Drug Treatments in Psoriasis
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Fig. L COMPOSITIONS and METHODS to INHIBIT STEM CELL and PROGENITOR CELL BINDING to LYMPHOID TISSUE and for REGENERATING GERMINAL CENTERS in LYMPHATIC TISSUES
(12) INTERNATIONAL APPLICATION PUBLISHED UNDER THE PATENT COOPERATION TREATY (PCT) (19) World Intellectual Property Organization International Bureau (10) International Publication Number (43) International Publication Date Χ 23 February 2012 (23.02.2012) WO 2U12/U24519ft ft A2 (51) International Patent Classification: AO, AT, AU, AZ, BA, BB, BG, BH, BR, BW, BY, BZ, A61K 31/00 (2006.01) CA, CH, CL, CN, CO, CR, CU, CZ, DE, DK, DM, DO, DZ, EC, EE, EG, ES, FI, GB, GD, GE, GH, GM, GT, (21) International Application Number: HN, HR, HU, ID, IL, IN, IS, JP, KE, KG, KM, KN, KP, PCT/US201 1/048297 KR, KZ, LA, LC, LK, LR, LS, LT, LU, LY, MA, MD, (22) International Filing Date: ME, MG, MK, MN, MW, MX, MY, MZ, NA, NG, NI, 18 August 201 1 (18.08.201 1) NO, NZ, OM, PE, PG, PH, PL, PT, QA, RO, RS, RU, SC, SD, SE, SG, SK, SL, SM, ST, SV, SY, TH, TJ, TM, (25) Filing Language: English TN, TR, TT, TZ, UA, UG, US, UZ, VC, VN, ZA, ZM, (26) Publication Language: English ZW. (30) Priority Data: (84) Designated States (unless otherwise indicated, for every 61/374,943 18 August 2010 (18.08.2010) US kind of regional protection available): ARIPO (BW, GH, 61/441,485 10 February 201 1 (10.02.201 1) US GM, KE, LR, LS, MW, MZ, NA, SD, SL, SZ, TZ, UG, 61/449,372 4 March 201 1 (04.03.201 1) US ZM, ZW), Eurasian (AM, AZ, BY, KG, KZ, MD, RU, TJ, TM), European (AL, AT, BE, BG, CH, CY, CZ, DE, DK, (72) Inventor; and EE, ES, FI, FR, GB, GR, HR, HU, IE, IS, ΓΓ, LT, LU, (71) Applicant : DEISHER, Theresa [US/US]; 1420 Fifth LV, MC, MK, MT, NL, NO, PL, PT, RO, RS, SE, SI, SK, Avenue, Seattle, WA 98101 (US). -
Targeted Therapies in B-Cell Non-Hodgkin Lymphomas
REVIEW Targeted therapies in B-cell non-Hodgkin lymphomas The incidence of non-Hodgkin lymphomas has risen in recent years. Although several chemotherapy regimens are efficacious in non-Hodgkin lymphoma, the addition of targeted therapies has become an indispensable part of their treatment. Monoclonal antibodies directed against lymphocytes in different stages of maturation have changed the treatment paradigm for lymphoma. Since these antibodies bind with high affinity to cell surface antigens, they target malignant cells and spare normal tissue, thereby causing less nonspecific toxicity. Rituximab, a monoclonal antibody directed against CD20, was the first antibody to be US FDA-approved for the treatment of lymphoma. Several clinical trials are ongoing that will help to establish the role of targeted agents in the treatment of non-Hodgkin lymphoma. This review provides a summary of targeted agents already approved or in clinical trials for the treatment of non-Hodgkin lymphoma. KEYWORDS: mAbs monoclonal antibodies non-Hodgkin lymphoma Sapna Khubchandani & radioimmunoconjugates rituximab targeted therapies Myron S Czuczman† †Author for correspondence: Roswell Park Cancer Institute, Non-Hodgkin lymphomas (NHLs) are increas- include: DLBCL and its variants, Burkitt lym- Elm and Carlton Streets, ing in incidence and will be diagnosed in more phoma, PTCL, immunodeficiency-associated Buffalo, NY 14263, USA than 55,000 individuals this year alone [1,2]. The lymphoproliferative disorder, precursor B lym- Tel.: +1 716 845 3221 13 most frequent -
Psoriasis and the New Biologic Agents: Interrupting a T-AP Dance
Review Synthèse Psoriasis and the new biologic agents: interrupting a T-AP dance Scott R.A. Walsh, Neil H. Shear Abstract corticosteroids, tar, anthralin, calcipotriol or tazarotene be- come cumbersome to apply as lesional surface area increases. PSORIASIS IS AN IMMUNE-MEDIATED SKIN DISEASE in which chronic T- Furthermore, potential side effects of these therapies increase cell stimulation by antigen-presenting cells (APC) occurs in the with the level of application. Nevertheless, topical treatment skin. This interplay between the T-cell and APC has been likened remains an adjunct in more severe disease to limit the re- to a “T-AP dance” where specific steps must occur in sequence to quirement for more aggressive therapies. Phototherapy is a result in T-cell activation and the disease phenotype; otherwise T- popular option in the treatment of more widespread disease. cell anergy would occur. Several novel engineered proteins de- However, ultraviolet light is generally only available in larger signed to block specific steps in immune activation (biologic treatment centres, requires a major time commitment (2–3 agents) have demonstrated efficacy in the treatment of psoriasis. times per week for many months) and can be associated with These agents include fusion proteins, monoclonal antibodies and an increased risk of cutaneous neoplasms.6 For moderate to recombinant cytokines. These medications act at specific steps during the T-AP dance either to inhibit T-cell activation, costimu- severe disease, oral systemic immunosuppressives such as lation and subsequent proliferation of T-cells, lead to immune de- methotrexate and cyclosporine or oral retinoids are generally viation or induce specific cytokine blockades. -
Autoinvolutive Photoexacerbated Tinea Corporis Mimicking a Subacute Cutaneous Lupus Erythematosus
Letters to the Editor 141 low-potency steroids had no eŒect. Our patient was treated 4. Jarrat M, Ramsdell W. Infantile acropustulosis. Arch Dermatol with a modern glucocorticoid which has an improved risk– 1979; 115: 834–836. bene t ratio. The antipruritic and anti-in ammatory properties 5. Kahn G, Rywlin AM. Acropustulosis of infancy. Arch Dermatol of the steroid were increased by applying it in combination 1979; 115: 831–833. 6. Newton JA, Salisbury J, Marsden A, McGibbon DH. with a wet-wrap technique, which has already been shown to Acropustulosis of infancy. Br J Dermatol 1986; 115: 735–739. be extremely helpful in cases of acute exacerbations of atopic 7. Mancini AJ, Frieden IJ, Praller AS. Infantile acropustulosis eczema in combination with (3) or even without topical revisited: history of scabies and response to topical corticosteroids. steroids (8). Pediatr Dermatol 1998; 15: 337–341. 8. Abeck D, Brockow K, Mempel M, Fesq H, Ring J. Treatment of acute exacerbated atopic eczema with emollient-antiseptic prepara- tions using ‘‘wet-wrap’’ (‘‘wet-pyjama’’) technique. Hautarzt 1999; REFERENCES 50: 418–421. 1. Vignon-Pennam en M-D, Wallach D. Infantile acropustulosis. Arch Dermatol 1986; 122: 1155–1160. Accepted November 24, 2000. 2. Duvanel T, Harms M. Infantile Akropustulose. Hautarzt 1988; 39: 1–4. Markus Braun-Falco, Silke Stachowitz, Christina Schnopp, Johannes 3. Oranje AP, Wolkerstorfer A, de Waard-van der Spek FB. Treatment Ring and Dietrich Abeck of erythrodermic atopic dermatitis with ‘‘wet-wrap’’ uticasone Klinik und Poliklinik fu¨r Dermatologie und Allergologie am propionate 0,05% cream/emollient 1:1 dressing. -
Siplizumab Induces NK Cell Fratricide Through Antibody-Dependent Cell
ORIGINAL RESEARCH published: 11 February 2021 doi: 10.3389/fimmu.2021.599526 Siplizumab Induces NK Cell Fratricide Through Antibody- Dependent Cell-Mediated Cytotoxicity Christian Binder 1,2*, Felix Sellberg 1,2, Filip Cvetkovski 2, Stefan Berg 2, Erik Berglund 2,3 and David Berglund 1,2 1 Department of Immunology, Genetics and Pathology, Section of Clinical Immunology, Uppsala University, Uppsala, Sweden, 2 Research and Development, ITB-Med AB, Stockholm, Sweden, 3 Division of Transplantation Surgery, Department of Clinical Science, Intervention and Technology (CLINTEC), Karolinska Institute and Karolinska University Hospital, Stockholm, Sweden The glycoprotein CD2 is expressed on T and NK cells and contributes to cell-cell conjugation, agonistic signaling and actin cytoskeleton rearrangement. CD2 has Edited by: previously been shown to have an important function in natural NK cell cytotoxicity but Carsten Watzl, to be expendable in antibody-mediated cytotoxicity. Siplizumab is a monoclonal anti-CD2 Leibniz Research Centre for Working fi Environment and Human Factors IgG1 antibody that is currently undergoing clinical trials in the eld of transplantation. This (IfADo), Germany study investigated the effect of CD2 binding and Fc g receptor binding by siplizumab (Fc- Reviewed by: active) and Fc-silent anti-CD2 monoclonal antibodies in allogeneic mixed lymphocyte John Pradeep Veluchamy, reaction and autologous lymphocyte culture. Further, induction of NK cell fratricide and VU University Medical Center, Netherlands inhibition of natural cytotoxicity as well as antibody-dependent cytotoxicity by these Kerry S. Campbell, agents were assessed. Blockade of CD2 via monoclonal antibodies in the absence of Fc g Fox Chase Cancer Center, United States receptor binding inhibited NK cell activation in allogeneic mixed lymphocyte reaction. -
Viral Rashes: New and Old Peggy Vernon, RN, MA, CPNP, DCNP, FAANP C5
Viral Rashes: New and Old Peggy Vernon, RN, MA, CPNP, DCNP, FAANP C5 Disclosures •There are no financial relationships with commercial interests to disclose Viral Rashes: New and Old •Any unlabeled/unapproved uses of drugs or products referenced will be disclosed Peggy Vernon, RN, MA, CPNP, DCNP, FAANP ©Pvernon2021 ©Pvernon2021 Restrictions Objectives • Permission granted to the 2021 National Nurse • Identify a potential sequelae from hand, foot and Practitioner Symposium and its attendees mouth disease • Describe the pattern of distribution and lesion • All rights reserved. No part of this presentation may description of varicella be reproduced, stored, or transmitted in any form or • Identify a precursor of Henoch Schonlein Purpura by any means without written permission of the author •Contact Peggy Vernon at [email protected] ©Pvernon2021 ©Pvernon2021 Viral Exanthems Morbilliform Exanthems •Morbilliform • Measles (rubeola) •Papular-nodular • Rubella •Vesiculobullous • Roseola •Petechial • Erythema Infectiosum •Purpuric • Pityriasis Rosea • Infectious Mono ©Pvernon2021 ©Pvernon2021 1 Viral Rashes: New and Old Peggy Vernon, RN, MA, CPNP, DCNP, FAANP C5 Measles (Rubeola) MEASLES (RUBEOLA) • Prodrome: fever, malaise, cough, DIFFERENTIAL DIAGNOSIS conjunctivitis. Patient appears quite ill •Other morbilliform eruptions: Rubella, • Koplik’s spots: bluish-white erythema infectiosum, pityriasis rosea, elevations on buccal mucosa infectious mono • Exanthem: erythematous •DRUG maculopapular eruption, from scalp to forehead, posterior -
Pustular Psoriasis in Children- a Review
Vol. 10, No. 1, 2012 Review Article Pustular Psoriasis in Children- a Review Malathi M 1, Thappa DM 2 1Senior Resident, 2Professor and Head, Department of Dermatology and STD, Jawaharlal Institute of Postgraduate Medical Education and Research (JIPMER), Pondicherry-605006, India Abstract Pustular psoriasis is a rare form of psoriasis in the pediatric population with the acute generalized and annular variants being the most common. There are two groups of pustular psoriasis one with a history of psoriasis vulgaris and the other without a history of psoriasis vulgaris which differ in various aspects including the age at onset and triggering factors. Several triggering factors have been implicated in generalized pustular psoriasis, the removal or treatment of which can allow the process to settle, which include upper respiratory tract and urinary tract infections, abrupt cessation of oral steroids and cyclosporine, sunburn, tar therapy, hypocalcemia and vaccination. But, generalized pustular psoriasis may present with potential life threatening complications warranting aggressive approach with various treatment modalities like retinoids, methotrexate, cyclosporine, dapsone and biologics which are frequently being used in children. However, the management issues in the pediatric age group are challenging pertaining to a host of precipitating factors, limited clinical experience with the optimal use of these agents in children, long term safety profile of these agents in the long run in children and the lack of long term follow up studies. Key words: Pustular psoriasis; children; complications; retinoids; methotrexate; cyclosporine; dapsone; biologics Correspondence: Dr. DM Thappa Professor and Head, Department of Dermatology and STD, Jawaharlal Institute of Postgraduate Medical Education and Research (JIPMER), Pondicherry-605006, India Email : [email protected] NJDVL - 1 Vol. -
Modifications to the Harmonized Tariff Schedule of the United States To
U.S. International Trade Commission COMMISSIONERS Shara L. Aranoff, Chairman Daniel R. Pearson, Vice Chairman Deanna Tanner Okun Charlotte R. Lane Irving A. Williamson Dean A. Pinkert Address all communications to Secretary to the Commission United States International Trade Commission Washington, DC 20436 U.S. International Trade Commission Washington, DC 20436 www.usitc.gov Modifications to the Harmonized Tariff Schedule of the United States to Implement the Dominican Republic- Central America-United States Free Trade Agreement With Respect to Costa Rica Publication 4038 December 2008 (This page is intentionally blank) Pursuant to the letter of request from the United States Trade Representative of December 18, 2008, set forth in the Appendix hereto, and pursuant to section 1207(a) of the Omnibus Trade and Competitiveness Act, the Commission is publishing the following modifications to the Harmonized Tariff Schedule of the United States (HTS) to implement the Dominican Republic- Central America-United States Free Trade Agreement, as approved in the Dominican Republic-Central America- United States Free Trade Agreement Implementation Act, with respect to Costa Rica. (This page is intentionally blank) Annex I Effective with respect to goods that are entered, or withdrawn from warehouse for consumption, on or after January 1, 2009, the Harmonized Tariff Schedule of the United States (HTS) is modified as provided herein, with bracketed matter included to assist in the understanding of proclaimed modifications. The following supersedes matter now in the HTS. (1). General note 4 is modified as follows: (a). by deleting from subdivision (a) the following country from the enumeration of independent beneficiary developing countries: Costa Rica (b). -
The Management of Psoriasis in Adults
DORSET MEDICINES ADVISORY GROUP THE MANAGEMENT OF PSORIASIS IN ADULTS Psoriasis is a common, genetically determined, inflammatory and proliferative disorder of the skin, the most characteristic lesions consisting of chronic, sharply demarcated, dull-red, scaly plaques, particularly on the extensor prominences and in the scalp. Self-care advice Many people's psoriasis symptoms start or become worse because of a certain event, known as a trigger. Common triggers include: • an injury to skin such as a cut, scrape, insect bite or sunburn (this is known as the Koebner response) • drinking excessive amounts of alcohol • smoking • stress • hormonal changes, particularly in women (for example during puberty and the menopause) • certain medicines such as lithium, some antimalarial medicines, anti-inflammatory medicines including ibuprofen, ACE inhibitors (used to treat high blood pressure) and beta blockers (used to treat congestive heart failure) • throat infections - in some people, usually children and young adults, a form of psoriasis called guttate psoriasis (which causes smaller pink patches, often without a lot of scaling) develops after a streptococcal throat infection, although most people who have streptococcal throat infections do not develop psoriasis • other immune disorders, such as HIV, which cause psoriasis to flare up or to appear for the first time Advice for patients can be found here Management pathway For people with any type of psoriasis assess: • disease severity • the impact of disease on physical, psychological and social wellbeing • whether they have psoriatic arthritis • the presence of comorbidities. • Consider using the Dermatology quality of life assessment: www.pcds.org.uk/p/quality-of-life Assess the severity and impact of any type of psoriasis: • at first presentation • before referral for specialist advice and at each referral point in the treatment pathway • to evaluate the efficacy of interventions. -
Dermatologic Nuances in Children with Skin of Color
5/21/2019 Dermatologic Nuances in Children with Skin of Color Candrice R. Heath, MD, FAAP, FAAD Director, Pediatric Dermatology LKSOM Temple University @DrCandriceHeath Advisory Board – Pfizer, Regeneron-Sanofi Consultant –Marketing – Unilever, Proctor & Gamble Speaker’s Bureau - Pfizer I do not intend to discuss on-FDA approved or investigational use of products in my presentation. • Recognize common hair, scalp and skin disorders that may present differently in children with skin of color • Select appropriate treatment options based upon common cultural preferences to increase adherence • Establish treatment algorithm for challenging cases 1 5/21/2019 • 2050 : Over half of the United States population will be people of color • 2050 : 1 in 3 US residents will be Hispanic • 2023 : Over half of the children in the US will be people of color • Focuses on ethnic and racial groups who have – similar skin characteristics – similar skin diseases – similar reaction patterns to those skin diseases Taylor SC et al. (2016) Defining Skin of Color. In Taylor & Kelly’s Dermatology for Skin of Color. 2016 Type I always burns, never tans (palest) Type II usually burns, tans minimally Type III sometimes mild burn, tans uniformly Type IV burns minimally, always tans well (moderate brown) Type V very rarely burns, tans very easily (dark brown) Type VI Never burns (deeply pigmented dark brown to darkest brown) 2 5/21/2019 • Black • Asian • Hispanic • Other Not so fast… • Darker skin hues • The term “race” is faulty – Race may not equal biological or genetic inheritance – There is not one gene or characteristic that separates every person of one race from another Taylor SC et al. -
Pityriasis Rosea
BMJ 2015;351:h5233 doi: 10.1136/bmj.h5233 (Published 29 October 2015) Page 1 of 6 Practice PRACTICE PRACTICE POINTER Pityriasis rosea Samantha Eisman consultant dermatologist, Rodney Sinclair professor in dermatology Sinclair Dermatology, Melbourne, VIC, 3002, Australia Pityriasis rosea is an acute exanthem that may cause patients great anxiety but is self limiting and resolves within one to three How does pityriasis rosea present? months.1 It is a distinctive erythematous oval scaly eruption of Pityriasis rosea begins in 40-76% of patients with a single herald the trunk and limbs, with minimal constitutional symptoms. patch—an asymptomatic thin oval scaly plaque often on the What causes pityriasis rosea? trunk (fig 1⇓).7 Multiple herald patches may also occur.8 The patch is usually well demarcated, 2-4 cm in diameter, The cause of pityriasis rosea is uncertain but epidemiological erythematous, salmon coloured, or hyperpigmented. A fine (seasonal variation and clustering in communities) and clinical collarette of scale is attached to the periphery of the plaque with features suggest an infective agent. Light and electron its free edge extending internally. Within days to three weeks microscopy findings suggest infection with human herpesviruses 2 the second phase begins—the appearance of numerous smaller 6 and 7 (HHV-6/7). These viral antigens have been detected lesions, which are similar in configuration but occur along the in skin lesions by immunohistochemistry and their DNA has lines of cleavage of the trunk (Christmas tree pattern; figs 2⇓ been isolated from non-lesional skin, peripheral blood 3 and 3⇓). The rash typically lasts five weeks; it resolves within mononuclear cells, serum, and saliva samples. -
Immune Response Patterns in Non‐Communicable Inflammatory Skin
DOI: 10.1111/jdv.14673 JEADV REVIEW ARTICLE Immune response patterns in non-communicable inflammatory skin diseases K. Eyerich,1,* S. Eyerich2 1Department of Dermatology and Allergy, Technical University of Munich, Munich, Germany 2ZAUM – Center of Allergy and Environment, Technical University and Helmholtz Center Munich, Munich, Germany *Correspondence: K. Eyerich. E-mail: [email protected] Abstract Non-communicable inflammatory skin diseases (ncISD) such as psoriasis or atopic eczema are a major cause of global disease burden. Due to their impact and complexity, ncISD represent a major challenge of modern medicine. Dermatol- ogy textbooks describe more than 100 different ncISD based on clinical phenotype and histological architecture. In the last decades, this historical description was complemented by increasing molecular knowledge – and this knowledge is now being translated into specific therapeutics. Combining the enormous advances made in lymphocyte immunology and molecular genetics with clinical and histological phenotyping reveals six immune response patterns of the skin – type I immune cells cause the lichenoid pattern characterized by immune-mediated cell death of keratinocytes; type II immune cells underlie the eczematous pattern with impaired epidermal barrier, infection and eosinophils as well as the bullous pattern with loss of epithelial integrity; Th17 cells and ILC3 mediate the psoriatic pattern characterized by acan- thosis, high metabolic activity and neutrophils; dysbalance of regulatory T cells causes either the fibrogenic pattern with rarefication of cells and dermal thickening or the granulomatous pattern defined by formation of granulomas. With more and more specific therapeutic agents approved, classifying ncISD also according to their immune response pattern will become highly relevant.