Search

Introduction: Complications following COVID-19 are starting to emerge; neurological disorders are already described in the literature., Case Report: This case is about a 20-year old male with a severe COVID-19, hospitalized in a Reanimation and Intensive Care Unit with an Acute Respiratory Distress Syndrome, thromboembolic complication and secondary bacterial infection. This patient had a non-specific neurological disorder with a pseudobulbar palsy, (MRI, ENMG and lumbar puncture were normal), associated 4 months later with persistent left shoulder motor deficit and respiratory failure. Respiratory and neurological check-up led to a diagnosis of the Parsonage-Turner syndrome or neuralgic amyotrophy affecting C5-C6 nerve roots, the lateral pectoral and phrenic nerves at the origin of the scapular belt, amyotrophy and left diaphragm paralysis., Conclusions: This case shows that persistant dyspnoea after COVID 19 infection should lead to a search for a diaphragmatic cause which is not always the result of Reanimation Neuropathy but may also indicate a neuralgic amyotrophy. It is the fourth case of neuralgic amyotrophy following COVID-19. This brings the medical community to consider the risk of diaphragm paralysis apart from critical illness polyneuropathy. Respiratory muscle evaluation and diaphragmatic ultrasound should be considered in case of persistent dyspnoea., (Copyright © 2021 SPLF. Published by Elsevier Masson SAS. All rights reserved.)

Introduction: Anti-tumoral immunotherapy is currently the basis of a profound modification of therapeutic concepts in oncology, in particular since the arrival of immune checkpoint inhibitors (ICI). In addition to their efficacy profile, these immune-targeted agents also generate adverse events. With the increasing use of ICI for a growing number of tumor types, awareness of immunotherapy-related adverse events is essential to ensure prompt diagnosis and effective management of these potentially serious adverse events., Background: Cytotoxic T-lymphocyte antigen 4 (CTLA4) and programmed cell death protein 1 (PD1) are two co-inhibitory receptors that are expressed on activated T cells against which therapeutic blocking antibodies have reached routine clinical use. Immune checkpoint blockade can induce inflammatory adverse effects, termed immune-related adverse events (irAEs), which resemble autoimmune disease. Though severe irAEs remain rare, they can be fatal if not diagnosed and treated in an appropriate manner., Outlook and Conclusion: Additional studies are needed to better understand the clinical characteristics and chronology of these adverse effects and to clarify their pathophysiological mechanisms., (Copyright © 2018 SPLF. Published by Elsevier Masson SAS. All rights reserved.)

Introduction: Immune checkpoint inhibitors are becoming a standard treatment for many different cancers. Their toxicities are variable and include organ-specific dysimmune injuries and the development of systemic diseases., Case Report: We report 3 cases of sarcoid-like granulomatosis that occurred during treatment of various types of primary cancer by immune checkpoint inhibitors: lung adenocarcinoma, small cell lung cancer and melanoma. The clinical presentation, radiologic pattern and severity of this toxicity were variable. The diagnosis was made on biopsy with pathological examination and exclusion of differential diagnoses, particularly infection. In such cases, immunotherapy should be discontinued and subsequent rechallenge discussed later. Systemic corticosteroids should be considered depending on the severity of symptoms., Conclusions: Knowledge of this toxicity is crucial as the clinical signs and radiological patterns may suggest tumour progression., (Copyright © 2018 SPLF. Published by Elsevier Masson SAS. All rights reserved.)

Introduction: Primary mediastinal tumors are rare diseases including a broad spectrum of pathologies ranging from the well-known, such as lymphoma, thymoma or germ-line tumors to some very unusual presentations., Case Report: We describe a solitary mediastinal mass compressing the bronchial and vascular system in a patient suffering from chronic dyspnea. Diagnosis, obtained by means of a CT-guided biopsy, was a melanoma without any sign of a primary cutaneous lesion which harbored the BRAF V600E mutation., Conclusions: An exclusive mediastinal presentation of a malignant melanoma is exceptional and, in the context of BRAF mutation needs to be considered and diagnosed given the potential therapeutic impact., (Copyright © 2013 SPLF. Published by Elsevier Masson SAS. All rights reserved.)

Thymidylate synthase (TS) is an enzyme, which catalyzes the methylation of deoxyuridylate to deoxythymidylate using 5.10-methylenetetrahydrofolate as a cofactor. For this reason, TS has been widely investigated and is one of the best-known drug targets in the anticancer area. Antimetabolites have been developed to target TS and among them, pemetrexed is now considered as part of the standard treatment for lung cancer and mesothelioma. Intratumoral expression of TS mRNA has been shown to be associated with prognosis and with the response to 5-FU therapy in patients with breast, colorectal, head and neck cancer types. Recent findings suggest that TS might be a biomarker for NSCLC treated with pemetrexed, as lower response rates in squamous cell carcinoma and small cell carcinoma may be due to a higher expression of TS. Specific validation for this use as a biomarker is awaited. All these recent findings suggest that TS could be a useful predictive marker of the treatment efficacy of antifolate drugs and indicate that both Real-Time PCR and immuno-histochemistry might be used to assess TS expression levels. This may help in defining the best therapeutic strategy., (Copyright © 2011 SPLF. Published by Elsevier Masson SAS. All rights reserved.)

Introduction: Rates of lung cancer in women have been increasing continually for several years. The basic surgical management of this condition is the same in both sexes but a number of differences are apparent., Methods: We analysed data entered onto the Epithor database between June 2002 and June 2006 concerning 8535 surgical resections performed in primary lung cancer., Results: 22.5 percent of patients were women. They were significantly younger (59.6 years vs 62.7 years) and had a lower BMI (24.7 kg x m(-2) vs 25.5 kg x m(-2)). They were in a better physical condition in terms of American Society of Anaesthesiology score and performance status, with better preserved lung function and fewer co-morbidities (1.8 vs 2.1) compared to men. The percentage of adenocarcinomas was higher in women and a higher proportion had early stage disease. 30 day mortality was three times as high in men who also experienced much greater post-operative morbidity. Multivariate analysis revealed an odds ratio of 0.49 (95% CI 0.3-0.8) for mortality and 0.54 (95% CI 0.4-0.6) for morbidity in women compared to men., Conclusion: Women with lung cancer have less risk of post-operative morbidity and mortality than men. These data suggest that they might be able to benefit from more aggressive perioperative therapy.

Total and differential cells counts from 173 bronchoalveolar lavages (BAL) carried out in 19 lung transplanted recipients have been analysed. The patients were separated into seven groups: (a) those without detectable complications (86 BAL); (b) those with acute rejection (AR) (26 BAL); (c) those with bronchiolitis obliterans (BO) (21 BAL); (d) those with intra-alveolar cytomegalovirus (CMV) but asymptomatic (11 BAL); (e) those with an associated intra-alveolar CMV and AR (7 BAL); (f) those with CMV pneumonia (11 BAL); (g) those with infectious pneumonia excluding CMV (11 BAL). The alveolar cytological data were compared to those from control subjects who were smokers (7 BAL) or non-smokers (8 BAL). Excluding the BO group, the total cell count from the BAL of transplanted patients was significantly higher than in the non-smoking controls and was approaching that of the smoking controls. The lymphocytes count was significantly higher in transplanted patients without complication and in the AR group than in the controls, but there was no significant difference between the two groups. There was a significantly greater eosinophilia at the time of AR than either before or after. Eosinophilia was also higher in grade 3 AR than in grade 1 or 2 AR. These data stress the absence of any correlation between the lymphocyte count in the BAL and the existence of AR. Alternatively, the alveolar eosinophilia observed at the time of AR does not allow the possibility of an infection to be elimitated with certainty.

Pulmonary fibrosis corresponds to an accumulation of collagens and other proteins of the extracellular matrix in the interstitium and alveoli. Biochemical and cellular mechanisms of pulmonary fibrogenesis remain poorly understood. The cells of the alveolitis (macrophages, lymphocytes and neutrophils) play a key role in producing the factors which regulate the proliferation, chemotactism and secretory activity of the fibroblasts. Amongst these factors the cytokines (interleukins, interferons and growth factors) play a definite but very complex role. Certain cytokines stimulate in vitro the attraction and activation of cells of the alveolitis, as well as the multiplication, migration and secretory activity of fibroblasts. The following cytokines are involved: tumour necrosis factor alpha: (TNF alpha), interleukin 1 (IL-1), interleukin 6 (IL-6) interleukin 8 (IL-8) transforming growth factor beta (TGF beta), platelet derived growth factor (PDGF), insulin like growth factor 1 (IGF-1), fibronectin, monocyte chemotactic protein 1: (MCP-1). Other cytokines, principally the interferons (of alpha, beta or gamma type: IFN alpha, IFN beta, IFN gamma) inhibit in vitro and in vivo the proliferation and the production of collagen by fibroblasts. During the course of human pulmonary fibrosis or in experimental situations, the majority of the cytokines mentioned above are produced in excess in the lung. Without doubt they play an important role in the pathogenesis of fibrosis, even if it is not yet very well known how they interact and contribute in vitro to the process of fibrogenesis. Certain cytokines potentially regulating in the fibrosis are yet to be identified. In the future the use of cytokines and of their inhibitors will perhaps provide new therapies in pulmonary fibrosis.

We report a case of pneumonia with hypoxaemia and a swinging fever which was resistant to antibiotics, but was associated with a hypereosinophilia (44%) noted in the bronchoalveolar lavage. Investigations as to the cause of the eosinophilic pneumonia were negative; a lung biopsy confirmed the eosinophilic infiltration and the absence of any angiitis. There was a rapid and favourable clinical outcome following steroid therapy, which was maintained for three months. No relapse has been noted in the ten months of follow up since ceasing the cortico-steroids. The diagnosis appears to be that of a sub-acute, idiopathic eosinophilic pneumonia. The similarities and differences between this case and the chronic idiopathic eosinophilic pneumonia of Carrington were discussed.

Plasma extravasation (EP) is an important phenomenon during the course of inflammation. In asthmatic subjects, EP is produced not only in the walls of the airways, but also in the lumen. This has consequences for the bronchial calibre and the qualitative and quantitative characteristics of the secretions. Numerous experimental methods have been developed in animals in order to study EP induced in the airways by different stimuli. For the most part these are inapplicable in man where EP is generally validated in an indirect fashion by measuring the quantity of certain plasma proteins, such as albumin in the secretions or the bronchoalveolar lavage. EP is linked to an increase in the permeability of the vessels, notably this is situated in the subepithelial zone. It is influenced by the appearance of disruption between the endothelial cells and possibly amplified by an increased blood flow linked to vasodilatation. It is the association of these phenomena of epithelial hyperpermeability which favours the appearance of EP in the lumen. In experimental systems the greater part of the mediators implicated in the pathophysiology of asthma are capable of inducing EP in the airways. The perfecting of reliable and non-invasive methods of study is, however, necessary to achieve a perfect understanding of the role of EP in the pathophysiology of asthma or other inflammatory diseases of the bronchi and to assess the efficacy of this parameter of different therapeutic techniques.