Literature DB >> 33217613

Overview of STING-Associated Vasculopathy with Onset in Infancy (SAVI) Among 21 Patients.

Marie-Louise Frémond1, Alice Hadchouel2, Laureline Berteloot3, Isabelle Melki4, Violaine Bresson5, Laura Barnabei6, Nadia Jeremiah7, Alexandre Belot8, Vincent Bondet9, Olivier Brocq10, Damien Chan11, Rawane Dagher12, Jean-Christophe Dubus13, Darragh Duffy9, Séverine Feuillet-Soummer14, Mathieu Fusaro15, Marco Gattorno16, Antonella Insalaco17, Eric Jeziorski18, Naoki Kitabayashi19, Mireia Lopez-Corbeto20, Françoise Mazingue21, Marie-Anne Morren22, Gillian I Rice23, Jacques G Rivière24, Luis Seabra19, Jérôme Sirvente25, Pere Soler-Palacin26, Nathalie Stremler-Le Bel13, Guillaume Thouvenin27, Caroline Thumerelle28, Eline Van Aerde29, Stefano Volpi16, Sophie Willcocks30, Carine Wouters31, Sylvain Breton3, Thierry Molina32, Brigitte Bader-Meunier33, Despina Moshous34, Alain Fischer35, Stéphane Blanche36, Frédéric Rieux-Laucat6, Yanick J Crow37, Bénédicte Neven38.   

Abstract

BACKGROUND: Gain-of-function mutations in STING1 underlie a type I interferonopathy termed SAVI (STING-associated vasculopathy with onset in infancy). This severe disease is variably characterized by early-onset systemic inflammation, skin vasculopathy, and interstitial lung disease (ILD).
OBJECTIVE: To describe a cohort of patients with SAVI.
METHODS: Assessment of clinical, radiological and immunological data from 21 patients (17 families) was carried out.
RESULTS: Patients carried heterozygous substitutions in STING1 previously described in SAVI, mainly the p.V155M. Most were symptomatic from infancy, but late onset in adulthood occurred in 1 patient. Systemic inflammation, skin vasculopathy, and ILD were observed in 19, 18, and 21 patients, respectively. Extensive tissue loss occurred in 4 patients. Severity of ILD was highly variable with insidious progression up to end-stage respiratory failure reached at teenage in 6 patients. Lung imaging revealed early fibrotic lesions. Failure to thrive was almost constant, with severe growth failure seen in 4 patients. Seven patients presented polyarthritis, and the phenotype in 1 infant mimicked a combined immunodeficiency. Extended features reminiscent of other interferonopathies were also found, including intracranial calcification, glaucoma and glomerular nephropathy. Increased expression of interferon-stimulated genes and interferon α protein was constant. Autoantibodies were frequently found, in particular rheumatoid factor. Most patients presented with a T-cell defect, with low counts of memory CD8+ cells and impaired T-cell proliferation in response to antigens. Long-term follow-up described in 8 children confirmed the clinical benefit of ruxolitinib in SAVI where the treatment was started early in the disease course, underlying the need for early diagnosis. Tolerance was reasonably good.
CONCLUSION: The largest worldwide cohort of SAVI patients yet described, illustrates the core features of the disease and extends the clinical and immunological phenotype to include overlap with other monogenic interferonopathies.
Copyright © 2020 American Academy of Allergy, Asthma & Immunology. Published by Elsevier Inc. All rights reserved.

Entities:  

Keywords:  Interstitial lung disease; JAK inhibitors; Lymphopenia; Polyarthritis; STING1; Stimulator of interferon genes; Type I interferonopathy; Vasculopathy

Mesh:

Substances:

Year:  2020        PMID: 33217613     DOI: 10.1016/j.jaip.2020.11.007

Source DB:  PubMed          Journal:  J Allergy Clin Immunol Pract


  24 in total

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