The respiratory system in connective tissue disorders

Crestani, Bruno

doi:10.1111/j.1398-9995.2005.00761.x

Cited by 98 publications

(112 citation statements)

References 166 publications

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“…Importantly, however, as of today no effective treatment directed against any kind of pulmonary fibrosis is available. 3 Histologically, several distinct patterns of pulmonary fibrosis can be detected and are associated with different DPLDs. A commonly occurring pattern is nonspecific interstitial pneumonia (NSIP), 1,4 which is characterized by relatively homogenous primarily inflammatory and fibrotic alterations, visible as accumulation of connective tissue in the alveolar septa.…”

mentioning

confidence: 99%

Extracellular matrix alterations and acute inflammation; developing in parallel during early induction of pulmonary fibrosis

Rydell‐Törmänen

Andréasson

Hesselstrand

et al. 2012

Laboratory Investigation

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Pulmonary fibrosis is a hallmark of several systemic diseases such as systemic sclerosis. Initiation and early development is not well characterized, as initiation usually is unnoticed in patients, yet fibrosis has been considered a late event, occurring after an inflammatory phase. By utilizing an animal model, the starting point can be defined and the initiation process and early development thoroughly investigated. To investigate these processes from a systemic perspective, we choose a systemic administration route, instead of the more commonly used local administration. The aim of this work was to study the initiation of pulmonary fibrosis in an animal model and to investigate early alterations in connective tissue, cell turnover and acute immune response in lung parenchyma. Animals were injected subcutaneously with bleomycin, three times a week (w) for 1-4w (controls received saline). Total collagen was histologically assessed by Picro Sirius Red and Masson's Trichrome, collagen production by antibodies directed against N-terminal of procollagens I and III, proliferation by labeling with proliferating cell nuclear antigen, apoptosis by TUNEL and innate immunity by detecting neutrophils and macrophages. Total collagen was significantly increased at 1, 2 and 4w compared with controls. Procollagen I, was increased at 1w and remained increased, whereas procollagen III-staining was increased at 2w, compared with controls. Myofibroblasts were increased at all times as were proliferation, whereas apoptosis was increased from 2w. Neutrophils peaked at 1w (2779±820 cells/mm 2 ) and gradually decreased, whereas macrophages peaked at 2w (135±29 cells/mm 2 ). Subcutaneously administered bleomycin induces rapid alterations in connective tissue and cell turnover, suggesting a plasticity of the connective tissue. A transient neutrophilia is detected and increased number of macrophages likely represents a clearance process of said neutrophils. The study suggests fibrosis initiation and acute inflammation to occur in parallel in this model. (2012) 92, 917-925; Laboratory Investigation

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confidence: 99%

Extracellular matrix alterations and acute inflammation; developing in parallel during early induction of pulmonary fibrosis

Rydell‐Törmänen

Andréasson

Hesselstrand

et al. 2012

Laboratory Investigation

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“…Rates of ILD differ between these CTDs. Using high-resolution computed tomography (HRCT) to detect ILD in CTD patient cohorts (cohort sizes ranging , prevalence varies from 19% in RA to 67% and 85% in MCTD and diffuse SSc, respectively [1][2][3]. Intermediate prevalence, in the range 23-38%, is found in SLE and DM/PM.…”

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confidence: 99%

Pivotal clinical dilemmas in collagen vascular diseases associated with interstitial lung involvement

Antoniou¹,

Margaritopoulos²,

Economidou³

et al. 2009

European Respiratory Journal

149

122

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The connective tissue disorders (CTDs), also called collagen vascular diseases (CVDs), represent a heterogeneous group of immunologically mediated inflammatory disorders with a large variety of affected organs. Individuals with a CTD (rheumatoid arthritis, systemic lupus erythematosus, systemic sclerosis, Sjögren's syndrome, polymyositis/dermatomyositis and mixed connective tissue disease) are susceptible to respiratory involvement. When the lungs are affected, an increasing mortality and morbidity in CVDs occurs. Interstitial lung disease (ILD) is established as a clinical corollary across the spectrum of CTDs, with an overall incidence estimated at 15%.Therefore, pivotal clinical dilemmas remain in the evaluation and management of ILD involvement in CVDs. Critical questions are the presence of fibrosis and whether the disease is clinically significant. Moreover, the clinician has to decide if treatment is warranted and which is the best therapeutic approach. The use of additional tests, such as pulmonary function tests, high-resolution computed tomography scan, bronchoalveolar lavage fluid and surgical lung biopsy, deserves better discussion. The present review focuses on establishing the diagnosis of ILD in CTD, and on evaluating disease activity and prognosis. This will provide the basis for therapeutic decisions that will be discussed, including an overview of recent advances.

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“…Patients also have an increased risk of opportunistic infections, often favoured by corticosteroids and/or immunosuppressive or immunomodulatory therapy [1,2]. The respective frequency of manifestations, their clinical and radiological presentations, response to treatment, and outcome are dependent on the underlying CTD.…”

mentioning

confidence: 99%

Interstitial lung disease: are we missing formes frustes of connective tissue disease?

Cottin¹

2006

European Respiratory Journal

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The respiratory system in connective tissue disorders

Cited by 98 publications

References 166 publications

Extracellular matrix alterations and acute inflammation; developing in parallel during early induction of pulmonary fibrosis

Extracellular matrix alterations and acute inflammation; developing in parallel during early induction of pulmonary fibrosis

Pivotal clinical dilemmas in collagen vascular diseases associated with interstitial lung involvement

Interstitial lung disease: are we missing formes frustes of connective tissue disease?

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