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Olsen Handout 7/16/14 TELOGEN EFFLUVIUM DIFFUSE HAIR LOSS IN CHILDREN AND ADOLESCENTS Physical exam: • Global decrease in hair density – Confirm by performing midline Elise A. Olsen, M.D part in back and top of scalp Professor of Dermatology and Medicine —should be similar Director, Hair Disorders • Preservation of follicular ostia on Research and Treatment Center scalp and scalp is generally normal Duke University Medical Center EAOlsen Society for Pediatric Dermatology Annual Meeting Coeur d’Alene, Idaho, July 2014 Hair Loss Evaluation in Etiology of Telogen Effluvium Telogen Effluvium: Hair Pull • Look for causes that occurred 3-6 months prior to onset • Grasp a small clump of hair at the roots and – Stress gently pull through to the ends. Be very gentle with this in young children. EAOlsen – Medical or surgical event especially thyroid related • Repeat in representative areas of entire scalp – Medications Telogen hairs including occiput. Hair pull in TE should be – Nutritional positive in all areas. 3-4 hairs/ pull is abnormal. • Perform microscopic hair exam of proximal ends • Protein (kwashiokor) of hairs EAOlsen • Calories (maramus) – All hairs in an adolescent with TE should be • Vitamins telogen hairs--any anagen hairs are abnormal Loose Anagen Hair – In children less than 5 years, one can artificially – Biotin induce “loose anagen” like hairs on too firm hair – Zinc pull which can confuse picture – Iron EAOlsen Telogen Effluvium and Medications Biotin Deficiency • Relationship to hair loss raised because of the biotin • Any medication can cause TE but ones of particular responsive hair loss associated with hereditary forms of biotin deficiency (holocarboxylase and biotinidase) concern in children/adolescents • Acquired forms of biotin deficiency – Isotretinoin – Parental alimentation – Vitamin A doses of >15,000 IU – Egg white diet – Lithium (evaluate for lithium hypothyroidism) – Gastric disease – Sodium valproate—alters zinc and selenium – IBD homeostasis and causes hyperandrogenism so may – Chronic hemodialysis also promote AGA – Medications: Lipoic acid, certain anticonvulsants – Amphetamine for weight loss (carbamazepine, phenobarbital, phenytoin) – Medications for ADHD – Antidepressants 1 7/16/14 Biotin Deficiency Zinc Deficiency • Hereditary: AR, abnormal gene SLC39A4 on Chromosome 824.3 Clinical Picture: which encodes Zip 4 transporter important in GI absorption • Full blown: infancy; neurological defects, dermatitis • Acquired especially periorificial, keratoconjunctivitis, hair loss – Abnormal absorption • Pancreatitis • Partial: later childhood, less severe symptoms-- • Intestinal bypass or short bowel syndrome seborrhea or eczema, depression, lethargy, • Crohn’s disease or ulcerative colitis paresthesias, thin hair +/- loss of hair color • Celiac disease Diagnosis: • Diet high in phytates (refined cereals), fiber • Biotin level, +/-ketoacidosis and lactic acidosis, organic – Certain drugs: sodium valproate, penicillamine, diueretics acidosis – Inadequate diet • Biotinidase <5% in severe, 15-30% NL in partial – Increased urinary excretion related to alcohol Treatment: Biotin 10 mg/day. Oral and topical EFA – Chronic renal disease noted to help – Sickle cell disease – Liver disease Acquired Zinc Deficiency Zinc Deficiency Clinical findings • Treatment: • Poor appetite – Supplemental zinc: 0.5-1 mg/kg/day x up to 6 months. • Mild growth retardation UL tolerated dose=40 mg/day • Hypogonadism (low T) – Monitor both zinc, copper/ceruloplasm and iron levels as • “Rough” skin zinc will depress copper absorption through induction • Mental lethargy metallothionein and can lead to a non-iron responsive • Taste abnormality microcytic anemia and neutropenia and also impair iron • Impaired wound healing absorption • Increased susceptibility to infections • Maintenance zinc: • Hair loss • 1-10 years: 10 mg/day Diagnosis: Serum zinc <70 ug/dL. Have drawn fasting and • >10 years: 15 mg/day off of supplements containing zinc • Potential for high zinc levels: Zinc lozenges for colds: doses range from 5-14 mg per Iron Deficiency (ID) and Hair Loss Identification of Iron Deficiency • Many publications have linked either low levels of iron or lower ferritin levels in hair loss patients compared to controls • Most studies use serum ferritin which is an excellent – Difficulties in proving the interrelatedness of ID and hair indicator of iron stores in healthy patients as only iron loss have included: deficiency causes low serum ferritin • Definition of ID is not uniform across all previous • Acute phase reactant with elevation in the face of studies (ferritin <10 ug/L to <70 ug/L used) inflammation • Many publications without control population • Serum levels used to identify ID: • Control populations have been drawn from varied • <10-15 ng/mL: sensitivity 75%, specificity 98% populations, of small numbers (largest =46 subjects • <40 ng/mL has sensitivity 98%, specificity 98% prior to Duke study of 96) and not necessarily screened • <70 ng/mL is reasonable level to define ID in patients for hair loss with underlying inflammatory disease. • Many articles disputing relationship of hair loss and ID >70 ng/mL is the benchmark for assuring adequate BM • No well controlled trials showing whether treatment of ID affects hair growth iron stores 2 7/16/14 Iron Deficiency in Children and Adolescents Duke Study on Iron Deficiency in FPHL, CTE and Controls* • Risk Factors • All subjects were Caucasian women who had not been – Rapid body growth pregnant in the past year and on no anticoagulants – Heavy menses • Controls – Pregnancy – Selected from volunteers who were screened for normal hair growth, good health, and who had serum ferritin, ESR – GI bleeding: Aspirin, NSAID (1 ml blood=0.5 mg iron) and hemoglobin obtained in absence of iron – Inadequate diet supplementation – Erythrodermic skin conditions • Hair loss subjects: – Poor absorption—celiac disease one cause – Olsen Hair Disorders Database utilized to identify those with established diagnosis of FPHL or CTE who had a – Genetic deficiency of key iron enzyme. Note ferritin is serum ferritin and hemoglobin an unreliable indicator of these conditions – History on iron supplementation at time of blood draw unknown and no ESR available majority *Olsen EA, Reed KB, Cacchio PC, Caudill L: Iron deficiency in female pattern hair loss, chronic telogen effluvium, and control groups. J Am Acad Dermatol. 63(6):991-9, 2010. Results of Duke Iron Deficiency Study Treatment of Iron Deficiency Serum Ferritin Levels • Increase heme iron in diet (meat, poultry, fish—2-3x Number Group absorption over iron-fortified or foods with non- subjects heme iron ≤ 15 µg/L ≤ 40 µg/L ≤ 70 µg/L • Absorption of iron supplements varies with type of Controls N=76) 21.1% 52.6% 81.6% iron: – 20% ferrous sulfate. 325 mg of ferrous sulfate CTE N=121 11.5% 53.1% 75.0% delivers about 60 mg of elemental iron. – 12% ferrous gluconate FPHL N=285 7.7% 45.6% 75.4% – 33% ferrous fumerate. Olsen EA, Reed KB, Cacchio PC, Caudill L: Iron deficiency in female pattern hair loss, chronic telogen effluvium, and control groups. J Am Acad Dermatol. 63(6):991-9, 2010. Treatment of Iron Deficiency Screening Labs for Telogen Effluvium • Divide total dose into multiple doses on an empty stomach and start with ferrous sulfate • Ideally do all tests off of any vitamin supplements for at (GI irritation/absorption best) least 24 hours • Absorption increased in mildly acidic medium— • CBC with diff Vitamin C, no food • TSH and free T4 • Absorption decreased with: antacids, proton pump • Ferritin inhibitors, levothyroxine, levodopa, • Iron/TIBC (% transferrin sat) or ESR as further screen for cholestyramine, calcium and certain foods [soy potential inflammation skewing ferritin products, tannates (tea)] • If severe dietary issues, consider a fasting zinc and biotin • Treatment should try to replace to normal levels ie level in healthy subject to serum ferritin 40 ug/L 3 7/16/14 Diffuse Alopecia Areata Loose Anagen Syndrome* Alopecia areata may present with diffuse loss that can mimic telogen effluvium or severe FPHL EAOlsen Estimated incidence <3% of children (Katsarou A. JAAD 2014) Type A Type B Type C Key features are the positive hair pull for EAOlsen EAOlsen EAOlsen dystrophic anagen hairs and presence EAOlsen - Diffuse thinning of “exclamation point” hairs on - Short and very slow-growing physical exam - +/- change in hair texture Yellow dots common on dermoscopy EAOlsen -Onset usually < 8 y. o. EAOlsen Look for nail abnormalies and hair loss -+ Hair pull for primarily LA EAOlsen on body, eyebrows or eyelashes EAOlsen - hairs, some telogen hairs Biopsy may only show miniaturization *Olsen EA, Bettencourt MS, Cote N: The presence of loose anagen hairs obtained by hair pull in the normal population. J Investig Dermatol Symp Proc (suppl) 4:258-260, 1999. Short Anagen Syndrome* Androgenetic Alopecia in Adolescents • Young children • Presents as decreased • Clinical Clues density, increased shedding – Both girls and boys: widened part may be only and inability to grow hair sign long – Absolute sparing occiput • Etiology is short anagen EAOlsen – Bitemporal recession phase – Hair pull: negative except in affected areas and • Hair pull is key: telogen hairs only – Proximal ends: may be – Variability in hair diameter central>occipital increased but only telogen scalp hairs – +/- perifollicular pigmentation on dermoscopy – Distal ends (if no hair cut): EAOlsen tapered ends *Antaya RJ, Sideridou E, Olsen EA.: Short anagen syndrome. JAAD, 53: S130-S134, 2005.
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