Hair Loss: Common Causes and Treatment T
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Pediatric and Adolescent Dermatology
Pediatric and adolescent dermatology Management and referral guidelines ICD-10 guide • Acne: L70.0 acne vulgaris; L70.1 acne conglobata; • Molluscum contagiosum: B08.1 L70.4 infantile acne; L70.5 acne excoriae; L70.8 • Nevi (moles): Start with D22 and rest depends other acne; or L70.9 acne unspecified on site • Alopecia areata: L63 alopecia; L63.0 alopecia • Onychomycosis (nail fungus): B35.1 (capitis) totalis; L63.1 alopecia universalis; L63.8 other alopecia areata; or L63.9 alopecia areata • Psoriasis: L40.0 plaque; L40.1 generalized unspecified pustular psoriasis; L40.3 palmoplantar pustulosis; L40.4 guttate; L40.54 psoriatic juvenile • Atopic dermatitis (eczema): L20.82 flexural; arthropathy; L40.8 other psoriasis; or L40.9 L20.83 infantile; L20.89 other atopic dermatitis; or psoriasis unspecified L20.9 atopic dermatitis unspecified • Scabies: B86 • Hemangioma of infancy: D18 hemangioma and lymphangioma any site; D18.0 hemangioma; • Seborrheic dermatitis: L21.0 capitis; L21.1 infantile; D18.00 hemangioma unspecified site; D18.01 L21.8 other seborrheic dermatitis; or L21.9 hemangioma of skin and subcutaneous tissue; seborrheic dermatitis unspecified D18.02 hemangioma of intracranial structures; • Tinea capitis: B35.0 D18.03 hemangioma of intraabdominal structures; or D18.09 hemangioma of other sites • Tinea versicolor: B36.0 • Hyperhidrosis: R61 generalized hyperhidrosis; • Vitiligo: L80 L74.5 focal hyperhidrosis; L74.51 primary focal • Warts: B07.0 verruca plantaris; B07.8 verruca hyperhidrosis, rest depends on site; L74.52 vulgaris (common warts); B07.9 viral wart secondary focal hyperhidrosis unspecified; or A63.0 anogenital warts • Keratosis pilaris: L85.8 other specified epidermal thickening 1 Acne Treatment basics • Tretinoin 0.025% or 0.05% cream • Education: Medications often take weeks to work AND and the patient’s skin may get “worse” (dry and red) • Clindamycin-benzoyl peroxide 1%-5% gel in the before it gets better. -
Clinical Presentation of Pili Torti - Case Report*
CASE REPORT 29 ▲ Clinical presentation of pili torti - Case report* Jeane Jeong Hoon Yang1 Karine Valentim Cade1 Flavia Cury Rezende1 José Marcos Pereira (In memoriam)1 José Roberto Pereira Pegas1 DOI: http://dx.doi.org/10.1590/abd1806-4841.20153540 Abstract: Pili torti also known as ‘twisted hairs’ (Latin: pili=hair; torti=twisted) is a rare, congenital or acquired clinical presentation, in which the hair shaft is fl attened at irregular intervals and twisted 180º along its axis. It is clinically characterized by fragile, brittle, coarse and lusterless hairs, due to uneven light refl ection on the twisted hair surface. Pili torti may be associated with neurological abnormalities and ectodermal dysplasias. There is no specifi c treatment for this condition, but it may improve spontaneously after puberty. We report a case of pili torti in a child who presented fragile, brittle, diffi cult to comb hair. The patient had no comorbidities. Keywords: Capillary fragility; Hair diseases; Rotation INTRODUCTION Pili torti is a congenital or acquired, dominant tion, audiometry and measurement of serum zinc were autosomal disease in which the hair shaft is fl attened performed. All results were within the normal range. at irregular intervals and twisted along its axis. It most The diagnostic hypothesis of pili torti was made. The commonly occurs in fair-haired girls, beginning in the patient remains in outpatient follow-up and shows second or third year of life. The hairs become dry, lus- age-appropriate neuropsychomotor development. terless, fragile and brittle. The condition may be asso- ciated with neurosensorial deafness1 and is probably caused by changes in the internal hair sheath. -
Alopecia Areata Part 1: Pathogenesis, Diagnosis, and Prognosis
Clinical Review Alopecia areata Part 1: pathogenesis, diagnosis, and prognosis Frank Spano MD CCFP Jeff C. Donovan MD PhD FRCPC Abstract Objective To provide family physicians with a background understanding of the epidemiology, pathogenesis, histology, and clinical approach to the diagnosis of alopecia areata (AA). Sources of information PubMed was searched for relevant articles regarding the pathogenesis, diagnosis, and prognosis of AA. Main message Alopecia areata is a form of autoimmune hair loss with a lifetime prevalence of approximately 2%. A personal or family history of concomitant autoimmune disorders, such as vitiligo or thyroid disease, might be noted in a small subset of patients. Diagnosis can often be made clinically, based on the characteristic nonscarring, circular areas of hair loss, with small “exclamation mark” hairs at the periphery in those with early stages of the condition. The diagnosis of more complex cases or unusual presentations can be facilitated by biopsy and histologic examination. The prognosis varies widely, and poor outcomes are associated with an early age of onset, extensive loss, the ophiasis variant, nail changes, a family history, or comorbid autoimmune disorders. Conclusion Alopecia areata is an autoimmune form of hair loss seen regularly in primary care. Family physicians are well placed to identify AA, characterize the severity of disease, and form an appropriate differential diagnosis. Further, they are able educate their patients about the clinical course of AA, as well as the overall prognosis, depending on the patient subtype. Case A 25-year-old man was getting his regular haircut when his EDITor’s KEY POINTS • Alopecia areata is an autoimmune form of barber pointed out several areas of hair loss. -
Short Anagen Syndrome: a Case Study
Journal of Cosmetics, Dermatological Sciences and Applications, 2012, 2, 14-15 http://dx.doi.org/10.4236/jcdsa.2012.21004 Published Online March 2012 (http://www.SciRP.org/journal/jcdsa) Short Anagen Syndrome: A Case Study Martina Alés Fernández, Francisco M. Camacho Martínez Department of Dermatology, Virgen Macarena University Hospital, Seville, Spain. Email: [email protected], [email protected] Received October 31st, 2011; revised November 18th, 2011; revised November 29th, 2011 ABSTRACT Short anagen syndrome is a relatively recently described entity. This syndrome is an unusual condition where the ana- gen growth phase of hair follicles is shorter than normal. Its clinical characteristics and trichogram findings contribute to the diagnosis of this trichosis. Keywords: Anagen Syndrome 1. Case Report Three-years-old girl with low density and slow growth scalp hair that had not been cut since birth. Her birth and medical history were unremarkable. The physical ex- amination revealed short and fine brown scalp hair with decreased density in frontoparietal areas (Figure 1). The rest of the physical examination was normal, without any abnormalities in eyelashes, eyebrows, teeth, nails or skin. The hair pull test was negative. The trichogram demon- strated some dystrophic hairs, but the most important data was an increased number of telogen hairs with a consistent decreased number of anagen hairs (Figure 2). The anagen to telogen ratio (7:28) was significantly re- duced with only 25% of hairs in anagen. 2. Discussion Short anagen syndrome is a relatively recently recog- nized entity poorly documented. Short hair due to a short anagen phase was described in 1987 by Kersey as part of tricho-dental syndrome [1]. -
Hypertrichosis in Alopecia Universalis and Complex Regional Pain Syndrome
NEUROIMAGES Hypertrichosis in alopecia universalis and complex regional pain syndrome Figure 1 Alopecia universalis in a 46-year- Figure 2 Hypertrichosis of the fifth digit of the old woman with complex regional complex regional pain syndrome– pain syndrome I affected hand This 46-year-old woman developed complex regional pain syndrome (CRPS) I in the right hand after distor- tion of the wrist. Ten years before, the diagnosis of alopecia areata was made with subsequent complete loss of scalp and body hair (alopecia universalis; figure 1). Apart from sensory, motor, and autonomic changes, most strikingly, hypertrichosis of the fifth digit was detectable on the right hand (figure 2). Hypertrichosis is common in CRPS.1 The underlying mechanisms are poorly understood and may involve increased neurogenic inflammation.2 This case nicely illustrates the powerful hair growth stimulus in CRPS. Florian T. Nickel, MD, Christian Maiho¨fner, MD, PhD, Erlangen, Germany Disclosure: The authors report no disclosures. Address correspondence and reprint requests to Dr. Florian T. Nickel, Department of Neurology, University of Erlangen-Nuremberg, Schwabachanlage 6, 91054 Erlangen, Germany; [email protected] 1. Birklein F, Riedl B, Sieweke N, Weber M, Neundorfer B. Neurological findings in complex regional pain syndromes: analysis of 145 cases. Acta Neurol Scand 2000;101:262–269. 2. Birklein F, Schmelz M, Schifter S, Weber M. The important role of neuropeptides in complex regional pain syndrome. Neurology 2001;57:2179–2184. Copyright © 2010 by -
Hair That Does Not Grow: Loose Anagen Hair Syndrome Versus Short Anagen Hair Syndrome
Central Annals of Pediatrics & Child Health Clinical Image *Corresponding author Norma E.Vázquez-Herrera, Hospital Zambrano Hellion Batallón San Patricio 112 Col. Real de San Agustín, San Hair That Does Not Grow: Pedro Garza García, México, Tel: 5281888880650; Email: Submitted: 03 March 2016 Loose Anagen Hair Syndrome Accepted: 29 April 2016 Published: 03 May 2016 Versus Short Anagen Hair Copyright © 2016 Vázquez-Herrera et al. Syndrome OPEN ACCESS Keywords Vázquez-Herrera NE1*, Sharma D2, Tosti A3 • Loose anagen hair syndrome • LAHS 1Departamen of MedicinaInterna, Tecnológico de Monterrey, México • Short anagen hair syndrome 2 Rutgers University, New Jersey Medical School, USA • SAHS 3 Department of Dermatology and Cutaneous Surgery, University of Miami, USA • Trichogram • Alopecia Abstract • Hair disorder • Pediatric hair loss Loose anagen hair syndrome (LAHS) is a hair disorder that is caused by defective • Painless extraction of hair anchorage of the hair shaft to the follicle and primarily affects children. Diagnosis is • Hair that will not grow made clinically by painless plucking of hair that does not grow long and confirmed • Short hair in child by a trichogram with distrophic anagen hairs. Short anagen hair syndrome (SAHS) is another hair condition in which anagen phase has a short duration and as a result, patients present with very short hair and often complain of increased shedding. In this second pathology, pull test shows extraction of telogen hairs with a pointed tip. Both of these diseases must be considered in pediatric patients that present with a complaint of hair that does not grow long. CLINICAL IMAGE encoding for companion layer keratin (K6HF) in patients with LAHS and wooly hair syndrome. -
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. -
Alopecia Areata: Evidence-Based Treatments
Alopecia Areata: Evidence-Based Treatments Seema Garg and Andrew G. Messenger Alopecia areata is a common condition causing nonscarring hair loss. It may be patchy, involve the entire scalp (alopecia totalis) or whole body (alopecia universalis). Patients may recover spontaneously but the disorder can follow a course of recurrent relapses or result in persistent hair loss. Alopecia areata can cause great psychological distress, and the most important aspect of management is counseling the patient about the unpredictable nature and course of the condition as well as the available effective treatments, with details of their side effects. Although many treatments have been shown to stimulate hair growth in alopecia areata, there are limited data on their long-term efficacy and impact on quality of life. We review the evidence for the following commonly used treatments: corticosteroids (topical, intralesional, and systemic), topical sensitizers (diphenylcyclopropenone), psor- alen and ultraviolet A phototherapy (PUVA), minoxidil and dithranol. Semin Cutan Med Surg 28:15-18 © 2009 Elsevier Inc. All rights reserved. lopecia areata (AA) is a chronic inflammatory condition caus- with AA having nail involvement. Recovery can occur spontaneously, Aing nonscarring hair loss. The lifetime risk of developing the although hair loss can recur and progress to alopecia totalis (total loss of condition has been estimated at 1.7% and it accounts for 1% to 2% scalp hair) or universalis (both body and scalp hair). Diagnosis is usu- of new patients seen in dermatology clinics in the United Kingdom ally made clinically, and investigations usually are unnecessary. Poor and United States.1 The onset may occur at any age; however, the prognosis is linked to the presence of other immune diseases, family majority (60%) commence before 20 years of age.2 There is equal history of AA, young age at onset, nail dystrophy, extensive hair loss, distribution of incidence across races and sexes. -
Dermatology Gp Booklet
These guidelines are provided by the Departments of Dermatology of County Durham and Darlington Acute Hospitals NHS Trust and South Tees NHS Foundation Trust, April 2010. More detailed information and patient handouts on some of the conditions may be obtained from the British Association of Dermatologists’ website www.bad.org.uk Contents Acne Alopecia Atopic Eczema Hand Eczema Intertrigo Molluscum Contagiosum Psoriasis Generalised Pruritus Pruritus Ani Pityriasis Versicolor Paronychia - Chronic Rosacea Scabies Skin Cancers Tinea Unguium Urticaria Venous Leg Ulcers Warts Topical Treatment Cryosurgery Acne Assess severity of acne by noting presence of comedones, papules, pustules, cysts and scars on face, back and chest. Emphasise to patient that acne may continue for several years from teens and treatment may need to be prolonged. Treatment depends on the severity and morphology of the acne lesions. Mild acne Comedonal (Non-inflammatory blackheads or whiteheads) • Benzoyl peroxide 5-10% for mild cases • Topical tretinoin (Retin-A) 0.01% - 0.025% or isotretinoin (Isotrex) Use o.d. but increase to b.d. if tolerated. Warn the patient that the creams will cause the skin to become dry and initially may cause irritation. Stop if the patient becomes pregnant- although there is no evidence of harmful effects • Adapalene 0.1% or azelaic acid 20% may be useful alternatives Inflammatory (Papules and pustules) • Any of the above • Topical antibiotics – Benzoyl peroxide + clindamycin (Duac), Erythromycin + zinc (Zineryt) Erythromycin + benzoyl peroxide (Benzamycin gel) Clindamycin (Dalacin T) • Continue treatment for at least 6 months • In patients with more ‘stubborn’ acne consider a combination of topical antibiotics o.d with adapalene, retinoic acid or isotretinoin od. -
Hirsutism and Polycystic Ovary Syndrome (PCOS)
Hirsutism and Polycystic Ovary Syndrome (PCOS) A Guide for Patients PATIENT INFORMATION SERIES Published by the American Society for Reproductive Medicine under the direction of the Patient Education Committee and the Publications Committee. No portion herein may be reproduced in any form without written permission. This booklet is in no way intended to replace, dictate or fully define evaluation and treatment by a qualified physician. It is intended solely as an aid for patients seeking general information on issues in reproductive medicine. Copyright © 2016 by the American Society for Reproductive Medicine AMERICAN SOCIETY FOR REPRODUCTIVE MEDICINE Hirsutism and Polycystic Ovary Syndrome (PCOS) A Guide for Patients Revised 2016 A glossary of italicized words is located at the end of this booklet. INTRODUCTION Hirsutism is the excessive growth of facial or body hair on women. Hirsutism can be seen as coarse, dark hair that may appear on the face, chest, abdomen, back, upper arms, or upper legs. Hirsutism is a symptom of medical disorders associated with the hormones called androgens. Polycystic ovary syndrome (PCOS), in which the ovaries produce excessive amounts of androgens, is the most common cause of hirsutism and may affect up to 10% of women. Hirsutism is very common and often improves with medical management. Prompt medical attention is important because delaying treatment makes the treatment more difficult and may have long-term health consequences. OVERVIEW OF NORMAL HAIR GROWTH Understanding the process of normal hair growth will help you understand hirsutism. Each hair grows from a follicle deep in your skin. As long as these follicles are not completely destroyed, hair will continue to grow even if the shaft, which is the part of the hair that appears above the skin, is plucked or removed. -
Hair and Nail Disorders
Hair and Nail Disorders E.J. Mayeaux, Jr., M.D., FAAFP Professor of Family Medicine Professor of Obstetrics/Gynecology Louisiana State University Health Sciences Center Shreveport, LA Hair Classification • Terminal (large) hairs – Found on the head and beard – Larger diameters and roots that extend into sub q fat LSUCourtesy Health of SciencesDr. E.J. Mayeaux, Center Jr., – M.D.USA Hair Classification • Vellus hairs are smaller in length and diameter and have less pigment • Intermediate hairs have mixed characteristics CourtesyLSU Health of E.J. Sciences Mayeaux, Jr.,Center M.D. – USA Life cycle of a hair • Hair grows at 0.35 mm/day • Cycle is typically as follows: – Anagen phase (active growth) - 3 years – Catagen (transitional) - 2-3 weeks – Telogen (preshedding or rest) about 3 Mon. • > 85% of hairs of the scalp are in Anagen – Lose 75 – 100 hairs a day • Each hair follicle’s cycle is usually asynchronous with others around it LSU Health Sciences Center – USA Alopecia Definition • Defined as partial or complete loss of hair from where it would normally grow • Can be total, diffuse, patchy, or localized Courtesy of E.J. Mayeaux, Jr., M.D. CourtesyLSU of Healththe Color Sciences Atlas of Family Center Medicine – USA Classification of Alopecia Scarring Nonscarring Neoplastic Medications Nevoid Congenital Injury such as burns Infectious Systemic illnesses Genetic (male pattern) (LE) Toxic (arsenic) Congenital Nutritional Traumatic Endocrine Immunologic PhysiologicLSU Health Sciences Center – USA General Evaluation of Hair Loss • Hx is -
Case of Persistent Regrowth of Blond Hair in a Previously Brunette Alopecia Areata Totalis Patient
Case of Persistent Regrowth of Blond Hair in a Previously Brunette Alopecia Areata Totalis Patient Karla Snider, DO,* John Young, MD** *PGYIII, Silver Falls Dermatology/Western University, Salem, OR **Program Director, Dermatology Residency Program, Silver Falls Dermatology, Salem, OR Abstract We present a case of a brunette, 64-year-old female with no previous history of alopecia areata who presented to our clinic with diffuse hair loss over the scalp. She was treated with triamcinolone acetonide intralesional injections and experienced hair re-growth of initially white hair that then partially re-pigmented to blond at the vertex. Two years following initiation of therapy, she continued to have blond hair growth on her scalp with no dark hair re-growth and no recurrence of alopecia areata. Introduction (CBC), comprehensive metabolic panel (CMP), along the periphery of the occipital, parietal and Alopecia areata (AA) is a fairly common thyroid stimulating hormone (TSH) test and temporal scalp), sisaipho pattern (loss of hair in autoimmune disorder of non-scarring hair loss. antinuclear antibody (ANA) test. All values were the frontal parietotemporal scalp), patchy hair unremarkable, and the ANA was negative. The loss (reticular variant) and a diffuse thinning The disease commonly presents as hair loss from 2 any hair-bearing area of the body. Following patient declined a biopsy. variant. Often, “exclamation point hairs” can be hair loss, it is not rare to see initial growth of A clinical diagnosis of alopecia areata was seen in and around the margins of the hair loss. depigmented or hypopigmented hair in areas made. The patient was treated with 5.0 mg/mL The distal ends of these hairs are thicker than the proximal ends, and they are a marker of active of regrowth in the first anagen cycle.