Pulmonary Sarcoidosis

Lynch, Joseph P.; Kazerooni, Ella A.; Gay, Steven

doi:10.1016/s0272-5231(05)70417-2

Cited by 253 publications

(239 citation statements)

References 168 publications

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“…Chest radiographs were analyzed independently by two readers and classi®ed in a standard manner according to the traditional roentgenographic stages [2,5]. The pulmonary function tests included measurements of the vital capacity (VC), dynamic lung compliance (CL,dyn), lung transfer for CO (TL,CO), and arterial blood gases.…”

Section: Initial Evaluationmentioning

confidence: 99%

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Pulmonary sarcoidosis in children: a follow-up study

et al. 2001

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Progression of pulmonary sarcoidosis in children remains poorly documented. The aim of this work was to gather follow-up information on pulmonary outcomes in children with sarcoidosis and to obtain data of relevance to a discussion of the optimal length and regimen of glucocorticoid therapy.In the present study, the authors experience of pulmonary sarcoidosis in 21 children referred to the paediatric pulmonary department over a 10-yr period is reported with a documented follow-up of at least 4 yr. Evaluation of the disease during the follow-up included analysis of clinical manifestations, chest radiographs, pulmonary function tests with measurements of the vital capacity (VC), dynamic lung compliance (CL,dyn), lung transfer for CO (TL,CO), and arterial blood gases, as well as bronchoalveolar lavage (BAL) with determination of total and differential cell counts.After initial evaluation the decision was a careful observation of four children without therapy. Corticosteroid treatment was initiated in 17 children. Analysis of results indicated that after 6±12 months of treatment most clinical manifestations of the disease and chest radiograph abnormalities disappeared, and bene®cial effects on VC and TL,CO were apparent. After 18 months of steroids no bene®t on pulmonary function tests could be noticed, with mainly persistence of alterations of CL,dyn. Results of BAL studies documented the presence of an alveolitis with increased lymphocyte populations throughout the follow-up. Relapses were observed in four children during tapering of prednisone; they were not reported after discontinuation of steroid therapy.Taken together data obtained in the presented population can lead to the following suggestions for the management of pulmonary sarcoidosis in children. BAL should be performed at the initial evaluation to document alveolitis; however, nothing seems to be gained from repeating this investigation during follow-up in the absence of speci®c reasons. Once the decision to initiate glucocorticoid therapy is made, 18 months may be a reasonable treatment duration. Discontinuation of therapy can be decided even if the pulmonary function tests remain abnormal, but the child should then be carefully monitored for a relapse.

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Section: Initial Evaluationmentioning

confidence: 99%

“…The decision to treat pulmonary sarcoidosis in adults remains dif®cult, as there is no consensus on which patients should receive treatment [2,5,6]. This is because the disease can stabilize or resolve without therapy.…”

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confidence: 99%

Pulmonary sarcoidosis in children: a follow-up study

et al. 2001

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“…P ulmonary sarcoidosis is an inflammatory disorder characterised by the accumulation of activated lymphocytes and macrophages in the lung, resulting in the formation of granulomas [1,2]. A key role in granuloma formation is played by interferon (IFN)-c [3] and Thelper (Th) type-1 cells accumulating in the sarcoid lungs, which express chemokine receptor CXC chemokine receptor (CXCR)3 [4].…”

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confidence: 99%

T-helper cell type-1 transcription factor T-bet is upregulated in pulmonary sarcoidosis

Kriegová¹,

Fillerová²,

Tománková³

et al. 2011

Eur Respir J

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Upregulation of genes for interferon (IFN)-γ and CXC chemokine receptor (CXCR)3 expression, two crucial molecules in sarcoid inflammation and granuloma formation, is directly controlled by the T-helper (Th)1 transcription factor T-bet (T-box, expressed in T-cells). However, there is no information on T-bet expression in sarcoidosis or its relationship with “sarcoidosis-associated” genes.Therefore, we investigated expression of T-bet mRNA and, in parallel, a spectrum of genes known to be involved in sarcoidosis pathogenesis. Transcripts were determined in bronchoalveolar lavage (BAL) cells from 62 sarcoidosis patients and 25 controls by quantitative RT-PCR; T-bet protein was localised by immunohistochemistry.Patient’s BAL cells expressed higher mRNA T-bet levels than those of controls (mean±sdfold change 3.64±1.72; p=0.00006). T-bet mRNA expression did not vary between clinical phenotypes as assessed by chest radiography stage, presence/absence of Löfgren's syndrome, extrapulmonary/pulmonary involvement or progressing/remitting disease (p>0.05). T-bet mRNA expression correlated with expression of IFN-γ, CC chemokine ligand 5, CXC chemokine ligand (CXC)10, interleukin (IL)-2 receptor/IL-15 receptor β, CXCR3 and CXCR6 (p<0.01). T-bet protein was localised to alveolar macrophages and lymphocytes, tissue multinucleated giant cells, macrophages and lymphocytes.In pulmonary sarcoidosis, T-bet upregulation is associated with changes in expression of IFN-γ, CXCR3 and chemokines/receptors involved in the pathogenesis of sarcoidosis, which suggests a role for T-bet in this Th1 disease, including modulation of some sarcoidosis-associated genes.

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“…Although vitamin D has a low-risk profile and a broad therapeutic window, we suggest that the use of vitamin D in healthy individuals outside of clear indications or clinical trials should be questioned for two reasons: first, there are currently no large prospective randomised controlled trials showing that vitamin D supplementation leads to beneficial outcomes; and, secondly, because of the potential risk of calcitriol-mediated hypercalcaemia that may arise from a variety of potentially unrecognised or asymptomatic conditions, as in the present patient. Asymptomatic sarcoidosis, especially in stage I, is not uncommon [7]. Vitamin D and calcium metabolism is abnormal in sarcoidosis.…”

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confidence: 99%