Effects of treatment for psoriasis on circulating levels of leptin, adiponectin and resistin: a systematic review and meta-analysis

Kyriakou, Aikaterini; Patsatsi, Aikaterini; Sotiriadis, D.; Goulis, Dimitrios G.

doi:10.1111/bjd.16437

Cited by 24 publications

(26 citation statements)

References 67 publications

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“…Anti-psoriatic treatment with secukinumab or etanercept did not alter adiponectin levels in the present study. This is in line with our finding that adiponectin levels are not significantly associated with psoriasis severity (PASI) and with other studies analyzing topical and/or systemic treatments other than secukinumab or other anti-IL17 inhibitors (20). It remains an open question whether the combination of biologic treatment with lifestyle interventions can improve the metabolic profile of psoriasis patients, including adiponectin levels.…”

Section: Discussionsupporting

confidence: 92%

Adiponectin levels in a large pooled plaque psoriasis study population

Gerdes

Pinter

Biermann

et al. 2019

Journal of Dermatological Treatment

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Background: Adiponectin is an adipocyte-secreted protein potentially relevant in the context of cardiometabolic comorbidity of psoriasis patients. Objective: This post-hoc analysis aimed to assess the impact of obesity, metabolic syndrome, psoriasis severity and treatment with secukinumab/etanercept on adiponectin. Methods: Three phase III trials in moderate to severe plaque psoriasis were included. Correlations of Psoriasis Area and Severity Index (PASI), body mass index (BMI), and associated comorbidity with adiponectin levels as well as the impact of secukinumab, etanercept, and placebo were analyzed. Results: Data of 3010 patients were included of whom 71.2% had a BMI >25. Adiponectin levels were significantly higher in patients with lower BMI (r ¼ À0.23; p < .0001) and in patients without metabolic syndrome compared to patients with higher BMI and with metabolic syndrome. PASI score was negatively associated with adiponectin levels (r ¼ À0.065; p ¼ .0004). However, the correlation was extremely weak and thus clinically irrelevant. During treatment with secukinumab or etanercept over 52 weeks adiponectin levels remained stable. Conclusion: Metabolic syndrome and BMI are key determinants of adiponectin levels in psoriasis patients. Psoriasis severity and anti-psoriatic treatment had no relevant impact on adiponectin levels.

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Section: Discussionsupporting

confidence: 92%

Adiponectin levels in a large pooled plaque psoriasis study population

Gerdes

Pinter

Biermann

et al. 2019

Journal of Dermatological Treatment

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“…On the other hand, meta-analysis performed by Kyriakou et al suggests a lack of the influence of an anti-cytokine therapy on the expressive profile of leptin. However, these authors do not wholly negate the possibilities of changes in the concentration of leptin under the influence of drugs used in psoriasis, at a time when the weight of the patients also decreases [50]. Nevertheless, the analysis of the influence of adalimumab conducted within the framework of the present work, indicates that this anti-TNF drug also exerts its influence through signaling pathways connected with leptin.…”

Section: Discussioncontrasting

confidence: 52%

Evaluation of the Influence of Adalimumab on the Expression Profile of Leptin-Related Genes and Proteins in Keratinocytes Treated with Lipopolysaccharide A

Grabarek

Kasela²,

Adwent³

et al. 2021

IJMS

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Psoriasis is a disease with a proinflammatory base, in which an increased expression of leptin, tumor necrosis factor alpha (TNF-α), interleukin (IL) IL-12/23, IL-6, is observed. A drug used in the treatment of psoriasis of moderate and acute strength is the monoclonal antibody anti-TNF–adalimumab. The goal of this study was to evaluate the influence of adalimumab on changes in the expression profile of leptin-related genes in human keratinocyte cells exposed to lipopolysaccharide A and analyze if adalimumab acts via leptin pathways. The evaluation of changes of the pattern of genes connected with leptin and proteins coded by them was marked in a culture of human keratinocytes (HaCaT) exposed to 1 µg/mL lipopolysaccharide A (LPS) for 8 h in order to induce the inflammatory process, then to 8 µg/mL of adalimumab for 2.8 and 24 h in comparison with the control (cells not treated with the substances). The techniques used were mRNA microarray, Real-Time Quantitative Reverse Transcription Reaction (RTqPCR), Enzyme-Linked Immunosorbent Assay (ELISA), as well as transfections of HaCaT culture with leptin small interfering RNA (siRNA) in order to see whether adalimumab works through pathways dependent on leptin. A statistically lower expression of leptin and its receptors was observed under the influence of the drug, independent of the exposition time of keratinocytes to adalimumab. In the cells transfected with leptin siRNA, a lower concentration of JAK2 and STAT3 proteins was observed, which confirms that adalimumab works through pathways dependent on leptin. Adalimumab has a modulatory effect on the gene expression pattern and the proteins coded by them connected with leptin in keratinocytes treated with LPS in vitro.

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“…Resistin signaling upregulates the production of proinflammatory cytokines from mononuclear cells, thus forming a vicious inflammatory circle [ 135 ]. Plasma resistin levels are correlated with the severity of psoriatic skin lesions, and its levels can decrease as the skin lesions improve following an appropriate treatment approach [ 141 , 142 ]. While serum resistin levels are closely correlated to the PASI score and to the involved body surface area percentage (%BSA) in psoriasis cases before anti-TNF therapy, its levels do not always decrease with the improvement in PASI and %BSA after adalimumab therapy [ 143 ].…”

Section: Biomarkers In Psoriasis Treatmentmentioning

confidence: 99%

Molecular Pathogenesis of Psoriasis and Biomarkers Reflecting Disease Activity

Honma

Nozaki

2021

JCM

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Psoriasis is a chronic inflammatory skin disease induced by multifactorial causes and is characterized by bothersome, scaly reddish plaques, especially on frequently chafed body parts, such as extensor sites of the extremities. The latest advances in molecular-targeted therapies using biologics or small-molecule inhibitors help to sufficiently treat even the most severe psoriatic symptoms and the extra cutaneous comorbidities of psoriatic arthritis. The excellent clinical effects of these therapies provide a deeper understanding of the impaired quality of life caused by this disease and the detailed molecular mechanism in which the interleukin (IL)-23/IL-17 axis plays an essential role. To establish standardized therapeutic strategies, biomarkers that define deep remission are indispensable. Several molecules, such as cytokines, chemokines, antimicrobial peptides, and proteinase inhibitors, have been recognized as potent biomarker candidates. In particular, blood protein markers that are repeatedly measurable can be extremely useful in daily clinical practice. Herein, we summarize the molecular mechanism of psoriasis, and we describe the functions and induction mechanisms of these biomarker candidates.

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Effects of treatment for psoriasis on circulating levels of leptin, adiponectin and resistin: a systematic review and meta-analysis

Abstract: There is no evidence that treatment for psoriasis modifies leptin and adiponectin concentrations. However, treatment intervention reduces resistin concentrations, a finding that is expected to be of clinical importance.

Cited by 24 publications

References 67 publications

Adiponectin levels in a large pooled plaque psoriasis study population

Adiponectin levels in a large pooled plaque psoriasis study population

Evaluation of the Influence of Adalimumab on the Expression Profile of Leptin-Related Genes and Proteins in Keratinocytes Treated with Lipopolysaccharide A

Molecular Pathogenesis of Psoriasis and Biomarkers Reflecting Disease Activity

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