Successful Treatment Of Psoriasis Research Articles

Successful Treatment of Psoriasis With Apremilast in a Kidney Transplant Recipient.

Successful Treatment of Psoriasis With Apremilast in a Kidney Transplant Recipient.

Successful treatment of psoriasis and lichen planus with tildrakizumab

Successful treatment of psoriasis and lichen planus with tildrakizumab

Pilihan Pengobatan Pada Pasien Psoriasis Dengan HIV: Sebuah Tinjauan Sistematik

Psoriasis is a disease related to the immunity, usually inherited genetically and is chronic and recurring. When patients with psoriasis are infected with the Human Immunodeficiency Virus (HIV), the theory is that there is a paradoxical relationship that affects the two diseases. HIV can be a trigger for psoriasis and psoriasis can appear as an early symptom of HIV infection. The successful treatment of Psoriasis with HIV positive must be done appropriately according to the patient's condition. Here we discuss several Psoriasis therapy options in HIV positive patients based on several case reports that have a variety of different diseases. The research design is a literature review and refers to the PRISMA method. Scientific articles searchable on PubMed. There were 13 scientific articles related to Psoriasis patients who were HIV positive and met the inclusion criteria. Initial treatment of Psoriasis using biological therapy such as Risankizumab and Secukimab 300 mg subcutaneously, can change the response rate of the Psoriasis Area and Severity Index to 100 or the total loss of psoriasis lesions after a few weeks. In addition, the treatment of psoriasis together with High-active antiretroviral therapy (HAART) also affects the improvement of Psoriasis.

Pilihan Pengobatan pada Pasien Psoriasis dengan HIV: Sebuah Tinjauan Sistematik

Psoriasis is a disease related to the immunity, usually inherited genetically and is chronic and recurring. When patients with psoriasis are infected with the Human Immunodeficiency Virus (HIV), the theory is that there is a paradoxical relationship that affects the two diseases. HIV can be a trigger for psoriasis and psoriasis can appear as an early symptom of HIV infection. The successful treatment of Psoriasis with HIV positive must be done appropriately according to the patient's condition. Here we discuss several Psoriasis therapy options in HIV positive patients based on several case reports that have a variety of different diseases. The research design is a literature review and refers to the PRISMA method. Scientific articles searchable on PubMed. There were 13 scientific articles related to Psoriasis patients who were HIV positive and met the inclusion criteria. Initial treatment of Psoriasis using biological therapy such as Risankizumab and Secukimab 300 mg subcutaneously, can change the response rate of the Psoriasis Area and Severity Index to 100 or the total loss of psoriasis lesions after a few weeks. In addition, the treatment of psoriasis together with High-active antiretroviral therapy (HAART) also affects the improvement of Psoriasis.

Ultraviolet Measurements and Photoclimatotherapy for Psoriasis at the Dead Sea: 25 Years of Experience.

Background: The Dead Sea basin is the lowest terrestrial site on the globe and is internationally recognized as a photoclimatotherapy center. Since the last century, questions were raised regarding a possible presence of unique incident ultraviolet irradiation, allowing the successful treatment of psoriasis, atopic dermatitis and other dermatological diseases. Aim: This research study aims to determine the characteristics of solar ultraviolet irradiation and to understand the mechanism of action of photoclimatotherapy while applying results to clinical protocols of treatments. Methods: A meteorological station was established at the Dead Sea basin to continuously measure global, UVB and UVA irradiation. The same irradiation parameters are also monitored continuously by a set of identical ultraviolet irradiation instruments installed on the campus of the Ben-Gurion University of the Negev in Beer Sheva. Results: This study details the results of these long-term measurements, as well as their correlation with the success obtained by clinicians treating psoriasis patients. Conclusions: A database of more than 25 years has enabled medical staff to establish tailor-made protocols for sun-exposure time intervals as a function of particular month and hour of day. The availability of such information significantly improved the results of photoclimatotherapy for psoriasis and simultaneously increased the safety of sun exposure at the Dead Sea.

Synergistic induction of IL-23 by TNFα, IL-17A, and EGF in keratinocytes

IL-23 is an inflammatory cytokine that plays an essential role in Th17 immunity by enhancing Th17 cell proliferation and survival, and Th17 cytokine production. IL-23 has pathogenic roles in the development of Th17-mediated inflammatory diseases including psoriasis. Despite successful treatment of psoriasis by blocking IL-23, the regulation of IL-23 expression in psoriasis patients is largely unknown. Dendritic cells are generally considered to be the primary source of IL-23 in psoriasis. While high levels of IL-23 are found in psoriatic epidermis, IL-23 expression in psoriatic keratinoctyes remains a controversial issue. In this study, we demonstrated that IL-23 production is induced by a combination of TNFα and IL-17A in human keratinocytes. Additionally, this IL-23 induction by TNFα and IL-17A is further increased in psoriatic keratinocytes and is enhanced by EGFR signaling. Although IL-23 is also robustly induced by toll-like receptor agonists in dendritic cells and macrophages, IL-23 expression in these cell types is not regulated by TNFα, IL-17A, and EGFR signaling. Given that IL-23 is essential for maintaining Th17 activation, IL-23 induction by TNFα, IL-17A, and EGF in keratinocytes could play an important pathological role in psoriasis pathogenesis as well as the cutaneous rash associated with EGFR inhibition therapy.

The tryptophan metabolism enzyme L-kynureninase is a novel inflammatory factor in psoriasis and other inflammatory diseases

Many human diseases arise from or have pathogenic contributions from a dysregulated immune response. One pathway with immunomodulatory ability is the tryptophan metabolism pathway, which promotes immune suppression through the enzyme indoleamine 2,3-dioxygenase (IDO) and subsequent production of kynurenine. However, in patients with chronic inflammatory skin disease, such as psoriasis and atopic dermatitis (AD), another tryptophan metabolism enzyme downstream of IDO, L-kynureninase (KYNU), is heavily upregulated. The role of KYNU has not been explored in patients with these skin diseases or in general human immunology. We sought to explore the expression and potential immunologic function of the tryptophan metabolism enzyme KYNU in inflammatory skin disease and its potential contribution to general human immunology. Psoriatic skin biopsy specimens, as well as normal human skin, blood, and primary cells, were used to investigate the immunologic role of KYNU and tryptophan metabolites. Here we show that KYNU(+) cells, predominantly of myeloid origin, infiltrate psoriatic lesional skin. KYNU expression positively correlates with disease severity and inflammation and is reduced on successful treatment of psoriasis or AD. Tryptophan metabolites downstream of KYNU upregulate several cytokines, chemokines, and cell adhesions. By mining data on several human diseases, we found that in patients with cancer, IDO is preferentially upregulated compared with KYNU, whereas in patients with inflammatory diseases, such as AD, KYNU is preferentially upregulated compared with IDO. Our results suggest that tryptophan metabolism might dichotomously modulate immune responses, with KYNU as a switch between immunosuppressive versus inflammatory outcomes. Although tryptophan metabolism is increased in many human diseases, how tryptophan metabolism is proceeding might qualitatively affect the immune response in patients with that disease.

Successful treatment of psoriasis with ustekinumab in patients with multiple sclerosis

Psoriasis is a chronic inflammatory disease, evolving from a complex interplay of genetic and environmental factors. In the recent years, we have seen much progress in understanding the immunopathogenesis of psoriasis, paving the way for new therapies with biologics. Currently, the most commonly used biologics in psoriasis are TNF inhibitors etanercept, infliximab and adalimumab, and the IL-12/23 inhibitor ustekinumab. As TNF inhibitors are contraindicated in patients with multiple sclerosis, ustekinumab remained the only biologic available for these patient before the recent approval of Secukinumab, an IL-17A inhibitor. Herein we report two patients with multiple sclerosis and comorbid psoriasis successfully treated with ustekinumab without progression of their multiple sclerosis. Our cases demonstrate that ustekinumab is a reasonably safe choice in this patient population. We also briefly reviewed new therapies currently under investigation, which will undoubtedly further expand our armamentarium for the treatment of psoriasis in patients with neuromuscular diseases.

Successful treatment of psoriasis with low-dose per os interleukins 4, 10, and 11.

Successful treatment of psoriasis with low-dose per os interleukins 4, 10, and 11.

High-Density Lipoprotein Cholesterol Function Improves after Successful Treatment of Psoriasis: A Step Forward in the Right Direction

There is epidemiological evidence that high-density lipoprotein (HDL) concentrations, or HDL "levels," exert protection from atherosclerosis, suggesting that HDL plays a role in vascular diseases. More accurate measures of HDL "function" are emerging, such as HDL efflux assays, which measure removal of cholesterol from peripheral tissues. Using this assay, we have demonstrated that psoriasis is associated with decreased HDL "levels" and HDL "function." The study by Holzer et al. in this issue demonstrates in an open-label, uncontrolled study that HDL function is impaired in psoriasis and improves after successful treatment of psoriasis. These findings underscore the notion that treatment of psoriasis likely extends beyond the skin and that a randomized controlled clinical trial is needed to confirm these findings.

Epidermal IL-15Rα acts as an endogenous antagonist of psoriasiform inflammation in mouse and man

Stromal cells at epithelial surfaces contribute to innate immunity by sensing environmental danger signals and producing proinflammatory cytokines. However, the role of stromal cells in controlling local inflammation is unknown. We show that endogenous soluble IL-15 receptor α (IL-15Rα) derived from epidermal stroma, notably keratinocytes, protects against dendritic cell/IL-15-mediated, T cell-driven skin inflammation in vivo, and is relevant to human psoriasis. Selective lack of IL-15Rα on stromal epidermal cells exacerbated psoriasiform inflammation in animals. Epidermal IL-15Rα was shed by keratinocytes via proteolytic cleavage by matrix metalloproteinases upon stimulation with proinflammatory cytokines to counteract IL-15-induced proliferation of IL-17(+) αβ and γδ T cells and production of TNF, IL-23, IL-17, and IL-22 during skin inflammation. Notably, administration of soluble IL-15Rα was able to repress secretion of IL-1β, IL-6, and TNF by keratinocytes, dampen expansion of IL-17(+) αβ and γδ T cells in vivo, and prevent psoriasis in two mouse models, including human xenograft AGR mice. Serum levels of soluble IL-15Rα negatively correlated with disease severity, and levels rose upon successful treatment of psoriasis in patients. Thus, stressed epidermal stromal cells use soluble IL-15Rα to dampen chronic inflammatory skin disease.

Successful treatment of psoriasis with interrupted adalimumab use: A case report

Successful treatment of psoriasis with interrupted adalimumab use: A case report

T helper type 17 in psoriasis: From basic immunology to clinical practice

Psoriasis is a chronic inflammatory disease mediated by a complex interplay between immune system and keratinocytes. Initially considered as a keratinocyte proliferation/differentiation disorder, an immune dysregulation was confirmed after the successful treatment of psoriasis with cyclosporine. The ying–yang theory, or T helper type 1 (Th1)/Th2 concept, was then introduced to explain the rarity of atopic dermatitis in patients with psoriasis and the aggravation of psoriasis after interferon-γ treatment. However, recent advances have revised the Th1/Th2 paradigm after the discovery of a novel subset of T cells, called Th17 cells. Th17 cells produce interleukin (IL)-17 and IL-22, and have other important downstream proinflammatory effects on skin, leading to clinical and pathological features typical of psoriasis. Nowadays, emerging evidence suggests integrative and complicated inflammatory circuits among Th1 and Th17 cells and keratinocytes in the pathogenesis of psoriasis, with Th17 cells playing a central role. Herein, we review the biology of Th17 cells as well as the reciprocal interplay between Th17 and regulatory T cells in psoriasis. Integration of the IL-23/Th17 axis into a revised concept of psoriasis has already been translated into novel therapeutic strategies. Studies investigating the effect and molecular mechanism of conventional and biological therapy for psoriasis on the IL-23/Th17 pathway were also discussed.

Safety of anti‐tumour necrosis factor‐α agents in psoriasis patients who were chronic hepatitis B carriers: a retrospective report of seven patients and brief review of the literature

Issues concerning the potential risks of reactivating chronic hepatitis B virus arise when the use of anti-Tumour Necrosis Factor-α (TNFα) agents is imperative in patients with concurrent psoriasis and hepatitis B virus infection. The aim of this study was to report the experience regarding safety in the management of patients with coexisting psoriasis and chronic hepatitis B with the anti-TNFα agents: infliximab, etanercept and adalimumab. The psoriasis outpatient database of our dermatological department was searched for psoriasis and hepatitis B diagnoses and the medical records of these patients were reviewed for use of anti-TNFα agents. Seven cases (four women and three men) were identified, with mean age of 51years (34-65years). Three patients received adalimumab, three patients were given etanercept and one infliximab. All patients received lamivudin, 100mg/day, which started 2weeks before the initiation of anti-TNFα medication and went on during the whole treatment period. Follow-up period extended from 6-24months. All patients were inactive HbsAg (+) carriers. Liver function tests - at baseline and at the end of follow-up period - were within the normal range. There was no considerable rise in the viral load in any case, from baseline until the last available measurement, although a patient receiving infliximab showed an increase that reached 600 IU/mL. Successful treatment of psoriasis with anti-TNFα agents in patients who are inactive HBsAg carriers is possible and could be safe under the conditions of concomitant lamivudin administration and intensive monitoring. Larger randomized controlled studies are needed to confirm these findings.

Successful treatment of psoriasis with alefacept in patients with previous adverse reactions to anti-TNFα treatments: Three case studies

Successful treatment of psoriasis with alefacept in patients with previous adverse reactions to anti-TNFα treatments: Three case studies

Successful treatment of psoriasis and psoriatic arthritis with etanercept and methotrexate in a patient newly unresponsive to infliximab

A 30 year-old woman presented with moderate-to-severe psoriasis and psoriatic arthritis. Both her cutaneous and arthritic signs and symptoms were refractory to methotrexate, cyclosporine, or both of these drugs in combination. After receipt of infliximab her psoriasis cleared, yet her arthritic symptoms remained. After five infusions her psoriasis became refractory to infliximab. Infliximab was discontinued, and the patient was treated with a combination of methotrexate and etanercept. Twelve weeks later both her psoriasis and psoriatic arthritis had completely resolved. This case demonstrates that TNF inhibition represents a viable option in patients with psoriasis and psoriatic arthritis unresponsive to either methotrexate or cyclosporine, or both drugs in combination. Further, etanercept in combination with methotrexate may be an effective option for patients with psoriasis and psoriatic arthritis who become refractory to infliximab.

A new generation of retinoid drugs for the treatment of dermatological diseases

Dermatological diseases such as acne, psoriasis, and various skin cancers affect approximately 24 million people in the US (17 million acne, 6.4 million psoriasis and 0.7 million skin cancer). In many cases, particularly for acne and psoriasis, these diseases have exhibited favourable responses to single agent or adjuvant retinoid therapy. When administered as both chemotherapeutic and chemopreventive agents, they offer a viable alternative to classical cancer chemotherapy. Although retinoid treatment has shown considerable promise, certain side-effects have limited their utility for chronic administration. Accordingly, there is considerable interest in developing novel retinoids that exhibit improvements in the side-effect profile, particularly for diseases that require chronic administration. Retinoids are potent biological modulators that exert their effects through intracellular receptors (retinoic acid receptors [RARs] and retinoid X receptors [RXRs]) where they regulate cellular proliferation, differentiation and programmed cell death. Currently, using a combination of molecular biology and synthetic chemistry, efforts are underway to fully characterise the biological role of individual retinoid receptor subtypes. Using receptor-selective retinoids, recent discoveries have assisted in clarifying the mechanism and biological function of retinoids and their receptors. It now appears that the RARs are implicated in the regulation of cellular proliferation and differentiation, whereas the RXRs function as modulators of programmed cell death or apoptosis. This suggests that diseases that are associated with abnormal proliferation and/or differentiation may be treatable with RAR active compounds. In fact, the data are supported by successful treatment of psoriasis, epithelial cancer and leukaemia with retinoids that preferentially activate the RARs. In contrast, retinoids that preferentially activate RXRs may be desirable for treatment of diseases for which enhancement of apoptosis is required. For example, they are potentially useful for treatment of cutaneous T-cell lymphoma and as chemopreventive agents [1]. The mechanisms of action of these RXR mediated effects are under investigation. Finally, certain receptor subtypes are implicated in retinoid side-effects. For example, it has become increasingly evident that side-effects such as triglyceridaemia [2] and teratogenesis [3,4] can be correlated to activation of the RARs and not the RXR. These findings offer opportunities for developing a new generation of retinoids which exhibit improved therapeutic indices. Recently, novel treatment strategies have evolved including the application of receptor-selective synthetic retinoids, combination therapies with other hormones or chemotherapeutic agents, and novel formulations. This has resulted in a new generation of retinoids and retinoid treatments which are in clinical development and which exhibit improvements in the therapeutic index.

An hypothesis explaining the successful treatment of psoriasis with thermal biofeedback: A case report

This is a single case report of a 56-year-old Caucasian female referred for biofeedback by her dermatologist after seven years of failed standard medical treatment for psoriasis. Patient's presenting complaint was the embarrassing psoriasis lesions on her arms. Following 13 weekly one-hour finger/hand thermal biofeedback treatments, all 11 presenting psoriasis lesions (2-6 cm) had disappeared. Interestingly, any new psoriasis lesions that surfaced during our treatment disappeared without leaving palpable or visible scarring, unlike lesions that were present prior to biofeedback treatment. Patient was unmedicated for psoriasis during our treatment and continues to be unmedicated and asymptomatic at 12-month follow-up.

Assessment of the activation pathways of the complement in psoriatic patients by use of complement fragment C4d and Bb measurements.

We have measured the complement fragment C4d and Bb levels in the plasma of 51 psoriatic patients and 54 normal controls. The C4d and Bb levels were not significantly elevated in the plasma of the psoriatic patients when compared with those of controls, except in patients with more than 60% skin involvement who exhibited an increase in Bb levels. C4d levels, however, did decrease slightly after successful treatment of psoriasis. Although these results suggest that the C4d and Bb levels partly reflect the complement activation in vivo, they do not seem to be suitable parameters to clarify the mechanism of complement activation in psoriasis.

Successful treatment of psoriasis with topical application of active vitamin D3 analogue, 1 alpha,24-dihydroxycholecalciferol.

We treated 11 psoriatic patients with topical 1 alpha,24-dihydroxycholecalciferol, a new synthetic analogue of active vitamin D3. In 10 of 15 tests the lesions cleared completely within 1-4 weeks, although some relapses occurred shortly after cessation of treatment. There were no side-effects. We suggest that 1 alpha, 24(OH)2D3 merits further investigation as a potentially useful topical therapy for psoriasis.