Necrotizing granulomatous inflammation: what does it mean if your special stains are negative?

Aubry, Marie Christine

doi:10.1038/modpathol.2011.155

Cited by 53 publications

(42 citation statements)

References 13 publications

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“…4,6 In children, Takayasu's arteritis and Kawasaki disease are the most common forms of coronary artery vasculitis. The inflammatory cell infiltrate varies depending on the aetiological cause with neutrophilic infiltrates commonly seen with Wegner's granulomatosis 7,11 and eosinophils or plasma cells more commonly seen in cases associated with ChurgeStrauss syndrome, rheumatoid arteritis or SLE. In all cases of vasculitis the coronary arteries show little or no evidence of atheroma.…”

Section: Discussionmentioning

confidence: 99%

Pseudotumour formation in atheromatous coronary arteries

Treacy

Norita

Ingram³

et al. 2015

Journal of Forensic and Legal Medicine

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Section: Discussionmentioning

confidence: 99%

Pseudotumour formation in atheromatous coronary arteries

Treacy

Norita

Ingram³

et al. 2015

Journal of Forensic and Legal Medicine

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“…Histologically, necrotizing vasculitis and inflammation consisting of histiocytes, lymphocytes, plasma cells, and multinucleated giant cells surrounding geographic areas of basophilic necrosis with granuloma formation is characteristic of nasal involvement in GPA . Differentially expressed genes identified in the nasal mucosa of patients with GPA suggest the importance of innate immunity, granulocyte and agranulocyte migration and diapedesis, extracellular matrix composition, and epithelial barrier integrity in the pathogenesis of nasal disease in GPA.…”

Section: Discussionmentioning

confidence: 99%

Brief Report: Defining the Nasal Transcriptome in Granulomatosis With Polyangiitis (Wegener's)

Grayson

Steiling

Platt

et al. 2015

Arthritis & Rheumatology

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Objectives To determine whether disease processes related to granulomatosis with polyangiitis (GPA) are reflected in gene expression profiles of nasal mucosa. Methods Nasal brushings of the inferior turbinate were obtained from 32 patients with GPA (10 with active nasal disease, 13 with prior nasal disease, 9 with no history of nasal disease) and a composite comparator group with and without inflammatory nasal disease (12 healthy people, 15 with sarcoidosis, 8 with allergic rhinitis). Differential gene expression was assessed between subgroups of GPA and comparators. Results 339 genes were differentially expressed between the GPA and comparator groups (absolute fold change > 1.5; false discovery rate < 0.05). Top canonical pathways upregulated in nasal brushings from patients with GPA include granulocyte adhesion and diapedesis (p=8.6 E-22), agranulocyte adhesion and diapedesis (p=1.3 E-14), interleukin 10 signaling (3.0 E-11), and TREM1 signaling (9.0 E-11). A set of genes differentially expressed in GPA independent of nasal disease activity status included genes related to epithelial barrier integrity (fibronectin 1, desmosomal proteins) and several matricellular proteins (e.g. osteonectin, osteopontin). Significant overlap of differentially expressed genes was observed between active and prior nasal disease GPA subgroups. Peripheral blood neutrophil and mononuclear gene expression levels associated with GPA were similarly altered in the nasal gene expression profiles of patients with active or prior nasal disease. Conclusions Profiling the nasal transcriptome in GPA reveals gene expression signatures related to innate immunity, inflammatory cell chemotaxis, extracellular matrix composition, and epithelial barrier integrity. Airway-based expression profiling is feasible and informative in GPA.

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“…Various infections can mimic many of these patterns: viral infection can produce a cellular NSIP pattern, resolving bacterial pneumonia can produce an OP pattern, and invasive fungal or mycobacterial infection can produce necrotizing granulomas resembling those seen in granulomatosis with polyangiitis. 67 Pulmonary toxicity from certain medications can produce many of these injury patterns, particularly OP, cellular NSIP, and DAD. Many therapies for CTD including immunosuppressive agents such as methotrexate, cyclophosphamide, and possibly tumor necrosis factor (TNF)-a inhibitors can give rise to pulmonary pathologies and Vivero & Padera can present years after the offending drug has been discontinued.…”

Section: Histologic Differential Diagnosis Of Lung Disease In Connectmentioning

confidence: 99%