Cases of systemic lupus erythematosus (SLE) following psoriatic arthritis (PsA) or vice versa are uncommon. Due to the complexity of autoimmune diseases and the rarity of such cases, comprehensive global data on the co-occurrence of these conditions are limited. Moreover, the pathophysiology concerning the coexistence of SLE and PsA has yet to be fully understood. Interestingly, the progression of both diseases appears to be significantly influenced by the key interleukin (IL) 17, particularly IL-17A. Here, we report 7 cases of SLE and PsA coexistence. In 5 of these cases, PsA occurred before the development of SLE, while in the remaining 2 cases, SLE was diagnosed before PsA. The PsA was characterized mainly by peripheral arthritis without any axial involvement, while the manifestations of SLE varied, with 3 developing systematic severe manifestations. Therapeutic challenges were posed in all cases, as treating one condition could worsen the other. Finally, we review the literature providing the current knowledge on the coexistence of these conditions. Overall, all reported cases emphasize the importance of personalized treatment and careful monitoring for patients with both SLE and PsA.

BACKGROUND: Tumor necrosis factor alpha (TNFα) is a pivotal cytokine involved in the pathogenesis of certain inflammatory diseases, such as rheumatoid arthritis (RA), spondyloarthropathies, and inflammatory bowel diseases. In the last two decades, TNFα inhibitors (TNFi) have revolutionized the treatment and outcome of the above disorders. However, the use of TNFi has been associated with the development of many autoimmune phenomena and paradoxical skin manifestations that may present as the same type of clinical indications for which the TNFi effectively used. Thus, they may display as arthritis, uveitis, colitis, psoriasis, and several other cutaneous clinical manifestations, among them the development of morphea, a localized scleroderma skin lesion.
METHODS: We describe a 58-year-old woman with seronegative RA, refractory to methotrexate, who was treated with ABP-501 (Hefiya), an adalimumab (ADA) biosimilar and developed an oval-shaped, deep skin lesion of approximately 3.5cm in size, affecting the left part of her back compatible with morphea 3 months after the initiation of therapy. ADA biosimilar was discontinued and two months later, she had substantial skin improvement.
CONCLUSIONS: This is the first report of morphea manifestation during TNFi biosimilar since the patient had no other trigger factors for morphea development like trauma and infections. Physicians dealing with patients treated with TNFi biosimilars should be aware of paradoxical skin reactions, among them morphea; thus, close monitoring, a minute and careful clinical examination, and a follow- up check are required.

BACKGROUND: Herbal medicines have been used for the preparation of numerous pharmaceutical products for the treatment of human disorders. Plant-derived products have been used in medicine, nutraceuticals, perfumery, beverages, and cosmetics industries for different purposes. Herbal medicines are mainly derived from different parts of plant materials. Phellodendron bark has been widely known as one of the fundamental herbs of traditional Chinese medicine. Phellodendron bark contains phellodendrine as a main active phytochemical. Phellodendrine ((7S,13aS)-3,10-dimethoxy-7-methyl-6,8,13,13atetrahydro-5H-isoquinolino[2,1-b]isoquinolin-7- ium-2,11-diol), is a quaternary ammonium alkaloid.
METHODS: This present study aimed to investigate the biological potential and therapeutic effectiveness of phellodendrine in medicine through scientific data analysis of different research works on phellodendrine. The therapeutic value of phellodendrine was analyzed in the present work through scientific data available in Google, Google Scholar, ScienceDirect, and PubMed. All the scientific data on phellodendrine were collected from these databases using the terms herbal drugs and phellodendrine. Pharmacological and analytical data of phellodendrine were analyzed in the present work in order to know the medicinal importance of phellodendrine.
RESULTS: Scientific data analysis of phellodendrine in the present work signified the biological importance of phellodendrine in medicine. Phellodendrine has numerous beneficial aspects in medicine due to its potential benefits in ulcerative colitis, inflammation, pancreatic cancer, nephritis, immune response, acetylcholinesterase activity, psoriasis, arthritis, atopic dermatitis, and oxidative stress. However, it also has significant effects on eicosanoid generation, neuraminidase-1, inflammasome generation, cytochrome p450, taste receptors, and hepatic gluconeogenesis. Furthermore, scientific data has indicated the presence of phellodendrine in different natural sources, including Phellodendri cortex. Analytical data on phellodendrines has signified their importance in the isolation and separation of pure phytochemicals in medicine. Pharmacokinetic parameters have highlighted the tissue distribution of phellodendrine in different tissue of human beings and higher animals.
CONCLUSIONS: In the present work, scientific data analysis has indicated the biological importance, pharmacological activities, and analytical aspects of phellodendrine in medicine.

Psoriasis is a chronic inflammatory skin disease associated with multiple comorbidities and complex pathogenesis. Long non-coding RNAs (lncRNAs) play an important regulatory role in many diseases, including psoriasis. In this study, We aimed to investigate the role and mechanism of lncRNA GDA-1 (GDA) in M5-treated psoriatic keratinocytes. GDA expression was significantly upregulated in psoriatic tissues and M5-treated keratinocytes. By silencing and overexpressing GDA in NHEKs and Ker-CT cells, we showed that GDA regulated proliferation and cell cycle and increased secretion of interleukin-1β (IL-1β), IL-6, and chemokine ligands 2 and 20 (CCL2 and CCL20). RNA sequencing after GDA silencing led to the identification of a close regulatory relationship between GDA and Forkhead Box M1 (FOXM1). GDA significantly influenced FOXM1 expression at both mRNA and protein levels and activated STAT3/NF-κB signaling pathways. STAT3 and NF-κB inhibition abrogated GDA effects on keratinocyte proliferation and inflammation. In conclusion, our study is the first to report that Lnc-GDA-1 distinctly regulates FOXM1 expression and mediates proliferation and inflammation of psoriatic keratinocytes through the STAT3/NF-κB signaling pathway, which may be a potent target for psoriasis treatment.

BACKGROUND: Drug hypersensitivity reactions to infliximab have been reported in pediatric patients. At times, these patients may need infliximab administration in spite of hypersensitivity. However, only a few reports of desensitization protocols are available in the literature in pediatric patients.
METHODS: We report a case of immediate hypersensitivity reaction to intravenous infliximab in a 13-year-old child suffering from pustular psoriasis who eventually underwent a 14 step desensitization protocol for the administration of infliximab in a pediatric intensive care unit.
CONCLUSIONS: Although our desensitization protocol was safe and effective, we recommend the entire desensitization procedure to be performed under the supervision of experienced personnel in a pediatric intensive care unit. Future studies with larger sample size are needed to confirm our findings.

Lichen planus pemphigoides (LPP) is an autoimmune disease characterised by evolution of subepidermal blisters on normal and lichen planus affected skin. We describe a case of LPP in a 54-year-old Chinese woman. The patient presented with psoriasiform plaques and was diagnosed with guttate psoriasis. Narrowband ultraviolet B (NBUVB) therapy was commenced, and she experienced a generalised eruption of violaceous papules, bullae over the lower limbs, and Wickham\'s striae over the buccal mucosa. Histology from a plaque revealed interface dermatitis, while a specimen from a blister showed subepidermal bulla. Direct immunofluorescence showed linear deposition of IgG and C3 along the basement membrane. A diagnosis of LPP was made on clinicopathological grounds. This is the first case report of NBUVB alone in unmasking LPP. In this case report, we describe the pathological mechanism of NBUVB in the development of LPP and key features distinguishing LPP from bullous lupus erythematosus, bullous lichen planus, bullous pemphigoid, and psoriasis.

Psoriasis (PsO) is T-cell-mediated disease resulting from aberrant activation of both innate and adaptive immunity. Perforin is a multi-domain, pore-forming protein. It is located within the cytoplasm of CD 8 cytotoxic T cells (CTLs) and natural killer cells (NK). The aim of this study was to evaluate the immunohistochemical (IHC) expression of perforin in lesional and perilesional skin of chronic plaque psoriatic patient and correlate its expression with the standard clinico-pathological variables. This prospective case-control study was conducted on 50 PsO patients and 30 age- and gender-matched healthy subjects as a control group. There were high-significant differences between lesional and perilesional skin of plaque PsO patients as regards to IHC perforin status and localization (p < 0.001 for both). There was a high-significant difference between positive and negative perforin cases as regards to psoriasis area severity index (PASI) (p < 0.000). There were significant differences between mild and moderate-to-severe intensity of IHC perforin expression as regards to triggering factors and PASI (p = 0.02 and 0.03, respectively). Localization of IHC perforin positive lymphocytes in both epidermis and dermis was significantly associated with higher degree of acanthosis and higher degree of inflammatory infiltrates in comparison with positive cells located in dermis (p = 0.001 for both). Perforin might have a putative signaling in early and late plaque PsO. Plaque psoriatic patients with positive perforin expression could be a candidate for a future target therapy to stop the proposed scenario and achieve a therapeutic response.

BACKGROUND: In recent years, research on psoriasis has focused on the identification of biomarkers for the diagnosis, pathogenesis, prognosis, or therapeutic response of the disease. These studies could provide insights into the susceptibility and natural history of psoriasis. The identification of biomarkers related to comorbidities in psoriasis, such as arthritis, cardiovascular disease, and the metabolic syndrome, is of special clinical interest.
METHODS: We performed an extensive review on psoriasis biomarkers, including cytokine and growth factors, in the literature published between 1997 and 2013, including cross-references of any retrieved articles. We also included some data from our own studies.
RESULTS: This review presents current knowledge of soluble biomarkers in psoriasis, including cytokines, chemokines, proangiogenic mediators, growth factors, antimicrobial proteins, neuropeptides, and oxidative stress markers.
CONCLUSIONS: In conclusion, a number of studies have been conducted with the aim of establishing soluble biomarkers for psoriasis. Most of the biomarkers that have been studied do not meet the criteria for a clinically useful biomarker. Further work is needed to establish a role for soluble biomarkers in the diagnosis and treatment of psoriasis, with a special focus on biomarkers for psoriasis comorbidities, such as arthritis, cardiovascular disease, and the metabolic syndrome.