5 Allergic Diseases (And Differential Diagnoses)
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Clinical Practice Statements-Oral Contact Allergy
Clinical Practice Statements-Oral Contact Allergy Subject: Oral Contact Allergy The American Academy of Oral Medicine (AAOM) affirms that oral contact allergy (OCA) is an oral mucosal response that may be associated with materials and substances found in oral hygiene products, common food items, and topically applied agents. The AAOM also affirms that patients with suspected OCA should be referred to the appropriate dental and/or medical health care provider(s) for comprehensive evaluation and management of the condition. Replacement and/or substitution of dental materials should be considered only if (1) a reasonable temporal association has been established between the suspected triggering material and development of clinical signs and/or symptoms, (2) clinical examination supports an association between the suspected triggering material and objective clinical findings, and (3) diagnostic testing (e.g., dermatologic patch testing, skin-prick testing) confirms a hypersensitivity reaction to the suspected offending material. Originators: Dr. Eric T. Stoopler, DMD, FDS RCSEd, FDS RCSEng, Dr. Scott S. De Rossi, DMD. This Clinical Practice Statement was developed as an educational tool based on expert consensus of the American Academy of Oral Medicine (AAOM) leadership. Readers are encouraged to consider the recommendations in the context of their specific clinical situation, and consult, when appropriate, other sources of clinical, scientific, or regulatory information prior to making a treatment decision. Originator: Dr. Eric T. Stoopler, DMD, FDS RCSEd, FDS RCSEng, Dr. Scott S. De Rossi, DMD Review: AAOM Education Committee Approval: AAOM Executive Committee Adopted: October 17, 2015 Updated: February 5, 2016 Purpose The AAOM affirms that oral contact allergy (OCA) is an oral mucosal response that may be associated with materials and substances found in oral hygiene products, common food items, and topically applied agents. -
White Lesions of the Oral Cavity and Derive a Differential Diagnosis Four for Various White Lesions
2014 self-study course four course The Ohio State University College of Dentistry is a recognized provider for ADA, CERP, and AGD Fellowship, Mastership and Maintenance credit. ADA CERP is a service of the American Dental Association to assist dental professionals in identifying quality providers of continuing dental education. ADA CERP does not approve or endorse individual courses or instructors, nor does it imply acceptance of credit hours by boards of dentistry. Concerns or complaints about a CE provider may be directed to the provider or to ADA CERP at www.ada.org/goto/cerp. The Ohio State University College of Dentistry is approved by the Ohio State Dental Board as a permanent sponsor of continuing dental education ABOUT this FREQUENTLY asked COURSE… QUESTIONS… Q: Who can earn FREE CE credits? . READ the MATERIALS. Read and review the course materials. A: EVERYONE - All dental professionals in your office may earn free CE contact . COMPLETE the TEST. Answer the credits. Each person must read the eight question test. A total of 6/8 course materials and submit an questions must be answered correctly online answer form independently. for credit. us . SUBMIT the ANSWER FORM Q: What if I did not receive a ONLINE. You MUST submit your confirmation ID? answers ONLINE at: A: Once you have fully completed your p h o n e http://dent.osu.edu/sterilization/ce answer form and click “submit” you will be directed to a page with a . RECORD or PRINT THE 614-292-6737 unique confirmation ID. CONFIRMATION ID This unique ID is displayed upon successful submission Q: Where can I find my SMS number? of your answer form. -
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. -
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. -
Introduction to Bacteriology and Bacterial Structure/Function
INTRODUCTION TO BACTERIOLOGY AND BACTERIAL STRUCTURE/FUNCTION LEARNING OBJECTIVES To describe historical landmarks of medical microbiology To describe Koch’s Postulates To describe the characteristic structures and chemical nature of cellular constituents that distinguish eukaryotic and prokaryotic cells To describe chemical, structural, and functional components of the bacterial cytoplasmic and outer membranes, cell wall and surface appendages To name the general structures, and polymers that make up bacterial cell walls To explain the differences between gram negative and gram positive cells To describe the chemical composition, function and serological classification as H antigen of bacterial flagella and how they differ from flagella of eucaryotic cells To describe the chemical composition and function of pili To explain the unique chemical composition of bacterial spores To list medically relevant bacteria that form spores To explain the function of spores in terms of chemical and heat resistance To describe characteristics of different types of membrane transport To describe the exact cellular location and serological classification as O antigen of Lipopolysaccharide (LPS) To explain how the structure of LPS confers antigenic specificity and toxicity To describe the exact cellular location of Lipid A To explain the term endotoxin in terms of its chemical composition and location in bacterial cells INTRODUCTION TO BACTERIOLOGY 1. Two main threads in the history of bacteriology: 1) the natural history of bacteria and 2) the contagious nature of infectious diseases, were united in the latter half of the 19th century. During that period many of the bacteria that cause human disease were identified and characterized. 2. Individual bacteria were first observed microscopically by Antony van Leeuwenhoek at the end of the 17th century. -
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. -
SAMPLE REPORT - STANDARD 150 We Hope That the Test Result & Report Will Give You Satisfactory Information and That It Enables You, to Make Informed Decisions
Independent Alternative Allergy Specialist Tripenhad, Tripenhad Road, Ferryside, SA17 5RS, Wales/UK 0345 094 3298 | [email protected] | www.allergylink.co.uk Combination Allergy & Intolerance Test Food Intolerance & Substance Sensitivity - Standard 150 - Ref No: AL#438 Name: SAMPLE Date: 15 January 2020 SSAAMMPPLLEE RREEPPOORRTT -- SSTTAANNDDAARRDD 115500 ©©CCooppyyrriigghhtt –– 22000044--22002200 AAlllleerrggyy LLiinnkk Updated: 15.01.2020 www.allergylink.co.uk ©2004-2020 Allergy Link SAMPLE REPORT - STANDARD 150 We hope that the Test Result & Report will give you satisfactory information and that it enables you, to make informed decisions. Content & Reference: Part 1: Test -Table 3 Low Stomach Acid / Enzyme deficiency 18 Part 2: About your Report 4-5 Other possible cause of digestive problems 19-20 About Allergies and Intolerances 5-7 Non-Food Items & Substances Part 3: Allergen’s and Reactions Explained 8 Pet Allergies, House dust mite & Pollen 20-21 Dairy / Lactose 8 Environmental toxins 21 Eggs & Chicken 9 Pesticides and Herbicides 21 Fish, Shellfish, Glucosamine 9 Fluoride (now classified as a neurotoxin) 22 Coffee, Caffeine & Cocoa / Corn 10 Formaldehyde, Chlorine 22 Gluten / Wheat 10 Toiletries / Preservatives MI / MCI 23 Yeast & Moulds 11 Perfume / Fragrance 23 Alcohol - beer, wine 11 Detergents & Fabric conditioners 23-24 Fruit , Citrus fruit 12 Aluminium, Nickel, Teflon, Latex 24 Fructose / FODMAPs | Cellery 12 Vegetables | Nightshades, Tomato 13 Part 4: Beneficial Supplementing of Vitamins & Minerals Soya , bean, products -
ALLERGY Fish/Seafood Allergy Means an Adverse Reaction to Proteins Found in Different Marine Species
PATIENT INFORMATION BROCHURE FISH AND SEAFOOD ALLERGY Fish/Seafood allergy means an adverse reaction to proteins found in different marine species. The immune system of sensitised/allergic individuals produces lgE antibodies, which causes release of histamine and harmful substances when the food is eaten. FISH Globally fish and seafood play an important role in human nutrition. The move to healthier eating habits and the substitution of meat with seafood in the diet has meant that more fish being ingested. In Southern Africa there are 2 000 different species of fish. SEAFOOD is the broad term used to describe 2 groups of marine animals: Crustaceans shrimp, rock lobster, prawns. Molluscs mussels, oysters, squid, calamari and octopus. If you are allergic to fish, you are not necessarily allergic to seafood. If you are allergic to crustaceans, you are not necessarily allergic to molluscs, and vice versa. WHAT ARE THE SYMPTOMS OF FISH/SEAFOOD ALLERGY? Allergy to seafood /fish could result in almost any allergy symptoms and sign, but some are more common than others. Common symptoms include skin rashes/swelling, nausea/vomiting and breathing difficulty. Respiratory symptoms may occur in sensitive subjects following inhalation of fumes from the cooked or braaied fish Most symptoms develop within 2 hours after eating, smelling or handling fish. Severe allergy can cause life-threatening anaphylaxis and needs to be treated with adrenaline. Fish/Seafood Allergy does not mean Iodine allergy! HOW COMMON IS SEAFOOD ALLERGY? True seafood allergy is more common in adults than children, but is more likely to persist in into adulthood, when present in a child. -
UC Davis Dermatology Online Journal
UC Davis Dermatology Online Journal Title Penicillamine-associated cutis laxa and milia en plaque - case report and review of cutaneous changes associated with penicillamine Permalink https://escholarship.org/uc/item/47p4d8zv Journal Dermatology Online Journal, 22(5) Authors Vajdi, Tina Lee, Wiggin Wu Paravar, Taraneh Publication Date 2016 DOI 10.5070/D3225030951 License https://creativecommons.org/licenses/by-nc-nd/4.0/ 4.0 Peer reviewed eScholarship.org Powered by the California Digital Library University of California Volume 22 Number 5 May 2016 Photo Vignette Penicillamine-associated cutis laxa and milia en plaque - case report and review of cutaneous changes associated with penicillamine Tina Vajdi1, Wiggin Wu Lee2, Taraneh Paravar2 Dermatology Online Journal 22 (5): 12 1University of California, San Diego School of Medicine 2Department of Dermatology, University of California, San Diego Correspondence: Taraneh Paravar, MD Assistant Clinical Professor Department of Dermatology University of California, San Diego 8899 University Center Lane, Suite 350 San Diego, California 92122, USA Tel. (858) 657-8322 E-mail: [email protected] Abstract Penicillamine-induced skin changes are rare and include: hypersensitivity reactions, autoimmune reactions, and cutaneous elastoses. We report a case of a 73-year-old man with cystinuria taking penicillamine for over 50 years who presented with penicillamine-induced cutis laxa and milia en plaque. A brief review of penicillamine induced skin changes, specifically cutis laxa and milia en plaque, is presented. Key Words: penicillamine, elastic tissue, cystinuria, cutis laxa, milia en plaque Introduction Penicillamine is a chelating agent commonly used to treat cystinuria and Wilson disease. Cystinuria is a genetic disorder in which patients lack the cysteine amino acid transporter. -
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. -
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. -
Anetoderma Secondary to Mid-Dermal Elastolysis
Anetoderma Secondary to Mid-dermal Elastolysis Gabriela A. Maloney, BS,* Jane James, MD, PhD,** Michael Welsch, MD,** Marylee Braniecki, MD** *Midwestern University, Downers Grove, IL **Pathology Department, University of Illinois Hospital & Health Sciences System, Chicago, IL Abstract Anetoderma usually presents as circumscribed, 1 cm to 2 cm patches and plaques of flaccid skin secondary to loss of dermal elastic tissue. Lesions often occur in the neck, upper extremities, chest, and back. On histopathology, one sees complete loss of dermal elastin involving the papillary and reticular dermis, with infiltration of plasma cells and histiocytes. A 40-year-old female with no significant medical history presented with multiple round, 1 cm to 2 cm lesions scattered on her upper back and chest. Skin biopsy demonstrated elastic-fiber loss localized to the mid-dermis along with a lymphohistiocytic infiltrate with elastophagocytosis and active inflammatory phase in the papillary and mid-reticular dermis. The histopathological findings were consistent with mid-dermal elastolysis with advancing inflammation, and the clinical features were consistent with anetoderma. The microscopic examination revealed an active inflammatory phase of mid-dermal elastolysis, supporting the postulated theory that MDE may be part of a continuous spectrum with anetoderma. Case Report by lax, wrinkled skin with underlying palpable biopsy and elastic-fiber staining demonstrated A 40-year-old female with no significant medical depression (Figure 1). They were often preceded elastic-fiber loss in the mid-dermis along with history presented with multiple round, 1 cm to by two to six months of local erythema and had a lymphohistiocytic infiltrate with evidence 2 cm lesions scattered throughout the upper increased in number over the past two years.