Biomarkers of Inflammation in Obesity-Psoriatic Patients

Table 1

Treatment of psoriasis.

	Mechanisms of action	Administration via
Conventional therapies
Methotrexate [36]	Inhibits replication of T and B lymphocytes and suppresses secretion of various cytokines, including IL-1 (interleukin-1), interferon-gamma, and TNF-alpha.	Oral and subcutaneous
Cyclosposrin A [34, 36]	Inhibits T cell activation by inhibiting interleukin-2 (IL-2) and interferon-gamma production through inhibition of calcineurin.	Oral
Acitretin [36]	Is a second-generation monoaromatic retinoid. It acts by modulating proliferation of epidermal keratinocytes, joining the nuclear receptor RAR or RXR.	Oral
Phototherapy [33, 36]	Causes alteration of the antigen-presenting cell population (Langerhans cells) and modifies intra- and intercellular signalling mechanisms, leading to development of Th2 preferentially to Th1 responses. It also causes apoptosis of activated T lymphocytes.	Ultraviolet A and B radiation
Biological treatments
Infliximab [35, 37]	Mouse antibody to TNF-alpha	Intravenous
Etanercept [35, 37]	Competitive inhibitor of tumour necrosis factor-alpha. It binds to TNF-alpha to inactivate it.	Subcutaneous
Adalimumab [38]	Anti-TNF IgG1 antibody of an entirely human nature, produced in genetically modified CHO cells.	Subcutaneous
Ustekinumab [39]	Is a fully human IgG1κ monoclonal antibody that binds with high affinity and specificity to the p40 protein subunit of the human cytokines IL-12 and IL-23.	Subcutaneous
Ixekizumab [40]	Is a humanized monoclonal antibody. The substance acts by blocking interleukin-17, reducing inflammation. The antibody has affinity to the homodimer IL-17A and heterodimer IL-17A/F.	Subcutaneous
Secukinumab [41]	Is a recombinant monoclonal antibody, entirely human, selective to interleukin-17A.	Subcutaneous
Others
Apremilast [42]	Is a novel phosphodiesterase 4 inhibitor.	Oral