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Relationships between Adipose Tissue and Psoriasis, with or without Arthritis.

Toussirot E, Aubin F, Dumoulin G - Front Immunol (2014)

Bottom Line: Adipokines may link the adipose tissue to the obesity-related complications of Pso and PsA.Indeed, altered circulating levels of the adipokines leptin, adiponectin, visfatine, and resistin have been found in patients with Pso or PsA.In addition, an excess of adipose tissue may compromise the therapeutic response to traditional drugs or biological agents in Pso and PsA.

View Article: PubMed Central - PubMed

Affiliation: Clinical Investigation Center for Biotherapy INSERM CIC-1431, University Hospital of Besançon , Besançon , France ; Department of Rheumatology, University Hospital of Besançon , Besançon , France ; Department of Therapeutics, University of Franche Comté , Besançon , France ; UPRES EA 4266 "Pathogens and Inflammation", University of Franche Comté , Besançon , France ; LabEX LipSTIC, ANR-11-LABX-0021 , Besançon , France.

ABSTRACT
Psoriasis (Pso) is a common chronic cutaneous inflammatory disease involving the skin that is associated with serious comorbidities. Comorbidities in Pso include psoriatic arthritis (PsA), reduced quality of life, malignancy, depression, but also a constellation of associated conditions that enhance the cardiovascular (CV) risk. Indeed, obesity is common in patients with Pso or PsA and is considered to be a risk factor for the onset of these diseases. Patients with Pso and PsA share common obesity-related complications such as metabolic syndrome (MetS), dyslipidemia, diabetes or insulin resistance, and CV diseases. Chronic inflammation in Pso and PsA partially explains the development of atherosclerosis and CV diseases. In parallel, body composition is disturbed in patients with Pso or PsA, as suggested by anthropometric measurements, while an excess of abdominal adiposity is observed in PsA, enhancing the risk of MetS and CV diseases. Adipokines may link the adipose tissue to the obesity-related complications of Pso and PsA. Indeed, altered circulating levels of the adipokines leptin, adiponectin, visfatine, and resistin have been found in patients with Pso or PsA. In addition, an excess of adipose tissue may compromise the therapeutic response to traditional drugs or biological agents in Pso and PsA. This paper reviews the comorbidities that contribute to enhanced CV risk, the body composition results, and the potential role of adipokines in systemic inflammation and energetic balance in Pso and PsA.

No MeSH data available.


Related in: MedlinePlus

Interrelationships between fat tissue, psoriasis (Pso), and psoriatic arthritis (PsA) are shown. Obesity is a predisposing factor the development of both Pso and PsA. Pso and PsA are associated with obesity-related complications such as metabolic syndrome, dyslipidemia, diabetes, or insulin resistance, which all enhance the cardiovascular (CV) risk. Body composition is disturbed in Pso or PsA, especially in patients with PsA who have an excess of abdominal adiposity, contributing to increase the risk of metabolic syndrome and CV diseases. Adipokines may link the adipose tissue to the obesity-related complications of Pso and PsA: altered circulating levels of the adipokines leptin, adiponectin, visfatin, resistin omentin, and retinol-binding protein-4 (RBP-4) have been found in patients with Pso or PsA. Leptin has pro-inflammatory effects and may contribute to skin and joint inflammation. Adiponectin promotes insulin sensitivity and its reduced level in Pso may drive insulin resistance and may lead to impaired cardiac and vascular protective effects, thus contributing to the CV risk. In addition, the excess of adipose tissue in Pso and PsA may compromise the therapeutic response to biological agents in Pso and PsA. Finally, anti-TNFα agents have been associated with weight gain in patients with Pso or PsA.
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Figure 1: Interrelationships between fat tissue, psoriasis (Pso), and psoriatic arthritis (PsA) are shown. Obesity is a predisposing factor the development of both Pso and PsA. Pso and PsA are associated with obesity-related complications such as metabolic syndrome, dyslipidemia, diabetes, or insulin resistance, which all enhance the cardiovascular (CV) risk. Body composition is disturbed in Pso or PsA, especially in patients with PsA who have an excess of abdominal adiposity, contributing to increase the risk of metabolic syndrome and CV diseases. Adipokines may link the adipose tissue to the obesity-related complications of Pso and PsA: altered circulating levels of the adipokines leptin, adiponectin, visfatin, resistin omentin, and retinol-binding protein-4 (RBP-4) have been found in patients with Pso or PsA. Leptin has pro-inflammatory effects and may contribute to skin and joint inflammation. Adiponectin promotes insulin sensitivity and its reduced level in Pso may drive insulin resistance and may lead to impaired cardiac and vascular protective effects, thus contributing to the CV risk. In addition, the excess of adipose tissue in Pso and PsA may compromise the therapeutic response to biological agents in Pso and PsA. Finally, anti-TNFα agents have been associated with weight gain in patients with Pso or PsA.

Mentions: There is compelling evidence suggesting that both Pso and PsA are associated with an excess of fat tissue (8, 20) (Figure 1). Moreover, obesity-related comorbidities accumulate in both conditions, especially, CV and metabolic comorbidities, leading to an increased CV burden. Pro-inflammatory cytokines, such as TNFα and IL-6, and the adipokines leptin, resistin, and visfatin produced by fat tissue are contributing and probably synergistic factors to a pro-inflammatory state in these conditions. Both Pso and PsA are associated with body composition changes, mainly in PsA. One unanswered question is the timing of adipose tissue changes: BMI and weight in early adulthood seem to predict Pso and PsA and conversely, patients with established disease (Pso or PsA) are characterized by excess fat mass. In other words, it remains to be clarified whether fat mass plays a role at the beginning (or before onset) of the disease, or whether the systemic inflammation in these chronic conditions may govern weight modification and fat redistribution.


Relationships between Adipose Tissue and Psoriasis, with or without Arthritis.

Toussirot E, Aubin F, Dumoulin G - Front Immunol (2014)

Interrelationships between fat tissue, psoriasis (Pso), and psoriatic arthritis (PsA) are shown. Obesity is a predisposing factor the development of both Pso and PsA. Pso and PsA are associated with obesity-related complications such as metabolic syndrome, dyslipidemia, diabetes, or insulin resistance, which all enhance the cardiovascular (CV) risk. Body composition is disturbed in Pso or PsA, especially in patients with PsA who have an excess of abdominal adiposity, contributing to increase the risk of metabolic syndrome and CV diseases. Adipokines may link the adipose tissue to the obesity-related complications of Pso and PsA: altered circulating levels of the adipokines leptin, adiponectin, visfatin, resistin omentin, and retinol-binding protein-4 (RBP-4) have been found in patients with Pso or PsA. Leptin has pro-inflammatory effects and may contribute to skin and joint inflammation. Adiponectin promotes insulin sensitivity and its reduced level in Pso may drive insulin resistance and may lead to impaired cardiac and vascular protective effects, thus contributing to the CV risk. In addition, the excess of adipose tissue in Pso and PsA may compromise the therapeutic response to biological agents in Pso and PsA. Finally, anti-TNFα agents have been associated with weight gain in patients with Pso or PsA.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4129363&req=5

Figure 1: Interrelationships between fat tissue, psoriasis (Pso), and psoriatic arthritis (PsA) are shown. Obesity is a predisposing factor the development of both Pso and PsA. Pso and PsA are associated with obesity-related complications such as metabolic syndrome, dyslipidemia, diabetes, or insulin resistance, which all enhance the cardiovascular (CV) risk. Body composition is disturbed in Pso or PsA, especially in patients with PsA who have an excess of abdominal adiposity, contributing to increase the risk of metabolic syndrome and CV diseases. Adipokines may link the adipose tissue to the obesity-related complications of Pso and PsA: altered circulating levels of the adipokines leptin, adiponectin, visfatin, resistin omentin, and retinol-binding protein-4 (RBP-4) have been found in patients with Pso or PsA. Leptin has pro-inflammatory effects and may contribute to skin and joint inflammation. Adiponectin promotes insulin sensitivity and its reduced level in Pso may drive insulin resistance and may lead to impaired cardiac and vascular protective effects, thus contributing to the CV risk. In addition, the excess of adipose tissue in Pso and PsA may compromise the therapeutic response to biological agents in Pso and PsA. Finally, anti-TNFα agents have been associated with weight gain in patients with Pso or PsA.
Mentions: There is compelling evidence suggesting that both Pso and PsA are associated with an excess of fat tissue (8, 20) (Figure 1). Moreover, obesity-related comorbidities accumulate in both conditions, especially, CV and metabolic comorbidities, leading to an increased CV burden. Pro-inflammatory cytokines, such as TNFα and IL-6, and the adipokines leptin, resistin, and visfatin produced by fat tissue are contributing and probably synergistic factors to a pro-inflammatory state in these conditions. Both Pso and PsA are associated with body composition changes, mainly in PsA. One unanswered question is the timing of adipose tissue changes: BMI and weight in early adulthood seem to predict Pso and PsA and conversely, patients with established disease (Pso or PsA) are characterized by excess fat mass. In other words, it remains to be clarified whether fat mass plays a role at the beginning (or before onset) of the disease, or whether the systemic inflammation in these chronic conditions may govern weight modification and fat redistribution.

Bottom Line: Adipokines may link the adipose tissue to the obesity-related complications of Pso and PsA.Indeed, altered circulating levels of the adipokines leptin, adiponectin, visfatine, and resistin have been found in patients with Pso or PsA.In addition, an excess of adipose tissue may compromise the therapeutic response to traditional drugs or biological agents in Pso and PsA.

View Article: PubMed Central - PubMed

Affiliation: Clinical Investigation Center for Biotherapy INSERM CIC-1431, University Hospital of Besançon , Besançon , France ; Department of Rheumatology, University Hospital of Besançon , Besançon , France ; Department of Therapeutics, University of Franche Comté , Besançon , France ; UPRES EA 4266 "Pathogens and Inflammation", University of Franche Comté , Besançon , France ; LabEX LipSTIC, ANR-11-LABX-0021 , Besançon , France.

ABSTRACT
Psoriasis (Pso) is a common chronic cutaneous inflammatory disease involving the skin that is associated with serious comorbidities. Comorbidities in Pso include psoriatic arthritis (PsA), reduced quality of life, malignancy, depression, but also a constellation of associated conditions that enhance the cardiovascular (CV) risk. Indeed, obesity is common in patients with Pso or PsA and is considered to be a risk factor for the onset of these diseases. Patients with Pso and PsA share common obesity-related complications such as metabolic syndrome (MetS), dyslipidemia, diabetes or insulin resistance, and CV diseases. Chronic inflammation in Pso and PsA partially explains the development of atherosclerosis and CV diseases. In parallel, body composition is disturbed in patients with Pso or PsA, as suggested by anthropometric measurements, while an excess of abdominal adiposity is observed in PsA, enhancing the risk of MetS and CV diseases. Adipokines may link the adipose tissue to the obesity-related complications of Pso and PsA. Indeed, altered circulating levels of the adipokines leptin, adiponectin, visfatine, and resistin have been found in patients with Pso or PsA. In addition, an excess of adipose tissue may compromise the therapeutic response to traditional drugs or biological agents in Pso and PsA. This paper reviews the comorbidities that contribute to enhanced CV risk, the body composition results, and the potential role of adipokines in systemic inflammation and energetic balance in Pso and PsA.

No MeSH data available.


Related in: MedlinePlus