Psoriatic Flare Research Articles

Stress and psoriasis: Exploring the link through the prism of hypothalamo-pituitary-adrenal axis and inflammation

BackgroundPsoriasis is an immune-mediated, chronic inflammatory disease affecting mainly the skin. Chronic stress leads to the blunted hypothalamic-pituitary-adrenal axis (HPA) that might induce pro-inflammatory conditions. Hence, we assessed the blood levels of the HPA hormones and interleukin-17 (IL-17) and the effect of stress and emotional distress to understand the link between stress and psoriasis better. MethodsThis cross-sectional study included 45 patients with psoriasis and 45 age and gender-matched apparently healthy volunteers (n = 45). IL-17, cortisol, and adrenocorticotrophic hormone (ACTH) levels were assessed in both groups. Psoriasis Area Severity Index (PASI) was used to assess disease severity. Presumptive Stressful Life Events scale [PSLE], Perceived Stress scale [PSS] and Daily Hassles and Uplifts Scale [DHUS] scoring were used to assess stress levels and emotional distress. ResultsPatients with psoriasis had higher levels of IL-17 and ACTH and lower levels of cortisol, as compared to controls. Stress scores (PSS, PSLE & DHUS) were significantly elevated in cases, as compared to the controls. IL-17, ACTH and stress scores showed a significant positive correlation with one another and a significant negative correlation with cortisol levels. They also showed a significant positive correlation with PASI, while cortisol levels showed a significant negative correlation. ConclusionPsoriasis patients having high ACTH, IL-17 and stress scores had lower levels of cortisol, indicating a dysregulated HPA axis with the pro-inflammatory state. This might lead to exacerbation of psoriatic flares, which needs investigation in further prospective studies.

Tozinameran (Pfizer-BioNTech COVID-19 vaccine)-induced AGEP-DRESS syndrome

Dear Editor, A 40-year-old woman with scalp psoriasis was maintained on topical mometasone furoate therapy from 2019 with no major psoriatic flares until she presented with one week of an acute generalised pustular eruption and fever in June 2021. Physical examination revealed numerous discrete and confluent pustules studded on her scalp, trunk and limbs, on

S3267 A Case of Spontaneous Resolution of Malignant Peritoneal Mesothelioma

Introduction: Malignant peritoneal mesothelioma (MPM) is an aggressive tumor of the peritoneum. Few cases have been reported in the literature describing spontaneous regression possibly related to immune reconstitution. Here in, we report a unique case of peritoneal mesothelioma that regressed over time. Case Description/Methods: A case of 44 y/o female with a history of severe psoriasis (on Humira) and NASH, coccidioidomycosis in 2018 (on ketoconazole) presented with jaundice and abdominal distention in September 2020. She was diagnosed with cirrhosis secondary to NASH, and DILI with a MELD score of 30. Ketoconazole and Humira were held. She was medically managed with furosemide and spironolactone. Her MELD score improved to 18. In January 2021, an orthotopic liver transplant (OLTx) was attempted but due to incidental finding of extensive peritoneal mesothelioma, this was aborted. MPM was confirmed on biopsy with cytokeratin 7+, calretinin+, WT1+, and p53 reactivity. The patient was not considered a candidate for cytoreductive surgery/hyperthermic intraperitoneal chemotherapy. She had multiple psoriatic flares which were managed with prednisone. A PET scan done in June 2022 revealed mild FDG uptake in sub-centimeter bilateral axillary and pelvic LN, cirrhotic liver, and splenomegaly. The patient denied the use of alternative medicine, except for the Atkins diet. She is now being considered for OLTx Discussion: We present a unique case of spontaneous regression of MPM and its association with psoriatic flare. Previous case reports suggest a co-relation of immune-mediated response with spontaneous regression.1 The immunologically relevant cytokines IF-alpha, IF-gama, and TNF-alpha can directly inhibit the growth of mesothelioma.2 These cytokines are elevated in psoriasis, which this case highlights. Trials with immunomodulatory agents e.g. CTLA-4 inhibitor have shown promising outcomes.3 However, little information is available about regression without any chemo/radiation/biologic therapy and the role of the innate immune response leading to tumor regression.

31047 Erythrodermic psoriasis secondary to the COVID-19 Moderna vaccine

Vaccination is an unusual trigger for dermatologic autoimmune conditions like psoriasis. Although a plausible association has been dilucidated between certain vaccines and psoriasis flares, to date, there have been no reports of psoriasis flares secondary to COVID vaccines. To our knowledge, we present the first case of a psoriasis flare secondary to the Moderna COVID-19 vaccine. Our patient is a 31-year-old Latino man with a medical history of well-controlled plaque psoriasis whose psoriasis flared 6 days after receiving the second dose of the Moderna COVID-19 vaccine. Upon presentation, he had approximately 15% body surface area (BSA) involvement. Interestingly, the patient had a severe COVID-19 infection 1 year prior to this but at that time had not flared from his psoriasis. He was treated with topical steroids, nbUVB, and oral prednisone, while awaiting risankizumab approval. During this time, the patient became erythrodermic. Once the patient started risankizumab injections, he achieved almost complete clearance by week 10 of treatment. The Moderna vaccine is an mRNA COVID-19 vaccine that induces a strong CD8 T cell response, along with a balanced Th1-Th2 antibody isotype response. In psoriasis, Th1 cells and CD8 T cells play a key role in keratinocyte proliferation; this upregulation in T cells by the Moderna vaccine could lead to a psoriatic flare. Clinicians should be aware of this side effect of the COVID-19 vaccine and advise patients to be compliant with psoriasis treatment and to inform their dermatologist if any worsening of their psoriasis occurs following the COVID-19 vaccination period.

Safety of SARS-CoV-2 vaccines in psoriatic patients treated with biologics: A real life experience.

Vaccination is the most effective method to prevent and control the SARS‐CoV‐2 infection and biologics are not considered a contraindication for vaccination. The burning question is that safety data are lacking since patients taking drugs affecting the immune system were excluded from clinical trials leading to vaccine approbation. Moreover, it seems that vaccination could worsen psoriasis. We conducted a survey to investigate the safety of SARS‐CoV‐2 vaccines in psoriatic patients treated with biologics. A total of 150 patients with stable plaque psoriasis treated with biologics for at least 2 months were evaluated in a 3 months period. Fifty patients (22 F/28 M; age: 33–83 years) only underwent the first and second doses of SARS‐CoV‐2 vaccines. All patients discontinued their biological agents 10 days before and 10 days after each dose of vaccine. Of these, 24 patients were treated with anti‐TNF, 14 with anti‐IL17, 7 with anti‐IL12‐23, and 5 with anti‐IL23. After the vaccines, all patients were evaluated at day 2, 7, and 14 for local and/or systemic side effects and/or adverse drug reactions to SARS‐CoV‐2 vaccines. None of the patients experienced any side effects or a psoriatic flare. Only one patient treated with infliximab biosimilar referred an exacerbation of psoriasis after vaccine. The remaining 100 patients reported that they did not get the vaccine yet. Our preliminary data confirm that SARS‐CoV‐2 mRNA vaccines are safe for patients with chronic plaque psoriasis treated with biologics and did not trigger psoriasis, although these data should be validated in a larger population. We encourage an early SARS‐CoV‐2 vaccines administration in all psoriatic patients on immunosuppressant drugs.

EP19 Renal sarcoidosis associated with certolizumab pegol treatment for psoriatic arthritis: a case report

EP19 Renal sarcoidosis associated with certolizumab pegol treatment for psoriatic arthritis: a case report

Psoriatic flare after the concomitant administration of L-methylfolate and methotrexate

Psoriatic flare after the concomitant administration of L-methylfolate and methotrexate

Etanercept as prophylactic psoriatic therapy before interferon-α and ribavirin treatment for active hepatitis C infection

Patients with psoriasis and chronic hepatitis C virus (HCV) infection are a therapeutic challenge. Systemic psoriasis treatment with methotrexate and acitretin can be hepatotoxic, and interferon (IFN)-alpha for treatment of HCV can worsen psoriasis. Etanercept can be successfully used in patients with psoriasis and HCV. To our knowledge, this is the first case report of etanercept used prophylactically to prevent a psoriatic flare in a patient with HCV treated with IFN-alpha and ribavirin.

Effectiveness of chondroitin sulphate in patients with concomitant knee osteoarthritis and psoriasis: a randomized, double-blind, placebo-controlled study

The aim of the trial was to assess the efficacy of chondroitin sulphate (CS) on symptomatic knee osteoarthritis (OA) associated to psoriasis. In this randomized, double-blind, placebo (PBO)-controlled clinical trial 129 patients with symptomatic knee OA and concomitant psoriasis were randomized into two groups receiving 800 mg daily of CS or PBO for 3 months. The primary efficacy outcome for knee OA was the Huskisson's visual analogue scale (VAS) and for psoriasis was the Psoriasis Area and Severity Index (PASI). Additionally, other secondary efficacy criteria for both conditions were assessed. After 3 months of treatment, CS was more effective than PBO, relieving pain VAS (CS -26.9+/-24.8 vs PBO -14.23+/-20.8mm, P<0.01), decreasing the Lequesne index (CS -4.8+/-3.4 vs PBO -3.3+/-3.5, P<0.05) and reducing the number of patients using acetaminophen as rescue medication (CS 43% vs PBO 64%, P<0.05). Regarding PASI, Overall Lesion Severity Scale and Physician's Global Assessment of Change no statistically significant changes were detected in front of PBO. However, CS improved plantar psoriasis compared to PBO (CS 87% vs PBO 27%, P<0.05). Quality of life improved significantly in CS-treated patients according to the Short Form-36 health survey and the Dermatology Life Quality Index (DLQI). CS tolerability was excellent. Adverse events were infrequent and evenly distributed among groups. The incidence of psoriatic flares did not increase after treatments. This study confirms the efficacy and safety of CS as a symptomatic slow-acting drug in patients with knee OA and shows that CS improves plantar psoriasis. The use of CS could represent a special benefit in patients with both pathologies since non-steroidal anti-inflammatory drugs have been reported to induce or exacerbate psoriasis.

Clinical Application of National Psoriasis Foundation Findings for Management of Psoriasis in Patients with Coexisting Hepatitis C Infection

Treating psoriasis in patients with concomitant hepatitis C infection presents an intricate challenge. Interferon (IFN) therapy, a mainstay of therapy for hepatitis C virus infection, often exacerbates psoriasis. Moreover, many psoriatic therapies are contraindicated in chronic liver infections due to their potential hepatotoxicity and immunosuppressive effects. The National Psoriasis Foundation (NPF) recently issued a consensus statement regarding the treatment of psoriasis in patients infected with hepatitis C virus (HCV) with the aim of standardizing treatment options and optimally managing psoriasis while minimizing adverse risks for the patients. A patient case is presented here for which the evidence-based treatment guidelines are applied and discussed. By managing psoriasis in patients with coexisting hepatitis C infection in a step-wise manner based on the currently recommended treatments, potential negative complications such as exacerbation of liver disease and dangerous psoriatic flares may be minimized.

Effective management of a psoriatic flare with narrowband UVB phototherapy during efalizumab therapy without discontinuing treatment

Effective management of a psoriatic flare with narrowband UVB phototherapy during efalizumab therapy without discontinuing treatment

Psoriatic Erythroderma Associated With Enalapril

A 59-year-old man with a 35-year personal and positive family history of psoriasis was admitted to our department for treatment of psoriatic erythroderma. The patient had commenced therapy with enalapril 10 mg b.i.d. for the treatment of hypertension approximately 6 weeks before hospitalization. Five weeks after the initiation of enalapril, his psoriasis began to flare, and for a period of about 1 week it reached the extent of erythroderma. The patient did not associate the psoriatic flare with other factors such as infections, trauma, or stress. The patient presented with diffuse erythema and pronounced desquamation covering his entire trunk, scalp, and extremities (Figure). Nearly 100% of the body surface area was involved. The palms and soles were also affected, displaying erythema, hyperkeratosis, and painful fissures. The nails showed pits, oil spots, and subungual hyperkeratosis. The patient also had psoriatic arthritis affecting the interphalangeal joints of his fingers. Laboratory tests revealed an elevated erythrocyte sedimentation rate, an elevated creatinine level of 180 mmol/L, a blood urea nitrogen level of 10.8 mmol/L, and a uric acid level of 716 mmol/L. Urinalysis showed proteinuria of 1.5 g/24 h. The patient's renal condition was diagnosed as chronic tubulointerstitial nephritis, most probably related to his dermatologic disease. Allopurinol and dietary measures were recommended. Following treatment with methotrexate and replacement of enalapril therapy, the erythema and scaling gradually subsided and became confined to his pre-eruptive chronic plaques (approximately 5% of body surface area). Rechallenge with enalapril was not performed.

Psoriasis herpeticum: Three cases of Kaposi's varicelliform eruption in psoriasis

Kaposi's varicelliform eruption (KVE), first described in 1887 by Moritz Kaposi, refers to a disseminated cutaneous infection with herpesvirus type 1 or 2, vaccinia virus, or coxsackievirus A16 in a patient with another underlying dermatosis. When herpesvirus type 1 or 2 is the pathogenic virus, the term "eczema herpeticum" is used, independent of the underlying dermatologic diagnosis that preceded the eruption. KVE is most often seen in patients with underlying atopic dermatitis, but has also been seen in association with other papulosquamous and acantholytic disorders. However, eczema herpeticum rarely occurs in patients with psoriasis. We present the clinical and laboratory findings of three patients in whom KVE developed during inpatient hospitalization for a psoriatic flare. These patients each had comorbidities that may have increased susceptibility to KVE. KVE may rarely occur in patients with psoriasis. Erythroderma, systemic sepsis, therapy with immunosuppressant drugs, such as methotrexate and systemic steroids, and therapy with systemic retinoids may possibly increase susceptibility to KVE.

Pustular psoriasis and the Köbner phenomenon caused by allergic contact dermatitis from zinc pyrithione‐containing shampoo

Zinc pyrithione is a shampoo ingredient that has been shown to be safe and effective for dandruff and scalp psoriasis. It is thought to decrease the cell turnover rate in hyperproliferative dermatoses such as psoriasis, and also has fungistatic and antimicrobial activity, although its exact mode of action is unknown. In psoriasis, external factors, such as trauma, infection and drugs, may provoke aggravated manifestations of psoriatic skin lesions. Rarely, irritant or allergic mechanisms are likely causes of psoriatic flare and Kobnerization. A patient had had stable psoriasis for 25 years and no any other skin disease. Within 20 days, she developed an aggravated scaly erythematous patch on the scalp, where a shampoo had been applied, and simultaneously developed pustular psoriasis on both forearms. Patch testing showed a relevant sensitization to zinc pyrithione, and we observed symptomatic aggravation by provocation testing with zinc pyrithione shampoo. We report a rare case of psoriasis aggravated by the induction of allergic contact dermatitis from zinc pyrithione after using antidandruff shampoo.

PSORIASIS SHOULD NOT BE A CONTRAINDICATION TO INTERFERON THERAPY IN PATIENTS WITH CHRONIC HEPATITIS C

Purpose: The purpose of the study was to determine the safety and efficacy of interferon therapy on psoriasis in hepatitis C patients treated with interferon. Psoriasis, as an autoimmune condition, has been considered a contraindication to interferon therapy in chronic hepatitis C. Methods: A retrospective review of 100 charts of patients with Hepatitis C at an outpatient tertiary liver clinic was performed. 6 patients were identified who had psoriasis and received interferon therapy. A systematic chart review was performed; age, sex, and biopsy results were obtained. The type and duration of therapy was also reviewed including the response to treatment and psoriatic flares during treatment. Results: Of the 6 patients, 4 were male and 2 were females. The majority of patients had advanced liver disease, either bridging fibrosis (2) or cirrhosis (3). Treatment duration ranged from 24 to 96 weeks with either conventional interferon 3/week or pegylated interferon, or both. 3/6 patients had a sustained virologic response (SVR) with therapy. While 2 patients had a worsening of their psoriasis, it had little impact on their treatment since they were able to complete a full course of treatment. One patient who had a SVR has actually had complete resolution of his psoriasis while on treatment that has still not reappeared 6 months after stopping treatment. Conclusions: Interferon therapy for Hepatitis C patients did not have a clinically significant impact on their psoriasis. Patients were able to tolerate the standard duration of therapy and obtain a SVR in 33% of those treated. Patients with psoriasis and Hepatitis C, especially those with advanced his-tologic liver disease, should be considered for interferon therapy in order to prevent progression to cirrhosis and its deadly consequences. Psoriasis should not be considered a contraindication to interferon therapy in patients with hepatitis C.Table 1

Initiating Narrow-band UVB for the Treatment of Psoriasis

Narrow-band UVB is effective for the treatment of psoriasis. 3,8,10 The numerous protocols available in the literature may make it challenging for a practitioner, wishing to initiate narrow-band therapy, to choose the appropriate protocol. This article is a review of the literature on narrow-band UVB protocols and a guide to initiate therapy. To commence therapy, a protocol that best suits the practi- tioner's expertise level and the type of staff the practitioner has is chosen. The two main types of narrow-band protocols presented in this review are the Skin Type and MED (minimal erythema dose) protocols. MED and skin type testing to determine the dose of narrow-band UVB to begin treatment are detailed in a step-by-step process. Subsequent treatment doses are based on the skin's response to the previous treatment. 11 Further adjustments in light dose can accommodate missed treatments. Narrow-band light treatments are continued until psoriasis clears or almost clears, followed by tapering maintenance treatments. The goals of therapy are to establish and maintain control over psoriatic flares, and to balance the risks and benefits of narrow-band treatment. Narrow-band ultraviolet B (NB-UVB) was introduced in 1976 and has been widely used for psoriasis, especially in Europe and Australia. It became available in the United States in 1996. NB- UVB emits a wavelength between 311-313 nm, which is most phototherapeutic for the clearance of psoriasis. NB-UVB has been shown to be more effective than broad-band ultraviolet B (BB-UVB) 1,2,3 and almost as effective as PUVA for the treatment of psoriasis, but with a shorter remission time, and possibly with a lower risk of skin cancer. 4,5,6 No standardized protocol has yet

Vitiligo following the resolution of psoriatic plaques during PUVA therapy

Vitiligo Is an acquired idiopathic disorder, involving 1–4% of tiie world population and characterized by depigmented white patches of the skin that lack the dopa‐positive melanocytes.It has been associated with physicai trauma and, systemic and cutaneous diseases. Among the many dermatoses, psoriasis has been reported to be associated with vitiiigo in the same individuals independently, or vitiligo may precede the formation of psoriasis at the same location. Currently, psoralen plus ultraviolet A iight (PUVA) is one of the efficacious treatments of psoriasis and vitiligo with side‐effects of hypopigmentation and vitiligo‐like lesions. We describe a patient with psoriasis vuigaris in whom vitiligo appeared in the same areas and configurations as his psoriatic plaques as they resolved while being treated with topicai PUVA.A 19‐year‐old Caucasian man was referred for treatment of his psoriatic flare. His medical history revealed a vitiiigo patch on his right calf at age five. At age 14, he developed initially psoriatic plaques on his knees and elbows which then gradually spread to the legs, arms, hands, trunk, scalp, and the genitai area. The only therapy used was a mid‐potency topical steroid ointment with some reiief. Recently the condition had deteriorated enough to seek medical attention.Physical examination revealed sharply demarcated erythematous, silvery‐white scaly papules, patches and plaques of various sizes on trunk, extremities, palms, buttocks, and penis. The patient received topical PUVA with 0.1% trimethoxalen cream for 3 months. Uitravioiet A light (UVA) was applied at 0.1 J/cm with an increment of 0.1 J/cm at each session as tolerated. At approximately the tenth session, depigmented lesions were noted around the margins of the regressing psoriatic plaques. This progressed continually until the vitiligous‐like lesions completely replaced the resolved psoriatic piaques in exactiy the same configurations (Fig. 1).Skin biopsies of the depigmented areas revealed parakeratosis, hypogranulosis, acanthosis, and a sparse iymphocytic infiitrate around dilated tortuous capillaries in the upper corium (Fig. 2). Also a Fontana‐Masson stain showed an absence of melanocytes as may be seen in vitiligo (Fig. 3).

The Place of Cyclosporin in the Treatment of Severe Psoriasis

The degree of efficacy of cyclosporin in psoriasis is dose related. While doses of 2.5 to 5 mg/kg/day result in significant clearing of psoriasis within 4 to 8 weeks, response to treatment is more rapid and dramatic with higher doses (> 5 mg/kg/day). A gradual recurrence of psoriasis, without rebound, usually occurs within weeks to months after discontinuation of therapy. Tachyphylaxis has not been reported. An initial dose of 3 to 5 mg/kg/day is recommended for the treatment of severe psoriasis and 5 mg/kg/day for the treatment of erythrodermic psoriasis, because it maximises the probability of therapeutic efficacy while minimising the likelihood of significant adverse effects. Although there appears to be no correlation between cyclosporin whole blood trough concentrations and clinical response, the drug concentrations in skin appear to approximate the peak plasma concentrations. Cyclosporin has been shown to be more effective than systemic retinoids in the treatment of psoriasis vulgaris. Psoriatic erythroderma may respond extremely rapidly to oral cyclosporin. Psoriatic arthropathy and nail disease also improve during cyclosporin therapy. Patients on cyclosporin treatment must be carefully selected and monitored for renal function, with due consideration given to drug interactions. The currently available formulation of cyclosporin does not ensure constant and predictable drug exposure because its gastrointestinal absorption is affected by biliary secretion, ingested food and gastrointestinal motility. A new microemulsion-based formulation (Neoral®)1 capable of guaranteeing more consistent bioavailability has been developed, and is under investigation. There is no significant cyclosporin-sparing effect when etretinate and UVB are used adjunctively. Furthermore, the combination of cyclosporin-UVB should be used with caution because of an increased risk of nonmelanoma skin cancer. The addition of topical corticosteroids results in more rapid clearing of psoriasis plaques, although relapse rates remain unchanged. The combination with calcipotriol has been evaluated in a placebo-controlled study, and it seems to have a cyclosporin-sparing effect. Cyclosporin is useful in short term intermittent therapy to control acute psoriatic flares and/or to induce a remission. Alternative agents can then be used for maintenance treatment, thus reducing the risk of toxicity associated with long term cyclosporin therapy.

Angiotensin-converting enzyme inhibitors as possible exacerbating drugs in psoriasis

Angiotensin-converting enzyme (ACE) inhibitors are approved for the treatment of hypertension. ACE inhibitors block the conversion of angiotensin I to angiotensin II, a potent vasopressor, by competing with kininase II, the converting enzyme, for binding sites in the lung. As a result of this competitive inhibition, increased levels of biologically active kininase II are present. This is significant because kininase II prevents the catabolism of bradykinin, an enzyme that promotes vasodilatation. Bradykinin is part of the complex kinin system responsible for the delayed phase of acute inflammatory responses. [-4 Thus ACE inhibitors may have an indirect proinflammatory effect that may flare preexisting psoriasis. Several cutaneous adverse effects have been reported with the use ofACE inhibitors. These include a maculopapular eruption with eosinophilia, which is usually mild, transient, and responds to a reduction in dose or treatment with antihistamines, a bullous pemphigoid-like eruption, and rosacea. Angioedema of the extremities, face, lips, tongue, and larynx has also been described.i There are several isolated reports of a pityriasis rosea-like eruption.' and exfoliative dermatitis. ACE inhibitors have not been reported to exacerbate psoriasis. The following case reports suggest that psoriatic flares may be induced by ACE inhibitor use.

Psoriasis and Bullous Pemphigoid

To the Editor.— Bullous pemphigoid was described as a distinct clinical entity by Lever 1 in 1953 and has been reported to have occurred with several autoimmune diseases, ie, systemic lupus erythematosus (SLE), 2 polymyositis, 3 and rheumatoid arthritis. 4 It has also been occasionally reported with other cutaneous diseases: Kaposi sarcoma, 5 lichen planus, 6 and pemphigus. 7 We report here on a patient with psoriasis in whom bullous pemphigoid developed after ultraviolet exposure. Report of a Case.— A 59-year-old man was hospitalized in June 1975 with a six-month history of psoriasis. Two weeks before admission he had a generalized psoriatic flare that evolved into an exfoliative erythroderma. Past medical history was unremarkable. Physical examination revealed generalized erythroderma, with distinct psoriatic plaques on the elbows, knees, legs, back, and chest. Laboratory studies were as follows: hemoglobin, 13.6 gm/100 ml; hematocrit, 42.9%; total leukocyte count 9.6%, with 25% band forms,