The clinical and immunologic features of pulmonary fibrosis in sarcoidosis

Patterson, Karen; Hogarth, Kyle; Husain, Aliya N.; Sperling, Anne I.; Niewold, Timothy B.

doi:10.1016/j.trsl.2012.03.005

Cited by 49 publications

(37 citation statements)

References 86 publications

(109 reference statements)

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“…In our study, booster challenge with PA induced activation of the Th1 immune response including expression of IFN-γ and TNF-α, which may have induced fibrosis and also activation of TGF-β1. BALF lymphocytes and ACE expression are both important in clinical assessments of sarcoidosis [5, 27]. In the present study, the number of inflammatory cells, especially lymphocytes, in the BALF increased from days 21 to 70.…”

Section: Discussionsupporting

confidence: 56%

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Pulmonary fibrosis in a mouse model of sarcoid granulomatosis induced by booster challenge withPropionibacterium acnes

et al. 2016

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Pulmonary fibrosis (PF) associated with chronic sarcoidosis remains poorly understood, and no experimental model is currently available for this condition. Previous studies have shown that Propionibacterium acnes (PA) was associated with sarcoidosis and induced granuloma formation in mice. Here, we investigated whether repeated challenge with PA induces persistent inflammation leading to sarcoidosis followed by PF in mice. Specifically, C57BL/6 mice were inoculated intraperitoneally and subjected to intratracheal challenge with PA, and then were booster-challenged with either PA or phosphate-buffered saline on day 28. Inflammation, granulomata, and features of fibrosis were evaluated every 7 days until day 70. Complete remission of lung granulomata was apparent on day 42 in the sarcoid-remission group. However, granulomata was present from days 21 to 70 in mice that received PA boosting. Inflammatory cell counts and Th1 cytokine levels in lung lavage fluids were elevated up to day 70. Furthermore, fibrotic changes in the lungs were observed around granulomatous and peribronchovascular regions after PA boosting. Taken together, these findings suggest that development of PF following sarcoidosis may result from continuous PA infection and inflammation. Repeated boosting with PA to induce PF might be a useful model for future studies of sarcoidosis-associated PF.

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Section: Discussionsupporting

confidence: 56%

“…It remains unclear whether or not progressive fibrosis results from persistent granulomatous inflammation [27]. In the sarcoid-remission group of the present study, no lung fibrosis was observed after the initial PA challenge.…”

Section: Discussionmentioning

confidence: 55%

Pulmonary fibrosis in a mouse model of sarcoid granulomatosis induced by booster challenge withPropionibacterium acnes

et al. 2016

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“…Furthermore, questions remain whether the process is early or late stage. [28**] Research is necessary to determine whether and when immunosuppression may alter the clinical course. Generally, it is recommended that if accompanying granulomatous inflammation is suspected, immunosuppression should be initiated to prevent further organ damage.…”

Section: Morbiditymentioning

confidence: 99%

“…Generally, it is recommended that if accompanying granulomatous inflammation is suspected, immunosuppression should be initiated to prevent further organ damage. [28**]…”

Section: Morbiditymentioning

confidence: 99%

Morbidity and mortality in sarcoidosis

Gerke

2014

Current Opinion in Pulmonary Medicine

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Purpose of Review Chronic sarcoidosis is a complex disease with numerous comorbid conditions and can be fatal in some cases. Recognizing causes of morbidity and mortality is important to effectively select treatments, manage symptoms, and improve outcomes. The purpose of this review is to examine emerging knowledge on morbidity and mortality in sarcoidosis. Recent Findings Approximately one to five percent of patients with sarcoidosis die from complications of sarcoidosis. Recent population studies indicate that mortality may be increasing over the past decade. The reasons behind these trends are unclear, but could include increasing incidence, detection rates, severity of disease, or age of the population. Morbidity of sarcoidosis is reflected by a trend of increased hospitalizations over recent years and increased use of healthcare resources. Morbidity can be caused by organ damage from granulomatous inflammation, treatment complications, and psychosocial effects of the disease. Recent studies are focused on morbidity related to cardiopulmonary complications, bone health, and aging within the sarcoidosis population. Last, sarcoidosis is associated with autoimmune diseases, pulmonary embolism, and malignancy; however, the underlying mechanisms linking diseases continue to be debated. Summary Morbidity in sarcoidosis is significant and multifactorial. Mortality is infrequent, but may be increasing over the years.

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“…Compared to patients with IPF, pulmonary fibrosis in sarcoidosis is characterised by a chronic course, often involving the upper lobe, and is predominantly of the nonhoneycombing type. Conversely, IPF progresses quickly, is mostly located peripherally or in the lower lobe, with a predominance of honeycombing [15]. This might lead to increased traction on the PA in IPF.…”

mentioning

confidence: 99%

Pulmonary artery diameter to predict pulmonary hypertension in pulmonary sarcoidosis

et al. 2015

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Pulmonary hypertension (PH) is a known complication of pulmonary sarcoidosis with a prevalence ranging from 5% to 74% [1]. The aetiology of PH in sarcoidosis is not fully understood. Usually, it is attributed to the destruction of the distal capillary bed by lung fibrosis and/or chronic hypoxaemia. However, the severity of PH does not correlate consistently with the degree of pulmonary fibrosis, and PH exists in sarcoidosis patients without fibrosis, suggesting a multifactorial mechanism. The presence of PH is associated with a poor prognosis, and early diagnosis and treatment might improve outcome [1]. Echocardiography should always be performed when PH is suspected [2]. However, the accuracy of echocardiography in patients with interstitial lung diseases is often limited due to poor image quality and unreliable tricuspid regurgitation signal to measure the right ventricular systolic pressure (RVSP) [3]. Further invasive investigation with the gold standard, right heart catheterisation (RHC), is often required. In order to optimise the noninvasive diagnostic approach, there is a need for more accurate predictors of PH. Computed tomography (CT) may raise suspicion of PH in symptomatic patients or those examined for unrelated indications by showing an increased pulmonary artery (PA) diameter (⩾29 mm) and PA diameter/ascending aorta diameter (AAD) ratio (⩾1.0) [2]. Similarly, PA diameter indexed to body surface area (BSA) has been suggested as possible predictor of PH. However, these parameters have never been investigated in pulmonary sarcoidosis specifically.In this study, PA diameter measurements on chest CT were retrospectively evaluated as predictors of PH. Patients suspected of PH and referred for analysis between November 2007 and May 2014 were included in cases with a consensus diagnosis of pulmonary sarcoidosis, aged ⩾18 years, with availability of chest CT within 1 year of PH analysis. The analysis protocol was based on the European PH guideline [2], and consisted of an ECG, laboratory testing, and echocardiographic assessment of RVSP and secondary parameters. Subsequently, patients were classified as "PH likely" (RVSP >50 mmHg), "PH possible" (RVSP of 36-50 mmHg or presence of secondary signs with normal/absent RVSP signal) or "PH unlikely" (RVSP <36 mmHg or absence of signal without secondary signs). RHC was performed if PH was possible or likely. PH was defined as an invasively measured mean PA pressure (mPAP) ⩾25 mmHg. Patients were divided into three groups: "PH confirmed by RHC", "no PH confirmed by RHC" and "no PH based on echocardiography".

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The clinical and immunologic features of pulmonary fibrosis in sarcoidosis

Cited by 49 publications

References 86 publications

Pulmonary fibrosis in a mouse model of sarcoid granulomatosis induced by booster challenge withPropionibacterium acnes

Pulmonary fibrosis in a mouse model of sarcoid granulomatosis induced by booster challenge withPropionibacterium acnes

Morbidity and mortality in sarcoidosis

Pulmonary artery diameter to predict pulmonary hypertension in pulmonary sarcoidosis

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