RECHERCHE BIBLIOGRAPHIQUE Nov-Dec 2009
Med Clin North Am. 2009 Nov;93(6):1291-303.
Evaluation and management of psoriasis: an internist's guide.
Levine D, Gottlieb A.
Department of Dermatology, Tufts Medical Center, Tufts University School of Medicine, 800 Washington Street, Boston, MA 02111, USA.
Psoriasis is a debilitating chronic skin condition that afflicts millions of patients worldwide. Patients experiencing psoriasis report a magnitude of impaired quality of life that is often similar to that of patients who have heart failure and cancer. Many patients who have psoriasis are even themselves at risk for developing heart disease, metabolic syndrome, certain cancers, and psychiatric illness. Therefore, primary care physicians must appreciate the current psoriatic disease model and share a basic understanding of psoriasis management. This article reviews the epidemiology, clinical features, pathogenesis, comorbidities, and treatment of psoriasis, with special emphasis placed on the new class of medications, biologics, which are revolutionizing the management of the disease.
J Am Acad Dermatol. 2009 Dec;61(6):1033-43.
Pain associated with aminolevulinic acid-photodynamic therapy of skin disease.
Warren CB, Karai LJ, Vidimos A, Maytin EV.
Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland Clinic, Cleveland, Ohio 44195, USA.
BACKGROUND: Pain during topical aminolevulinic acid (ALA)-mediated photodynamic therapy (PDT) limits the use of this treatment of skin diseases. OBJECTIVE: We sought to summarize the effectiveness of interventions to reduce ALA-PDT-related pain, and to explore factors contributing to pain induction. METHODS: A PubMed search was performed to identify all clinical PDT trials (2000-2008) that used ALA or methyl-ALA, enrolled at least 10 patients per trial, and used a semiquantitative pain scale. RESULTS: In all, 43 articles were identified for review. Pain intensity is associated with lesion size and location and can be severe for certain diagnoses, such as plaque-type psoriasis. Results are inconsistent for the correlation of pain with light source, wavelength of light, fluence rate, and total light dose. Cooling represents the best topical intervention. LIMITATIONS: Pain perception differs widely between patients and can contribute to variability in the reported results. CONCLUSION: Gamma-aminobutyric acid receptors, cold/menthol receptors (transient receptor potential cation channel, subfamily M, member 8), and vanilloid/capsaicin receptors (transient receptor potential cation channel, subfamily V, member 1) may be involved in pain perception during ALA-PDT and are therefore worthy of further investigation.
Arch Dermatol. 2009 Nov;145(11):1262-6.
Alefacept for severe alopecia areata: a randomized, double-blind, placebo-controlled study.
Strober BE, Menon K, McMichael A, Hordinsky M, Krueger G, Panko J, Siu K, Lustgarten JL, Ross EK, Shapiro J.
Department of Dermatology, New York University Medical Center, 550 First Ave, TCH-158, New York, NY 10016, USA.
OBJECTIVE: To assess the efficacy of alefacept for the treatment of severe alopecia areata (AA). DESIGN: Multicenter, double-blind, randomized, placebo-controlled clinical trial. SETTING: Academic departments of dermatology in the United States. PARTICIPANTS: Forty-five individuals with chronic and severe AA affecting 50% to 95% of the scalp hair and resistant to previous therapies. Intervention Alefacept, a US Food and Drug Administration-approved T-cell biologic inhibitor for the treatment of moderate to severe plaque psoriasis. Main Outcome Measure Improved Severity of Alopecia Tool (SALT) score over 24 weeks. RESULTS: Participants receiving alefacept for 12 consecutive weeks demonstrated no statistically significant improvement in AA when compared with a well-matched placebo-receiving group (P = .70). Conclusion Alefacept is ineffective for the treatment of severe AA.
J Allergy Clin Immunol. 2009 Nov;124(5):1022-10.e1-395.
Effective treatment of psoriasis with etanercept is linked to suppression of IL-17 signaling, not immediate response TNF genes.
Zaba LC, Suárez-Fariñas M, Fuentes-Duculan J, Nograles KE, Guttman-Yassky E, Cardinale I, Lowes MA, Krueger JG.
Laboratory for Investigative Dermatology, Rockefeller University, New York, NY 10065, USA.
BACKGROUND: TNF inhibitors have revolutionized the treatment of psoriasis vulgaris as well as psoriatic and rheumatoid arthritis and Crohn disease. Despite our understanding that these agents block TNF, their complex mechanism of action in disease resolution is still unclear. OBJECTIVE: To analyze globally the genomic effects of TNF inhibition in patients with psoriasis, and to compare genomic profiles of patients who responded or did not respond to treatment. METHODS: In a clinical trial using etanercept TNF inhibitor to treat psoriasis vulgaris (n = 15), Affymetrix gene arrays were used to analyze gene profiles in lesional skin at multiple time points during drug treatment (baseline and weeks 1, 2, 4, and 12) compared with nonlesional skin. Patients were stratified as responders (n = 11) or nonresponders (n = 4) on the basis of histologic disease resolution. Cluster analysis was used to define gene sets that were modulated with similar magnitude and velocity over time. RESULTS: In responders, 4 clusters of downregulated genes and 3 clusters of upregulated genes were identified. Genes downmodulated most rapidly reflected direct inhibition of myeloid lineage immune genes. Upregulated genes included the stable dendritic cell population genes CD1c and CD207 (langerin). Comparison of responders and nonresponders revealed rapid downmodulation of innate IL-1beta and IL-8 sepsis cascade cytokines in both groups, but only responders downregulated IL-17 pathway genes to baseline levels. CONCLUSION: Although both responders and nonresponders to etanercept inactivated sepsis cascade cytokines, response to etanercept is dependent on inactivation of myeloid dendritic cell genes and inactivation of the T(H)17 immune response.
South Med J. 2009 Nov;102(11):1133-40.
Adverse cutaneous reactions induced by TNF-alpha antagonist therapy.
Borrás-Blasco J, Navarro-Ruiz A, Borrás C, Casterá E.
Pharmacy Department, Hospital de Sagunto, Sagunto, Spain.
OBJECTIVE: To review adverse cutaneous drug reactions induced by tumor necrosis factor alpha (TNF-alpha) antagonist therapy. METHODS: A literature search was performed using PubMed (1996-March 2009), EMBASE, and selected MEDLINE Ovid bibliography searches. All language clinical trial data, case reports, letters, and review articles identified from the data sources were used. RESULTS: Since the introduction of TNF-alpha antagonist, the incidence of adverse cutaneous drug reactions has increased significantly. A wide range of different skin lesions might occur during TNF-alpha antagonist treatment. New onset or exacerbation of psoriasis has been reported in patients treated with TNF-alpha antagonists for a variety of rheumatologic conditions. TNF-alpha antagonist therapy has been associated with a lupus-like syndrome; most of these case reports occurred in patients receiving either etanercept or infliximab. Serious skin reactions such as erythema multiforme, Stevens-Johnson syndrome, and toxic epidermal necrolysis have been reported rarely with the use of TNF-alpha antagonists. CONCLUSIONS: As the use of TNF-alpha antagonists continues to increase, the diagnosis and management of cutaneous side effects will become an increasingly important challenge. In patients receiving TNF-alpha antagonist treatment, skin disease should be considered, and clinicians need to be aware of the adverse reactions of these drugs.
Lupus: affection inflammatoire auto-immune;
Erythème polymorphe: peut être une réaction à l’ingestion d’un médicament, pathogénie mal connue;
Si touche les muqueuses trachéaux-bronchiques = syndrome de Stevens-Johnson.
J Invest Dermatol. 2009 Nov;129(11):2604-12.
Cancer risk evaluation in psoriasis: in search of the Holy Grail?
Paul CF, Gourraud PA.
Paul Sabatier University, Toulouse, France.
Benefit-risk assessment of systemic treatment in psoriasis is a dynamic process. Long-term safety of psoriasis therapies has been questioned, with the spectrum of systemic immunosuppression potentially leading to increased cancer risk. In this issue, Brauchli et al. report on a population-based analysis of cancer risk in a large cohort of psoriasis patients, most of whom had not been treated with systemic agents. The study prepares the ground for future prospective long-term cohort studies in psoriasis patients treated with systemic therapies, including biological agents.
J Am Acad Dermatol. 2009 Dec;61(6):1044-55. Epub 2009 Oct 7.
Treatment of psoriasis in patients with hepatitis C: from the Medical Board of the National Psoriasis Foundation.
Frankel AJ, Van Voorhees AS, Hsu S, Korman NJ, Lebwohl MG, Bebo BF Jr, Gottlieb AB; National Psoriasis Foundation.
Department of Dermatology, Tufts Medical Center, Boston, Massachusetts 02111, USA.
BACKGROUND: Treating psoriasis in patients with concomitant hepatitis C virus (HCV) infection presents a special challenge. Not only is psoriasis exacerbated by interferon therapy, the standard of care for HCV, but many psoriasis therapies are potentially hepatotoxic, immunosuppressive, or both, which has been generally thought to be a contraindication in chronic infections such as HCV. OBJECTIVE: Our aim was to arrive at a consensus on treating psoriasis in patients with concomitant HCV infection. METHODS: Reports in the literature were reviewed regarding common psoriasis therapies and liver toxicity. RESULTS: Topical therapies are first-line therapy for patients with limited psoriasis and HCV. Ultraviolet B phototherapy may be considered as a second-line treatment when needed. Ultraviolet B phototherapies in combination with topical therapies are first line for patients with moderate to severe psoriasis, and are considered safe in those patients with concomitant HCV infection. Other systemic therapies, such as acitretin, etanercept, and, possibly, other tumor necrosis factor inhibitors, are considered second line. Psoralen plus ultraviolet A should also be considered a second-line therapy. LIMITATIONS: There are few evidence-based studies on treating psoriasis with systemic therapy in patients with pre-existing liver disease. CONCLUSIONS: There are no large double-blind clinical trials addressing the treatment of psoriasis in patients with HCV infection and more studies are needed.
Clin Rheumatol. 2009 Nov;28(11):1349-50. Epub 2009 Aug 20.
Psoriatic arthritis and chronic lymphoedema: treatment efficacy by adalimumab.
Tong D, Eather S, Manolios N.
Department of Rheumatology, Westmead Hospital, Sydney, NSW 2145, Australia.
Lymphoedema is a rare complication of psoriatic arthritis (PsA) and inflammatory joint disease, with no response noted to disease-modifying drugs. However, reports are emerging of a beneficial effect on lymphoedema in patients treated with tumor necrosis factor-alpha antagonists for PsA (Etanercept), rheumatoid arthritis (Etanercept) and ankylosing spondylitis (Infliximab). We describe a psoriatic arthritis patient whose lymphoedema greatly improved following commencement of adalimumab.
Mesenteric and splenic cat-scratch disease during etanercept therapy.
Schiffmann A, Pers YM, Lukas C, Combe B, Morel J.
Rheumatology (Oxford). 2009 Nov;48(11):1461-2. Epub 2009 Aug 18. No abstract available. PMID: 19690129 [PubMed - indexed for MEDLINE]Related articles
Comment on: Liver fibrosis in patients with psoriasis and psoriatic arthritis on long-term, high cumulative dose methotrexate therapy.
Boffa MJ, Smith A, Chalmers RJ.
Rheumatology (Oxford). 2009 Nov;48(11):1464; author reply 1465. Epub 2009 Aug 11. No abstract available. PMID: 19671697 [PubMed - indexed for MEDLINE]Related articles
Clin Rheumatol. 2009 Nov;28(11):1337-40. Epub 2009 Aug 10.
Acute bilateral phrenic neuropathy following treatment with adalimumab.
Alexopoulou A, Koskinas J, Soultati A, Katsaounis P, Kilidireas K, Papageorgiou C, Antoniou C, Katsambas A, Archimandritis A.
2nd Department of Medicine, University of Athens Medical School, Hippokration General Hospital, 40 Konstantinoupoleos Street, 16342 Athens, Greece.
The recombinant human IgG1 monoclonal antibody specific for human TNF-a adalimumab (Humira) has been recently introduced for the treatment of moderate/severe psoriasis. Neurological diseases have been rarely described as adverse events of anti-TNF agents. A case of acute respiratory failure due to diaphragmatic weakness following adalimumab therapy for psoriasis is described. A 65-year-old female patient presented with jaundice followed 2 days later by severe dyspnea and tachypnea which worsened when patient was lying flat, 1 week after the fourth dose of adalimumab. Isoniazid and vitamin B6 were co-administered with adalimumab. A symmetric elevation of diaphragms was shown on radiography and fluoroscopy. A pulmonary restrictive defect with a prominent decline of forced vital capacity (FVC) when the patient was on supine position was recorded. In the absence of specific limb electrophysiological abnormalities, acute bilateral symmetric phrenic neuropathy was diagnosed. The patient was a borderline candidate for mechanical ventilation for 3 weeks. Conservative treatment with oxygen was administered and both respiratory and liver disorder resolved 4 weeks following admission. A causal relationship of phrenal neuropathy with adalimumab is herein discussed.
J Am Acad Dermatol. 2009 Nov;61(5):841-56. Epub 2009 Aug 6.
Complementary and alternative medicine for psoriasis: a qualitative review of the clinical trial literature.
Smith N, Weymann A, Tausk FA, Gelfand JM.
Department of Dermatology, University of Rochester, Rochester, New York, USA.
BACKGROUND: Patients with psoriasis often inquire about complementary and alternative medicine in an effort to do everything possible to control the disease. OBJECTIVE: We sought to review the clinical trial literature regarding complementary and alternative medicine for the treatment of psoriasis. METHODS: We conducted qualitative systematic review of randomized, clinical trials. RESULTS: Although many randomized controlled trials were found, both the results and the quality of the studies varied. LIMITATIONS: The main limitations were the relatively low quality of studies (as assessed by Jadad scores), lack of inclusion of unpublished studies, and the fact that only one author determined inclusion of studies and assignment of Jadad scores. CONCLUSION: There is a large body of literature in regard to complementary and alternative medicine for the treatment of psoriasis. More work is necessary before these modalities should be recommended to our patients.
J Invest Dermatol. 2009 Dec;129(12):2747-50.
FOXP3+CD25- tumor cells with regulatory function in Sézary syndrome.
Heid JB, Schmidt A, Oberle N, Goerdt S, Krammer PH, Suri-Payer E, Klemke CD.
Tumor Immunology Program, Division of Immunogenetics (D030), German Cancer Research Center, Heidelberg, Germany.
Cutaneous T-cell lymphoma (CTCL) has been suggested by in vitro experiments to represent a malignant CD4+ T-cell proliferation with a regulatory T-cell (Treg) phenotype (CD4+CD25+FOXP3+). We investigated percentages of FOXP3+ and CD25+ cells in the blood of 15 Sézary, 14 mycosis fungoides (MF), and 10 psoriasis (Pso) patients and 20 normal healthy donors (NHDs). We found similar numbers of FOXP3+ cells in MF (10.4% of blood CD4+ cells) and Pso (11.1%) patients and NHDs (9.8%). In 8 of 15 (53%) Sézary patients, significantly reduced percentages of FOXP3+ cells were seen in blood (2.9%) and skin (10.4%). Interestingly, 6 of 15 (40%) Sézary patients showed significantly increased percentages of FOXP3+ cells (39.7% (blood), 20.3% (skin)); however, these cells did not express CD25. In these latter patients, clone-specific TCR-Vbeta-chain antibodies were used to demonstrate that these FOXP3+CD25- cells were monoclonal CTCL tumor cells. FOXP3+CD25- CTCL tumor cells showed a highly demethylated status of the foxp3 gene locus similar to Treg cells, and they were functionally able to suppress IL-2 mRNA induction in TCR-stimulated conventional T cells. Thus, FOXP3+CD25- CTCL tumor cells with functional features of Treg cells define a subgroup of Sézary patients who might carry a different prognosis and might require differential treatment.
J Invest Dermatol. 2009 Nov;129(11):2552-66. Epub 2009 May 28.
Chemokine receptors in T-cell-mediated diseases of the skin.
Lonsdorf AS, Hwang ST, Enk AH.
Department of Dermatology, University Hospital Heidelberg, Heidelberg, Germany.
The chemokine/chemokine receptor network is an integral element of the complex system of homeostasis and immunosurveillance. Initially studied because of their role in coordinating tissue-specific migration and activation of leucocytes, chemokines have been implicated in the pathogenesis of various malignancies and diseases with strong inflammatory components. We discuss recent findings suggesting a critical involvement of chemokine receptor interactions in the immunopathogenesis of classical inflammatory skin disorders such as psoriasis and atopic dermatitis, as well as neoplastic diseases with a T-cell origin, such as mycosis fungoides. A deeper understanding of the underlying contribution of the chemokine network in the disease processes is key for the development of selective targeted immunotherapeutics that may meet the delicate balance between efficacy and safety.
Chemokine: famille de petites cytokines secrétées par la peau.
Discussion sur le rôle éventuel des récepteurs aux Chemokines dans la pathogénie de troubles inflammatoires de la peau, tel que le psoriasis.
J Invest Dermatol. 2009 Nov;129(11):2604-12. Epub 2009 May 14.
Psoriasis and risk of incident cancer: an inception cohort study with a nested case-control analysis.
Brauchli YB, Jick SS, Miret M, Meier CR.
Division of Clinical Pharmacology and Toxicology, University Hospital, Basel, Switzerland.
Psoriasis has been associated with lymphohematopoietic and solid cancers; however, reports have been inconsistent. Cancer incidence was compared between psoriasis and psoriasis-free patients, and the roles of psoriasis duration and treatment were explored in this observational study using the UK General Practice Research Database. Among 67,761 patients, 1,703 patients had incident cancer; of whom 54% had a history of psoriasis. Incidence rate ratios for lymphohematopoietic and pancreatic cancers were 1.81 (95% confidence interval (CI) 1.35-2.42) and 2.20 (95% CI 1.18-4.09), respectively. In a nested case-control analysis, adjusted odds ratios (ORs) for cancer overall were 1.50 (95% CI 1.30-1.74) for psoriasis of >or=4 years duration and 1.53 (95% CI 0.97-2.43) for patients receiving systemic treatment (marker of disease severity). Lymphohematopoietic malignancy risk was highest in patients with systemic treatment. The OR for patients without systemic treatment was 1.59 (95% CI 1.01-2.50) for psoriasis of <2 years and 2.12 (95% CI 1.45-3.10) for that of >or=2 years duration. Risks of bladder/kidney and colorectal cancers were increased with longer-duration psoriasis. Psoriasis patients may have an increased overall risk of incident cancer (mainly lymphohematopoietic and pancreatic). Longer-term psoriasis and more severe disease may increase the risk of some cancers. These observations need further confirmation, particularly because of the potential of findings by chance in observational studies with subgroup analyses.
Clin Exp Dermatol. 2009 Jul;34(5):e177-9. Epub 2009 Dec 15.
Superimposed linear psoriasis: differential therapeutic response of linear and nonlinear lesions.
Seitz CS, Garbaraviciene J, Bröcker EB, Hamm H.
Department of Dermatology, Venereology and Allergology, University of Würzburg, Würzburg, Germany.
Linear psoriasis is a very unusual clinical variation of psoriasis. Typical clinical features include early onset of erythematosquamous lesions along Blaschko's lines, ability to elicit psoriatic features, absence of pruritus and positive family history for psoriasis. Recently, the term 'superimposed linear psoriasis' was coined for cases with development of nonlinear psoriatic lesions at predilection sites in later life. We report a 19-year-old woman meeting all criteria for the diagnosis of superimposed linear psoriasis including typical histological features. Remarkably, treatment with topical steroids and dithranol cleared the psoriatic lesions on predilection sites whereas the linear lesions were resistant to topical therapy. Linear psoriatic lesions are believed to be caused by genetic alterations in early embryogenesis leading to loss of heterozygosity at a gene locus involved in the pathogenesis of psoriasis. Comparison of mosaic keratinocytes derived from linear lesions with wild-type keratinocytes from the same person may therefore allow identification of key regulatory genes.