Incidental Focal Acantholytic Dyskeratosis in the Setting of Rosacea
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Paraneoplastic Syndrome Presenting As Giant Porokeratosis in a Patient with Nasopharyngeal Cancer
Paraneoplastic Syndrome Presenting As Giant Porokeratosis in A Patient with Nasopharyngeal Cancer Fitri Azizah, Sonia Hanifati, Sri Adi Sularsito, Lili Legiawati, Shannaz Nadia Yusharyahya, Rahadi Rihatmadja Department of Dermatology and Venereology, Faculty of Medicine Universitas Indonesia / Dr. Cipto Mangunkusumo National General Hospital Keywords: porokeratosis, giant porokeratosis, paraneoplastic syndrome, nasopharyngeal Abstract: Giant porokeratosis is a rare condition in which the hyperkeratotic plaques of porokeratosis reach up to 20 cm in diameter. Porokeratosis is characterized clinically by hyperkeratotic papules or plaques with a thread-like elevated border. Although rare, porokeratosis has been reported in conjunction with malignancies suggesting a paraneoplastic nature. Associated malignancies reported were hematopoietic, hepatocellular, and cholangiocarcinoma. We report a case of giant porokeratosis in a patient with nasopharyngeal cancer responding to removal of the primary cancer by chemoradiotherapy. 1 INTRODUCTION regress completely after the treatment of malignancy, suggestive of paraneoplastic syndrome. Porokeratosis is a chronic progressive disorder of keratinization, characterized by hyperkeratotic papules or plaques surrounded by a thread-like 2 CASE elevated border corresponds to a typical histologic hallmark, the cornoid lamella . O regan, 2012) There Mr. SS, 68-year-old, was referred for evaluation of are at least six clinical variants of porokeratosis pruritic, slightly erythematous plaques with raised, recognized with known genetic disorder.1 Some hyperpigmented border of one and a half year clinical variant of porokeratosis has been reported in duration on the extensor surface of both legs. The the setting of immunosuppressive conditions, organ lesions shown minimal response to potent topical transplantation, use of systemic corticosteroids, and corticosteroids and phototherapy given during the infections, suggesting that impaired immunity may last 8 months in another hospital. -
Features of Reactive White Lesions of the Oral Mucosa
Head and Neck Pathology (2019) 13:16–24 https://doi.org/10.1007/s12105-018-0986-3 SPECIAL ISSUE: COLORS AND TEXTURES, A REVIEW OF ORAL MUCOSAL ENTITIES Frictional Keratosis, Contact Keratosis and Smokeless Tobacco Keratosis: Features of Reactive White Lesions of the Oral Mucosa Susan Müller1 Received: 21 September 2018 / Accepted: 2 November 2018 / Published online: 22 January 2019 © Springer Science+Business Media, LLC, part of Springer Nature 2019 Abstract White lesions of the oral cavity are quite common and can have a variety of etiologies, both benign and malignant. Although the vast majority of publications focus on leukoplakia and other potentially malignant lesions, most oral lesions that appear white are benign. This review will focus exclusively on reactive white oral lesions. Included in the discussion are frictional keratoses, irritant contact stomatitis, and smokeless tobacco keratoses. Leukoedema and hereditary genodermatoses that may enter in the clinical differential diagnoses of frictional keratoses including white sponge nevus and hereditary benign intraepithelial dyskeratosis will be reviewed. Many products can result in contact stomatitis. Dentrifice-related stomatitis, contact reactions to amalgam and cinnamon can cause keratotic lesions. Each of these lesions have microscopic findings that can assist in patient management. Keywords Leukoplakia · Frictional keratosis · Smokeless tobacco keratosis · Stomatitis · Leukoedema · Cinnamon Introduction white lesions including infective and non-infective causes will be discussed -
Review an Overview of the Pale and Clear Cells of the Nipple Epidermis
Histol Histopathol (2009) 24: 367-376 Histology and http://www.hh.um.es Histopathology Cellular and Molecular Biology Review An overview of the pale and clear cells of the nipple epidermis M.F. Garijo, D. Val and J.F. Val-Bernal Department of Anatomical Pathology, Marqués de Valdecilla University Hospital, Medical Faculty, University of Cantabria, Santander, Spain Summary. The stratified squamous epithelium of the exterior. In the non-lactating breast these duct openings nipple-areola complex may contain pale or clear cells are usually filled with plugs of keratin. The nipple and including: Paget’s disease cells (PDCs), Toker cells areola are covered by keratinizing stratified squamous (TCs), and so-called clear cells (CCs). Paget’s disease is epithelium similar to that seen in the epidermis an uncommon presentation of breast carcinoma. PDCs elsewhere in the body. The collecting ducts show a are large, atypical, have abundant, pale-staining double epithelial and myoepithelial lining. The cytoplasm that may contain mucin secretion vacuoles epithelium is columnar and the myoepithelial cells lie and bulky heterochromatic nuclei. They are commonly between the epithelial layer and the basal lamina. A concentrated along the basal layer and stain for EMA, cross section of the major ducts shows an irregular, CAM5.2, cytokeratin 7, and HER2/neu oncoprotein. TCs pleated or serrated outline and an investment with are bland cells with roundish and scant chromatin nuclei. muscular tissue. The areola dermis contains numerous They are found incidentally and are reactive for EMA, sebaceous glands. Some of them open directly onto the CAM5.2, and cytokeratin 7, but show negativity for surface, whereas others drain into a collecting duct or HER2/neu oncoprotein. -
An Update on the Biology and Management of Dyskeratosis Congenita and Related Telomere Biology Disorders
Expert Review of Hematology ISSN: 1747-4086 (Print) 1747-4094 (Online) Journal homepage: https://www.tandfonline.com/loi/ierr20 An update on the biology and management of dyskeratosis congenita and related telomere biology disorders Marena R. Niewisch & Sharon A. Savage To cite this article: Marena R. Niewisch & Sharon A. Savage (2019) An update on the biology and management of dyskeratosis congenita and related telomere biology disorders, Expert Review of Hematology, 12:12, 1037-1052, DOI: 10.1080/17474086.2019.1662720 To link to this article: https://doi.org/10.1080/17474086.2019.1662720 Accepted author version posted online: 03 Sep 2019. Published online: 10 Sep 2019. Submit your article to this journal Article views: 146 View related articles View Crossmark data Citing articles: 1 View citing articles Full Terms & Conditions of access and use can be found at https://www.tandfonline.com/action/journalInformation?journalCode=ierr20 EXPERT REVIEW OF HEMATOLOGY 2019, VOL. 12, NO. 12, 1037–1052 https://doi.org/10.1080/17474086.2019.1662720 REVIEW An update on the biology and management of dyskeratosis congenita and related telomere biology disorders Marena R. Niewisch and Sharon A. Savage Clinical Genetics Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA ABSTRACT ARTICLE HISTORY Introduction: Telomere biology disorders (TBDs) encompass a group of illnesses caused by germline Received 14 June 2019 mutations in genes regulating telomere maintenance, resulting in very short telomeres. Possible TBD Accepted 29 August 2019 manifestations range from complex multisystem disorders with onset in childhood such as dyskeratosis KEYWORDS congenita (DC), Hoyeraal-Hreidarsson syndrome, Revesz syndrome and Coats plus to adults presenting Telomere; dyskeratosis with one or two DC-related features. -
Progressive Widespread Warty Skin Growths
DERMATOPATHOLOGY DIAGNOSIS Progressive Widespread Warty Skin Growths Patrick M. Kupiec, BS; Eric W. Hossler, MD Eligible for 1 MOC SA Credit From the ABD This Dermatopathology Diagnosis article in our print edition is eligible for 1 self-assessment credit for Maintenance of Certification from the American Board of Dermatology (ABD). After completing this activity, diplomates can visit the ABD website (http://www.abderm.org) to self-report the credits under the activity title “Cutis Dermatopathology Diagnosis.” You may report the credit after each activity is completed or after accumu- lating multiple credits. A 33-year-old man presented with progres- sive widespread warty skin growths that had been present copysince 6 years of age. Physical examination revealed numerous verrucous papules on the face and neck along with Figure 1. H&E, original magnification ×40. Figure 2. H&E, original magnification ×40. verrucous, tan-pink papules and plaques diffuselynot scattered on the trunk, arms, and legs. A biopsy of a lesion on the neck Dowas performed. H&E, original magnification ×200. The best diagnosisCUTIS is: a. condyloma acuminatum b. epidermodysplasia verruciformis c. herpesvirus infection d. molluscum contagiosum e. verruca vulgaris PLEASE TURN TO PAGE 99 FOR DERMATOPATHOLOGY DIAGNOSIS DISCUSSION Mr. Kupiec is from the State University of New York (SUNY) Upstate Medical University, Syracuse. Dr. Hossler is from the Departments of Dermatology and Pathology, Geisinger Medical Center, Danville, Pennsylvania. The authors report no conflict of interest. Correspondence: Patrick M. Kupiec, BS, 50 Presidential Plaza, Syracuse, NY 13202 ([email protected]). 82 CUTIS® WWW.CUTIS.COM Copyright Cutis 2017. No part of this publication may be reproduced, stored, or transmitted without the prior written permission of the Publisher. -
Cutaneous Adverse Reaction to Infliximab: Report of Psoriasis Developing in 3 Patients
THERAPEUTICS FOR THE CLINICIAN Cutaneous Adverse Reaction to Infliximab: Report of Psoriasis Developing in 3 Patients Gregg A. Severs, DO; Tara H. Lawlor, DO; Stephen M. Purcell, DO; Donald J. Adler, DO; Robert Thompson, MD Infliximab is a chimeric immunoglobulin G1k nfliximab is a chimeric immunoglobulin monoclonal antibody against tumor necrosis fac- G1k monoclonal antibody (75% human and tor a (TNF-a), a proinflammatory cytokine that I 25% mouse origin) against tumor necrosis participates in both normal immune function and factor a (TNF-a). It neutralizes the biologic activity the pathogenesis of many autoimmune disorders. of TNF-a by directly binding to soluble and trans- Treatment with infliximab reduces the biologic membrane TNF-a molecules in the plasma and activities of TNF-a and thus is indicated in the on the surface of macrophages and T cells in dis- treatment of rheumatoid arthritis, Crohn disease, eased tissue. The binding destroys these TNF-a ankylosing spondylitis, psoriatic arthritis, plaque molecules via antibody-dependent cellular toxicity psoriasis, and ulcerative colitis. and complement-dependent cytotoxic mechanisms. To our knowledge, there have been 13 case Thus, infliximab decreases the actions of TNF-a, reports of new-onset psoriasis, psoriasiform der- which include induction of proinflammatory cyto- matitis, and palmoplantar pustular psoriasis that kines such as interleukins (IL) 1 and 6; enhancement developed during treatment with infliximab. We of leukocyte migration by increasing endothelial layer report 3 additional cases of biopsy-proven new- permeability and expression of adhesion molecules onset psoriasis that developed while the patients by endothelial cells and leukocytes; activation of underwent treatment with infliximab for inflamma- neutrophil and eosinophil functional activity; induc- tory bowel disease. -
Diffuse Drug-Induced Dermatitis Following Sclerotherapy for Telangiectasias Libby MW, Caitlin WH, Deniz OA and Heller JA*
Case Report iMedPub Journals Journal of Vascular and Endovascular Surgery 2016 http://www.imedpub.com/ Vol.1 No.3:17 DOI: 10.21767/2573-4482.100017 Diffuse Drug-Induced Dermatitis following Sclerotherapy for Telangiectasias Libby MW, Caitlin WH, Deniz OA and Heller JA* Department of Surgery, Johns Hopkins Vein Center, Johns Hopkins Medical Centers, Baltimore, USA *Corresponding author: Jennifer A Heller, 10755 Falls Road, Pavilion 1 Suite 360, Lutherville, MD 21903, Tel: 4105500415; Email: [email protected] Received date: June 14, 2016; Accepted date: July 26, 2016; Published date: August 02, 2016 Copyright: © 2016 Libby MW, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Abstract Sclerotherapy is an effective treatment modality for the management of lower extremity telangiectasias. Although localized dermatologic reactions are known complications of this procedure, systemic reactions are rare. Here, we present a case of a diffuse drug eruption following sclerotherapy for the treatment of bilateral lower extremity telangiectasias. Salient clinical and physical exam findings are described. Management strategies for the treatment of drug eruptions are outlined. This is the first case report that we know of describing a diffuse drug eruption associated with sclerotherapy. It is important to recognize the possibility of diffuse drug eruptions secondary to sclerotherapy treatment so that expectant management may be initiated expeditiously in affected patients. Figure 1: Drug eruption following sclerotherapy. The patient was referred for evaluation by a dermatologist, Case Report who initially diagnosed diffuse dermatitis based on clinical A 64-year-old woman with hypertension and bilateral lower exam. -