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Frailty is a syndrome characterized by the decline in the physiologic reserve and function of several systems, leading to increased vulnerability and adverse health outcomes. While common in the elderly, recent studies have underlined the higher prevalence of frailty in chronic diseases, independent of age. The pathophysiological mechanisms that contribute to frailty have not been completely understood, although significant progresses have recently been made. In this context, chronic inflammation is likely to play a pivotal role, both directly and indirectly through other systems, such as the musculoskeletal, endocrine, and neurological systems. Rheumatic diseases are characterized by chronic inflammation and accumulation of deficits during time. Therefore, studies have recently started to explore the link between frailty and rheumatic diseases, and in this review, we report what has been described so far. Frailty is dynamic and potentially reversible with 8.3%-17.9% of older adults spontaneously improving their frailty status over time. Muscle strength is likely the most significant influencing factor which could be improved with training thus pointing at the need to maintain physical activity. Not surprisingly, frailty is more prevalent in patients affected by rheumatic diseases than in healthy controls, regardless of age and is associated with high disease activity to affect the clinical outcomes, largely due to chronic inflammation. More importantly, the treatment of the underlying condition may prevent frailty. Scales to assess frailty in patients affected by rheumatic diseases have been proposed, but larger casuistries are needed to validate disease-specific indexes, which could allow more accurate prognostic estimates than demographic and diseaserelated variables alone. Frail patients can be more vulnerable and more difficult to treat, due to the risk of side effects, therefore frailty should be taken into account in clinical decisions. Clinical trials addressing frailty could identify patients who are less likely to tolerate potentially toxic medications and might benefit from more conservative regimens. In conclusion, the implementation of the concept of frailty in rheumatology will allow a better understanding of the patient global health, a finest risk stratification and a more individualized management strategy.

The immune system is the central regulator of tissue homeostasis, ensuring tissue regeneration and protection against both pathogens and the neoformation of cancer cells. Its proper functioning requires homeostatic properties, which are maintained by an adequate balance of myeloid and lymphoid responses. Aging progressively undermines this ability and compromises the correct activation of immune responses, as well as the resolution of the inflammatory response. A subclinical syndrome of “homeostatic frailty” appears as a distinctive trait of the elderly, which predisposes to immune debilitation and chronic low-grade inflammation (inflammaging), causing the uncontrolled development of chronic and degenerative diseases. The innate immune compartment, in particular, undergoes to a sequela of age-dependent functional alterations, encompassing steps of myeloid progenitor differentiation and altered responses to endogenous and exogenous threats. Here, we will review the age-dependent evolution of myeloid populations, as well as their impact on frailty and diseases of the elderly.

HLA-B27 status was obtained in only 21 (31.8%) patients, of which one in the polyarthritis subgroup tested positive.Most patients were treated with glucocorticoids (50%-78%), non-steroidal anti-inflammatory drugs (33%-52%) or analgesics (14%-28%), while disease-modifying antirheumatic drugs were used in five (28%) patients with polyarthritis, five (24%) patients with oligoarthritis and only three (11%) patients with PMR-like presentation.Despite the limitation of a very short follow-up, the clinical course seemed excellent in patients with PMR-like onset with 74% achieving full remission of symptoms after 2 weeks; on the other hand, 67% of patients with polyarthritis had active disease after an average follow-up of 6 weeks.In conclusion, despite the fact that a clear cause-effect relationship is far to be ascertained, our data suggest that inflammatory musculoskeletal symptoms may occasionally develop in close temporal association with COVID-19 vaccine administration. However, even assuming a direct causal relationship, we feel that the overall safety of COVID-19 vaccines remains unaffected, and the benefits of vaccination largely outweigh the minimal risks associated with such uncommon inflammatory complications, probably reflecting a transient reactogenic response to the vaccine rather than a structured, chronic inflammatory joint disease.

SARS-CoV-2 vaccination has proven effective in inducing an immune response in healthy individuals and is progressively us allowing to overcome the pandemic. Recent evidence has shown that response to vaccination in some vulnerable patients may be diminished, and it has been proposed a booster dose. We tested the kinetic of development of serum antibodies to the SARS-CoV-2 Spike protein, their neutralizing capacity, the CD4 and CD8 IFN-γ T-cell response in 328 subjects, including 131 immunocompromised individuals (cancer, rheumatologic, and hemodialysis patients), 160 health-care workers (HCW) and 37 subjects older than 75 yr, after vaccination with two or three doses of mRNA vaccines. We stratified the patients according to the type of treatment. We found that immunocompromised patients, depending on the type of treatment, poorly respond to SARS-CoV-2 mRNA vaccines. However, an additional booster dose of vaccine induced a good immune response in almost all of the patients except those receiving anti-CD20 antibody. Similarly to HCW, previously infected and vaccinated immunocompromised individuals demonstrate a stronger SARS-CoV-2–specific immune response than those who are vaccinated without prior infection.