Nailfold Changes As a Sign of Underlying Systemic Illnesses
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Idiopathic Spiny Keratoderma: a Report of Two Cases and Literature Review
Idiopathic Spiny Keratoderma: A Report of Two Cases and Literature Review Jessica Schweitzer, DO,* Matthew Koehler, DO,** David Horowitz, DO*** *Intern, Largo Medical Center, Largo, FL **Dermatology Resident, Third Year, College Medical Center/Western University, Long Beach, CA ***Dermatology Residency Program Director, College Medical Center/Western University, Long Beach, CA Abstract Spiny keratoderma is a rare and likely underreported condition that presents with punctate hyperkeratotic growths localized to the palms and soles. We present two cases of clinically diagnosed spiny keratoderma. Although the lesions were asymptomatic, patients are at risk of an underlying internal malignancy with this condition, so diagnosis is crucial. Neither men were seeking treatment for the lesions when they were discovered, suggesting that this condition may be much more common than reported. Patients with histories of manual labor, increased UV exposure, and non-melanoma skin cancer (NMSC) may also be at higher risk for developing spiny keratoderma.1 The epidemiology, histopathologic features, differential diagnosis, and current treatments for spiny keratoderma are reviewed. Introduction Case 2 enthusiast for his entire life, spending significant Spiny keratoderma is a rare palmoplantar A 67-year-old Caucasian male presented with a time using his hands to maintain and fire his keratoderma that presents with keratotic, pinpoint one-year history of insidiously growing, pinpoint weapons and many hours outside without sun papules on the palms and soles. There are both hyperkeratotic papules projecting from his palms protection. The patient was referred back to his hereditary and acquired forms. When found, bilaterally (Figures 4-5). He presented to the clinic primary care physician for internal evaluation. -
Chapter 3 Bacterial and Viral Infections
GBB03 10/4/06 12:20 PM Page 19 Chapter 3 Bacterial and viral infections A mighty creature is the germ gain entry into the skin via minor abrasions, or fis- Though smaller than the pachyderm sures between the toes associated with tinea pedis, His customary dwelling place and leg ulcers provide a portal of entry in many Is deep within the human race cases. A frequent predisposing factor is oedema of His childish pride he often pleases the legs, and cellulitis is a common condition in By giving people strange diseases elderly people, who often suffer from leg oedema Do you, my poppet, feel infirm? of cardiac, venous or lymphatic origin. You probably contain a germ The affected area becomes red, hot and swollen (Ogden Nash, The Germ) (Fig. 3.1), and blister formation and areas of skin necrosis may occur. The patient is pyrexial and feels unwell. Rigors may occur and, in elderly Bacterial infections people, a toxic confusional state. In presumed streptococcal cellulitis, penicillin is Streptococcal infection the treatment of choice, initially given as ben- zylpenicillin intravenously. If the leg is affected, Cellulitis bed rest is an important aspect of treatment. Where Cellulitis is a bacterial infection of subcutaneous there is extensive tissue necrosis, surgical debride- tissues that, in immunologically normal individu- ment may be necessary. als, is usually caused by Streptococcus pyogenes. A particularly severe, deep form of cellulitis, in- ‘Erysipelas’ is a term applied to superficial volving fascia and muscles, is known as ‘necrotiz- streptococcal cellulitis that has a well-demarcated ing fasciitis’. This disorder achieved notoriety a few edge. -
Lepromatous Leprosy with Erythema Nodosum Leprosum Presenting As
Lepromatous Leprosy with Erythema Nodosum Leprosum Presenting as Chronic Ulcers with Vasculitis: A Case Report and Discussion Anny Xiao, DO,* Erin Lowe, DO,** Richard Miller, DO, FAOCD*** *Traditional Rotating Intern, PGY-1, Largo Medical Center, Largo, FL **Dermatology Resident, PGY-2, Largo Medical Center, Largo, FL ***Program Director, Dermatology Residency, Largo Medical Center, Largo, FL Disclosures: None Correspondence: Anny Xiao, DO; Largo Medical Center, Graduate Medical Education, 201 14th St. SW, Largo, FL 33770; 510-684-4190; [email protected] Abstract Leprosy is a rare, chronic, granulomatous infectious disease with cutaneous and neurologic sequelae. It can be a challenging differential diagnosis in dermatology practice due to several overlapping features with rheumatologic disorders. Patients with leprosy can develop reactive states as a result of immune complex-mediated inflammatory processes, leading to the appearance of additional cutaneous lesions that may further complicate the clinical picture. We describe a case of a woman presenting with a long history of a recurrent bullous rash with chronic ulcers, with an evolution of vasculitic diagnoses, who was later determined to have lepromatous leprosy with reactive erythema nodosum leprosum (ENL). Introduction accompanied by an intense bullous purpuric rash on management of sepsis secondary to bacteremia, Leprosy is a slowly progressive disease caused by bilateral arms and face. For these complaints she was with lower-extremity cellulitis as the suspected infection with Mycobacterium leprae (M. leprae). seen in a Complex Medical Dermatology Clinic and source. A skin biopsy was taken from the left thigh, Spread continues at a steady rate in several endemic clinically diagnosed with cutaneous polyarteritis and histopathology showed epidermal ulceration countries, with more than 200,000 new cases nodosa. -
C.O.E. Continuing Education Curriculum Coordinator
CONTINUING EDUCATION All Rights Reserved. Materials may not be copied, edited, reproduced, distributed, imitated in any way without written permission from C.O. E. Continuing Education. The course provided was prepared by C.O.E. Continuing Education Curriculum Coordinator. It is not meant to provide medical, legal or C.O.E. professional services advice. If necessary, it is recommended that you consult a medical, legal or professional services expert licensed in your state. Page 1 of 199 Click Here To Take Test Now (Complete the Reading Material first then click on the Take Test Now Button to start the test. Test is at the bottom of this page) 5 hr. Nail Structure and Growth & TCSG Health and Safety Outline Why Study Nail Structure and Growth? • The Natural Nail • Nail Anatomy • Nail Growth • Know Your Nails Objectives After completing this section, you should be able to: C.O.E.• Describe CONTINUING the structure and composition of nails. EDUCATION • Discuss how nails grow. • Identify diseases and disorders of the nail All Rights Reserved. Materials may not be copied, edited, reproduced, distributed, imitated in any way without written permission from C.O. E. Continuing Education. The course provided was prepared by C.O.E. Continuing Education Curriculum Coordinator. It is not meant to provide medical, legal or professional services advice. If necessary, it is recommended that you consult a medical, legal or professional services expert licensed in your state. 1 CONTINUING EDUCATION All Rights Reserved. Materials may not be copied, edited, reproduced, distributed, imitated in any way without written permission from C.O. -
Leprosy in Two Patients with Relapsing Remitting Multiple Sclerosis Treated with Fingolimod Alfred Balasa, M.D.1 and George J
Leprosy in Two Patients with Relapsing Remitting Multiple Sclerosis Treated with Fingolimod Alfred Balasa, M.D.1 and George J. Hutton, M.D.2 1 Department of Pediatrics, Section of Pediatric Neurology and Developmental Neuroscience; 2 Department of Neurology; Baylor College of Medicine, Houston, Texas Background A B Leprosy (Hansen’s disease) is a chronic infection caused by Mycobacterium leprae. The disease develops over months to years and may cause extensive damage to the skin and peripheral nervous system. A B In multiple sclerosis (MS), fingolimod treatment is Figure 3. Immune response in the polar clinical forms of leprosy. known to increase the risk for infections. There is one prior reported case of leprosy while on [A] In tuberculoid leprosy (TT) patients, the innate immune response is activated by M. leprae through toll-like receptors (TLR2/1). IL-15 fingolimod for relapsing remitting multiple sclerosis stimulates the vitamin D-dependent antimicrobial program in macrophages and inhibits phagocytosis of mycobacteria. These events (RRMS). We report two further cases of leprosy in promote a Th1 T-cell cytokine response (IFN-γ, IL-2, TNF, and IL-15) that contains the infection in well-formed granulomas, and a Th17 patients with RRMS and treated with fingolimod. C D response (IL-17A, IL-17F, IL-21 and IL-22) that leads to tissue inflammation and destruction, neutrophil recruitment, macrophage activation, and enhancement of Th1 effector cells. [B] In lepromatous leprosy (LL) patients, IL-4, IL-10, leukocyte immunoglobulin-like receptor subfamily A member 2 (LILRA2), and oxidized phospholipids inhibit TLR2/1-induced cytokine responses but preserve IL-10 release. -
An Unusual Course in Bullous Morphea
Case Report An Unusual Course in Bullous Morphea İlknur Kıvanç Altunay, MD, Hilal Kaya Erdoğan*, MD, Nurhan Döner, MD, Damlanur Sakız,1 MD. Address: Dermatology and 1Pathology Departments, Şişli Etfal Training and Research Hospital, Istanbul, 34377, Turkey. * Corresponding Author: Dr. Hilal Kaya Erdoğan, Şisli Etfal Training and Research Hospital. Istanbul, 34377, Turkey. E-mail: [email protected] Published: J Turk Acad Dermatol 2010; 4 (4): 04401c This article is available from: http://www.jtad.org/2010/4/jtad04401c.pdf Key Words: bullous morphea, drug reaction Abstract Observations: We report a 75-year-old woman with bullous morphea characterized by disseminated erythemato-pigmentous plaques and a few blisters on some morphea plaques at the beginning of first visit. While she was under narrow band UV therapy, she discontinued the treatment and refused to have any more after 13 sessions. One month later, she reapplied with extensive bullae and facial edema with severe itching. We learned that she had taken naproxen sodium one a day for two days ten days ago. Bullous drug reaction was diagnosed and systemic cortisone was started. She was in remission after fifteen days. The patient had very different clinical picture on her second visit with extensive, large and cadaverous bullae, facial eryhtema and edema. It seems to be a bullous drug reaction based on bullous morphea. However, it remains a mystery whether this clinical presentation is a peculiar drug reaction or is really a mere exacerbation of existed bullous morphea. Introduction noprost eye drop and tolterodine. These medicati- ons had been used for over a year. Her family his- Bullae formation in lesions of morphea is an tory was unremarkable. -
Immunological Aspects of Leprosy with Special Reference to Autoimmune Diseases 0
'Bull. Org. mond. Sante 1969, 41, 793-804 Bull. Wld Hlth Org. Immunological Aspects of Leprosy with Special Reference to Autoimmune Diseases 0. WAGER1 Leprosy, particularly lepromatous leprosy, is associated with a multitude of (auto) immune aberrations, and its clinical features also have much in common with the collagen diseases. Immunopathological studies of the 2 groups of diseases may thus elucidate the basic mechanisms of both. The reported evidencefor a genetically determined hyporeactivity ofcell-mediated (CM) immunity in lepromatous subjects is reviewed; most, but not all, of the findings fit such a hypothesis well. The possibility remains that the observed hyporeactivities may be secondary to direct effects of Mycobacterium leprae. Evidencefor a general hyperreactivity of the antibody-mediated (AM) immunity in lepromatous leprosy is then reviewed and considered to be fragmentary. The concept and general criteria of autoimmunity are discussed briefly and the high incidence in lepromatous leprosy of various (auto)immune aberrations, resembling those in systemic lupus erythematosus (SLE) and in rheumatoid arthritis is reviewed. Although autoantibodies are not likely to be directly deleterious to the host, immune complexes containing autoantibodies may be pathogenic. Mixed cryoimmunoglobulins, consisting of 2 (IgG-IgM or IgG-IgA) or 3 immunoglo-. bulins, and occasionally also containing measurable amounts of complement components, have recently been encountered in SLE and its variants and also in a number of microbial diseases with autoimmune features (syphilis, streptococcal nephritis and endocarditis, mononucleosis, Mycoplasma pneumoniae pneumonia). They may represent circulating immune complexes, analogous to the IgM (IgA) rheumatoid factors in combination with their IgG reactants. In leprosy also, the existence of pathogenic immune complexes is indirectly suggested by mixed cryoglobulinemia andfurther by a number of other features reviewed in this article. -
Oral Frictional Hyperkeratosis (FK)
Patient information Oral frictional hyperkeratosis (FK) What is oral frictional hyperkeratosis? Hyperkeratinisation - excessive growth of stubbornly attached keratin (a fibrous protein produced by the body) - may happen for a number of reasons, and may be genetic (runs in the family), physiological e.g. due to friction from a sharp tooth, pre-malignant (pre-cancerous) and malignant (cancerous). The change may result from chemical, heat or physical irritants. Friction (the constant rubbing of two surfaces against each other) in the mouth may result in benign (non-cancerous) white patches. Various names have been used to describe particular examples of FK, including those resulting from excessive tooth-brushing force (toothbrush keratosis), the constant rubbing of the tongue against the teeth (tongue thrust keratosis), and that produced by the habit of chronic cheek or lip biting (cheek or lip bite keratosis). What are the signs and symptoms of FK? Most patients with FK are free of symptoms. A patient may notice a thickening of an area of skin in the mouth, or FK may be discovered by accident during a routine oral examination. What are the causes of FK? The white patches of FK that develop in the mouth are formed in the same way that calluses form on the skin of hands and feet. The most common causes are long term tissue chewing (biting the inside of the cheek or lips), ill-fitting dentures, jagged teeth, poorly adapted dental fillings or caps, and constant chewing on jaws that have no teeth. The constant irritation encourages the growth of keratin, giving the skin involved a different thickness and colour. -
Investigating Biomarkers of Keloid Scarring
Investigating Biomarkers of Keloid Scarring Zoe Drymoussi 2015 A thesis presented for the degree of Doctor of Philosophy Centre for Cutaneous Research, Blizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary, University of London 1 Declaration I, Zoe Drymoussi, declare that the work presented in this thesis is my own and has not been submitted in any form for another degree or diploma at any university or other institute of tertiary education. Information derived from the published or unpublished work of others has been acknowledged in the text and a list of references is given. Zoe Drymoussi, PhD Student 1st August 2015 2 Abstract Keloids are fibroproliferative scars that form in response to abnormal healing processes. The extracellular matrix (ECM) remodelling of the dermis in the maturation phase of normal wound healing is insufficient in keloids, leading to excessive ECM proteins being deposited in the granulation tissue. Keloid scars are unique to humans, and show increased prevalence in darker skin types. Current treatments rarely lead to permanent regression, and despite decades of study, the key molecular processes responsible for keloid scarring are still largely elusive. The research presented in this thesis aims to investigate markers of keloid scars, and to examine the impact of both the dermis and epidermis in keloid pathogenesis. Histological examination of the keloid scars showed a thickened epidermis and densely collagenous dermis, both of which demonstrated a higher level of cell proliferation and myofibroblast expression, as compared to normal skin. Differences between the central and marginal regions of the scars were also noted. -
Hair Loss in Infancy
SCIENCE CITATIONINDEXINDEXED MEDICUS INDEX BY (MEDLINE) EXPANDED (ISI) OFFICIAL JOURNAL OF THE SOCIETÀ ITALIANA DI DERMATOLOGIA MEDICA, CHIRURGICA, ESTETICA E DELLE MALATTIE SESSUALMENTE TRASMESSE (SIDeMaST) VOLUME 149 - No. 1 - FEBRUARY 2014 Anno: 2014 Lavoro: 4731-MD Mese: Febraury titolo breve: Hair loss in infancy Volume: 149 primo autore: MORENO-ROMERO No: 1 pagine: 55-78 Rivista: GIORNALE ITALIANO DI DERMATOLOGIA E VENEREOLOGIA Cod Rivista: G ITAL DERMATOL VENEREOL G ITAL DERMATOL VENEREOL 2014;149:55-78 Hair loss in infancy J. A. MORENO-ROMERO 1, R. GRIMALT 2 Hair diseases represent a signifcant portion of cases seen 1Department of Dermatology by pediatric dermatologists although hair has always been Hospital General de Catalunya, Barcelona, Spain a secondary aspect in pediatricians and dermatologists 2Universitat de Barcelona training, on the erroneous basis that there is not much in- Universitat Internacional de Catalunya, Barcelona, Spain formation extractable from it. Dermatologists are in the enviable situation of being able to study many disorders with simple diagnostic techniques. The hair is easily ac- cessible to examination but, paradoxically, this approach is often disregarded by non-dermatologist. This paper has Embryology and normal hair development been written on the purpose of trying to serve in the diag- nostic process of daily practice, and trying to help, for ex- ample, to distinguish between certain acquired and some The full complement of hair follicles is present genetically determined hair diseases. We will focus on all at birth and no new hair follicles develop thereafter. the data that can be obtained from our patients’ hair and Each follicle is capable of producing three different try to help on using the messages given by hair for each types of hair: lanugo, vellus and terminal. -
Nails Develop from Thickened Areas of Epidermis at the Tips of Each Digit Called Nail Fields
Nail Biology: The Nail Apparatus Nail plate Proximal nail fold Nail matrix Nail bed Hyponychium Nail Biology: The Nail Apparatus Lies immediately above the periosteum of the distal phalanx The shape of the distal phalanx determines the shape and transverse curvature of the nail The intimate anatomic relationship between nail and bone accounts for the bone alterations in nail disorders and vice versa Nail Apparatus: Embryology Nail field develops during week 9 from the epidermis of the dorsal tip of the digit Proximal border of the nail field extends downward and proximally into the dermis to create the nail matrix primordium By week 15, the nail matrix is fully developed and starts to produce the nail plate Nails develop from thickened areas of epidermis at the tips of each digit called nail fields. Later these nail fields migrate onto the dorsal surface surrounded laterally and proximally by folds of epidermis called nail folds. Nail Func7on Protect the distal phalanx Enhance tactile discrimination Enhance ability to grasp small objects Scratching and grooming Natural weapon Aesthetic enhancement Pedal biomechanics The Nail Plate Fully keratinized structure produced throughout life Results from maturation and keratinization of the nail matrix epithelium Attachments: Lateral: lateral nail folds Proximal: proximal nail fold (covers 1/3 of the plate) Inferior: nail bed Distal: separates from underlying tissue at the hyponychium The Nail Plate Rectangular and curved in 2 axes Transverse and horizontal Smooth, although -
Georgia TCSG Health and Safety
Chapter 1: Georgia TCSG Health and Safety 3 CE Hours Copyright ©October 2002-2015 State of Georgia All rights reserved. Georgia. Developed for the Georgia State Board of Cosmetology No part of this manual may be reproduced or transmitted in any form and the Georgia State Barber Board by the Technical College System or by any means, electronic or mechanical, including photocopying, of Georgia Formerly the Georgia Department of Technical and Adult recording, or by any information storage and retrieval system, Education (DTAE) Publication #C121002, Published December without written permission from the Technical College System of 2002, Revised November 2008. COURSE TABLE OF CONTENTS SECTION 1: SKIN, DISEASES, DISORDERS ● Anatomy and Histology of the Skin ○ Nerves of the Skin ○ Glands of the Skin ○ Nourishment of the Skin ○ Functions of the Skin ○ Terminology ● Diseases and Disorders ○ Skin Conditions/Descriptions ○ Nail Diseases/Disorders ○ Hair Disease/Disorders ○ Skin Conditions/Descriptions SECTION 2: BLOODBORNE PATHOGENS ● What are Bloodborne Pathogens? ● Hepatitis B Virus (HBV) ● Human Immunodeficiency Virus (HIV) ● Signs and Symptoms ● Transmission ● Transmission Routes ● Risk Factors and Behaviors ● Personal Protective Equipment SECTION 3: DECONTAMINATION & STERILIZATION ● Common Questions ● HIV ● Precautions SECTION 4: DECONTAMINATION AND INFECTION CONTROL ● Professional Salon Environment ● Safety Precautions ● Material Safety Data Sheet (M.S.D.S.) ● Organizing an M.S.D.S. Notebook SECTION 5: GEORGIA STATE BOARD OF COSMETOLOGY SANITARY