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Idiopathic mediastinal fibrosis presenting as mediastinal compression syndrome  [cached]
Patil Prashant,Salkar H
Indian Journal of Medical Sciences , 2005,
Abstract: Mediastinal compression syndrome is a commonly seen entity. Mediastinal compression, mostly due to a space-occupying lesion, is distinct and different from mediastinitis/mediastinal fibrosis, which could also lead to superior vena cava syndrome. Idiopathic mediastinal fibrosis should also be considered as differential diagnosis of mediastinal structures with various radiological, CT and MRI and histological features if feasible. Medical therapy is disappointing while surgical cure has limitations. This interesting patient presented as mediastinal compression syndrome, which on investigation was postulated as idiopathic mediastinal fibrosis, as a diagnosis on exclusion of other causes, which is rare, hence is being reported.
Anterior Mediastinal Mass: A Rare Presentation of Tuberculosis  [PDF]
Gopi C. Khilnani,Neetu Jain,Vijay Hadda,Sudheer K. Arava
Journal of Tropical Medicine , 2011, DOI: 10.1155/2011/635385
Abstract: We report a case of a 14-year-boy who presented to us with a low-grade fever with evening rise for 9 months. Along with this, the patient also reported a reduction in his appetite and body weight. He had a mild dry cough but no respiratory symptoms otherwise. There was no other localization for fever on history. He received antitubercular therapy, based on abnormal chest radiograph. However, there was no relief in his symptoms. General physical examination revealed mild fever. Systemic examination was unremarkable. Blood investigations done for fever were noncontributory. Computed tomographic (CT) scan of the chest revealed a mediastinal mass compressing the trachea. The possibilities of lymphoma or germ cell tumour were considered. A biopsy from the mass under CT guidance was performed. The histopathology revealed multiple epithelioid cell granulomas with necrosis, and the diagnosis of tuberculosis was made. The clinical course of this patient and the relevant literature is presented in this paper. 1. Introduction The anterior mediastinal space is almost a virtual space. However, the multiplicity of the structures it contains and the diversity of disease processes affecting them make it a region of great clinical interest. This cavity encloses muscle, ligaments, fat tissue, and parenchymatous organs such as thymus, thyroid, and ectopic parathyroid gland. Mediastinal masses are commonly encountered in clinical practice. However, they represent a challenging and urgent diagnostic problem because the differential diagnoses range from absolutely benign to highly malignant conditions, and delay in diagnosis may be fatal. The common anterior masses include thymoma, lymphoma, and germ cell tumours [1, 2]. An isolated mediastinal mass without lung parenchymal lesion is an uncommon presentation of tuberculosis [3, 4]. Here, we present a case of anterior mediastinal mass compressing the trachea which was histopathologically diagnosed as tubercular and treated successfully with antituberculosis therapy (ATT). 2. Case Summary A 14-year-old boy presented to us in July 2009 with low-grade, evening rise fever since March 2008. He also complained of reduction in appetite and weight loss of 8?kg during this period. He had a mild dry cough. However, there was no history of shortness of breath, chest pain, hemoptysis, hoarseness of voice, or dysphagia. There was no other significant history to localize the cause of fever. He received antituberculosis therapy (ATT) for these symptoms and abnormal chest radiograph. He was treated for the first time for 4 months from March
Anterior mediastinal paraganglioma: A case for preoperative embolization
Murtaza Shakir, Geoff Blossom, John Lippert
World Journal of Surgical Oncology , 2012, DOI: 10.1186/1477-7819-10-134
Abstract: We report a case of anterior mediastinal paraganglioma that was embolized preoperatively, and was resected without the need for cardiopulmonary bypass and without major bleeding complications.We make a case to further the role of preoperative embolization in the treatment of mediastinal paragangliomas.
Imaging Manifestations of Mediastinal Fat Necrosis  [PDF]
Malay Y. Bhatt,Santiago Martínez-Jiménez,Melissa L. Rosado-de-Christenson,Kenneth R. Watson,Christopher M. Walker,Jeffrey R. Kunin
Case Reports in Radiology , 2013, DOI: 10.1155/2013/323579
Abstract: Mediastinal fat necrosis (MFN) or epipericardial fat necrosis, as it is commonly referred to in the literature, is a rare self-limiting cause of chest pain of unclear etiology. MFN affects previously healthy individuals who present with acute pleuritic chest pain. Characteristic computed tomography (CT) findings include a fat attenuation lesion with intrinsic and surrounding increased attenuation stranding. There is often associated thickening of the adjacent pericardium and/or pleural effusions. We present two cases of MFN manifesting as ovoid fat attenuation lesions demarcated by a soft tissue attenuation rim with intrinsic and surrounding soft tissue attenuation stranding and review the clinical and pathologic features of these lesions. Knowledge of the clinical presentation of patients with MFN and familiarity with the characteristic imaging findings of these lesions should allow radiologists to prospectively establish the correct diagnosis and suggest conservative management and follow-up. 1. Introduction Mediastinal fat necrosis (MFN) is a rare self-limiting cause of chest pain, with the first reported cases dating back to 1957 [1]. In the current literature, “epipericardial” or “epicardial” fat necrosis is the term used to identify this condition [2–4]. However, as the juxtapericardial mediastinal fat is characteristically affected, we propose that the term MFN is more appropriate given the anatomical location of the disease process. MFN classically affects previously healthy individuals who present with acute pleuritic chest pain that raises concern for an acute cardiopulmonary process including pulmonary thromboembolic and coronary artery diseases [1–12]. We present two cases of MFN and discuss their clinical, pathologic, and imaging findings. In both cases, the affected patients presented with severe chest pain and no associated physical examination findings or specific laboratory abnormalities. The presentation of acute pleuritic chest pain in association with CT findings of an ovoid juxtapericardial fat attenuation lesion with intrinsic and surrounding increased attenuation stranding, thickening of the adjacent pericardium, and resolution on follow-up imaging can be collectively used to establish the diagnosis [2]. Making the correct diagnosis prospectively mitigates unnecessary testing in favor of conservative management. 2. Case Reports Case 1. A 51-year-old man presented with dyspnea and left pleuritic chest pain that radiated to his back. His physical exam and laboratory tests were normal. PA and lateral chest radiographs showed a small
Idiopathic pulmonary fibrosis
Eric B Meltzer, Paul W Noble
Orphanet Journal of Rare Diseases , 2008, DOI: 10.1186/1750-1172-3-8
Abstract: Idiopathic pulmonary fibrosis (IPF).Synonym: cryptogenic fibrosing alveolitis (CFA) was the preferred term in Europe until terminology was simplified by consensus conference [1].Idiopathic pulmonary fibrosis (IPF) is a chronic disease that manifests over several years and is characterized by scar tissue within the lungs, in the absence of known provocation. Exercise-induced breathlessness and chronic dry cough are the prominent symptoms.IPF belongs to a family of lung disorders known as the interstitial lung diseases (ILD) or, more accurately, the diffuse parenchymal lung diseases (DPLD). Within this broad category of diffuse lung diseases, IPF belongs to the subgroup known as idiopathic interstitial pneumonia (IIP). By definition, the etiology of IIP is unknown. There are seven distinct IIPs, differentiated by specific clinical features and pathological patterns [2]. IPF is the most common form of IIP. It is associated with the pathologic pattern known as usual interstitial pneumonia (UIP); for that reason, IPF is often referred to as IPF/UIP. IPF is usually fatal, with an average survival of approximately three years from the time of diagnosis [3-5]. Older studies suggested that five-year mortality for IPF was only 50%, but this estimate was derived prior to the recognition of nonspecific interstitial pneumonia (NSIP), a pathological subtype of IIP that mimics IPF in its clinical presentation [6-8]. NSIP has a more favorable prognosis and the almost certain inclusion of NSIP cases in older studies of IPF mortality accounts for differences in observed outcome [9]. By definition, IPF/UIP must be discriminated from NSIP.The incidence and prevalence of IPF are difficult to determine because uniform diagnostic criteria have only recently been defined [1]. Historical information relating to vital statistics relied on population studies which utilized diagnostic coding data and death certificates to identify cases. The accuracy of this information can be questioned, espe
Idiopathic pulmonary fibrosis with bronchogenic carcinoma
Nair Girija,Swami Shivani,Mehta Ankur
Lung India , 2009,
Abstract: Idiopathic pulmonary fibrosis is essentially a benign disease. We present a case of 65-year-old female patient who presented with left-sided chest pain and breathlessness. Her CT thorax revealed idiopathic pulmonary fibrosis along with a left-sided pleural-based mass. Biopsy of the mass revealed a squamous cell carcinoma. She was exposed to home wood smoke while cooking on the chulla for many years, which was possibly responsible for both the diseases.
Autophagy in Idiopathic Pulmonary Fibrosis  [PDF]
Avignat S. Patel, Ling Lin, Alexander Geyer, Jeffrey A. Haspel, Chang Hyeok An, Jiaofei Cao, Ivan O. Rosas, Danielle Morse
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0041394
Abstract: Background Autophagy is a basic cellular homeostatic process important to cell fate decisions under conditions of stress. Dysregulation of autophagy impacts numerous human diseases including cancer and chronic obstructive lung disease. This study investigates the role of autophagy in idiopathic pulmonary fibrosis. Methods Human lung tissues from patients with IPF were analyzed for autophagy markers and modulating proteins using western blotting, confocal microscopy and transmission electron microscopy. To study the effects of TGF-β1 on autophagy, human lung fibroblasts were monitored by fluorescence microscopy and western blotting. In vivo experiments were done using the bleomycin-induced fibrosis mouse model. Results Lung tissues from IPF patients demonstrate evidence of decreased autophagic activity as assessed by LC3, p62 protein expression and immunofluorescence, and numbers of autophagosomes. TGF-β1 inhibits autophagy in fibroblasts in vitro at least in part via activation of mTORC1; expression of TIGAR is also increased in response to TGF-β1. In the bleomycin model of pulmonary fibrosis, rapamycin treatment is antifibrotic, and rapamycin also decreases expression of á-smooth muscle actin and fibronectin by fibroblasts in vitro. Inhibition of key regulators of autophagy, LC3 and beclin-1, leads to the opposite effect on fibroblast expression of á-smooth muscle actin and fibronectin. Conclusion Autophagy is not induced in pulmonary fibrosis despite activation of pathways known to promote autophagy. Impairment of autophagy by TGF-β1 may represent a mechanism for the promotion of fibrogenesis in IPF.
Smoking and Idiopathic Pulmonary Fibrosis  [PDF]
Chad K. Oh,Lynne A. Murray,Nestor A. Molfino
Pulmonary Medicine , 2012, DOI: 10.1155/2012/808260
Abstract: Idiopathic pulmonary fibrosis (IPF) is a disease of unknown etiology with considerable morbidity and mortality. Cigarette smoking is one of the most recognized risk factors for development of IPF. Furthermore, recent work suggests that smoking may have a detrimental effect on survival of patients with IPF. The mechanism by which smoking may contribute to the pathogenesis of IPF is largely unknown. However, accumulating evidence suggests that increased oxidative stress might promote disease progression in IPF patients who are current and former smokers. In this review, potential mechanisms by which cigarette smoking affects IPF, the effects of cigarette smoking on accelerated loss of lung function in patients with IPF, key genetic studies evaluating the potential candidate genes and gene-environment (smoking) interaction, diagnosis, and treatment with emphasis on recently closed and ongoing clinical trials are presented. 1. Introduction Idiopathic pulmonary fibrosis (IPF) is defined as a specific form of chronic, progressive fibrosing interstitial pneumonia of unknown cause, occurring primarily in older adults, limited to the lungs, and associated with the histopathologic and/or radiologic pattern of usual interstitial pneumonia (UIP) [1]. Current estimates of IPF prevalence and annual incidence in the United States range from 14 to 42.7 per 100 000 and 6.8–16.3 per 100 000, respectively [2]. There is a high unmet need for novel therapies as conventional therapy has limited efficacy or an unfavorable safety profile and there are no US Food and Drug Administration- (FDA-) approved therapies for IPF treatment. In a recent meta-analysis of observational studies examining environmental and occupational risk factors for IPF, significantly increased risk for IPF was associated with cigarette smoking and exposure [3]. Several environmental exposures also have been associated with increased risk for IPF. Occupational factors, primarily metal and wood dust exposure, adjusted for age and smoking, have been found to be significantly associated with IPF [4, 5]. Among these risk factors, cigarette smoking seems to be the most strongly associated risk factor in both sporadic IPF and familial pulmonary fibrosis [3, 6]. The prevalence of tobacco use in IPF ranges from 41% to 83%, depending on the case definition used in the studies [7, 8]. Current or former smokers have consistently been overrepresented in IPF [9–13]. In one case-control study, smoking was identified as a potential risk factor for the development of IPF (odds ratio [OR] = 1.6) [14]. The overall OR for
Non-traumatic anterior mediastinal abscess in childhood  [cached]
Kumar Sandeep,Kumar Virendra,Bishnoi Amit,Chadha Rajiv
Journal of Indian Association of Pediatric Surgeons , 2011,
Abstract: Anterior mediastinal abscesses (MAs) due to a non-traumatic etiology are extremely rare in childhood and only 13 such cases have been reported in the literature. We report a 5-year-old male child with disseminated staphylococcal infection and a large non-traumatic anterior MA, who had a successful recovery after surgical drainage of the abscess.
Mechanical induction of cough in Idiopathic Pulmonary Fibrosis
Richard M Jones, Simon Hilldrup, Benjamin DM Hope-Gill, Ronald Eccles, Nicholas K Harrison
Cough , 2011, DOI: 10.1186/1745-9974-7-2
Abstract: We studied 27 non-smoking subjects with IPF (63% male), mean (SD) age 71.7 (7) years and 30 healthy non-smokers. Quality of life (Leicester Cough Questionnaire), cough symptom scores and cough severity scores (visual analog scales) were recorded. Percussion stimulation was applied over the posterior lung base, upper anterior chest and manubrium sternum at sequential frequencies (20 Hertz (Hz), 40 Hz and 60 Hz) for up to 60 seconds and repeated twice at two minute intervals. The number of subjects achieving two and five-cough responses, total cough counts and cough latency were recorded. In separate experiments, the effect of mechanical stimulation on the pattern of breathing was determined in eight IPF subjects and five control subjects.In patients with IPF, we demonstrated strong correlations between subjective cough measurements, particularly the cough symptom score and Leicester Cough Questionnaire (r = -0.86; p < 0.001). Mechanical percussion induced a true cough reflex in 23/27 (85%) IPF subjects, but only 5/30 (17%) controls (p < 0.001). More patients with IPF reached the two-cough response at a lower frequency (20 Hz) posteriorly than at other positions. Highest mean cough totals were seen with stimulation at or above 40 Hz. Mechanical stimulation had no effect on respiratory rate but increased tidal volume in four (50%) subjects with IPF, particularly at higher frequencies. It was associated with increased urge to cough followed by a true cough reflex.This study demonstrates that patients with IPF show enhanced cough reflex sensitivity to mechanical stimulation of the chest wall whilst normal individuals show little or no response. The observation that low frequency stimulation over the lung base, where fibrosis is most extensive, induces cough in more patients than at other sites supports the hypothesis that lung distortion contributes to the pathogenesis of cough in IPF.Idiopathic pulmonary fibrosis (IPF) is a disease characterised by lung parenchymal dist
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