Copyrighted Material

Total Page:16

File Type:pdf, Size:1020Kb

Copyrighted Material Index Note: Page references in italics refer to Figures; those in bold refer to Tables 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) 87 future of 25–6 3β-hydroxysteroid dehydrogenase 45 grading xxvi-xxvii 4-n-butylresorcinol 140 management 21–4 5-aminolevulinic acid (ALA) 138 nicotine and 91 5-fluorouracil 107 photodamage in 91 5α-androstan-3β-ol-17-one 81 post-rupture 15 5α-androstanedione 81 pre-rupture 15 5α-androstene-3β, 17β-diol 81 punch ablation, debridement in 17 5α-dihydrotestosterone (5α-DHT) 48–9, 67 terminology xxiii–xxvi 5α-pregnan-3β-ol-20-one 81 therapeutic choices 185–6 5α-pregnanedione 69, 81, 148 unroofing technique 17, 18 5α-reductase 45, 48 vs acne vulgaris 18–21 5α-reductase inhibitors 147–8 acne keloidalis 63 7-dehydrocholesterol (7-DHC) 150 acne rosacea xiii, xxiv, 3–12 7α,11β-dimethyl-19-nortestosterone 87 adaptive immune reaction 4 11β-methyl-19-nortestosterone 87 classification and staging 187–9 17α-hydroxylase, 45 erythema in 4–6 17α-lyase 45 functional 4, 6 17β-hydroxysteroid dehydrogenase 45, 48, 49 inflammatory 4, 6 structural 4–6 abscess 153 fibrosis in 6–7 acamprosate 87 genetics 34 Accutane® 114, 124, 127, 128, 136, 171 grading xxvi Aché tribe, Paraguay inflammatory epiphenomena in 8–12 abhorrence of milk 80, 82, 89, 174 innate immune reaction 4 photodamage 163 ocular rosacea in 7 acitretin xiv, xiv, 127 pathogenesis 56–7 in acne keloidalis 63 terminology xxii–xxiii acne agminata 137 therapeutic choices 185 acne climacterica (menopausal acne) 75, 78 total sun avoidance 110 acne conglobata xxii, 135 ultraviolet A 7–8 acné excoriée des jeunes filles, l' 65–6,COPYRIGHTED 98 acne MATERIAL varioliformis 128, 132 acne fulminans xxii acne vulgaris xx, 1–3 acne inversa genetics 31–4 genetics 34 grading xxvi acne inversa/hidradenitis suppurativa (AI/HS) xiii, xxiii, xxv, incidence 1 12–26, 57–60 pathogenesis 54–6 avoiding recurrence 25 terminology xxi-xxii, 1–2 foreign materials in 15–18 therapeutic choices 184–5 Acne: Causes and Practical Management, First Edition. F. William Danby. © 2015 John Wiley & Sons, Ltd. Published 2015 by John Wiley & Sons, Ltd. 215 0002211741.indd 215 11/5/2014 11:16:10 AM 216 Index acneform eruptions 64, 87, 89 beta-lactoglobulin 106 acnegens 87–92 biologics 137 Acnomel® 121 bipolar disorder 124 actinic telangiectasia 4–6, 7, 8, 163 birth control pills (BCPs) 139, 141–2 Aczone® blackhead see open comedo in pregnancy 176, 178 blepharitis 133, 134–5, 134 adalimumab (Humira®) 22, 23 body dysmorphic disorder 125 adapalene xiv 119, 139 Botox® 132 adrenal corticotropic hormone (ACTH) 26–7 bovine somatotropin (BST) 112 adrenal glands 26 bovine spongiform encephalopathy 113 age, women, acne in 74–5 brentuximab 64, 65 aging 91 bromine 89 Akt kinase 50 bromoderma 36, 89 aldosterone 144 burning out of acne 3 all-trans retinoic acid 118 bystander suppression 164 alopecia, androgenic 75 alpha-hydroxy acids 120 calcium supplementation 114 alpha lactalbumin 106 Candida 11, 56, 58, 61, 98, 99 amoxicillin 94, 129 Candida albicans, radiation and 163 in acne keloidalis 63 Candida vulvovaginitis 62 ampicillin 94, 129 carbohydrates 115–16 anabolic steroids 45 versus dairy load 83–4 in mothers' milk 72–4 casein 90–1, 90 as muscle makers 74 cefadroxil in acne keloidalis 63 analgesics, narcotic 22 cheese 112 androgen receptor blockade 143–7 chloracne 87 androgens 40, 67–8 chocolate 89–90 antibiotic-resistant acne 94 ciprofloxacin 94 antibiotics as anti-inflammatories 128 clarithromycin 94 in acne vulgaris 128–9 Clearasil® 121 in acne rosacea 129 clindamycin 22, 60, 94, 128, 129 in acne inversa 129 closed comedo xiii, xx, xxi, xxii, 61 in dissecting terminal folliculitis (DTF) and acne retinoids 118, 118 keloidalis 129–30 surgery 151 as antibiotics 130 combination vacuum suction–phototherapy machine 152 antigens 55, 104 comedolytics 117–28 antihistamines 62 standard topical 118–20 anti-inflammatories 128–37 systemic 121–8 antimicrobials 128–37 unclassifed topicals 120–1 apocrine sweat glands 1 comedones (comedo) xiii–xiv, xv APSEA (Assessment of the Psychological and Social Effects see closed comedo; open comedo of Acne) 27 competitive inhibition 144 arbutin 141 Comprehensive Acne Severity Scale (CASS) xxvi atopic dermatitis 10, 11, 95, 97, 97 conglobate acne see acne conglobata Aureomycin® 128 contraceptives, oral 183 azelaic acid 94, 120–1 controversies azithromycin 94, 128–9 acne rosacea classification and staging 187–9 in pregnancy 177 dairy vs carbohydrate 189–91 corpus luteum Bacillus oleronius 9, 185 cyst 68 benzoyl peroxide xiv, 119–20 persistent 68 beta-hydroxy acid 120 cortexolone 17α-propionate 147 0002211741.indd 216 11/5/2014 11:16:10 AM Index 217 corticosteroids 135–7, 182–3 drospirenone xii, 75, 76–7, 142, 143, 144, 146–7 in pregnancy 178 ductal keratinocytes 38 corticotropin-releasing hormone (CRH) 26–7, 27 ductus seboglandularis (sebaceous gland duct).43 Corynebacterium acnes see Propionibacterium acnes dutasteride xii, 147–8, 149 Coumadin 131 in pregnancy 179 Crohn's disease 158 crotamiton 134, 185 eccrine sweat glands 1 cyproterone acetate 76, 142, 146 Elimite® 134 cytosol 50 emblica extract 141 end organ responsiveness 51 dairy intolerance 82–3 endocrine imitators and disruptors 87–8 dairy products xii, 112–15 endocrine-disrupting chemicals (EDCs) 87 see also milk endogenous hormones 45, 67–72 dairy vs carbohydrate controversy 191 Enovid® 74, 142 damage-associated molecular pattern molecules (DAMPs) 55 environmental contamination 88 dandruff 95 environmental management 109 dapsone xiv eosinophilic pustular folliculitis see Ofuji's disease in acne keloidalis 63 epidermal growth factor receptor inhibitor eruption 64–5 in Ofuji's disease 62 epidermal growth factor receptor (EGFR) inhibitors 87 oral 137 epidermoid cyst xxii, 16 in pregnancy 176, 178 epigenetics 33 topical 128 epinephrine (adrenalin) 26 dehiscence 159 epiphenomena 3, 105 dehydroepiandrosterone (DHEA) 67 erythematotelangiectatic rosacea xxii, 12, 187 dehydroepiandrosterone sulfate (DHEAS) 25, 67 erythromycin 60, 94, 128, 176 Demodecosis 12 in pregnancy 177 Demodex xxiv, 4, 9, 9, 56, 99–101 estradiol (E2) xii, 68, 142 sampling 100 estriol (E3) 68, 142 Demodex folliculorum 99–100 estrogens 68–9 desogestrel 75, 76 birth control pill 142, 74–5 diabetes 69–70, 144, 158, 159 side effects 142–3 Type I 70 estrone (E1) 68, 142 Type II 70, 71, 183 ethinyl estradiol (EE2) 74, 142 see also insulin etonogestrel 77 Diane® 35, 142, 146 Eurax® 134 Dianette® 146 exogenous hormones 45, 72–84, 72 diet xii, 111–17, 148–9 anabolic steroids 72–3 impact of 80–1 oral contraceptive hormones 74–84 see also dairy products; milk experienced-based medicine (XBM) 111 Differin® 119 diformazan 48 Favre–Racouchot syndrome (solar elastosis with dihydrotestosterone (DHT) 45, 47–9, 54, 67 comedones) 7–8, 41, 91 minimization 147–9 finasteride 147 dimethandrolone 87 in pregnancy 178 dioxins 47 fluconazole 129 diphtheria toxin 132 fluctuant nodule 153 dissecting folliculitis of the scalp xxv, xxv, 63, 135 flutamide 146 dissecting terminal folliculitis 63 in pregnancy 178–9 dl-norgestrel 75 follicle stimulating hormone (FSH) 142 Dowling–Degos disease lesions 158 follicular canal xix doxycycline 22, 60, 62, 94, 128, 129, 133, 139 follicular occlusion tetrad xxvi draining nodule 153 follicular tetrad 63 0002211741.indd 217 11/5/2014 11:16:11 AM 218 Index folliculitis 87 hair follicle xx folliculopapules 3 hidradenitis suppurativa see acne inversa/hidradenitis central facial xiii suppurativa monomorphic 61 high-fructose corn syrup (HFCS) 116 folliculopilosebaceous units (FPSUs) xv, xx, xxi, 1, 7, 31–52 hirsutism 75 anatomy 31, 32 history xviii biochemistry 44–5 homogentisic acid 140 embryology 36–7 hormone manipulations and therapy 141–50 epigenetics 35–6 hormone replacement therapy (HRT) 75 FoxO1 and mTORC1 49–52, 51 hormone-free milk 82 genetics 31–5 hormones xii-xiii acne vulgaris 31–4 Hurley's three-stage system xxvi, 17–18 acne rosacea 34 hydroquinone 139, 140 acne inversa 34 hyperinsulinemia 115–16 histology 38–42 hypertrophic scars xvi, xvii, xxii, xxiii, 107, 153 hormones, enzymes, receptors and intracrine system hypoxia-inducible factor 1 (HIF-1) 44, 93 45–9 physiology 42–4 iatrosacea 136 hair 42 ibuprofen 137 oil 42–3 in pregnancy 178 follicle 43–4 ice cream 81 folliculopustules xiii, xiv, xv, 3 Implanon® 77, 78 monomorphic 61 indomethacin 62 Follikel-Filament 1, 3 inflammatory response 103–7 foods 88–91 adaptive (acquired) immunity 104 see also dairy products; diet; milk allergy (shared antigens) 106 FoxO1 49–52, 51, 69 as primary acnegen 104–5 functional androgenic hyper-responsiveness to ACTH 26 innate immunity 103–4 fusidic acid 94 mediators, cellular and humoral, and neuroimmunology 105–6 gamma rays 163 pigment, and post-inflammatory hyperpigmentation 106–7 gene therapy 58 scarring 107 genetics xii infliximab (Remicade®) 137 genotype 33 insulin 69–71, 81–2 gestagens 141 insulin and IGF-1 stimulation (IIS) 51 gestodene 76 insulin resistance 70, 71, 117 glassy membrane 163 insulin-like growth factor-1 (IGF-1) 69, 72, 82, 84, 94, 110 Global Acne Grading System (GAGS) xxvi insulin-like growth factor-1 signaling (IIS) 83, 84 Global Acne Severity Scale (GEA Scale) xxvi intense pulsed light (IPL) 165 glucose-dependent insulinotropic polypeptide (GIP) 70–1, 82, interleukins 84, 115 IL-1 105 glutathione 141 IL-8 190 glycation 91 IL-17 22 glycemic index 83–4 IL-23 22 glycemic load 115–16 intracrine system 45, 46, 48–9 glycolic acid in pregnancy 177 intrafollicular flora 55 glycolysis 116 intrauterine devices 78 grading xx-xxvii intravaginal devices
Recommended publications
  • Blood Plasma Bromide Levels in Bromoderma' Lester W
    BLOOD PLASMA BROMIDE LEVELS IN BROMODERMA' LESTER W. KIMBERLY, M.D.2 (Received for publication May 16, 1939) The ordinary cutaneous manifestations of bromide eruptions are well known. Numerous reports have appeared in the litera- ture supporting various theories as to the development of cutane- ous lesions due to bromides but practically no one has studied the plasma bromide levels with relation to bromoderma. Hanes and Yates (1) found approximately 0.9 per cent of the total admissions to Duke Hospital had increased amounts of bromide in their plasma. They also found that 28 per cent of 64 patients with blood serum bromides above 200 mgm. had bromoderma. The percentage of patients with significantly elevated plasma bromides is even higher among patients admitted to psychopathic hospitals. Szadek (2) believed that the cutaneous eruption originated from an irritation of the sebaceous glands. Laudenheimer (3) and Von Wyss (4) thought that the ingestion of bromide led to a gradual retention of the drug in the tissues and the replacement of the chloride. Engman and Mook (5) felt that the lesions were more apt to occur at the site of previous inflammation and that trauma might play a part, thereby explaining the predilection of a bromoderma for old seborrheic or acne areas. Wile (6) stated that he was unable to demonstrate the drug in the content of the lesions and he believed that it was not present unless there was an admixture of blood serum. Bloch and Tenchio (7) considered bromoderma to be an idiosyncratic phenome- non of the skin and mucous membranes brought about by sensitization.
    [Show full text]
  • Nonbacterial Pus-Forming Diseases of the Skin Robert Jackson,* M.D., F.R.C.P[C], Ottawa, Ont
    Nonbacterial pus-forming diseases of the skin Robert Jackson,* m.d., f.r.c.p[c], Ottawa, Ont. Summary: The formation of pus as a Things are not always what they seem Fungus result of an inflammatory response Phaedrus to a bacterial infection is well known. North American blastomycosis, so- Not so well appreciated, however, The purpose of this article is to clarify called deep mycosis, can present with a is the fact that many other nonbacterial the clinical significance of the forma¬ verrucous proliferating and papilloma- agents such as certain fungi, viruses tion of pus in various skin diseases. tous plaque in which can be seen, par- and parasites may provoke pus Usually the presence of pus in or on formation in the skin. Also heat, the skin indicates a bacterial infection. Table I.Causes of nonbacterial topical applications, systemically However, by no means is this always pus-forming skin diseases administered drugs and some injected true. From a diagnostic and therapeutic Fungus materials can do likewise. Numerous point of view it is important that physi¬ skin diseases of unknown etiology cians be aware of the nonbacterial such as pustular acne vulgaris, causes of pus-forming skin diseases. North American blastomycosis pustular psoriasis and pustular A few definitions are required. Pus dermatitis herpetiformis can have is a yellowish [green]-white, opaque, lymphangitic sporotrichosis bacteriologically sterile pustules. The somewhat viscid matter (S.O.E.D.). Pus- cervicofacial actinomycosis importance of considering nonbacterial forming diseases are those in which Intermediate causes of pus-forming conditions of pus can be seen macroscopicaily.
    [Show full text]
  • Date: 1/9/2017 Question: Botulism Is an Uncommon Disorder Caused By
    6728 Old McLean Village Drive, McLean, VA 22101 Tel: 571.488.6000 Fax: 703.556.8729 www.clintox.org Date: 1/9/2017 Question: Botulism is an uncommon disorder caused by toxins produced by Clostridium botulinum. Seven subtypes of botulinum toxin exist (subtypes A, B, C, D, E, F and G). Which subtypes have been noted to cause human disease and which ones have been reported to cause infant botulism specifically in the United States? Answer: According to the cited reference “Only subtypes A, B, E and F cause disease in humans, and almost all cases of infant botulism in the United States are caused by subtypes A and B. Botulinum-like toxins E and F are produced by Clostridium baratii and Clostridium butyricum and are only rarely implicated in infant botulism” (Rosow RK and Strober JB. Infant botulism: Review and clinical update. 2015 Pediatr Neurol 52: 487-492) Date: 1/10/2017 Question: A variety of clinical forms of botulism have been recognized. These include wound botulism, food borne botulism, and infant botulism. What is the most common form of botulism reported in the United States? Answer: According to the cited reference, “In the United States, infant botulism is by far the most common form [of botulism], constituting approximately 65% of reported botulism cases per year. Outside the United States, infant botulism is less common.” (Rosow RK and Strober JB. Infant botulism: Review and clinical update. 2015 Pediatr Neurol 52: 487-492) Date: 1/11/2017 Question: Which foodborne pathogen accounts for approximately 20 percent of bacterial meningitis in individuals older than 60 years of age and has been associated with unpasteurized milk and soft cheese ingestion? Answer: According to the cited reference, “Listeria monocytogenes, a gram-positive rod, is a foodborne pathogen with a tropism for the central nervous system.
    [Show full text]
  • 5 Allergic Diseases (And Differential Diagnoses)
    Chapter 5 5 Allergic Diseases (and Differential Diagnoses) 5.1 Diseases with Possible IgE Involve- tions (combination of type I and type IVb reac- ment (“Immediate-Type Allergies”) tions). Atopic eczema will be discussed in a separate section (see Sect. 5.5.3). There are many allergic diseases manifesting in The maximal manifestation of IgE-mediated different organs and on the basis of different immediate-type allergic reaction is anaphylax- pathomechanisms (see Sect. 1.3). The most is. In the development of clinical symptoms, common allergies develop via IgE antibodies different organs may be involved and symp- and manifest within minutes to hours after al- toms of well-known allergic diseases of skin lergen contact (“immediate-type reactions”). and mucous membranes [also called “shock Not infrequently, there are biphasic (dual) re- fragments” (Karl Hansen)] may occur accord- action patterns when after a strong immediate ing to the severity (see Sect. 5.1.4). reactioninthecourseof6–12harenewedhy- persensitivity reaction (late-phase reaction, LPR) occurs which is triggered by IgE, but am- 5.1.1 Allergic Rhinitis plified by recruitment of additional cells and 5.1.1.1 Introduction mediators.TheseLPRshavetobedistin- guished from classic delayed-type hypersensi- Apart from being an aesthetic organ, the nose tivity (DTH) reactions (type IV reactions) (see has several very interesting functions (Ta- Sect. 5.5). ble 5.1). It is true that people can live without What may be confusing for the inexperi- breathing through the nose, but disturbance of enced physician is familiar to the allergist: The this function can lead to disease. Here we are same symptoms of immediate-type reactions interested mostly in defense functions against are observed without immune phenomena particles and irritants (physical or chemical) (skin tests or IgE antibodies) being detectable.
    [Show full text]
  • Rosacea with Extensive Extrafacial Lesions Teresa M
    CORE Metadata, citation and similar papers at core.ac.uk Provided by Repositório Comum CaseBlackwellOxford,IJDInternational0011-9059©XXX 2007 TheUK Publishing International Journal Ltdof Dermatology Society of Dermatology report RosaceaExtrafacialPereiraCase report et al. rosacea; Rosacea with extensive extrafacial lesions Teresa M. Pereira, Ana Paula Vieira, and A. Sousa Basto From the Department of Dermatology and Abstract Venereology, Hospital de São Marcos, Braga, Rosacea is a very common skin disorder in the clinical practice that primarily affects the convex Portugal areas of the face. Extrafacial rosacea lesions have occasionally been described, but extensive involvement is exceptional. In the absence of its typical clinical or histological features, the Correspondence Teresa M. Pereira, MD diagnosis of extrafacial rosacea may be problematic. We describe an unusual case of rosacea Department of Dermatology and Venereology with very exuberant extrafacial lesions, when compared with the limited involvement of the face. Hospital de São Marcos Apartado 2242 4701-965 Braga Portugal E-mail: [email protected] Bacteriological and mycological tests of the contents of Introduction the pustules were negative. Baseline investigations, including Rosacea is a skin disorder frequently observed in the clinical complete blood count, liver and renal functions, autoimmune practice. It is characterized by the primary involvement of screen, serology for human immunodeficiency virus, and urine convex areas of the face.1 However, a wide spectrum of clin- bromides and iodides levels were negative or normal. Photo- ical findings is often observed.2 We describe an unusual case testing with ultraviolet A (100 J/cm2 daily) and ultraviolet B of rosacea with exuberant extrafacial involvement.
    [Show full text]
  • (12) United States Patent (10) Patent No.: US 7,359,748 B1 Drugge (45) Date of Patent: Apr
    USOO7359748B1 (12) United States Patent (10) Patent No.: US 7,359,748 B1 Drugge (45) Date of Patent: Apr. 15, 2008 (54) APPARATUS FOR TOTAL IMMERSION 6,339,216 B1* 1/2002 Wake ..................... 250,214. A PHOTOGRAPHY 6,397,091 B2 * 5/2002 Diab et al. .................. 600,323 6,556,858 B1 * 4/2003 Zeman ............. ... 600,473 (76) Inventor: Rhett Drugge, 50 Glenbrook Rd., Suite 6,597,941 B2. T/2003 Fontenot et al. ............ 600/473 1C, Stamford, NH (US) 06902-2914 7,092,014 B1 8/2006 Li et al. .................. 348.218.1 (*) Notice: Subject to any disclaimer, the term of this k cited. by examiner patent is extended or adjusted under 35 Primary Examiner Daniel Robinson U.S.C. 154(b) by 802 days. (74) Attorney, Agent, or Firm—McCarter & English, LLP (21) Appl. No.: 09/625,712 (57) ABSTRACT (22) Filed: Jul. 26, 2000 Total Immersion Photography (TIP) is disclosed, preferably for the use of screening for various medical and cosmetic (51) Int. Cl. conditions. TIP, in a preferred embodiment, comprises an A6 IB 6/00 (2006.01) enclosed structure that may be sized in accordance with an (52) U.S. Cl. ....................................... 600/476; 600/477 entire person, or individual body parts. Disposed therein are (58) Field of Classification Search ................ 600/476, a plurality of imaging means which may gather a variety of 600/162,407, 477, 478,479, 480; A61 B 6/00 information, e.g., chemical, light, temperature, etc. In a See application file for complete search history. preferred embodiment, a computer and plurality of USB (56) References Cited hubs are used to remotely operate and control digital cam eras.
    [Show full text]
  • Histopathologic Evaluation of Acneiform Eruptions: Practical Algorithmic Proposal for Acne Lesions 141
    Provisional chapter Chapter 10 Histopathologic Evaluation of Acneiform Eruptions: HistopathologicPractical Algorithmic Evaluation Proposal of Acneiformfor Acne Lesions Eruptions: Practical Algorithmic Proposal for Acne Lesions Murat Alper and Fatma Aksoy Khurami Murat Alper and Fatma Aksoy Khurami Additional information is available at the end of the chapter Additional information is available at the end of the chapter http://dx.doi.org/10.5772/65494 Abstract Acneiform lesions are encountered in different chapters in various dermatology and der- matopathology textbooks. The most common titles used for these disorders are diseases of the hair, diseases of cutaneous appendages, folliculitis, acne, and inflammatory lesions of dermis and epidermis. In this chapter, first of all we will discuss folliculitis, and then acne vulgaris that is a kind of folliculitis will be described. After acne vulgaris, other acneiform eruptions and demodicosis will be studied. At the end, simple algorithmic schemes by assembling clinical, pathological, and microbiological data will be shared. Keywords: acneiform lesions, algorithm, histopathologic evaluation 1. Introduction 1.1. Histology of pilar unit Pilar unit is a structure generally made up of three subunits which are hair follicle, seba- ceous gland, and arrector pili muscle. Hair follicle is divided in to three parts: infundibulum, isthmus, and inferior part. Infundibulum extends between entrance of sebaceous gland duct to the follicular orifice in epidermis. Isthmus: extends between entrance of sebaceous duct to hair follicle and insertion of arrector pili muscle. The basal part of hair follicle is called the inferior segment or inferior part. Histologic structure and function of hair follicle is very intriguing. Demodex folliculorum mites, Staphylococcus epidermis, and yeast of pityrosporum can be seen and can be a normal component of pilosebaceous unit.
    [Show full text]
  • Pyoderma Gangrenosum: a Critical Appraisal
    DECEMBER 2017 CLINICAL MANAGEMENT extra Pyoderma Gangrenosum: A Critical Appraisal CME 1 AMA PRA ANCC Category 1 CreditTM 1.5 Contact Hours 0.5 Pharmacology Hours Eran Shavit, MD & Dermatologist, Clinical Fellow & Division of Dermatology, Department of Medicine & Women_s College Hospital, University of Toronto & Toronto, Ontario, Canada Afsaneh Alavi, MD, MSc, FRCPC & Assistant Professor & Division of Dermatology, Department of Medicine & Women_sCollege Hospital, University of Toronto & Toronto, Ontario, Canada R. Gary Sibbald, MD, DSc (Hons), MEd, BSc, FRCPC (Med)(Derm), FAAD, MAPWCA & Professor & Medicine and Public Health & University of Toronto & Toronto, Ontario, Canada & Director & International Interprofessional Wound Care Course & Masters of Science in Community Health (Prevention & Wound Care) & Dalla Lana Faculty of Public Health & University of Toronto & Past President & World Union of Wound Healing Societies & Clinical Editor & Advances in Skin & Wound Care & Philadelphia, Pennsylvania The authors, faculty, staff, and planners, including spouses/partners (if any), in any position to control the content of this CME activity have disclosed that they have no financial relationships with, or financial interests in, any commercial companies pertaining to this educational activity. To earn CME credit, you must read the CME article and complete the quiz online, answering at least 13 of the 18 questions correctly. This continuing educational activity will expire for physicians on December 31, 2018, and for nurses on December 31, 2019. All tests are now online only; take the test at http://cme.lww.com for physicians and www.nursingcenter.com for nurses. Complete CE/CME information is on the last page of this article. GENERAL PURPOSE: To provide information about pyoderma gangrenosum (PG), including pathophysiology, diagnostic criteria, and treatment.
    [Show full text]
  • Drug Eruptions
    DRUG ERUPTIONS E. W. NETHERTON, M.D. For practical purposes, the cutaneous manifestions of the toxic effects of drugs may be divided into two groups: (1) Those in which the injury is a result of external contact with the drug; as for example, sulphur, mercury, iodine and other drugs commonly used by the physician, and (2) eruptions which result from the introduction of drugs into the body by various methods, which most frequently is by ingestion. In the first group are classified the cases known as derma- titis venenata. Although individuals vary greatly in their suceptibil- ity to such drugs, their prolonged use, which commonly is by topical applications, produces irritation and if they are used for a long time or in a concentration which is too strong, they will produce dermatitis in a large percentage of patients. The second group is commonly spoken of as dermatitis medicamentosa. In this group there is, like- wise, an individual variation in susceptibility. Bromides, iodides, and arsenic when administered for a sufficiently long time will produce an eruption in a large number of patients, while other drugs such as quinine, phenolphthalein, and the various barbituric acid derivatives when ingested by the majority of individuals do not affect the skin, but in a few cases may produce fairly characteristic eruptions. There is a third group of cases in which it has been demonstrated that an eruption develops either after contact or by introduction into the body of a specific drug. Wise and Sulzberger1 observed a case in which a dermatitis was produced when quinine was applied externally to the skin or when it was taken by mouth.
    [Show full text]
  • A Case Report with Review of Literature on Pyoderma
    CASE REPORTS Year: 2018 I Volume: 1 I Issue: 3 I Page: 96-99 A CASE REPORT WITH REVIEW OF LITERATURE ON PYODERMA FACIALE IN PREGNANCY – A THERAPEUTIC DILEMMA Rahul Kumar Sharma1, Susanne Pulimood1, Dincy Peter1, Leni George1 1Department Of Dermatology Christian Medical College Vellore Corresponding Author: Dr. Rahul Kumar Sharma Consultant Dermatologist, Ajmer Email: [email protected] Abstract Pyoderma faciale is a rare facial dermatosis. It is characterized by a fulminating course of facial inflammation consisting of numerous pustules, cystic swellings and coalescing sinuses in young women. It has to be differentiated from acne and rosacea. The aetiopathogenesis of pyoderma faciale is not yet identified. It has been associated with pregnancy in a few cases. We report a case of a primigravida who presented with sudden onset of pustules and cystic swellings over the face with no prior similar history which was diagnosed as pyoderma faciale. In view of her pregnancy, systemic retinoids which is the treatment of choice was contraindicated and so was treated with tapering doses of oral steroids in combination with topical therapy. There was complete resolution of symptoms with treatment and a good obstetric outcome. Key words: pyoderma faciale, pregnancy Introduction Pyoderma faciale was formerly described by O'Leary and Kierland in 1940.1 It is a rare facial dermatosis characterized by the sudden onset of severe facial inflammation consisting of numerous pustules, cystic swellings and coalescing sinuses. Plewig et al considered it as an extreme form of rosacea and termed it as rosacea fulminans.2 But it is not yet clear whether this condition is a variant of rosacea or acne vulgaris or a separate entity.
    [Show full text]
  • Dermatological Problems of the Puberty
    Review paper Dermatological problems of the puberty Beata Bergler-Czop, Ligia Brzezińska-Wcisło Department of Dermatology, Silesian Medical University, Katowice, Poland Head: Prof. Ligia Brzezińska-Wcisło MD, PhD Postep Derm Alergol 2013; XXX, 3: 178 –187 DOI: 10.5114/pdia.2013.35621 Abstract Puberty is a period of life between childhood and adulthood. It is characterized by many changes in morphology and appearance of the body (biological maturation), in the psyche – development of personality (psychological mat - uration), and in the attitude towards one’s own and the opposite sex (psychosexual maturation), and in the social role (social maturation). Dermatological problems of adolescence are mainly related to fluctuations in hormone lev - els, mainly androgens. They include acne, hair problems and excessive sweating. Acne vulgaris is the most frequently diagnosed dermatosis in patients aged between 11 and 30 years. It is believed that it affects about 80% of persons in this age group or even, taking into account lesions of low intensity, 100% of young people. Excessive sweating is a condition characterised by excessive production of sweat, resulting from high activity of sweat glands. The sweat glands are localised in almost all areas of the body surface but on the hands, feet, armpits and around the groin they are found at the highest density. Seborrhoeic dermatitis of the scalp is a chronic, relapsing, inflammatory der - matosis, which currently affects about 5% of the population. It affects mostly young people, particularly men. Key words: puberty, acne, hyperhidrosis, hair. Introduction lieved that it affects about 80% of persons in this age group Puberty is a period of life between childhood and adult - or even, taking into account lesions of low intensity, 100% hood.
    [Show full text]
  • Hall (Editor), Gordon C
    Sauer's Manual of Skin Diseases 8th edition (January 15, 2000): by John C. Hall (Editor), Gordon C. Manual of Skin Diseases Sauer ByLippincott Williams & Wilkins Publishers By OkDoKeY Sauer’s Manual of Skin Diseases Contents Dedication Contributing Authors Preface to the First Edition (abridged) Preface Acknowledgments Chapter 1 Structure of the Skin Kenneth R. Watson, D.O. Chapter 2 Laboratory Procedures and Tests Kenneth R. Watson, D.O. Chapter 3 Dermatologic Diagnosis Chapter 4 Introduction to the Patient Chapter 5 Dermatologic Therapy Chapter 6 Physical Dermatologic Therapy Chapter 7 Fundamentals of Cutaneous Surgery Frank Custer Koranda, M.D. Chapter 8 Cosmetics for the Physician Marianne N. O’Donoghue,M.D. Chapter 9 Dermatologic Allergy Chapter 10 Dermatologic Immunology Richard S. Kalish, M.D., Ph.D. Chapter 11 Pruritic Dermatoses Chapter 12 Vascular Dermatoses Chapter 13 Seborrheic Dermatitis, Acne, and Rosacea Chapter 14 Papulosquamous Dermatoses Chapter 15 Dermatologic Bacteriology Chapter 16 Spirochetal Infections Chapter 17 Dermatologic Virology Chapter 18 Cutaneous Disease Associated with Human Immunodeficiency Virus M. Joyce Rico, M.D., and Neil S. Prose,M.D. Chapter 19 Dermatologic Mycology Chapter 20 Granulomatous Dermatoses Chapter 21 Dermatologic Parasitology Chapter 22 Bullous Dermatoses Chapter 23 Exfoliative Dermatitis Chapter 24 Pigmentary Dermatoses Chapter 25 Collagen Disease Chapter 26 The Skin and Internal Disease Warren R. Heymann, M.D., and Robin Levin,M.D. Chapter 27 Diseases Affecting the Hair Thelda Kestenbaum, M.D. Chapter 28 Diseases Affecting the Nails Thelda Kestenbaum, M.D. Chapter 29 Diseases of the Mucous Membranes Chapter 30 Dermatologic Reactions to Sun and Radiation Chapter 31 Genodermatoses Virginia P.
    [Show full text]