[Diagnostic and therapeutic clues in idiopathic pulmonary fibrosis].
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Biomedical subjects
Publications and source records attributed to Doina Todea.
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Langerhans' cell histiocytosis (LCH) encompasses a group of disorders with variable clinical features and prognosis that share in common the infiltration of involved tissues by numerous Langerhans' cell (LC), often organized in granulomas. In adults, pulmonary involvement with LCH is observed predominantly in young cigarette smokers. Lung involvement is usually an isolated or a predominant manifestation, and is characterized by LC granulomas entered on distal bronchioles. HRCT has proved to be very useful in the diagnosis of pulmonary LCT, showing in typical asess the association of nodules, cavitary nodules and cystic lesions with both thick and thin walls. The definite diagnosis of pulmonary LCT generally requires lung biopsy. The pathogenesis of pulmonary LCH is not well understood.
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Risk factors and patient stratification are important parameters in the assessment and management of patients with community-acquired pneumonia. In accordance to several guidelines, stratification of patients by various factors (severity of disease, presence of co-morbidities, modifying factors) are helpful in specific management decision such as site of care, extent of diagnostic testing and empirical antimicrobial therapy.
Fluid in the pleural cavity, parenchyma masses and consolidation provide excellent sonographic windows for scanning. Ultrasound has proven extremely useful in directing interventional procedures in the pleural space, pulmonary parenchyma and mediastinum. Ultrasound offers a number of advantages over other imaging methods, the most important being the capability to monitor continuously the interventional procedures, thus assuring maximum safety and benefit. We will discuss the indications, technique, performances and complications of ultrasound guided thoracic puncture in the pleural space, pulmonary parenchyma and mediastinum.
Although its real incidence is not clearly established, malignant pleural effusions is one of the more common problems that internists, pneumologists and oncologists face in their daily practice. Because the patients are already terminally ill, it is important to obtain a diagnosis expeditiously and formulate a treatment plan that optimizes quality of life.
Genic variability has a role in bronchial asthma susceptibility and the influence of its gravity, and also influences therapy efficacy. Clinical trials demonstrated that beta2 adrenoreceptors variability has an influence on the response to bronchodilator therapy. Some mutations induce resistance to bronchial asthma occurrence (Q27E which reduces down-regulation), others make subjects susceptible to asthma (D79N, T1641 and most of all R16G by an intensive down-regulation), and a third kind of mutations has no influence whatsoever on this disease (1159L, 1159F, K375R). A better understanding of the molecular processes involved in different pathways in asthma can lead to pathophysiological details, to find a more efficient treatment.
Pleuropulmonary manifestations in connective tissue diseases are frequent and variable. Pleural involvement is due especially to autoimmune inflammation and vasculitis, causing increased capillary permeability. Many of pleural effusions are asymptomatic, but with advancement in chest scanning techniques and immunohistology, pleuropulmonary abnormalities are increasingly being recognized in the early stages of a variety of connective tissue disease. The purpose of this article is to provide comprehensive information about incidence, pathophysiology, clinical manifestation and treatment for pleural diseases associated with connective tissue diseases.