339 a Acquired and Idiopathic Angioedema, 79 Acute Cutaneous

Total Page:16

File Type:pdf, Size:1020Kb

339 a Acquired and Idiopathic Angioedema, 79 Acute Cutaneous Index A management/prognosis, 332–335 Acquired and idiopathic angioedema, 79 nail findings, 329, 330 Acute cutaneous lupus erythematosus (ACLE), pathophysiology/genetics, 331–332 254, 255 Alopecia totalis, 329, 330 Allergic contact dermatitis (ACD). See also Alopecia universalis, 329 Rubber allergies American Contact Dermatitis Society, 156 armpit rash, 169–171 Amoxicillin, 27 chronic rash, 172–173 Angioedema definition, 173 ACE, 68 diagnostic patch testing, 174, 175 acute and chronic angioedema, 67 fragrance allergen series, 176–177 definition, 12 fragrance mix I and II, 175, 176 differential diagnosis, 67 ICDRG scale, 175 Hageman factor (XIIa), 68 pathophysiology, 174 idiopathic angioedema (see Idiopathic preservative angioedema) 2, 5-diazolidinylurea, 134–135 INH deficiency, 68 formaldehyde, 131–133 laboratory findings, 68–69 imidazolidinyl urea, 134 management, 69–70 MCI/MI, 135 mechanisms, 67 MDNG/phenoxyethanol, 135 vasoactive substance, 68 parabens, 135–136 without wheals, 18 quaternium-15, 133–134 Angiotensin converting enzyme (ACE) standard series patch test, 131 angioedema, 68 prevalence, 173–174 HAE, 81 red and splotchy rash, 171–172 laryngeal edema, 79 Alopecia areata Antigen presenting cells (APCs), 158, 174 definition, 329 Antihistamines, 21–22 epidemiology, 329 Aquagenic urticaria, 17 hair loss Asthma differential diagnosis, 324–328 clinical presentation, 25 hypothyroidism, 327 diagnosis, 27 medical history and medications, differential diagnosis, 26 323, 326 follow up, 27–28 physical examination, 324, 326, 327 physical examination, 26 hair pull tests, 329 treatment, 25–26 histopathology, 332, 333 urticaria and angioedema, 26 immune-mediated disease, 329, 331 work-up, 27 339 340 Index Atopic dermatitis B in adult, 193 Blue jean (nickel) ACD, 154 in childhood, 192 Bullous lupus, 256, 314 diagnosis, 195 Bullous pemphigoid, 314, 315 eczema differential diagnosis, 187–188 C impetiginized lesions, 188–189 Calcineurin inhibitors, 165 management and follow-up, 190–191 Candida albicans. See Recurrent vaginal medical and social history, 187 candidiasis physical examination, 187–191 C1 esterase inhibitor review of systems, 187 facial and throat swelling, 62, 63 seborrheic dermatitis, 190 HAE, 14, 19 subacute spongiotic dermatitis, 189 recurrent angioedema, 66 genetics, 193–194 Chronic cutaneous lupus erythematosus histology, 193 (CCLE), 254, 263 immunology, 194–195 Chronic dorsal foot eczema, 142–143 prevalence, 192 Chronic idiopathic angioedema, 69 rash Churg–Strauss syndrome, 226–228 autoimmune disease elimination, 186 C1-INH. See Complement 1 inhibitor differential diagnosis, 185 Clavulanic acid, 27 impetiginized lesions, 186 Cobalt allergy, 13–14 management and follow-up, 186–187 Cold stimulation time test (CSTT), 39 medical and surgical history, 183 Cold urticaria physical examination, 184, 185 asthma, 25–28 review of systems, 183 primary acquired (see Primary acquired risk factors, 192 cold urticaria) treatment syncopal and near-syncopal, 28–31 antibiotics, 197 Complement 1 inhibitor (C1-INH ), 76 calcineurin inhibitors, 197–198 Complement 4 (C4) level, 76 corticosteroids and Complete blood count (CBC) antihistamines, 197 femoral medial condyle, nail gun, 116 HEPA filter, 196 rashes, 186 immunosuppressants, 198 urticaria treatment, 22 phototherapy, 197 Comprehensive metabolic panel (CMP), 186 Staphylococcus aureus, 196 Contact urticaria syndrome (CUS) topical corticosteroids, 196–197 atopic dermatitis, 47–48 Autoimmune blistering diseases, causative agent, 55–56 skin and mucous membranes chamber and chamber prick test, 54 desquamative gingivitis ICU, 51 BP, 314, 315 IgE–allergen interaction, 17 bullous lupus erythematosus, 314 medical history, 48–49 differential diagnosis, 312–313 NICU direct immunofluorescence, epoxy (epoxid) resins, 51, 52 313–314 vs. ICU, 52, 53 EBA, 314–316 prostaglandin metabolism inhibition, 52 medical history and medications, 312 substances, 51 MMP, 314, 316–317 nonallergic IgE–independent group, 17 ocular findings, 317–318 open test, 54 physical examination, 312 prevalence, 49–51 treatment measures, 317 radioallergosorbent test (RAST), 55 lichenoid dermatitis (see Lichenoid staging, 53, 54 dermatitis) tachyphylaxis, 55 Autoimmune progesterone dermatitis, 19 treatment-resistant hand eczema, 45–47 Azathioprine, 198 use test, 54–55 Index 341 Corticosteroids Cyproheptadine, 40 ACD treatment, 149, 165 Cytomegalovirus (CMV), 202 chronic dorsal foot eczema, 142 Crohn’s disease, 76 Cryopyrin, 33 D CUS. See Contact urticaria syndrome Darier’s sign Cutaneous lupus differential diagnosis, 239 bullous lupus, 256 mast cell aggregation, 240 classification, 254, 256 physical examination, 238–239 clinical presentation, 256–257 pruritic lesions, 237 DH, 256 skin biopsy, 239 histologic features, 255 Delayed pressure urticaria, 16 pruritic rash Dermatitis herpetiformis (DH), 256 complete blood count and punch Dermatomyositis (DM), 290–291 biopsies, 260, 261 Diffuse cutaneous systemic sclerosis diagnosis, 258–260 (DcSSc), 292 skin examination, 259–260 Dimethyglyoxime (DMG) SCLE, 262–264 nickel-containing metal alloys, 164–165 SLE (see Systemic lupus peri-umbilical dermatitis, 154, 155 erythematosus) Diphenylcyclopropenone (DPCP), 335 TEN-like ACLE, 257 Doxepin, 21, 40 Cutaneous lymphocyte-associated antigen Duodenal ischemia, 76 (CLA), 194 Duodenal lymphoma/adenocarcinoma, 76 Cutaneous mastocytosis anaphylaxis, 247 Darier’s sign E differential diagnosis, 239 EACA. See Epsilon-aminocaproic acid mast cell aggregation, 240 Eczema. See Atopic dermatitis physical examination, 238–239 Edematous and erythematous lesions pruritic lesions, 237 autoimmune progesterone dermatitis, 11 skin biopsy, 239 chronic urticaria and angioedema, 9 diagnostic evaluation, 246–247 clinical presentation, 7 histopathological analysis, 246 differential diagnosis, 10 intramuscular epinephrine management and follow-up, 11 allergic reactions, 241 patient history, 10 IgE-mediated anaphylactic reaction, physical examination, 8–10 242–243 EIA. See Exercise-induced anaphylaxis medical and family history, 240 Enzyme-linked immunosorbent assays physical examination, 241 (ELISA), 218, 231 skin biopsy, 241–242 Epidermolysis bullosa acquisita, 314, 315 mediator release, symptoms, 244 Epidermolysis bullosa acquisita (EBA), 256 medical treatment, 247 Epigastric pain non-IgE-mediated mechanisms, 245–246 allergy service assessment, 76 physical examination, 246 bowel syndrome, 73 prognosis, 248 C4 level and C1-INH, 76 serum tryptase, 246 diagnosis, 77 telangiectasia macularis eruptiva perstans, medical and family history, 74 244, 245 pancreatitis, 76 transmembrane tyrosine kinase receptor, physical examination, 74–75 KIT, 243 PUD, 75–76 Cutaneous small-vessel vasculitis, 230–231 Epsilon-aminocaproic acid (EACA), 85 Cyclo-oxygenase 1(COX 1), 68 Erythema. See Toxic epidermal necrolysis Cyclooxygenase-2 inhibitor valdecoxib, 95 Erythema multiforme, 106–108, 115, 117 Cyclosporin, 191, 198 Erythrodermic psoriasis, 274 342 Index Excited skin syndrome (ESS), 173, 175 I Exercise-induced anaphylaxis (EIA), 17 ICDRG. See International Contact Dermatitis Research Group ICU. See Immunologic contact urticaria F Idiopathic angioedema Familial atypical cold urticaria (FACU), 32–33 facial and throat swelling Familial cold auto-inflammatory syndrome acquired angioedema, 63–64 (FCAS), 32–33 C1 esterase inhibitor, 62, 63 Familial delayed cold urticaria, 32–33 diagnostic testing, 60–62 Filaggrin (FLG) gene, 194 differential diagnosis, 62 food allergy, 63 HAE, 63 G IM epinephrine, 59–60 Ganser syndrome, 223 medical history, 60 Gastric antral vascular ectasia (GAVE), medication induced angioedema, 63 289–290 physical examination and Gold allergy, 160 medications, 60 Guillain-Barre syndrome, 222 review of system, 60 Guttate psoriasis, 274–275 treatment planning, 61 recurrent angioedema acquired angioedema, 66 H comprehensive laboratory evaluation, 66 HAE. See Hereditary angioedema differential diagnosis and testing, 65 Hair loss. See Alopecia areata doxepin, 64 Heat urticaria, 16 drug allergy, 64 Henoch-Schonlein purpura, 114 HAE type III, 66 Hereditary angioedema (HAE) medical history, 64 abdominal exacerbations, 83 medication induced angioedema, 66–67 C1 esterase inhibitor, 14, 19 physical examination, 65 epigastric pain (see Epigastric pain) review of system, 64 erythema marginatum, 83 treatment planning, 65 facial and throat swelling, 63 TSH, 66 gastrointestinal tract, 81–82 IGDA. See Interstitial granulomatous laryngeal edema, 77–80 dermatitis with arthritis management and treatment IgE receptors, 14, 68 danazol androgen and EACA, 85 IgE-specific enzyme-linked immunosorbent ecallantide (DX-88), 86 assay, 204 fresh frozen plasma, 85 IL-17 cytokine, 159 Rhucin, 85 Immediate pressure urticaria, 15 short-and long-term prophylaxis, 84–85 Immunologic contact urticaria (ICU), 51, 148 pathophysiology, 83 Interferon-gamma (IFN-g? cytokine, 160, 194 recurrent cramping/colicky abdominal International Contact Dermatitis Research pain, 83 Group (ICDRG) subcutaneous/submucosal swelling, 80 armpit rash, 170 type I, II & III, 80 atopic dermatitis, 48 Hereditary C1 inhibitor (INH), 68 chronic rash, 172 Herpes simplex virus (HSV), 202 dermatitis, 155 Hevea brasiliensis, 143 patch test scoring, 175 High efficiency particulate air (HEPA) filter, 196 red and splotchy rash, 171 Histocompatibility Complex Type II Receptor treatment-resistant hand eczema, 46 (MHC II), 136 Interstitial granulomatous dermatitis with Human papilloma virus (HPV), 202 arthritis (IGDA), 233–234 Human seminal plasma
Recommended publications
  • Photoaging & Skin Damage
    Use_for_Revised_OFC_Only_2006_PhotoagingSkinDamage 5/21/13 9:11 AM Page 2 PEORIA (309) 674-7546 MORTON (309) 263-7546 GALESBURG (309) 344-5777 PERU (815) 224-7400 NORMAL (309) 268-9980 CLINTON, IA (563) 242-3571 DAVENPORT, IA (563) 344-7546 SoderstromSkinInstitute.comsoderstromskininstitute.com FROMFrom YOUR Your DERMATOLOGISTDermatologist [email protected]@skinnews.com PHOTOAGING & SKIN DAMAGE Before You Worship The Sun Who’s At Risk? Today, many researchers and dermatologists Skin types that burn easily and tan rarely are believe that wrinkling and aging changes of the skin much more susceptible to the ravages of the sun on the are much more related to sun damage than to age! skin than are those that tan easily, rather than burn. Many of the signs of skin damage from the sun are Light complected, blue-eyed, red-haired people such as pictured on these pages. The decrease in the ozone Swedish, Irish, and English, are usually more suscep- layer, increasing the sun’s intensity, and the increasing tible to photo damage, and their skin shows the signs sun exposure among our population – through work, of photo damage earlier in life and in a more pro- sports, sunbathing and tanning parlors – have taken a nounced manner. Dark complexions give more protec- tremendous toll on our skin. Sun damage to the skin tion from light and the sun. ranks with other serious health dangers of smoking, alcohol, and increased cholesterol, and is being seen in younger and younger people. NO TAN IS A SAFE TAN! Table of Contents Sun Damage .............................................Pg. 1 Skin Cancer..........................................Pgs. 2-3 Mohs Micrographic Surgery ......................Pg.
    [Show full text]
  • 3628-3641-Pruritus in Selected Dermatoses
    Eur opean Rev iew for Med ical and Pharmacol ogical Sci ences 2016; 20: 3628-3641 Pruritus in selected dermatoses K. OLEK-HRAB 1, M. HRAB 2, J. SZYFTER-HARRIS 1, Z. ADAMSKI 1 1Department of Dermatology, University of Medical Sciences, Poznan, Poland 2Department of Urology, University of Medical Sciences, Poznan, Poland Abstract. – Pruritus is a natural defence mech - logical self-defence mechanism similar to other anism of the body and creates the scratch reflex skin sensations, such as touch, pain, vibration, as a defensive reaction to potentially dangerous cold or heat, enabling the protection of the skin environmental factors. Together with pain, pruritus from external factors. Pruritus is a frequent is a type of superficial sensory experience. Pruri - symptom associated with dermatoses and various tus is a symptom often experienced both in 1 healthy subjects and in those who have symptoms systemic diseases . Acute pruritus often develops of a disease. In dermatology, pruritus is a frequent simultaneously with urticarial symptoms or as an symptom associated with a number of dermatoses acute undesirable reaction to drugs. The treat - and is sometimes an auxiliary factor in the diag - ment of this form of pruritus is much easier. nostic process. Apart from histamine, the most The chronic pruritus that often develops in pa - popular pruritus mediators include tryptase, en - tients with cholestasis, kidney diseases or skin dothelins, substance P, bradykinin, prostaglandins diseases (e.g. atopic dermatitis) is often more dif - and acetylcholine. The group of atopic diseases is 2,3 characterized by the presence of very persistent ficult to treat . Persistent rubbing, scratching or pruritus.
    [Show full text]
  • 61497191.Pdf
    View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Repositório Institucional dos Hospitais da Universidade de Coimbra Metadata of the chapter that will be visualized online Chapter Title Phototoxic Dermatitis Copyright Year 2011 Copyright Holder Springer-Verlag Berlin Heidelberg Corresponding Author Family Name Gonçalo Particle Given Name Margarida Suffix Division/Department Clinic of Dermatology, Coimbra University Hospital Organization/University University of Coimbra Street Praceta Mota Pinto Postcode P-3000-175 City Coimbra Country Portugal Phone 351.239.400420 Fax 351.239.400490 Email [email protected] Abstract • Phototoxic dermatitis from exogenous chemicals can be polymorphic. • It is not always easy to distinguish phototoxicity from photoallergy. • Phytophotodermatitis from plants containing furocoumarins is one of the main causes of phototoxic contact dermatitis. • Topical and systemic drugs are a frequent cause of photosensitivity, often with phototoxic aspects. • The main clinical pattern of acute phototoxicity is an exaggerated sunburn. • Subacute phototoxicity from systemic drugs can present as pseudoporphyria, photoonycholysis, and dyschromia. • Exposure to phototoxic drugs can enhance skin carcinogenesis. Comp. by: GDurga Stage: Proof Chapter No.: 18 Title Name: TbOSD Page Number: 0 Date:1/11/11 Time:12:55:42 1 18 Phototoxic Dermatitis 2 Margarida Gonc¸alo Au1 3 Clinic of Dermatology, Coimbra University Hospital, University of Coimbra, Coimbra, Portugal 4 Core Messages photoallergy, both photoallergic contact dermatitis and 45 5 ● Phototoxic dermatitis from exogenous chemicals can systemic photoallergy, and autoimmunity with photosen- 46 6 be polymorphic. sitivity, as in drug-induced photosensitive lupus 47 7 ● It is not always easy to distinguish phototoxicity from erythematosus in Ro-positive patients taking terbinafine, 48 8 photoallergy.
    [Show full text]
  • Urticaria - Primary Care Treatment Pathway
    DORSET MEDICINES ADVISORY GROUP Urticaria - Primary Care Treatment Pathway Urticaria – also known as hives or nettle rash – is a raised, itchy rash that can occur on just one part of the body or be spread across large areas. The weals of urticaria last less than 24 hours although patients may develop new weals on a daily basis. If urticaria clears completely within six weeks, it is known as acute urticaria. Urticaria occurring for more than six weeks is referred to as chronic urticaria. Most cases of chronic disease occur without an obvious trigger (chronic spontaneous urticaria). Some urticaria has a physical trigger such as pressure (symptomatic dermographism or delayed pressure urticaria), cold or exercise (cholinergic urticaria), or may be drug induced (e.g. by NSAIDS, ACE inhibitors and opioids). All forms of urticaria can be treated with antihistamine although physical urticaria is less likely to respond to treatment than spontaneous urticaria. Most cases of urticaria settle spontaneously within two years but the condition can last for decades in some patients. Referral criteria Refer routinely to dermatology if patients are not responding to standard treatment (see primary care treatment below, up to step 4), they can then be considered for immunomodulation treatment such as ciclosporin (can be very useful for patients thought to have an autoimmune basis for their urticaria), methotrexate or omalizumab. The diagnosis of urticaria is primarily clinical therefore do not routinely refer for allergy testing. The British Association of Dermatologists (BAD) has produced a patient information leaflet which covers this in detail for patients. PRIOR TO SPECIALIST REFERRAL -conduct a full blood count (FBC), erythrocyte sedimentation rate (ESR), thyroid function tests (TFTs), liver function tests (LFTs), and Helicobacter pylori screening (if gastrointestinal symptoms are present).
    [Show full text]
  • Vibratory Urticaria
    Vibratory urticaria Description Vibratory urticaria is a condition in which exposing the skin to vibration, repetitive stretching, or friction results in allergy symptoms such as hives (urticaria), swelling ( angioedema), redness (erythema), and itching (pruritus) in the affected area. The reaction can be brought on by towel drying, hand clapping, running, a bumpy ride in a vehicle, or other repetitive stimulation. Headaches, fatigue, faintness, blurry vision, a metallic taste in the mouth, facial flushing, and more widespread swelling (especially of the face) can also occur during these episodes, especially if the stimulation is extreme or prolonged. The reaction occurs within a few minutes of the stimulation and generally lasts up to an hour. Affected individuals can have several episodes per day. Frequency Vibratory urticaria is a rare disorder; its prevalence is unknown. It belongs to a class of disorders called physical urticarias in which allergy symptoms are brought on by direct exposure to factors such as pressure, heat, cold, or sunlight. Physical urticarias have been estimated to occur in up to 5 per 1,000 people. Causes Vibratory urticaria can be caused by a mutation in the ADGRE2 gene. This gene provides instructions for making a protein found in several types of immune system cells, including mast cells. Mast cells, which are found in many body tissues including the skin, are important for the normal protective functions of the immune system. They also play a role in allergic reactions, which occur when the immune system overreacts to stimuli that are not harmful. The specific role of the ADGRE2 protein in mast cells is not well understood.
    [Show full text]
  • Photodermatoses  Update Knowledge and Treatment of Photodermatoses  Discuss Vitamin D Levels in Photodermatoses
    Ashley Feneran, DO Jenifer Lloyd, DO University Hospitals Regional Hospitals AMERICAN OSTEOPATHIC COLLEGE OF DERMATOLOGY Objectives Review key points of several photodermatoses Update knowledge and treatment of photodermatoses Discuss vitamin D levels in photodermatoses Types of photodermatoses Immunologically mediated disorders Defective DNA repair disorders Photoaggravated dermatoses Chemical- and drug-induced photosensitivity Types of photodermatoses Immunologically mediated disorders Polymorphous light eruption Actinic prurigo Hydroa vacciniforme Chronic actinic dermatitis Solar urticaria Polymorphous light eruption (PMLE) Most common form of idiopathic photodermatitis Possibly due to delayed-type hypersensitivity reaction to an endogenous cutaneous photo- induced antigen Presents within minutes to hours of UV exposure and lasts several days Pathology Superficial and deep lymphocytic infiltrate Marked papillary dermal edema PMLE Treatment Topical or oral corticosteroids High SPF Restriction of UV exposure Hardening – natural, NBUVB, PUVA Antimalarial PMLE updates Study suggests topical vitamin D analogue used prophylactically may provide therapeutic benefit in PMLE Gruber-Wackernagel A, Bambach FJ, Legat A, et al. Br J Dermatol, 2011. PMLE updates Study seeks to further elucidate the pathogenesis of PMLE Found a decrease in Langerhans cells and an increase in mast cell density in lesional skin Wolf P, Gruber-Wackernagel A, Bambach I, et al. Exp Dermatol, 2014. Actinic prurigo Similar to PMLE Common in native
    [Show full text]
  • Urticaria from Wikipedia, the Free Encyclopedia Jump To: Navigation, Search "Hives" Redirects Here
    Urticaria From Wikipedia, the free encyclopedia Jump to: navigation, search "Hives" redirects here. For other uses, see Hive. Urticaria Classification and external resourcesICD-10L50.ICD- 9708DiseasesDB13606MedlinePlus000845eMedicineemerg/628 MeSHD014581Urtic aria (or hives) is a skin condition, commonly caused by an allergic reaction, that is characterized by raised red skin wheals (welts). It is also known as nettle rash or uredo. Wheals from urticaria can appear anywhere on the body, including the face, lips, tongue, throat, and ears. The wheals may vary in size from about 5 mm (0.2 inches) in diameter to the size of a dinner plate; they typically itch severely, sting, or burn, and often have a pale border. Urticaria is generally caused by direct contact with an allergenic substance, or an immune response to food or some other allergen, but can also appear for other reasons, notably emotional stress. The rash can be triggered by quite innocent events, such as mere rubbing or exposure to cold. Contents [hide] * 1 Pathophysiology * 2 Differential diagnosis * 3 Types * 4 Related conditions * 5 Treatment and management o 5.1 Histamine antagonists o 5.2 Other o 5.3 Dietary * 6 See also * 7 References * 8 External links [edit] Pathophysiology Allergic urticaria on the shin induced by an antibiotic The skin lesions of urticarial disease are caused by an inflammatory reaction in the skin, causing leakage of capillaries in the dermis, and resulting in an edema which persists until the interstitial fluid is absorbed into the surrounding cells. Urticarial disease is thought to be caused by the release of histamine and other mediators of inflammation (cytokines) from cells in the skin.
    [Show full text]
  • Module Test № 1 on Dermatology
    THE MINISTRY OF HEALTHCARE OF THE RUSSIAN FEDERATION FEDERAL STATE BUDGETARY EDUCATIONAL INSTITUTION OF HIGHER PROFESSIONAL EDUCATION PIROGOV RUSSIAN NATIONAL RESEARCH MEDICAL UNIVERSITY DEPARTMENT OF DERMATOVENEROLOGY Gaydina T.A., Dvornikov A.S., Skripkina P.A., Nazhmutdinova D.K., Heydar S.A., Arutunyan G.B., Pashinyan A.G. MODULE TEST №1 ON DERMATOLOGY FOR STUDENTS OF INSTITUTES OF HIGHER MEDICAL EDUCATION ON SPECIALTY THERAPEUTIC FACULTY DEPARTMENT OF DERMATOVENEROLOGY Moscow 2016 ISBN УДК ББК A21 Module test №1 on Dermatology for students of institutes of high medical education on specialty «Therapeutic faculty» department of dermatovenerology: manual for students for self-training//FSBEI HPE “Pirogov RNRMU” of the ministry of healthcare of the russian federation, M.: (publisher) 2016, 144 p. The manual is a part of teaching-methods on Dermatovenerology. It contains tests on Dermatology on the topics of practical sessions requiring single or multiple choice anser. The manual can be used to develop skills of students during practical sessions. It also can be used in the electronic version at testing for knowledge. The manual is compiled according to FSES on specialty “therapeutic faculty”, working programs on dermatovenerology. The manual is intended for foreign students of 3-4 courses on specialty “therapeutic faculty” and physicians for professional retraining. Authors: Gaydina T.A. – candidate of medical science, assistant of dermatovenerology department of therapeutic faculty Pirogov RNRMU Dvornikov A.S. – M.D., professor of dermatovenerology department of therapeutic faculty Pirogov RNRMU Skripkina P.A. – candidate of medical science, assistant professor of dermatovenerology department of therapeutic faculty Pirogov RNRMU Nazhmutdinova D.K. – candidate of medical science, assistant professor of dermatovenerology department of therapeutic faculty Pirogov RNRMU Heydar S.A.
    [Show full text]
  • Etiology, Classification, and Treatment of Urticaria
    CONTINUING MEDICAL EDUCATION Etiology, Classification, and Treatment of Urticaria Kjetil Kristoffer Guldbakke, MD; Amor Khachemoune, MD, CWS GOAL To understand urticaria to better manage patients with the condition OBJECTIVES Upon completion of this activity, dermatologists and general practitioners should be able to: 1. Discuss the clinical classification of urticaria. 2. Recognize how to diagnose urticaria. 3. Identify treatment options. CME Test on page 50. This article has been peer reviewed and approved Einstein College of Medicine is accredited by by Michael Fisher, MD, Professor of Medicine, the ACCME to provide continuing medical edu- Albert Einstein College of Medicine. Review date: cation for physicians. December 2006. Albert Einstein College of Medicine designates This activity has been planned and imple- this educational activity for a maximum of 1 AMA mented in accordance with the Essential Areas PRA Category 1 CreditTM. Physicians should only and Policies of the Accreditation Council for claim credit commensurate with the extent of their Continuing Medical Education through the participation in the activity. joint sponsorship of Albert Einstein College of This activity has been planned and produced in Medicine and Quadrant HealthCom, Inc. Albert accordance with ACCME Essentials. Drs. Guldbakke and Khachemoune report no conflict of interest. The authors discuss off-label use of colchi- cine, cyclophosphamide, cyclosporine, dapsone, intravenous immunoglobulin, methotrexate, montelukast sodium, nifedipine, plasmapheresis, rofecoxib, sulfasalazine, tacrolimus, thyroxine, and zafirlukast. Dr. Fisher reports no conflict of interest. Urticaria is among the most common skin dis- autoimmune mechanisms are now recognized as a eases. It can be acute, chronic, mediated by a cause of chronic urticaria. A search of the PubMed physical stimulus, or related to contact with an database (US National Library of Medicine) for urticant.
    [Show full text]
  • Local Heat Urticaria
    Volume 23 Number 12 | December 2017 Dermatology Online Journal || Case Presentation DOJ 23 (12): 10 Local heat urticaria Forrest White MD, Gabriela Cobos MD, and Nicholas A Soter MD Affiliations: 1 New York University Langone Health, New York Abstract PHYSICAL EXAMINATION: A brisk, mechanical stroke elicited a linear wheal. Five minutes after exposure We present a 38-year-old woman with local heat to hot water, she developed well-demarcated, urticaria confirmed by heat provocation testing. Heat erythematous blanching wheals that covered the urticaria is a rare form of physical urticaria that is distal forearm and entire hand. triggered by exposure to a heat source, such as hot water or sunlight. Although it is commonly localized Conclusion and immediate, generalized and delayed onset forms Physical or inducible urticarias are a group of exist. Treatment options include antihistamines urticarias that are triggered by various external and heat desensitization. A brisk, mechanical stroke physical stimuli, such as mechanical stimuli, pressure, elicited a linear wheal. Five minutes after exposure cold, light, or temperature change. Urticarias due to hot water, she developed well-demarcated, to temperature change include heat urticaria (HU), erythematous blanching wheals that covered the cholinergic urticaria, and cold urticaria. distal forearm and entire hand. HU is a rare form of chronic inducible urticaria, with Keywords: urticaria, local heat urticaria, physical approximately 60 reported cases [1]. In HU, contact urticaria with a heat source such as hot water, sunlight, hot air, radiant heat, or hot objects results in wheal formation Introduction HISTORY: A 38-year-old woman presented to the Skin and Cancer Unit for the evaluation of recurrent, intensely pruritic eruptions that were precipitated by exposure to heat, which included hot water and sunlight.
    [Show full text]
  • Edderm101 CORE DISEASES V2.09
    ed.derm.101: core diseases almost everything you need to know to survive dermatology* “Two thirds of what we see is behind our eyes” “Explain, explain,” grumbled Étienne. “If you people can’t name something you’re incapable of seeing it.”— Cortázar, 1966, Hopscotch “Learning results from what the student does and thinks and only from what the student does and thinks. The teacher can advance learning only by influencing what the student does to learn.” Herbert Simon, Nobel Laureate. ! " *the first of many outright lies exaggerations. You need to know skincancer909 too, and ed.derm.101: core concepts, but these are also free. Professor Jonathan Rees FMedSci Grant Chair of Dermatology University of Edinburgh email me reestheskin.me: about me reestheskinblog.me: unreasonable views from the edge of education and medicine skincancer909: an online textbook of skin cancer for medical students V2.09, 25 September 2019 at 13:18 Distributed under a Creative Commons Attribution-Non Commercial ShareAlike 4.0 License !1 Preface The purpose of ed.derm.101: core diseases is to cover all the clinical material that we expect students to know, that is not covered in either ed.derm.101: core concepts or skincancer909. I assume you have already worked your way through ed.derm.101: core concepts (because what follows is heavily dependent on this foundational reading). A few words of advice about studying this aspect of dermatology and ed.derm.101: - It is hard to learn about a disease without some sort of mental image of what it looks like. In skincancer909 I was able to make use of a bespoke library of images that were developed as part of a research project funded by the Wellcome Trust.
    [Show full text]
  • Antihistamines in the Treatment of Chronic Urticaria I Jáuregui,1 M Ferrer,2 J Montoro,3 I Dávila,4 J Bartra,5 a Del Cuvillo,6 J Mullol,7 J Sastre,8 a Valero5
    Antihistamines in the treatment of chronic urticaria I Jáuregui,1 M Ferrer,2 J Montoro,3 I Dávila,4 J Bartra,5 A del Cuvillo,6 J Mullol,7 J Sastre,8 A Valero5 1 Service of Allergy, Hospital de Basurto, Bilbao, Spain 2 Department of Allergology, Clínica Universitaria de Navarra, Pamplona, Spain 3 Allergy Unit, Hospital La Plana, Villarreal (Castellón), Spain 4 Service of Immunoallergy, Hospital Clínico, Salamanca, Spain 5 Allergy Unit, Service of Pneumology and Respiratory Allergy, Hospital Clínic (ICT), Barcelona, Spain 6 Clínica Dr. Lobatón, Cádiz, Spain 7 Rhinology Unit, ENT Service (ICEMEQ), Hospital Clínic, Barcelona, Spain 8 Service of Allergy, Fundación Jiménez Díaz, Madrid, Spain ■ Summary Chronic urticaria is highly prevalent in the general population, and while there are multiple treatments for the disorder, the results obtained are not completely satisfactory. The second-generation H1 antihistamines remain the symptomatic treatment option of choice. Depending on the different pharmacokinetics and H1 receptor affi nity of each drug substance, different concentrations in skin can be expected, together with different effi cacy in relation to the histamine-induced wheal inhibition test - though this does not necessarily have repercussions upon clinical response. The antiinfl ammatory properties of the H1 antihistamines could be of relevance in chronic urticaria, though it is not clear to what degree they infl uence the fi nal therapeutic result. Before moving on to another therapeutic level, the advisability of antihistamine dose escalation should be considered, involving increments even above those approved in the Summary of Product Characteristics. Physical urticaria, when manifesting isolatedly, tends to respond well to H1 antihistamines, with the exception of genuine solar urticaria and delayed pressure urticaria.
    [Show full text]