developing severe respiratory insufficiency, they should also be considered for treatment as soon as an effective therapy for LCH is available.
STUDY OBJECTIVE: Airway obstruction (AO) in sarcoidosis is reported to be associated with respiratory symptoms, increased morbidity, and an increased mortality risk. Because AO in sarcoidosis may result from several causes, the therapeutic benefit of corticosteroids is difficult to determine. The aim of this study was to evaluate the therapeutic response of AO attributable to sarcoid granulomas in the bronchial wall. PATIENTS: We selected 11 patients who had sarcoidosis with AO (defined as FEV(1)/vital capacity [VC] < 70%) associated with sarcoid granulomas on an endobronchial biopsy. Exclusion criteria were history of asthma, smoker or ex-smoker, stage 4 disease, evidence of extrinsic compression by enlarged lymph nodes, and localized endobronchial stenosis seen during fiberoptic bronchoscopy. INTERVENTIONS: We compared the results of pulmonary function tests and clinical, radiologic, and biological findings at baseline with those obtained at the time of the last pulmonary function tests available, between the sixth and 12th months of treatment. Eight patients took oral corticosteroids (20 to 60 mg/d initially), one received IV methylprednisolone pulses, another took oral hydroxychloroquine, and the last one received IM methotrexate. MEASUREMENTS AND RESULTS: With treatment, FEV(1) and FEV(1)/VC significantly improved in eight patients (72%), normalized in four patients, and was unchanged in the remaining three patients. The mean FEV(1) increased from 60.8 +/- 10.8% to 76 +/- 13.7% of the predicted value (p < 0.02). VC did not change significantly. FEV(1)/VC increased from 76.1 +/- 6.4% to 87.6 +/- 10.7% of the predicted value (p < 0.01). Dyspnea on exertion and other clinical findings were attenuated in 10 patients; the chest radiograph improved in 9 patients, and normalized in 5 patients. The mean serum angiotensin-converting enzyme level decreased from 112 +/- 48 to 58 +/- 40 IU/mL (p < 0.05), and normalized in four patients. CONCLUSION: The present study indicates that AO caused by sarcoid granulomas in the bronchial wall can be either partially or completely reversed by treatment with a concomitant attenuation of pulmonary symptoms.
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