scholarly journals Radiation Patterns of Modern Sarcoidosis (Alphabet)

2021 ◽  
Author(s):  
Aleksandra Speranskaia
Keyword(s):  
Pulmonary Fibrosis ◽  
Pulmonary Sarcoidosis ◽  
Radiation Patterns ◽  
Radionuclide Studies

Radiation diagnostics of sarcoidosis in modern conditions is CT, supplemented by radionuclide studies (SPECT, PET), ultrasound, MRI. The paper describes the classic signs of pulmonary sarcoidosis (according to the Statement on Sarcoidosis, 1999), which have changed their characteristics due to the widespread use of CT: variants of lymphadenopathy, dissemination, interstitial involvement. New unfavorable forms of thoracic sarcoidosis are discussed: fibrous sarcoidosis (with a description of the variants of sarcoid fibrosis and their differences from other progressive pulmonary fibrosis) and progressive sarcoidosis (possible causes and patterns). Radiation semiotics of extrapulmonary and comorbid manifestations is touched upon.

Pulmonary Sarcoidosis after Ten to Twenty Years

1986 ◽  
Vol 31 (2) ◽  
pp. 72-78 ◽  
Author(s):  
R. N. Johnston
Keyword(s):  
Pulmonary Fibrosis ◽  
Autoimmune Diseases ◽  
Transfer Factor ◽  
Respiratory Function ◽  
Malignant Disease ◽  
Causes Of Death ◽  
Respiratory Function Tests ◽  
Pulmonary Sarcoidosis ◽  
Radiological Evidence

One hundred and fifty-nine patients with Pulmonary Sarcoidosis have been studied ten to 20 years after diagnosis with a 90 per cent follow-up of survivors. Among the 76 patients with a mean follow-up of 22.5 years there is radiological evidence of pulmonary fibrosis in 13 and respiratory function tests revealed 12 with a transfer factor of less than 80 per cent of predicted. Of the further 83 patients followed to ten years there was radiological evidence of pulmonary fibrosis in five and a reduced transfer factor in four. Thirty-one patients received Prednisolone for various complications due to Sarcoidosis. There is no evidence of late respiratory disability. The complications and causes of death at ten and 20 years are examined and among the latter eight developed various forms of malignant disease. Since 1973 a further 139 patients have been studied, i.e. a total of 298 and two of these died from progressive Sarcoidosis despite corticostroid treatment. Six patients have developed late autoimmune diseases.

Different Angiogenic Activity in Pulmonary Sarcoidosis and Idiopathic Pulmonary Fibrosis

CHEST Journal ◽  
2006 ◽  
Vol 130 (4) ◽  
pp. 982-988 ◽  
Author(s):  
Katerina M. Antoniou ◽  
Argyris Tzouvelekis ◽  
Michael G. Alexandrakis ◽  
Katerina Sfiridaki ◽  
Ioanna Tsiligianni ◽  
...  
Keyword(s):  
Idiopathic Pulmonary Fibrosis ◽  
Pulmonary Fibrosis ◽  
Pulmonary Sarcoidosis ◽  
Angiogenic Activity

scholarly journals Intracardiac hemodynamic abnormalities in patients with sarcoidosis

2018 ◽  
Vol 28 (5) ◽  
pp. 567-575
Author(s):  
E. I. Leonova ◽  
E. I. Shmelev ◽  
R. B. Amansakhedov
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Fibrosis ◽  
Right Ventricular ◽  
Diastolic Dysfunction ◽  
Systolic Function ◽  
Cor Pulmonale ◽  
Pulmonary Sarcoidosis ◽  
Right Heart ◽  
Lung Lesions ◽  
The Right

The aim of this study was to evaluate intracardiac hemodynamic abnormalities in patients with pulmonary sarcoidosis and to investigate relevant factors. Methods. The study involved 42 patients with chronic pulmonary sarcoidosis. Chest computed tomography (CT), echocardiography, body plethysmography, spirometry, 6-minute walking test, and measurements of lung diffusing capacity (DLCO), blood gases and blood C-reactive protein (CRP) were performed in all patients. Results. Chronic cor pulmonale was detected in 26.2% of patients. The right heart diastolic dysfunction was found in 14.3% of patients, the left heart diastolic dysfunction was found in 23.8% of patients, the mean pulmonary artery pressure (mPAP) was increased in 19% of patients. The right ventricular diameter was found to be related to the inspiratory bronchial resistance (Rin) (R = 0.480; p = 0.02), the intrathoracic gas volume (ITGV) (R = –0.670; p = 0.001), DLCO (R = 0.438; p = 0.013), and pulmonary fibrosis. The right heart systolic function (TAPSE) was related to DLCO (R = 0.518; p = 0.006), the total lung capacity (TLC) (R = 0.639; p = 0.001) and pulmonary fibrosis. The increased mPAP was related to the extension of disseminated lung lesions (R = 0.716; p = 0.018), blood oxygen partial pressure (R = 0.486; p = 0.017) and CRP level. The 6-min distance was related to Rin, the right ventricular diameter, parameters of the right heart diastolic function (tricuspid E / A ratio) (R = 0.486; p = 0.01), and ITGV (R = 0.494; p = 0.006). Conclusion. The development of cor pulmonale in patients with pulmonary sarcoidosis was related to DLCO, Rin and pulmonary fibrosis. The extension of disseminated lung lesions, hypoxemia and increased CRP were related to pulmonary hypertension. Different factors associated with cor pulmonale and pulmonary hypertension in sarcoidosis could prompt further investigation of different phenotypes of this disease with the intrinsic central hemodynamic abnormalities. 

scholarly journals Different Activity of the Biological Axis VEGF-Flt-1 (fms-Like Tyrosine Kinase 1) and CXC Chemokines between Pulmonary Sarcoidosis and Idiopathic Pulmonary Fibrosis: A Bronchoalveolar Lavage Study

2009 ◽  
Vol 2009 ◽  
pp. 1-8 ◽  
Author(s):  
Katerina M. Antoniou ◽  
Giannoula Soufla ◽  
Athanasia Proklou ◽  
George Margaritopoulos ◽  
Christiana Choulaki ◽  
...  
Keyword(s):  
Idiopathic Pulmonary Fibrosis ◽  
Pulmonary Fibrosis ◽  
Tyrosine Kinase ◽  
Bronchoalveolar Lavage ◽  
Mrna Expression ◽  
Normal Subjects ◽  
Lavage Fluid ◽  
Pulmonary Sarcoidosis ◽  
Mrna Levels ◽  
Vegf Mrna

Background. We have previously shown a different local and systemic angiogenic profile of CXC chemokines in Idiopathic Pulmonary Fibrosis (IPF) patients compared to sarcoidosis. In particular, sarcoidosis showed an angiostatic microenvironment, as compared with the angiogenic cytokine milieu seen in IPF.Purpose of the Study. Our aim was to further investigate the aforementioned finding by measuring the expression of different chemokines in granulomatous and fibrotic diseases. We estimated the levels of vascular endothelial growth factor (VEGF) and its high-affinity receptor, Flt-1 (fms-like tyrosine kinase 1), in bronchoalveolar lavage fluid (BALF) of patients with IPF and pulmonary sarcoidosis. We have also investigated the mRNA expression of angiogenetic chemokines' receptors such as CXCR2 and CXCR3 and the biological axis of stromal derived factor-1 (SDF-1 or CXCL12/CXCL12) and receptor, CXCR4.Methods. We studied prospectively three groups of patients: (i) one group of 18 patients with IPF, (ii) one group of 16 patients with sarcoidosis, and (iii) 10 normal subjects.Results. A statistically significant increase has been detected in VEGF mRNA expression in IPF in comparison with pulmonary sarcoidosis . In addition, a significant increase has been measured in CXCL12 in sarcoidosis in comparison to IPF . Moreover, a statistically significant decrease has been found in Flt-1 protein levels in pulmonary sarcoidosis in comparison with IPF . A significant increase in VEGF and CXCR4 mRNA levels has been also detected in sarcoidosis' patients when compared with healthy controls.Conclusions. Our data suggest that increased expression of Flt-1 and downregulation of CXCL12 in IPF may further support the hypothesis of a different angiogenetic profile between fibrotic and granulomatous diseases. However, further studies are needed in order to better investigate these enigmatic diseases.

Advanced Pulmonary Sarcoidosis

2020 ◽  
Vol 41 (05) ◽  
pp. 700-715
Author(s):  
Rohit Gupta ◽  
Robert P. Baughman
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Fibrosis ◽  
Structural Changes ◽  
Advanced Disease ◽  
Respiratory Infections ◽  
Pulmonary Sarcoidosis ◽  
Emission Tomography ◽  
Specific Therapy ◽  
New Techniques ◽  
Positron Emission

AbstractAt least 5% of sarcoidosis patients die from their disease, usually from advanced pulmonary sarcoidosis. The three major problems encountered in advanced pulmonary sarcoidosis are pulmonary fibrosis, pulmonary hypertension, and respiratory infections. Pulmonary fibrosis is the result of chronic inflammation, but other factors including abnormal wound healing may be important. Sarcoidosis-associated pulmonary hypertension (SAPH) is multifactorial including parenchymal fibrosis, vascular granulomas, and hypoxia. Respiratory infections can be cause by structural changes in the lung and impaired immunity due to sarcoidosis or therapy. Anti-inflammatory therapy alone is not effective in most forms of advanced pulmonary sarcoidosis. New techniques, including high-resolution computer tomography and 18F-fluorodeoxyglucose positron emission tomography (PET) have proved helpful in identifying the cause of advanced disease and directing specific therapy.

scholarly journals Improvement of pulmonary sarcoidosis following sleeve gastrectomy

2019 ◽  
Vol 7 (1) ◽  
pp. 1
Author(s):  
Natalie E. Hassell ◽  
Ewa Grzeszczak ◽  
Ryan C. Adams ◽  
Wonder P. Drake
Keyword(s):  
Bariatric Surgery ◽  
Risk Factor ◽  
Sleeve Gastrectomy ◽  
Pulmonary Fibrosis ◽  
Effective Treatment ◽  
Clinical Improvement ◽  
Sex Hormones ◽  
Pulmonary Sarcoidosis ◽  
Growing Body

Pulmonary sarcoidosis is unlikely to resolve if it persists for greater than five years. A growing body of literature supports the involvement of the microbiome in sarcoidosis and a role for sex hormones in pulmonary fibrosis. Additionally, obesity is a risk factor for the development of sarcoidosis. Bariatric surgery is an effective treatment for obesity and can lead to microbial and endocrine changes. Here, we report the clinical improvement of longstanding pulmonary sarcoidosis following sleeve gastrectomy.

Oligo-2′,5′-Adenylate Synthetase in Pulmonary Sarcoidosis and Idiopathic Pulmonary Fibrosis

CHEST Journal ◽  
1994 ◽  
Vol 105 (2) ◽  
pp. 496-500 ◽  
Author(s):  
Masatoshi Amaya ◽  
Noriharu Shijubo ◽  
Nobuhiro Fujii ◽  
Keiji Oguma ◽  
Shosaku Abe
Keyword(s):  
Idiopathic Pulmonary Fibrosis ◽  
Pulmonary Fibrosis ◽  
Pulmonary Sarcoidosis
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