Outcome measures for primary Sjögren’s syndrome

Séror, Raphaèle; Bootsma, Hendrika; Bowman, Simon; Döerner, Thomas; Gottenberg, Jacques-Éric; Mariette, Xavier; Ramos-Casals, Manuel; Ravaud, Philippe; Theander, Elke; Tzioufas, Athanasios G.; Vitali, Claudio

doi:10.1016/j.jaut.2012.01.013

Cited by 47 publications

(23 citation statements)

References 32 publications

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“…Participants reported no upper respiratory symptoms at the time of data collection. Participants completed the Voice Handicap Index and the EULAR (European League Against Rheumatism) Sjögren's Syndrome Patients Reported Index—a measure of disease severity—prior to data collection. The University of Utah Institutional Review Board approved all study‐related procedures (#555046).…”

Section: Methodsmentioning

confidence: 99%

Comparing nebulized water versus saline after laryngeal desiccation challenge in Sjögren's Syndrome

et al. 2013

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Section: Methodsmentioning

confidence: 99%

Comparing nebulized water versus saline after laryngeal desiccation challenge in Sjögren's Syndrome

et al. 2013

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“…In fact, 30% to 70% of patients develop systemic involvement before or after the diagnosis of pSS [21-24]. In addition, it must be considered that this group of patients more commonly has circulating anti-Ro and anti-La autoantibodies, in comparison with the group of patients with sicca-limited disease [25].…”

Section: Introductionmentioning

confidence: 99%

Novel aspects of Sjögren’s syndrome in 2012

Tincani

Andréoli

Cavazzana

et al. 2013

BMC Med

145

138

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Sjögren’s syndrome (SS) is a systemic progressive autoimmune disease characterized by a complex pathogenesis requiring a predisposing genetic background and involving immune cell activation and autoantibody production. The immune response is directed to the exocrine glands, causing the typical ‘sicca syndrome’, but major organ involvement is also often seen. The etiology of the disease is unknown. Infections could play a pivotal role: compared to normal subjects, patients with SS displayed higher titers of anti-Epstein-Barr virus (EBV) early antigens, but lower titers of other infectious agent antibodies such as rubella and cytomegalovirus (CMV) suggest that some infections may have a protective role against the development of autoimmune disease. Recent findings seem to show that low vitamin D levels in patients with SS could be associated with severe complications such as lymphoma and peripheral neuropathy. This could open new insights into the disease etiology. The current treatments for SS range from symptomatic therapies to systemic immunosuppressive drugs, especially B cell-targeted drugs in cases of organ involvement. Vitamin D supplementation may be an additional tool for optimization of SS treatment.

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“…The exocrine glands become functionally bereft due to compromised secretory activity. With the persistent inflammatory foci, fibrosis, atrophy and fatty changes that underscore lymphocytic adenitis and degeneration of the exocrine glands, it is important to decipher these pathways[68], since once fibrosis sets in, response to therapy becomes limited. The effect of therapy on salivary secretion is reported to be more marked in patients having moderate lymphocytic infiltration and moderate or less severe acinar atrophy and intralobular fibrosis at baseline [69].…”

Section: 0 Discussionmentioning

confidence: 99%

A link between interferon and augmented plasmin generation in exocrine gland damage in Sjögren's syndrome

Gliozzi

Greenwell-Wild

Jin

et al. 2013

Journal of Autoimmunity

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Sjögren’s syndrome is an autoimmune disease that targets exocrine glands, but often exhibits systemic manifestations. Infiltration of the salivary and lacrimal glands by lymphoid and myeloid cells orchestrates a perpetuating immune response leading to exocrine gland damage and dysfunction. Th1 and Th17 lymphocyte populations and their products recruit additional lymphocytes, including B cells, but also large numbers of macrophages, which accumulate with disease progression. In addition to cytokines, chemokines, chitinases, and lipid mediators, macrophages contribute to a proteolytic milieu, underlying tissue destruction, inappropriate repair, and compromised glandular functions. Among the proteases enhanced in this local environment are matrix metalloproteases (MMP) and plasmin, generated by plasminogen activation, dependent upon plasminogen activators, such as tissue plasminogen activator (tPA). Not previously associated with salivary gland pathology, our evidence implicates enhanced tPA in the context of inflamed salivary glands revolving around lymphocyte-mediated activation of macrophages. Tracking down the mechanism of macrophage plasmin activation, the cytokines IFNγ and to a lesser extent, IFNα, via Janus kinase (JAK) and signal transducer and activator of transcription (STAT) activation, were found to be pivotal for driving the plasmin cascade of proteolytic events culminating in perpetuation of the inflammation and tissue damage, and suggesting intervention strategies to blunt irreversible tissue destruction.

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Outcome measures for primary Sjögren’s syndrome

Cited by 47 publications

References 32 publications

Comparing nebulized water versus saline after laryngeal desiccation challenge in Sjögren's Syndrome

Comparing nebulized water versus saline after laryngeal desiccation challenge in Sjögren's Syndrome

Novel aspects of Sjögren’s syndrome in 2012

A link between interferon and augmented plasmin generation in exocrine gland damage in Sjögren's syndrome

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