Psoriatic arthritis (PsA) is a chronic disease affecting a variety of organs and tissues such as skin, joints, eyes and gut. The most prevalent comorbidities in PsA include cardiovascular diseases, metabolic syndromes (diabetes, obesity), inflammatory bowel disease, depression and anxiety. These comorbidities are so diffused in PsA patients that they can be considered part of the psoriatic disease itself. In fact, systemic inflammation, involving low-grade inflammatory activity in the vascular wall, is pivotal in the pathogenesis of atherosclerosis. The concept of a common pathogenic mechanism resulted in the increased importance of an integrated multidisciplinary approach to optimize the screening and the therapies for patients with PsA. A variety of experimental studies demonstrated that inhibition of proinflammatory cytokines, such as tumour necrosis factor (TNF), interleukin (IL)-1 and IL-6, had beneficial effects on cardiac function and outcome. Other experimental studies showed that IL-12 family cytokines, including IL-12, IL-23, IL-27, and IL-35 were involved in the crosstalk among major immune cell types driving the pro-inflammatory and anti-inflammatory responses in atherosclerosis. Such pleiotropic role in atherosclerosis was also reported for IL-17, with some experimental studies suggesting a proatherogenic effect, and others sugesting an atheroprotective role. Moreover, the presence of subclinical intestinal inflammation in the new pathogenetic hypotheses for the disease confirms the intestine being the site where the innate immune system is activated, as a result of interaction with the bacterial microenvironment.
In recent years, several drugs have been approved for PsA but little data is available on the impact of these drugs on comorbidities and eventually on the influence of comorbidities on the choice of the specific drug. Drugs that target the inflammatory cytokines responsible for the pathogenetic mechanism (TNF, IL23, IL17) could also have a benefit on comorbidities. However, although on a theoretical point of view this may be valid, in reality, there are no experimental data on the impact of these drugs on the comorbidities.
The aim of this Research Topic is to evaluate the impact of the biological therapies on the comorbidities of PsA. Its final scope is to identify which are the possible aspects of the comorbidities which could affect and modify the response of the patients to the drug.
Our purpose is to define the weight of comorbidities in the management of psoriatic arthritis. Also, we would like to evaluate the impact of treatment on comorbidities both in terms of disease activity and of disease evolution.
Topics which are welcome to this article collection include, but are not limited to, the following:
• comorbidities in patients with PsA
• personalized therapy for PsA based on comorbidities
• therapeutic efficacy of biological drugs in patients with comorbidities
Psoriatic arthritis (PsA) is a chronic disease affecting a variety of organs and tissues such as skin, joints, eyes and gut. The most prevalent comorbidities in PsA include cardiovascular diseases, metabolic syndromes (diabetes, obesity), inflammatory bowel disease, depression and anxiety. These comorbidities are so diffused in PsA patients that they can be considered part of the psoriatic disease itself. In fact, systemic inflammation, involving low-grade inflammatory activity in the vascular wall, is pivotal in the pathogenesis of atherosclerosis. The concept of a common pathogenic mechanism resulted in the increased importance of an integrated multidisciplinary approach to optimize the screening and the therapies for patients with PsA. A variety of experimental studies demonstrated that inhibition of proinflammatory cytokines, such as tumour necrosis factor (TNF), interleukin (IL)-1 and IL-6, had beneficial effects on cardiac function and outcome. Other experimental studies showed that IL-12 family cytokines, including IL-12, IL-23, IL-27, and IL-35 were involved in the crosstalk among major immune cell types driving the pro-inflammatory and anti-inflammatory responses in atherosclerosis. Such pleiotropic role in atherosclerosis was also reported for IL-17, with some experimental studies suggesting a proatherogenic effect, and others sugesting an atheroprotective role. Moreover, the presence of subclinical intestinal inflammation in the new pathogenetic hypotheses for the disease confirms the intestine being the site where the innate immune system is activated, as a result of interaction with the bacterial microenvironment.
In recent years, several drugs have been approved for PsA but little data is available on the impact of these drugs on comorbidities and eventually on the influence of comorbidities on the choice of the specific drug. Drugs that target the inflammatory cytokines responsible for the pathogenetic mechanism (TNF, IL23, IL17) could also have a benefit on comorbidities. However, although on a theoretical point of view this may be valid, in reality, there are no experimental data on the impact of these drugs on the comorbidities.
The aim of this Research Topic is to evaluate the impact of the biological therapies on the comorbidities of PsA. Its final scope is to identify which are the possible aspects of the comorbidities which could affect and modify the response of the patients to the drug.
Our purpose is to define the weight of comorbidities in the management of psoriatic arthritis. Also, we would like to evaluate the impact of treatment on comorbidities both in terms of disease activity and of disease evolution.
Topics which are welcome to this article collection include, but are not limited to, the following:
• comorbidities in patients with PsA
• personalized therapy for PsA based on comorbidities
• therapeutic efficacy of biological drugs in patients with comorbidities