Value of serum soluble Interleukin-2 Receptor as a diagnostic and predictive biomarker in sarcoidosis.
Conclusion: High levels of sIL-2R are suggestive of sarcoidosis, although a broad overlap exists in sIL-2R levels across sarcoidosis, cHP and IPF. High levels of sIL-2R might serve as a prognostic biomarker for chronicity. PMID: 32248706 [PubMed - as supplied by publisher]
Condition: Sarcoidosis Intervention: Sponsor: University of Aarhus Recruiting
Conclusion The results of the study show that VAM should be used because of its high diagnostic benefit in mediastinal lymphadenopathies, which are difficult to diagnose, or mediastinal lesions located in the paratracheal region. Despite the increase in the number of new diagnostic modalities, VAM is still the most effective method and a gold standard. [...] Georg Thieme Verlag KG Stuttgart · New YorkArticle in Thieme eJournals: Table of contents | Abstract | Full text
Conclusion: The diagnosis of NS requires a high degree of suspicion, coupled with exclusion of alternate diagnosis. It commonly precedes the onset of systemic sarcoidosis. Central nervous system involvement in sarcoidosis is associated with poor clinical outcomes.
Diagnosis of extra-pulmonary sarcoidosis can be difficult, and a biopsy is usually required. We evaluated the utility of endobronchial ultrasound-transbronchial needle aspiration (EBUS-TBNA) in patients with suspected extra-pulmonary sarcoidosis with thoracic lymph nodes ≤10 mm on chest computed tomography (CT) and no or minimal pulmonary infiltrates.
Authors: Takada S, Saito MK, Kambe N Abstract Blau syndrome, or early-onset sarcoidosis, is hereditary juvenile-onset systemic granulomatosis. Clinical symptoms appear before the age of 4 years and mainly affect the skin, joints, and eyes. The symptoms are progressive and cause severe complications, such as joint destruction and blindness. Although tumor necrosis factor alpha (TNFα) antagonists are effective for controlling some of the symptoms of Blau syndrome, there is no specific curative treatment. Heterozygous mutations in nucleotide-binding oligomerization domain 2 (NOD2) were identified as the cause of...
Conclusion: KL-6 is predictive biomarker useful in the clinical management of ILD patients, in particular in patients with severe fibrotic lung disorders. PMID: 32613855 [PubMed - as supplied by publisher]
Authors: Arai T, Kasai T, Shimizu K, Kawahara K, Katayama K, Sugimoto C, Hirose M, Okamoto H, Tachibana K, Akira M, Inoue Y Abstract Autoimmune pulmonary alveolar proteinosis (APAP) is caused by macrophage dysfunction due to anti-granulocyte-macrophage colony-stimulating factor (GM-CSF) autoantibody. We experienced 2 cases of APAP complicated with sarcoidosis in a 42-year-old woman and a 51-year-old man (age at the sarcoidosis diagnosis). APAP preceded sarcoidosis in the woman, and both diseases were diagnosed simultaneously in the man. Sarcoidosis lesions were observed in the lung, skin, and eyes, and the patholog...
A sarcoidosis patient may be refractory to corticosteroid therapy. This may be because corticosteroids are ineffective in relieving the sarcoidosis patient's symptoms/dysfunction or because the clinician has determined that the risks of corticosteroids outweigh their benefits. Interestingly, when corticosteroids truly fail to improve a sarcoidosis patient's condition, it is very rarely because of failure of the drug as an anti-granulomatous agent; rather, it is usually because the patient's symptoms were unrelated to active sarcoid granulomas.
Publication date: Available online 1 July 2020Source: Joint Bone SpineAuthor(s): S Cadiou, F Robin, R Guillin, A Perdriger, S Jouneau, N Belhomme, G Coiffier, P Guggenbuhl
We report on three Mexican patients clinically diagnosed with BS who exhibited a likely pathogenic variant in NOD2 as revealed by whole-exome sequencing (WES) and Sanger sequencing: two variants (c.1000 C > T/p.Arg334Trp and c.1538 T > C/p.Met513Thr) lie in the ATP/Mg2+ binding site, whereas the other (c.3019dupC/p.Leu1007ProfsTer2) introduces a premature stop codon disrupting the last LRR domain (LRR9) formation; all three variants are consistent with gain-of-function changes. Interestingly, all these patients presented concomitant likely pathogenic variants in other inflammatory disease-...