Ioannides D, Tosti A (eds): Alopecias – Practical Evaluation and Management. Curr Probl Dermatol. Basel, Karger, 2015, vol 47, pp 55–66 (DOI: 10.1159/000369405) Hair Loss in Children Rubina Alves · Ramon Grimalt Department of Dermatology, Universitat Internacional de Catalunya, Barcelona, Spain Abstract Introduction Hair diseases represent frequent complaints in dermatol- ogy clinics, and they can be caused by a number of condi- Hair loss in children occurs in a wide range of tions reflected by specific diagnoses. Hair loss is not un- conditions that may be congenital or acquired. A common in the pediatric group, but its patterns in this congenital abnormality may be an isolated find- group are different from those seen in adults. Addition- ing in a healthy patient or may occur as a feature ally, in children, these disorders can have psychological of a multisystem syndrome. Recognition of a hair effects that can interfere with growth and development. disorder may enable the diagnosis of a particular Hair is easily accessible for examination, and dermatolo- syndrome. The clinical presentations of pediatric gists are in the enviable situation of being able to study hair disorders range from subtle to disfiguring. many disorders using simple diagnostic techniques. To Alopecia is not uncommon in the pediatric popu- fully understand hair loss during childhood, a basic com- lation but has patterns that are different from prehension of normal hair growth is necessary. Knowl- those seen in adults. The occurrence of these edge of the normal range and variation observed in the problems during childhood can cause psycholog- hair of children further enhances its assessment. This ical and emotional stress to both children and chapter has been written in an attempt to facilitate the their parents. A good knowledge of the normal diagnostic process during daily practice by helping to dis- hair cycle, embryology and clinical features is tinguish between acquired and congenital hair diseases. necessary. It can sometimes be difficult to differentiate between ab- normality and normality in neonatal hair aspects. Man- agement of hair disorders can be quite a daunting task Embryology and Normal Hair Development for the attending physician and mandates a holistic ap- proach to the patient. Some hair disturbances have no Hair follicles are derived from an interaction be- effective treatment, and for others, no single treatment is tween the embryological ectoderm and meso- 100% successful. If no effective treatment for a hair loss derm, which begins at 9 weeks of gestation. Pri- disease exists, a cosmetic approach is important. mary follicles first develop on the eyebrows, up- © 2015 S. Karger AG, Basel per lip and chin. Then, hair follicles develop over Downloaded by: UCONN Storrs 137.99.31.134 - 5/23/2015 4:42:42 PM the scalp in a frontal to occipital direction and tailed history is essential for an accurate diagno- progress over the body in a cephalocaudal direc- sis. The key points in a patient’s history are the tion [1]. By 18–20 weeks of gestation, the entire following: age of onset (congenital or acquired); initial population of follicles has formed, includ- onset of hair loss (sudden or insidious); extent of ing those on the scalp [2]. Each follicle is capable alopecia (localized or diffuse); physical and men- of producing three different types of hair as fol- tal development (underlying syndrome?); past lows: lanugo, vellus and terminal. Lanugo hair is medical history (surgery, autoimmune disease, nonmedullated, fine, soft, and usually nonpig- or medication); psychiatric disorders; and family mented, and it can be found on the bodies of history of alopecia [3, 5]. Similar to the history newborns. This type of hair is shed by 3–4 months evaluation, an exhaustive physical examination after birth. Vellus hair is short, fine, light-col- should be performed to assess the following ored, barely noticeable, and covers almost the components: type of alopecia (localized or gen- whole body. During puberty, the androgen hor- eralized/scarring or nonscarring); hypotrichosis mone causes most of vellus hair to turn into ter- or alopecia; hair shaft anomalies; hair quality; minal hair. Terminal hair is larger, thicker and and hair color. A thorough scalp examination strongly pigmented, and it is found on the scalp, is also important to evaluate the existence of eyebrows, axillary and pubic areas, chest and face erythema, edema, pustules, scaling, atrophy or [1]. scarring. Human hair grows in a continuous cyclic pat- The presence of short stature, abnormal bone tern known as the hair cycle. The hair cycle pres- development, defective hearing, dysmorphic fea- ents with different phases as follows: the anagen tures, impaired vision or other physical findings or growth phase (85–90% of hairs), the catagen or could indicate an underlying metabolic or auto- regression phase (<1% of hairs), the telogen or immune disease. resting phase (4–15% of hairs) and, finally, the Usually, the diagnosis of the most common shedding exogen phase. At birth, about 5 million forms of hair loss can be made only by clinical and hair follicles cover the human body, and approxi- physical examinations. A hair pull test distin- mately 100,000 are scalp hairs [2]. Newborn hairs guishes between loss from follicles and loss due to are all anagen, and during childhood, there is a hair shaft fragility. To perform this test, around gradual transition of scalp hairs from vellus to 50–60 hairs are grasped between the index finger terminal hairs [3]. and thumb and then lifted with gentle traction. The pull test is considered positive if more than 10% of hairs are released [5]. False positives can Diagnosis occur if the test is performed on a day in which hair has been washed. A newborn can have the following three presen- To confirm breakage of the hair shaft, a tug test tations of hair (normal variants): a full head of should be performed. The tug test consists of the hair, or little or no hair. The beginning of abnor- grasping of a hair between the finger and thumb mal hair growth sometimes occurs during infan- near its exit from the scalp and the pulling of the cy; thus, it is difficult to predict which newborn distal part [6]. If the hair is fragile, a fracture will will have a hair pathology. Knowledge of a pa- occur in the shaft. Trichoscopy, a noninvasive tient’s personal and family history, a thorough method, has emerged as a valuable tool in the dif- clinical examination, as well as general and spe- ferential diagnosis of most hair and scalp diseases. cific diagnostic procedures are important for a It is also important to evaluate the therapeutic re- correct diagnosis and early treatment [4]. A de- sponse of hair loss [7]. 56 Alves · Grimalt Ioannides D, Tosti A (eds): Alopecias – Practical Evaluation and Management. Curr Probl Dermatol. Basel, Karger, 2015, vol 47, pp 55–66 (DOI: 10.1159/000369405) Downloaded by: UCONN Storrs 137.99.31.134 - 5/23/2015 4:42:42 PM Alopecia Areata fect the scalp or any hair-bearing area on the body. This disorder is associated with nail in- Alopecia areata (AA) is a nonscarring, autoim- volvement, including nail pitting, trachyonychia, mune and inflammatory pattern of alopecia that brittle nails, onycholysis and koilonychia [16– occurs in both children and adults. It is a com- 18]. mon disorder, affecting different ethnicities with Trichoscopy examination reveals the pres- equal incidences between genders. The preva- ence of short ‘exclamation mark’ hairs at the pe- lence of AA is approximately 0.2% in the general riphery of the lesion (pathognomonic of AA) and population, and its lifetime risk is estimated to be ‘yellow dots’ in a follicular distribution. The hair approximately 1.7% [8]. Although AA has been pull test is typically positive in active AA with the considered rare in young infants, recent studies presence of telogen club hairs and dystrophic have suggested that this disorder could occur in anagen hairs [5, 19]. A scalp biopsy is usually un- 1–2% of patients less than 2 years of age [9]. In necessary to establish the diagnosis of AA, except children younger than 16 years of age, AA has in the case of diffuse shedding. The hallmark his- been reported to occur in 21–24% of patients [9, tological finding is a dense lymphocyte infiltrate 10]. comprising mainly T cells around the anagen The predisposition to AA is genetically deter- hair bulb matrix and the dermal papillae. The mined, with 5–25% of patients possessing a strong main differential diagnosis of AA in children in- family history [10, 11]. There is also an increased cludes tinea capitis, trichotillomania (TTM), frequency of AA in individuals with Down syn- transient neonatal hair loss (TNHL) and congen- drome [12–15]. AA may be seen in association ital triangular alopecia. with autoimmune disorders, such as atopic der- Tinea capitis is a common cause of patchy matitis, allergic rhinitis, asthma, vitiligo and au- hair loss in infants, although individuals of all toimmune thyroid disease [13]. ages are occasionally affected. This condition in- There are several clinical presentations of AA, volves the invasion of scalp hairs by dermato- which are usually classified according to the hair phyte fungi, including Trichophyton and Micros- loss pattern or extent. The classic presentations porum species. The clinical picture of this disease are as follows: patchy AA (the most common pat- varies according to host immunity, the degree of tern), alopecia totalis (the complete absence of inflammatory response and the type of hair inva- terminal scalp hair), and alopecia universalis (the sion by the pathogen. The key feature is patchy total loss of terminal scalp and body hair) [13]. hair loss with various degrees of inflammation Less frequent patterns of AA include the reticu- and scaling and the easy removal of hairs from lated pattern, ophiasis type, sisaipho type and dif- the affected area [19].