DERMATOLOGY

Professor: Ravelinda Soriano-Perez Trans by: Manlongat, Tangonan

TOPIC: HAIR DISORDERS

TOPIC OUTLINE
I. Alopecia II. Review Questions o Risk of male pattern baldness depends on the family
A. Androgenetic Alopecia III. References
history in the father, the mother, or the maternal
B. Telogen effluvium
C. Alopecia areata grandfather.
 Female AGA
I. Alopecia o Increased frequency of balding in first-degree male
CAUSES OF ALOPECIA relatives
 Nonscarring Alopecia ETIOLOGY
o Hair shafts are absent or miniaturized but hair  Multifactorial and polygenic.
follicles are preserved that is why nonscarring  Men
alopecia is reversible in nature. o Androgen hyperactivity. (Androgen-dependent trait)
o Primary Cutaneous Disorders  Dihydrotestosterone is the androgen chiefly
 Androgenetic Alopecia (AGA) responsible for the follicular pathology and acts
 Telogen effluvium primarily on dermal papilla.
 Alopecia areata  Women
 Traumatic Alopecia o Role of androgens in female AGA is less certain than
o Drugs in men, there is a subset of women with AGA.
o Systemic Diseases  Associated with hormonal dysregulation.
 Scarring Alopecia PATHOGENESIS
o Associated with fibrosis, inflammation, and loss of  Terminal hairs (large, pigmented hairs) are gradually
hair follicles. replaced by vellus hairs (fine, nearly invisible,
o Smooth scalp with decreased number of follicular colorless).
openings  There is gradual replacement of terminal hairs by vellus
o Discoid Lesions of Cutaneous Lupus is a classic hairs, called miniaturization.
example

Non scarring Scarring

A. Androgenetic Alopecia
EPIDEMIOLOGY
 Most common type of human hair loss.
 Increasing frequency with age (although the age of
onset may be at any age following puberty)
 Male > Female
o The frequency and severity of AGA is lower in women
than in men.
o 50%- 60% of men: age of 50 years
o 80% of men: ≥70 years
 Male AGA
o Strong paternal influence on the risk of balding
CLINICAL FEATURES
1. Male Pattern Hair Loss (MPHL), Hamilton-Norwood
Type
 Most frequent clinical pattern in men with AGA (only
occasionally observed in women).
 Characteristic Finding: Recession of the frontal hairline
(triangular pattern) → vertex thinning with progression
until the top of the scalp is completely bald
 Occipital area and sides of the scalp are spared.

1|P age
 FEMALE ANDROGENETIC ALOPECIA
 Elevation of circulating levels of androgens may be seen
as a result of ovarian or adrenal gland dysfunction or
neoplasm.
 Signs of virilization
o Deepened voice , Enlarged clitoris
2. Female Pattern Hair Loss (FPHL), Ludwig Type o Ovarian or adrenal gland tumor should be considered.
 Diffuse thinning of the centroparietal region with
maintenance of the frontal line.
 Most common type of AGA in women, occasionally
observed in men.
 Ludwig scale: three-point scale describing the pattern of
hair loss.

ASSOCIATED DISEASES
 Early vertex balding is associated with increased risk for:
o Coronary Heart Diseases
o Insulin Resistance
o Prostate Cancer

2|P age
DIAGNOSIS  Loss of Libido
 Generally, AGA is a clinical diagnosis.  Oral Finasteride & Minoxidil
 Longstanding, slowly progressing reduction of hair o Assess response to treatment at 6 months.
density (sometimes they don’t even notice) o In some men, it may not become evident before 12
 Hair thinning: months with oral finasteride.
o Accentuation of the frontal, parietal or vertex region o If successful, treatment should be continued to
o Diffuse thinning maintain efficacy.
o Initial signs: Pruritus and trichodynia  Finasteride
 Depending on the patient history and clinical evaluation, o Not indicated in women
further diagnostics may be necessary such as scalp o Contraindicated in pregnant women and women of
biopsy, however you have to get two specimens for the childbearing potential, because of the risk of
vertical and horizontal cut. Consider biopsy of the scalp as feminization of a male fetus.
bloody. Send the specimen to a dermatopathologist who’s o Finasteride-treated men must avoid donating their
trained on reading specimens on the scalp. blood.
CLINICAL COURSE AND PROGNOSIS  Cyproterone Acetate
 Naturally progressive.  Spironolactone
 Aim is the improvement or prevention of disease  17-estradiol
progression.  Low Level Light Therapy
o During the early, mild to moderate stages of the  Wigs and Hairpieces
disease.  Hair Restoration Surgery
 Significant distress, underestimated psychosocial impact. o Involves hair transplantation, less invasive.
 Extent of hair loss depends on the genetic predisposition. o Evolved into a microsurgical procedure.
TREATMENT o Follicular units of 1 to 4 hairs are transplanted in large
 Approved for the therapy of AGA in men: oral numbers and high densities.
Finasteride, topical Minoxidil o Result greatly depends on the skills of the surgical
 Minoxidil team and individual patient characteristics.
o Prevents further progression of the disease and leads o Hair surgery does not prevent the progression of AGA
to increase density and hair density and thickness in o In men, a combination of finasteride 1 mg and/or
both male and female patients older than 18 years old. topical minoxidil with follicular unit transplantation →
 Minoxidil 2% or 5% reduce postoperative progression of AGA.
o Biologic response modifier.
o Patients should be informed about transitory increased
telogen hair shedding usually appearing within the first
8 weeks of therapy initiation
o After end of therapy, increased hair loss follows.
 Lifelong treatment
 Main Side Effect: Hypertrichosis
 Others: Irritant and allergic contact dermatitis
 Advice patient to apply only on the bald part, because if
you apply it on unaffected area continuously, later on
you can see growing of hairs on that area
 Oral Finasteride
o Highly sensitive selective 5a-reductase type-2
inhibitor
o 1 mg/day, Male >18 years old (mild to moderate AGA)
o Combine with topical minoxidil → better efficacy
o Side Effects: Reduction of prostate-specific antigen
o Others: Impaired sexual function (should be explained
before considering this treatment, most patients
decline because of these side effects and prefer topical
minoxidil)
 Erectile Dysfunction
 Ejaculation Dysfunction
 Reduced Ejaculate Volume

3|P age
  Postpartum alopecia or telogen gravidarum
 Observed 2-3 months after childbirth
o Aging
 Diffuse hair loss in the scalp and body
o Weight loss (crash diet)
 Vigorous weight loss (11.7-24.75 kg within 3 week-3
months)  increase in telogen counts 25%-50%
 Calorie restriction of 0 to 1200 kcal per day
o Drugs (may cause CDTHL)
 Clinical Findings
o Sudden onset of massive shedding
o Anagen hairs are prematurely shifted into telogen hairs
o Normal anagen/telogen ratio of 90:10 can switch to
70:30
o “Bag sign”: bringing in bags with hair that have been
collected every day
B. Telogen Effluvium (TE)
 Premature termination of the anagen (growing) phase of
hair follicles → increase in telogen (resting) phase hairs
→ excessive and diffuse loss of club hairs

EPIDEMIOLOGY
 Females > Males
o Stronger awareness and more dynamic hormonal
changes (menstruation, gestation).
 Incidence in children: low
CLINICAL SUBTYPES
 Acute Telogen Effluvium (Acute TE)
 Chronic diffuse telogen hair loss (CDTHL)
 Chronic Telogen Effluvium (CTE) CHRONIC DIFFUSE TELOGEN HAIR LOSS (CDTHL)
ACUTE TELOGEN EFFLUVIUM (ATE)  Secondary to various causes.
 Most classic type of TE  Temporal insult triggers sudden-onset diffuse hair
 Acute and diffuse hair shedding, 2 to 4 months from shedding.
causative events  Recovers after the elimination of triggering-stress.
 No sign of inflammation or scarring.  Lasts > 6 months
 Regrowth of new anagen hairs by 3-6 months.  Possible triggers:
 Possible Triggers: o Thyroid disease
o Effluvium of the newborn o Aging
 Shedding starts within 4 mos after birth o Malnutrition
o Febrile illness o Iron Deficiency (controversial)
 Hair shedding 3-4 mos after illness and continues for o Zinc deficiency (severe cases)
3-4 weeks o Systemic illness
o Surgery – major surgery o Psychological stress (controversial)
o Pregnancy
4|P age
 o STI (HIV infection and syphilis)  Iron supplementation is recommended: ferritin level < 70
o Miscellaneous ng/mL
 It should be reversible and reproducible once the inciting  Topical 2% or 5% minoxidil solution: 1 mL twice daily
event has been managed. for women with prolonged hair loss with unknown triggers.
CHRONIC TELOGEN EFFLUVIUM (CTE) REPRESENTATIVE DRUGS CAUSE TELOGEN EFFLUVIUM
 Idiopathic form  Androgen hormone (testosterone, anabolic steroids,
 Middle-aged women, 4th to 6th decade proandrogenic supplements [DHEA], contraceptives
containing progesterone)
 > 6 months to several years with fluctuation
 Anticoagulants (heparins, warfarin, [possible;
 Telogen club hairs can be pulled out easily from the vertex dabigatran, rivaroxaban])
and occipital areas.  Antihistamines (cimetidine, ranitidine)
 Marked bitemporal recession of hair  Anti-infective agents
o Antifungals (clotrimazole, fluconazole, itraconazole,
terbinafine)
o Antivirals (acyclovir, imiquimod, indinavir)
o Antituberculosis (ethambutol, isoniazid)
o Antiparasitic drug (albendazole, mebendazole)
 Antimitotic agents (colchicine, methotrexate)
 Antithyroid agents (propylthiouracil, methimazole)
 Cardiovascular drugs
o ACE inhibitors (captopril, enalapril, moexipril,
HAIR EXAMINATION ramipril)
 Hair Appearance o Beta-adrenoceptor antagonists (metoprolol,
o global hair thickness and part width propranolol)
 Hair Loss Count  Disease-modifying antirheumatic drug (leflunomide)
 HPV vaccine
o Hair loss > 100, "gold standard"
 Dopamine precursor and agonists (levodopa,
 Hair Pull Test bromocriptine, pergolide pramipexole,)
o 40-60 hairs are grasped between the thumb and fingers  Interferons (Interferon a-2b, y)
and pulled firmly alongside with hair shafts.  Intravenous immunoglobulin
o Patient should not use shampoo for more than 24 hours  Metabolic disease therapeutics (allopurinol,
prior the examination. cholestyramine, clofibrate, fenofibrate, triparanol,
o At least 3 scalp areas (frontal, occipital, and temporal nicotinic acid)
regions).  Minoxidil (at initiation or withdrawal)
 Nonsteroidal antiinflammatories (ibuprofen, naproxen,
o Active hair shedding: > 10% of tested hairs were
salicylates)
collected.
 Oral contraceptives (cyproterone, drospirenone)
 Psychotropics
o Amphetamines
o Anticonvulsants (lamotrigine, phenytoin, valproic
acid)
o Antidepressants (fluoxetine, sertraline, tricyclic
antidepressants)
o Mood stabilizers (lithium, sodium valproate)
 Pyridostigmine bromide
 Retinoid, vitamin A and its derivatives (acitretin,
etretinate, isotretinoin)
 Spironolactone
 Sulfasalazine
CLINICAL COURSE AND PROGNOSIS SYSTEMIC DISEASES (TO RULE OUT)
 Variable  Lymphoproliferative disease
 Hair likely grows back around 6 months after removal  Advanced malignancy
of the initiating trigger.  Collagen disease (systemic lupus erythematosus and
 Favorable prognosis: no visible reduction, > 7-8 years hair dermatomyositis)
loss.  Hepatic disease
 Does not lead to complete baldness  Chronic renal failure
TREATMENT  Systemic amyloidosis
 Triggers identified and eliminated  Eosinophilia-myalgia syndrome
 Inflammatory bowel disease

5|P age
 C. Alopecia Areata
EPIDEMIOLOGY
 Male = Female
 Incidence at younger age is higher.
 Most common form of alopecia seen in children.
 Lifetime risk: 1.7%
 Familial occurrence is 15%

 Dermoscopy: “Black dots” (cadaver hairs, point noir

will confirm the diagnosis): resulting from hair that breaks
before it reaches the skin surface.

ETIOLOGY AND PATHOGENESIS

 Chronic, organ-specific autoimmune disease,
mediated by autoreactive CD8+ T-cells, which affects  Exclamation point hairs:
hair follicles. o With a blunt distal end and taper proximally.
 Melanogenesis-associated autoantigens: key target of o Appear when the broken hairs (black dots) are pushed
auto aggressive inflammation. out of the follicle.
 Many patients report the experience of major emotional
stress prior to the onset.
 Risk Factors:
o Genetic
 Positive family history: 10%-42% of cases
 Early-onset alopecia areata
o Major emotional stress
CLINICAL FINDINGS
 Presents with oval or round, well-circumscribed, bald
patches with a smooth surface in a diffuse distribution.

COURSE
 Very variable
 Irregular relapsing course
 Approximately 25% having solitary episode (single
episode)
PROGNOSIS
 5% risk → alopecia areata totalis
 1% risk → alopecia areata universalis
 Poor prognosis
o involvement of the occiput and/or hairline
o chronic relapsing course
o presence of nail changes
o childhood onset
 Nail involvement: nail pitting and sandpaper-like
appearance
6|P age
TREATMENT REFERENCE
 High rate of spontaneous remission  Dr. Perez’s Discussion and Powerpoint Presentation
 Topical corticosteroids: Super potent (class I) and  Trans 2023
potent (class II) clobetasol propionate, halobetasol
propionate, bethametasone dipropionate
 Intralesional corticosteroid injection: triamcinolone
acetonide 15- 40 mg/week x 4-6 weeks
 Systemic corticosteroid
 Topical minoxidil
 Anthralin
 Phototherapy
 Cyclosporine

REVIEW QUESTIONS
1. What do you call this sign of patients with hair loss?

Answer: “BAG SIGN” Bringing in bags with hair that have

been collected everyday

2. What is the most common MPHL?

Answer: Male pattern, Hamilton-Norwood type
3. What do you call these findings in alopecia areata?

Answer: Exclamation point hairs

4. Diagnosis

Answer: Alopecia Areata

7|P age