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PubMed2001

Keratinocytes from patients with atopic dermatitis and psoriasis show a distinct chemokine production profile in response to T cell-derived cytokines.

BACKGROUND: Atopic dermatitis (AD) and psoriasis are genetically determined inflammatory skin disorders. Keratinocytes actively participate in cutaneous inflammatory responses by elaborating various chemokines. OBJECTIVE: We investigated the capacity of IL-4, IFN-gamma, and TNF-alpha to modulate the expression of CCL and CXCL chemokines in cultured keratinocytes from patients and healthy individuals, as well as chemokine expression in situ. METHODS: Keratinocyte cultures were established from normal-looking skin of adult patients with AD or psoriasis vulgaris and from healthy subjects. Monocyte chemoattractant protein 1 (MCP-1)/CCL2, RANTES/CCL5, IL-8/CXCL8, and IFN-gamma-induced protein of 10 kd (IP-10)/CXCL10 production was evaluated at the mRNA and protein levels by using RNase protection assay and ELISA, respectively. The expression of the same chemokines was studied in chronic lesional skin by means of immunohistochemistry or in situ hybridization. RESULTS: Only IL-8 mRNA was detected in unstimulated ke-ratinocyte cultures. MCP-1 and IP-10 were potently induced by IFN-gamma, whereas IL-8 and RANTES were preferentially upregulated by TNF-alpha and, to a lesser extent, by IFN-gamma. IL-4 weakly induced IP-10, RANTES, and IL-8 but not MCP-1. Keratinocytes of patients with AD invariably responded with significantly earlier and higher RANTES expression. By contrast, keratinocytes of patients with psoriasis displayed much higher levels of both constitutive and induced IL-8 and a stronger induction of MCP-1 and IP-10. RANTES and MCP-1 mRNA(+) keratinocytes were detected in the basal layer of lesions of patients with AD and psoriasis. IP-10 and IL-8 were consistently upregulated in the epidermis of patients with psoriasis but not in lesions of patients with AD. CONCLUSIONS: Keratinocytes of patients with AD and psoriasis show an intrinsically abnormal and different chemokine production profile and may thus favor the recruitment of distinct leukocyte subsets into the skin.

Adult↗
PubMed2001

A multicenter dose-escalation trial with denileukin diftitox (ONTAK, DAB(389)IL-2) in patients with severe psoriasis.

BACKGROUND: Denileukin diftitox, a fusion protein targeting both malignant and normal activated lymphocytes, has been shown previously to have antipsoriatic activity. However, the ideal dosing regimen for treating psoriasis was not established. OBJECTIVE: We examined the safety and efficacy of denileukin diftitox in patients with severe plaque-type psoriasis. METHODS: This was a cohort dose-escalation trial. Patients were administered denileukin diftitox on 3 consecutive days every other week. Patients were evaluated for toxicity, improvement in psoriasis, immunogenicity, and serum levels. RESULTS: Thirty-five patients were treated at 3 dose levels. Eight patients had a 50% decrease or more in Psoriasis Area and Severity Index score from baseline (0/10 at 0.5 microg/kg per day, 1/10 at 1.5 microg/kg per day, and 7/15 at 5 microg/kg per day). Adverse events primarily consisted of constitutional events and skin reactions. CONCLUSIONS: The potential antipsoriatic activity of denileukin diftitox demonstrated in this study was comparable to that observed in other psoriasis studies with this agent. However, this dosing regimen was better tolerated than the dosing regimen used in the last study with denileukin diftitox in psoriasis patients.

Adult↗
PubMed2002

Clinical and histologic response to single-dose treatment of moderate to severe psoriasis with an anti-CD80 monoclonal antibody.

Pathologic T-cell activation is implicated in psoriasis progression. CD80, a costimulatory molecule involved in T-cell activation, likely plays a key role. IDEC-114, an IgG(1) anti-CD80 antibody, was evaluated for safety, pharmacokinetics, and preliminary clinical activity in this open-label, single-dose, dose-escalating study in patients with moderate to severe chronic plaque psoriasis. Twenty-four patients received IDEC-114 (0.05 mg/kg, 0.25 mg/kg, 1 mg/kg, 5 mg/kg, 10 mg/kg, or 15 mg/kg). Psoriasis Area and Severity Index, Physician's Global Psoriasis Assessment, and Psoriasis Severity Scale scores improved in the highest-dose groups. Average plaque thickness and plaque CD3+ and CD8+ T-cell counts decreased in the 10 mg/kg dose group. Adverse events were primarily mild, transient, constitutional symptoms; the most common related events were mild asthenia (29% of patients), chills (25%), and headache (21%). The serum half-life of IDEC-114 was approximately 13 days. A single dose of IDEC-114 appears to be safe and well tolerated and has promising clinical activity in psoriasis.

Adolescent↗
PubMed2003

Connections between psoriasis and Crohn's disease.

UNLABELLED: The prevalence of psoriasis in patients with Crohn's disease (CD) is higher than chance would allow if they were mutually exclusive diseases. A close examination reveals genetic and pathologic connections between these diseases. An appreciation for the role of tumor necrosis factor-alpha in both diseases has proven very important. Increased levels of this inflammatory cytokine have been measured in CD lesions, and in 1997 a clinical trial demonstrated the response of this disease to infliximab, a monoclonal antibody specific for tumor necrosis factor-alpha. A subsequent clinical trial evaluated infliximab in a patient with CD and psoriasis, another disease in which increased levels of tumor necrosis factor-alpha are seen in lesions. Scientists noticed the marked skin improvement of this patient and later demonstrated the efficacy of infliximab for psoriasis in a randomized, double-blind, placebo-controlled trial. Thus, an appreciation for connections between psoriasis and CD can suggest novel therapeutic strategies with ensuing benefits to patients. This article reviews epidemiologic, genetic, and pathologic connections between psoriasis and CD and discusses pharmaceuticals targeting inflammatory mediators common to each disease. (J Am Acad Dermatol 2003;48:805-21.) LEARNING OBJECTIVE: At the completion of this learning activity, participants should understand how psoriasis and Crohn's disease are related at epidemiologic, genetic, and pathological levels and should appreciate how to use this knowledge to treat these diseases.

Antibodies, Monoclonal↗
PubMed2000

Analysis of HLA antigens in Croatian patients with psoriasis.

In common with most autoimmune diseases, psoriasis is associated with some HLA antigens. We studied the distribution of HLA antigens in Croatian patients with psoriasis: 108 patients were divided into groups according to family history and age of disease onset. HLA antigens were analyzed serologically and HLA-C alleles were analyzed using polymerase chain reaction. We found significant increases in HLA-A2, -B17, -B37 and -B13 antigens and highly significant increases in HLA-Cw*0602 and DR7 antigens in psoriatic patients compared with controls. Patients with type I psoriasis (early onset, positive family history) showed highly significant associations with Cw*0602 [p < 0.00001; relative risk (RR) = 14.45] and DR7 (p < 0.00001; RR = 15.09) antigens. Patients with type II psoriasis (late onset, no family history) had a significant association with Cw*03 antigen (p = 0.008; RR = 0.17). In conclusion, HLA-B13, -B17, Cw*0602 and -DR7 antigens are associated with a significant risk of psoriasis in the Croatian population and the Cw*0602 allele has the strongest association, especially for type I psoriasis.

Adult↗
PubMed2005

Serum levels of parathyroid hormone and parathyroid-related peptide in psoriasis.

Psoriasis is a common skin disorder that may be triggered by hormonal disturbances, among other factors. Some studies have demonstrated an elevation of serum parathyroid hormone (PTH) levels in psoriasis and several other diseases of keratinization of unknown aetiology. PTH-related peptide (PTH-rp), on the other hand, is a potent inhibitor of epidermal cell growth factor and is not expressed in psoriatic skin. Serum levels of this peptide have not been reported in psoriasis. Immunoassay was used to measure serum PTH and PTH-rp in 22 patients with plaque-type psoriasis before and after treatment with mometasone furoate. Results were compared with a group of 20 healthy, non-psoriatic volunteers. Serum PTH levels were significantly elevated in the psoriatic group compared with the control group (p=0.001) and were significantly reduced after treatment (p=0.01). A correlation was found between pretreatment serum PTH levels and psoriasis area and severity scores (PASI) (r=0.42; p=0.01). In contrast, serum PTH-rp levels were not different between psoriatics and controls and were not affected by treatment. These findings indicate that serum PTH concentrations reflect disease activity in patients with psoriasis.

Adolescent↗
PubMed1998

Hepatic cytochrome P450 CYP2C activity in psoriasis: studies using proguanil as a probe compound.

Retinol and proguanil are metabolised by the same family of hepatic cytochrome P450, i.e. CYP2C. We used proguanil as a probe to study CYP2C activity, and by implication retinol metabolism, in psoriasis. In vitro studies showed that retinol competitively inhibited the hepatic metabolism of proguanil to cycloguanil. Proguanil metabolism was assessed in 82 patients with chronic plaque psoriasis. Following proguanil orally (200 mg), urine was analysed for proguanil and cycloguanil. A proguanil to cycloguanil ratio < 1 signified extensive metabolism and a ratio > 10 poor metabolism. A wider range of ratios was observed in psoriasis than previously reported for normal subjects. The proguanil to cycloguanil ratio was assessed in 10 cases each of know severe and mild psoriasis. Low CYP2C activity was associated with severe psoriasis, poor metaboliser status occurring in 50% of the severe group, but in none of the mild cases, p < 0.01. These findings may indicate differences in retinoid metabolism in psoriasis.

Administration, Oral↗
PubMed1999

Expression of the psoriasis-associated antigen, Pso p27, is inhibited by cyclosporin A.

The psoriasis-associated antigen, pso p27, can be isolated from psoriasis scale and is present in complement-activating immune complexes in psoriatic scale, and in serum from patients with psoriasis. The antigen is produced by tryptase-positive cells in the skin lesions and is shown to be a major antigen in the immune reactions in psoriasis. The synthesis of this particular antigen is reduced with the remission of inflammation in the skin lesions. In this study we followed 3 patients with severe plaque psoriasis during treatment with cyclosporin A. In all patients we observed a decrease in the expression of the antigen pso p27 during the therapy. The effectiveness of the therapy varied among the patients, but there was a clear correlation between disease activity and expression of the antigen pso p27 as demonstrated by immunofluorescence in biopsies from selected skin lesions. This observation strengthens our hypothesis that the pso p27 antigen plays an important role in the inflammation in psoriasis.

Adult↗
PubMed2005

Possible molecular mechanisms to account for the involvement of tryptase in the pathogenesis of psoriasis.

Tryptase has been suggested to take part in the pathophysiology of psoriasis mainly through the production of C3a by cleaving C3. However, studies using tryptase preparations of high purity do not support this notion. Therefore, although tryptase is unanimously believed to be involved in the immunopathogenesis of psoriasis, no convincing mechanism has been proposed for its role. This paper proposes several mechanisms by which this enyme may exert its role in the pathobiology of psoriasis. Tryptase is a mitogen for epithelial cells and stimulates IL-8 production and ICAM-1 expression by these cells. It also induces the expression of mRNA for IL-1beta and IL-8 and stimulates the selective release of IL-8 from endothelial cells and TNF-alpha, IL-1beta, and IL-6 from lymphocytes and monocytes. Besides itself being a chemoattractant for neutrophils, tryptase activates mast cells and generates kinins from kininogen, thereby playing a crucial role in leukocyte infiltration into psoriatic lesions. This enzyme also induces leukocyte infiltration partly through activating endothelial PAR-2, which contributes to leukocyte rolling, adherence and recruitment by inducing the release of endothelial platelet-activating factor. Through activating PAR-2, tryptase could also trigger the development of Langerhans cells which play a crucial role in the pathophysiology of psoriasis. This enzyme is a mitogen for fibroblasts, which are probably involved in the pathophysiology of psoriasis through production of insulin-like growth factor-I (IGF-I). Tryptase is a gelatinase and also activates stromelysin-1 (MMP-3), thereby contributing to the disruption of psoriatic basement membrane and to the joint damage seen in psoriatic arthritis. Increase of tryptase levels following trauma could also provide a mechanism for Koebner phenomenon seen in psoriasis.

Animals↗
PubMed2005

The comorbid state of psoriasis patients in a university dermatology practice.

BACKGROUND: Psoriasis treatment is frequently complicated by the various types and severities of disease as well as the large number of therapies available. Another critical consideration in treatment planning is the presence of comorbid diseases. PURPOSE: The purpose of this study was to evaluate the relative prevalence of major comorbid disease states in patients with psoriasis and to identify significant predictors of these concurrent diseases in such patients. METHODS: A retrospective chart review of 753 patients from an academic dermatology practice was performed. The patients were identified by ICD-9 code for psoriasis in billing records of patients seen between 1997 and 2000. Data on comorbidities were compiled from review of electronic chart notes from all physician visits in the university practice. RESULTS: Comorbid diagnoses were listed in 551 out of 753 (73%) charts. As would be expected, hypertension, dyslipidaemia, diabetes and heart disease were the most common comorbidities; renal failure and hepatitis were least likely. Hepatitis was associated with use of systemic therapies (odds ratio = 2.19) and non-white race. When compared with national prevalence estimates, psoriasis patients had increased heart disease, hypertension, diabetes and emphysema; however, these findings must be interpreted with some caution. CONCLUSIONS: Comorbid diseases are common in psoriasis patients and should be taken into account during treatment planning and surveillance; they may pose unique challenges in caring for patients with psoriasis, particularly those requiring systemic therapy.

Academic Medical Centers↗
PubMed2005

Systemic treatment for moderate to severe psoriasis: estimates of failure rates and direct medical costs in a north-eastern US managed care plan.

BACKGROUND: Estimates of US medical costs related to psoriasis treatment are limited and tend to understate the economic burden of moderate to severe psoriasis, which often requires the use of systemic agents, phototherapy or both. OBJECTIVE: To estimate treatment failure rates and direct medical costs associated with the use of systemic agents and phototherapy in US patients with psoriasis. METHODS: Claims records from a large New England-based health insurer were used to obtain patient-level data. Eligible patients with at least one claim listing an ICD-9-CM code for psoriasis (696.0; 696.1) were identified. Patients not receiving systemic treatments (methotrexate, cyclosporine, acitretin) or phototherapy (ultraviolet B with or without tar or petrolatum, psoralen and ultraviolet A [PUVA]) were excluded. Treatment failure was defined as a switch in therapy, augmentation with non-topical therapies, discontinuation following uptitration of dose or discontinuation following hospitalization. Medical costs included those related to pharmacy (over-the-counter medication excluded), institutional services (inpatient and outpatient) and professional services. RESULTS: A total of 2068 patients with moderate to severe psoriasis were included in the analysis. Over a 1-year period, approximately 20% of patients experienced treatment failure. The mean time to failure among patients who switched therapy ranged from 3 to 6 months. Mean annual pharmacy costs in the various treatment groups (categorized according to initial therapy received) ranged from 257 dollars to 1992 dollars per patient. Mean annual costs for institutional and professional services ranged from 156 dollars to 799 dollars and 183 dollars to 481 dollars per patient, respectively. The 99th percentile annual pharmacy and institutional costs exceeded 10,000 dollars and 18,000 dollars, respectively. CONCLUSION: Treatment of moderate to severe psoriasis with traditional systemic agents or phototherapy is associated with a high likelihood of treatment failure and a considerable economic burden.

Acitretin↗
PubMed2006

Death from psoriasis: representative US data.

OBJECTIVES: Psoriasis can be associated with severe, life-threatening exacerbations. We sought to approximate the mortality associated with hospitalizations for psoriasis. MATERIALS AND METHODS: We analyzed data from two sources to estimate a death rate associated with psoriasis. RESULTS: There were 471 hospital admissions for psoriasis from 1988 to 2001 with a corresponding mortality rate of 1.5%. Documented on nationwide death certificates, there were a total of 29, 33, and 25 deaths attributable to psoriasis in 2001, 2000, and 1999, respectively. CONCLUSIONS: Though effective therapies for severe psoriasis are available, access to them is not guaranteed. It is disturbing to think that the deaths observed here could, at least in part, be prevented with the appropriate use of treatments.

Adult↗
PubMed2026

Practical Saudi Guidelines on management of moderate-to-severe psoriasis: 2026 update.

BACKGROUND: Psoriasis is a chronic, immune-mediated inflammatory skin disease that affects approximately 5.3% of the population in the Kingdom of Saudi Arabia (KSA). Thus, we aim to develop updated evidence-based clinical practice guidelines for the management of adults and pediatric patients with moderate-to-severe plaque psoriasis in the KSA. METHODS: These guidelines followed the "Grading of Recommendations, Assessment, Development, and Evaluation" (GRADE) methodology. We conducted a systematic literature review of PubMed, EMBASE, and the Cochrane Library for high-quality evidence published between 2020 and 2026. The panel developed 31 PICO questions that address key treatment considerations for moderate-to-severe psoriasis. RESULTS: We established 27 evidence-based recommendations and 4 good-practice statements addressing key aspects of moderate-to-severe psoriasis management. These guidelines strongly recommend adopting the Psoriasis Area and Severity Index (PASI) 90 as the primary treatment goal over PASI 75. For adult patients, the guidelines recommend biologic therapies, including interleukin (IL)-17 inhibitors, IL-23 inhibitors, IL-12/23 inhibitors, and tumor necrosis factor (TNF)-&#x3b1; inhibitors, for better disease control. For pediatric patients, the guidelines recommend early initiation of biologic therapy, with etanercept, secukinumab, ixekizumab, and adalimumab as preferred options. CONCLUSION: These Saudi national guidelines offer a comprehensive, evidence-based framework for managing moderate-to-severe psoriasis in adults and pediatric patients.

Humans↗
PubMed2006

Drug-induced psoriasis: an evidence-based overview and the introduction of psoriatic drug eruption probability score.

Psoriasis is a common skin disorder that needs a long-term management, not only because, of its prevalence but also because of the profound impact it can have on patients quality of life. Drugs may result in exacerbation of a preexisting psoriasis, in induction of psoriatic lesions on clinically uninvolved skin in patients with psoriasis, or in precipitation of the disease in persons without family history of psoriasis or in predisposed individuals. The knowledge of the drugs that may induce, trigger, or exacerbate the disease is of primary importance in clinical practice. By reviewing the literature, there are many reports on drug-induced psoriasis, but the data are not univocal. We propose, when possible, the use of a probability score from the authors to obtain a better classification and further understanding of drug-induced psoriasis.

Adrenergic beta-Antagonists↗
PubMed2003

Case studies in severe psoriasis: A clinical strategy.

Individuals with moderate-to-severe psoriasis perceive that the disease exerts profound emotional, social and physical effects on their lives, and a significant percentage report that they do not consider their treatment sufficiently aggressive. A survey of individuals with a variety of chronic diseases reveals that those with psoriasis have the lowest estimation of their health-related quality of life, lower than that of patients with arthritis, congestive heart failure, chronic lung disease or depression. Although psoriasis can be treated effectively, many treatments are associated with long-term risks. Toxicity-sparing treatment strategies that include combination, rotational and sequential regimens can help to control moderate-to-severe psoriasis while reducing risk. Algorithms for the treatment of moderate-to-severe psoriasis detail possible options for specific types of psoriasis and for patients with specific needs. The purpose of the algorithms is to make optimum use of phototherapy, traditional cytotoxic and immunosuppressive agents, retinoids, and newer biologic agents.

Acitretin↗
PubMed1994

PUVA bath therapy strongly suppresses immunological and epidermal activation in psoriasis: a possible cellular basis for remittive therapy.

Psoriasis is characterized by alterations in both the epidermis and dermis of the skin. Epidermal keratinocytes display marked proliferative activation and differentiate along an "alternate" or "regenerative" pathway, while the dermis becomes infiltrated with leukocytes, particularly interleukin 2 (IL-2) receptor-bearing "activated" T cells. Psoralens, administered by the oral route, have therapeutic effects in psoriasis when photochemically activated by ultraviolet A light (PUVA therapy). Recently psoralen bath therapy has been introduced to more effectively deliver this agent to the diseased skin. We have correlated the efficacy of PUVA bath therapy with its effects on specific molecular and cellular parameters of disease, in 10 consecutive patients with recalcitrant psoriasis. Rapid clearing of lesions occurred in 8 out of 10 patients. Biopsies were taken from lesional and nonlesional skin before and after a single round of therapy, and observation was continued in our Clinical Research Center at The Rockefeller University. Enumeration of cycling keratinocytes with the Ki-67 monoclonal antibody showed that PUVA reduced cell proliferation by 73%. The pathological increase in insulin-like growth factor 1 (IGF-1) receptors was reversed, whereas epidermal growth factor (EGF) receptors, which are also increased in psoriasis, remained unchanged. Keratinocyte proteins that are expressed in abnormal sites of the epidermis during psoriasis, i.e., keratin 16, filaggrin, and involucrin, were, after PUVA treatment, localized to their normal sites. Epidermal and dermal T-lymphocytes (CD3+), as well as CD4+, CD8+, and IL-2 receptor+ subsets, were strongly suppressed by PUVA, with virtual elimination of IL-2 receptor+ T cells in some patients. Consistent with diminished lymphocyte activation, HLA-DR expression by epidermal keratinocytes was markedly reduced in treated skin. In comparison to cyclosporine treatment of psoriasis, PUVA therapy leads to more complete reversal of pathological epidermal and lymphocytic activation, changes which we propose to be the cellular basis for a more sustained remission of disease after PUVA treatment.

Adult↗
PubMed1999

Novel genetic association between the corneodesmosin (MHC S) gene and susceptibility to psoriasis.

Psoriasis is an inflammatory skin disease of unknown origin, but with a clear genetic component. The strongest genetic association has been found with the major histocompatibility complex (MHC) region, and specifically between susceptibility to familial early onset psoriasis and human leukocyte antigen (HLA)-Cw6. The basis of this association of the HLA-C locus with disease pathogenesis is, however, not clear, and it is possible that other genes, or a combination of genes, in the HLA region are of functional importance. The MHC S gene is expressed specifically in keratinocyte differentiation and, being located 160 kb telomeric of HLA-C, is a plausible candidate gene. We analysed the allelic distribution of two polymorphisms in the MHC S gene (at +619 and +1243) in a case-control association study. We could confirm a significant association between psoriasis and HLA-Cw6 [odds ratio (OR) = 7.75]. No association was found between disease (or any subtypes) and the MHC S gene polymorphism at position +619, despite its close proximity to HLA-C and the strong linkage disequilibrium between the loci. However, a significant trend with the rarer allele at MHC S (+1243) and psoriasis was detected in the overall data set (OR = 2. 66; P = 2 [times] 10(-)9). This effect was most pronounced in the type 1a (early onset) psoriatics (OR = 3.43). Furthermore, homozygosity for the associated allele at MHC S (+1243) increased the risk of disease over that for carriage of HLA-Cw6 alone (OR = 9. 38), suggesting that allele 2 of MHC S (+1243) provides an additional risk in psoriasis susceptibility. The strong association found here, coupled with the biological involvement of the MHC S gene product corneodesmosin in skin physiology, implicates this locus (or a haplotype across HLA-C and MHC S ) in the impaired desquamation characteristic of psoriasis.

Adult↗
PubMed2004

The genetics of psoriasis, psoriatic arthritis and atopic dermatitis.

Psoriasis and atopic dermatitis are chronic and relapsing inflammatory diseases of the skin associated with various immunologic abnormalities. Approximately 30% of psoriasis patients also have joint involvement, indicative of psoriatic arthritis. Genes and environment play a key role in the pathogenesis of these diseases. Genome-wide linkage scans have identified multiple loci linked to each disease and revealed overlap with psoriasis and atopic dermatitis susceptibility loci on chromosomes 1q21, 3q21, 17q25 and 20p12. The genes from these loci have not yet all been identified, or systematically tested for a role in psoriasis and atopic dermatitis; however, these locations suggest that some susceptibility factors lie within genes or gene families with common effects upon epithelial immunity. A strong HLA association is described for psoriasis, but not for atopic dermatitis. Knowledge of the genetic factors leading to these diseases will lead to an understanding of their variable age at onset, their waxing and waning and the variability of body surface environment. The effect of environmental triggers may also be understood once the altered pathways are elucidated. Genes implicated so far in atopic dermatitis are SPINK5, FcepsilonRI-beta and PHF11. Genes implicated in psoriasis so far are HLA-C, SLC9A3R1, NAT9, RAPTOR and SLC12A8. Genetic modifiers such as CARD15 may predispose to psoriatic arthritis.

Arthritis, Psoriatic↗