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Accelerated atherosclerosis is a distinct feature of some inflammatory and autoimmune disorders and several specific autoimmune mechanisms and persistent inflammation have been identified to exert a pivotal role in precocious atherosclerotic damage in these disorders. Although increased atherosclerotic risk has been well established in some rheumatic autoimmune systemic diseases, such as systemic lupus erythematosus and rheumatoid arthritis, reliable data regarding the prevalence and pathogenetic mechanisms associated with increased atherosclerotic damage in primary Sjögren's syndrome are scarse. Indeed, primary Sjögren's syndrome is an autoimmune disorder characterised by chronic inflammation and autoimmune dysregulation that shares many pathogenic mechanisms and clinical features with systemic lupus erythematosus and rheumatoid arthitis. Higher prevalence of subclinical atherosclerosis has been observed in primary Sjögren's syndrome patients and recent population-based studies demonstrated an increased risk of cardiovascular events in these patients in comparison to general population. Among mechanisms associated with atherosclerotic damage, the prevalence and the role of traditional cardiovascular risk factors have been poorly investigated. In particular, the issue of whether the presence of these cardiovascular risk factors is associated with an increased risk of cardiovascular events needs to be further explored.

Sjögren's syndrome is a complex and potentially disabling slow progressive, systemic disorder. During the last twelve months several original and important contributions have been published on the pathogenesis, diagnosis and therapy of the disease. This review, following the others of this series is aimed at summarising some of the most significant studies that have been recently published. Regarding the pathogenesis, we will specifically focus on novel insights on miRNA, gut microbiota, adaptive and innate autoimmunity and animal models. Concerning novelties in pSS diagnosis, we will focus on salivary gland ultrasonography and histology. Finally, we will conclude with an update of the clinical manifestations of the disease and with an overview of the future therapies.

Mucosal dryness is a key clinical feature in primary Sjögren's syndrome (pSS) and its assessment relies on both objective measurement of residual secretion and subjective symptoms reported by patients. However, while the objective assessment and grading of glandular dysfunction can be easily performed, the spectrum of clinical symptoms encompassed by the terms 'dry eye' and 'dry mouth' is wide and heterogeneous. Therefore, patient reported outcomes (PROs) for dryness in pSS poorly correlate with the amount of glandular secretion. In addition, subjective dryness is not correlated with the severity of systemic disease and severely affects the patient quality of life even in presence of active extraglandular manifestations. The purpose of this review article is to provide an overview of glandular dysfunction in pSS as well as the impact of discrepancy between objective assessment, subjective symptom and extraglandular disease activity on disease management.

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease that predominately affects women. It is characterised by a broad spectrum of clinical manifestations, however, its course and organ involvement are unpredictable. Although over the last few decades an improvement in survival for SLE patients has been observed, pathogenic mechanisms underlying this disease are still unclear. Comorbidities, due to both disease and treatment, as well as multiple aspects of SLE, are under intensive investigation. Following the previous annual reviews of this series, we hereby provide a critical digest of the recent papers on SLE focusing on pathogenesis, clinical and laboratory features, as well as current and new therapeutic strategies published over the last year.

Systemic lupus erythematosus (SLE) is a systemic autoimmune disease with a highly variable course and prognosis. The management of the disease is still a clinical challenge for the treating physicians as many aspects regarding the disease pathogenesis, clinical picture and outcomes remain to be elucidated. New and interesting data are emerging; here the recent literature on SLE pathogenesis, clinical and laboratory aspects, as well as treatments and comorbidities, are reviewed and the main findings summarised in order to provide a bird's eye on the relevant papers on these topics.

The pathogenesis of rheumatoid arthritis (RA) is a complex scenario that, to date, is not fully elucidated. However, scientific progress has enabled us to understand several mechanisms underlying the development of the disease. The breakdown of self-tolerance in genetically predisposed individuals and the aberrant activation of innate and adaptive immune responses culminate in synovial hyperplasia and bone destruction. In addition, extra-articular manifestations, as well as the burden of increased cardiovascular risk (CVR), in patients with RA represent another interesting aspect of RA pathogenesis under intense investigation. The purpose of this review article is to provide an overview of the new insights in RA pathogenesis summarising the most relevant studies published over the last year.