Dermatology & Coronavirus Disease 2019 (COVID- 19)

Home   »   Dermatology & Coronavirus Disease 2019 (COVID- 19)

Dermatology & Coronavirus Disease 2019 (COVID- 19)

Hair loss is a very common problem nowadays. Stress, hectic lifestyle, lack of hair care and nutritional deficiency are the common avoidable causes. Hair fall is not uncommon in the paediatric age group, but the patterns of it are quite different in children. It can cause psychological and emotional stress to both children and family.

To understand more of Dermatology & Coronavirus Disease 2019 (COVID- 19), first you need to know about normal hair development, types of hair and hair cycle.

Hair Development

Hair follicles are derived from interaction between embryological ectoderm and mesoderm, which begins at 9 weeks of gestation. Primary hair follicles first develop on eyebrows, upper lip and chin; then on scalp (frontal to occipital) and progress over body (cephalocaudal direction). By 18-20 weeks of gestation, entire body hair follicles are formed.

There are three types of hair

  • Lanugo hair- Nonmedullated, fine, soft and usually nonpigmented. Found on bodies of new born, shed in 3-4 months after birth.
  • Vellus hair- Short, fine, light-coloured, barely noticeable. Body hair are vellus hair. During puberty, androgen hormone turns most of vellus hair into terminal hair.
  • Terminal hair- Larger, thicker, strongly pigmented, found on scalp, eyebrows, axilla, pubic areas, chest and face (beard area).

During childhood, there is gradual transition of scalp hairs from vellus to terminal hairs.

Human hair grows in a continuous cyclic pattern known as Hair cycle. Different phases of hair cycle are:

  • Anagen or growth phase (85-90% of hairs; 2-6 years). Mitotically active matrix cells in the hair bulb differentiate and divide, resulting in hair growth.
  • Catagen or regression phase (< 1% of hairs; 3 weeks)
  • Telogen or resting phase (4-15% of hairs; 3 months)
  • Exogen phase or shedding phase.

New born can normally have a full head of hair, little or no hair.


Patient’s history-

  • Age of onset (congenital or acquired)
  • Onset of hair loss (sudden or insidious)
  • Extend of alopecia (localized or diffuse)
  • Physical and mental development (underlying syndrome)
  • Past medical history (surgery, autoimmune disease or medication)
  • Psychiatric disorders
  • Family history of alopecia

Physical examination

  • Type of alopecia (localized or generalized/ scarring or nonscarring)
  • Hypotrichosis or alopecia
  • Hair shaft anomalies
  • Hair quality and hair colour

Scalp examination

  • Presence of erythema, edema, pustules, scaling, atrophy or scarring.

Presence of short stature, abnormal bone development, defective hearing, dysmorphic features, and impaired vision suggest metabolic or autoimmune disease.

Hair pull test

  • Around 50-60 hairs are grasped between index finger and thumb and then lifted with gentle traction.
  • Should be performed at the vertex, parietal and occipital areas.
  • It is considered positive if >10% of hairs are released.
  • False positive result can occur if patient has washed hair on same day.
  • It chiefly distinguishes between loss from hair follicle and loss due to hair shaft fragility

Tug test

  • Grasp the hair between finger and thumb and near its exit from the scalp and pulling of the distal part
  • If hair is fragile, fracture will occur in the shaft.


  • Non-invasive
  • Used for differential diagnosis of most of hair and scalp diseases.
  • It is also useful for evaluating therapeutic response of hair loss management.

Alopecia Areata

Etiology: –

  • Prevalence- 1-2% in < 2 years; 21-24% in < 16 years of age.
  • Genetic- 5-25% has strong family history. Increased frequency in Down syndrome.

Association with autoimmune disorders- Atopic dermatitis, allergic rhinitis, asthma, vitiligo and autoimmune thyroid disease.

Clinical presentations: –

  • Classic presentations- Patchy AA (most common), alopecia totalis (complete absence of terminal scalp hair) and alopecia universalis (total loss of terminal scalp and body hair).
  • Less frequent patterns- Reticulated pattern, ophiasis type, sisaipho type and diffuse thinning over a part of or the total scalp.
  • Typical appearance- Well-demarcated localized single or multiple patches, asymptomatic, round or oval with smooth surface (no associated epidermal changes, such as scaling or erythema).
  • Nail involvement- Nail pitting, trachyonychia, brittle naily, onycholysis and koilonychia.

Diagnosis: –

  • Trighoscopy- Short ‘Exclamation mark’ hairs at the periphery of the lesion (pathognomonic of AA) and ‘yellow dots’ in follicular distribution.
  • Hair pull test- Positive in active AA with presence of telogen club hairs and dystrophic anagen hairs.
  • Scalp biopsy- Usually unnecessary, except in case of diffuse shedding. Hallmark histological finding is a dense lymphocyte infiltrate, comprising mainly T cells, around the anagen hair bulb matrix and the dermal papilla.

Differential diagnosis: –

  • Tinea capitis- Caused by dermatophytes Trichophyton or Microsporum species. Clinically patchy hair loss with various degrees of inflammation and scaling, and easily removal of hairs from the affected area. Trichoscopic hallmark is presence of comma hairs.
  • Trichotillomania (TTM) – Repetitive and self-induced compulsive hair pulling.
  • Transient neonatal hair loss (TNHL) – Also known as ‘Neonatal occipital alopecia’ – is a bald patch on occipital region. Initially, it was thought to be secondary to friction due to babies sleeping in supine position. It is physiological and appear from birth until second month of life. It resolves spontaneously.
  • Congenital triangular alopecia- Also known as ‘Temporal triangular alopecia’ or ‘Brauer nevus’. It is localized, congenital, nonscarring alopecia present at birth or acquired during the first 10 years of life. Lesions are triangular or lancet shaped, hairless or with very fine vellus hair, unilateral or bilateral, confined to front temporal region.

Treatment: –

  • Its natural history is uncertain. No consistently reliable treatment available. Spontaneous remission occurs within 1 year.
  • Topical corticosteroids (potent fluorinated corticosteroids), Systemic corticosteroids (for widespread AA or refractory AA) and Topical Minoxidil.
  • Topical immunotherapy- by provoking allergic contact dermatitis (with dinitrochlorobenzene, squaric acid dibutylester and diphencyprone), anthralin (induces inflammatory irritant dermatitis), phototherapy, immunosuppressants and immunomodulators.
  • Poor prognosis is there in presence of immune disease, atopy, family history of AA, young age of onset, nail involvement, excessive hair loss and ophiasis pattern.
  • Course of AA is totally unpredictable.

Androgenetic alopecia (AGA) in children

For development of androgenetic alopecia, presence of androgens is necessary in combination with genetically susceptible hair follicles. So it is not expected to occur in prepubertal child without abnormal androgen levels. Endocrine evaluation is recommended in such cases.

AGA is not uncommon in adolescents. Minoxidil topical solution is a well-tolerated and effective treatment option. Finasteride should be avoided in children below 18 years.

Disturbances of Hair cycle

Anagen Effluvium

Occurs within 1-2 weeks of insult.

Causes: –

  • Radiotherapy
  • Systemic chemotherapy (e.g. doxorubicin, cyclophosphamide, vincristine, or bleomycin)
  • Toxic agents’ intoxication (mercury, colchicine, boric acid intoxication; e.g. exposure or ingestion of household pesticides)
  • Ingestion of certain plants (Lecythis ollaria, Leucaena glauca)
  • Severe protein malnutrition

Diagnosis- By clinical history and presence of dystrophic anagen hairs.

Treatment- Remove the insult, normal hair regrowth will occur, because hair cycle was only temporary interrupted.

Loose Anagen Syndrome

The anchoring of growing anagen hairs to follicles is impaired, with a lack of adhesion of the hair shaft to the hair follicle.

At birth, the hair are normal, at the age of 2-3 years, it becomes unruly and remains so until it spontaneously become normal at the age of 5-7 years.


  • Clinically parents complain that there is no need for haircut, as hair does not grow long in such children.
  • Light microscopy- shows distorted anagen roots without inner root sheaths and ruffled cuticles.
  • Trichogram- Reveals preponderance of anagen haris (>97%).

No treatment is required, as there is spontaneous recovery.

Telogen Effluvium

It is a reaction pattern to pathologic or physiologic alteration in the health condition, in which a percentage of hairs move prematurely from anagen to telogen, resulting in diffuse increase in hair shedding.

It is less frequent in children, especially due to some sudden disease or trauma or nutritional cause (protein-calorie malnutrition, zinc deficiency, or starvation).

Diagnosis- Detailed history and clinical examination. Hair pull test is positive with >20% telogen hairs.

Treatment- of underlying disorder and hair supplements.


Traumatic Alopecia

Trichotillomania (TTM)

Repetitive and self-induced compulsive hair pulling. In infancy and early childhood, there is male predominance; while during puberty and adults, there is strong female predominance.

Clinically- Different shapes of areas of alopecia, with irregular borders and presence of hairs of different lengths. Typically there is no scaling, but some excoriations can be seen, and if hair are plucked persistently it may result in scarring.

Hair density is normal and hair pull test is negative. Trichoscopy reveals the presence of ‘flame hairs’ with the v-sign and tulip hairs, which are specific for TTM.

In children at preschool age, TTM is usually a habit comparable to thumb sucking. It has self-limited and benign course, with regrowth of hair by managing the condition conservatively.

In preadolescents to young adults (age 9-13 years), it is related to stress. These patients tend to have more chronic and relapsing courses. Patient without associated psychiatric conditions are benefited from behaviour modification programs. If associated with psychological/psychiatric disorders, referral to a psychiatrist is recommended. Serotonin-specific re-uptake inhibitors, Tricyclic antidepressants and N-acetylcysteine are prescribed.

Traction alopecia

It is caused by physical trauma, induced as a consequence of constant traction while hair styling (e.g. tight ponytails, cornrows or rollers).

Clinically patient presents with hair thinning, focal decrease in hair density and perifollicular erythema. Short broken hairs, folliculitis and follicular papules are seen. With prolonged traction, perifollicular scarring and cicatricial alopecia develop, which is more evident along the hairline.

During the early stage, alopecia is reversible with change in hairstyling methods. If patient maintains continuous traction, permanent hair loss occurs due to loss of hair follicle.

Hair shaft disorders

It can be inherited or acquired. They can be a marker, and hence aid in diagnosis of underlying disease.

  1. Hair shaft abnormalities with increased fragility and breakage
  • Trichorrhexis nodosa
  • Monilethrix (beaded hair)
  • Pili torti
  • Trichorrhexis invaginate (bamboo hair)
  • Trichothiodystrophy
  1. Hair shaft abnormalities Without increased fragility
  • Pili annulate (ringed hair)
  • Woolly hair syndrome
  • Uncombable hair (pili trianguli and canaliculi)

Special disorders with Hypotrichosis in children

  1. Congenital Atrichia and Hypotrichosis

Atrichia congenita is a rare form of irreversible alopecia with autosomal recessive mode of inheritance. It is associated with mutation in human hairless gen located on chromosome 8. There is follicular agenesis or programmed follicular destruction. Hair is sparse (or inexistent or lanugo hair) at birth and progress to total and permanent absence over the first few months to 5 years, and are never replaced. It occurs as isolated phenomenon or in association with some syndrome.

Congenital hypotrichosis is less severe form of atrichia congenita, in which hair is not absent but is diffusely thinned. There is profound reduction in number of hair follicles on the scalp. It is noticed clinically at the age of 2 years, because of variation in quality and quantity of hair normally present at birth. It occurs as an isolated defect.

  1. Marie-Unna Hereditary Hypotrichosis

It is a rare autosomal dominant condition, characterized by isolated progressive alopecia. At birth, the hair is normal or sparse. Around the third year of life, it becomes coarse and twisted, resembling an ‘ill-fitting wig’. During puberty, hair is gradually lost from the crown, causing complete baldness due to destruction of the follicles with scarring. Eyelashes, eyebrows and body hair are also sparse or absent.

  1. Ectodermal Dysplasia

It is a heterogenous group of inherited disorders affecting more than on ectoderm-derived tissue, leading to abnormalities of the hair, nails, epidermis, teeth and eccrine glands. Scalp hair is fine and short but silky in texture. Eyebrows and/or eye lashes are also affected.

Dr. Milap Jolapara
founder of SPARSH MD Skin & VD