**6. Clinical findings**

**5. Functional types of telogen effluvium**

**5.1. Immediate anagen release**

**5.2. Delayed anagen release**

**5.3. Immediate telogen release**

**5.4. Delayed telogen release**

cause is seasonal hair loss [2, 16].

isolated disorder in otherwise healthy children [2, 16].

**5.5. Short anagen phase**

telogen early [14].

128 Hair and Scalp Disorders

release, delayed telogen release, and short anagen phase [2].

telogen hair can be seen after a couple of months of delivery [2, 15].

paradoxical phenomenon occurs, by stimulated anagen phase [2].

Headington defined five types of functional TE, according to the different follicular cycles. These include the immediate anagen release, delayed anagen release, immediate telogen

It is a common form of TE which is related to physiological stress, severe illness, and drug use. During stress, the cytokines induce apoptosis of hair follicle keratinocytes, first with catagen, followed by telogen [2]. Therefore, follicles, which are induced to leave the anagen, enter

It typically occurs in women with postpartum hair loss, and when the oral contraceptives are discontinued. It is also known as telogen gravidarum. It is caused by high levels of circulating placental estrogen, which prolongs the anagen phase, result in a full head of hair during pregnancy. The withdrawal of these hormones during delivery stimulates the overdue anagen hair to enter into the catagen phase simultaneously. As a result, an increased shedding of

Drug-induced shortening of telogen results in follicles with the reentry of the anagen prematurely [14]. Hair follicles typically release the club hair 100 days later. It is caused by a shortened normal telogen cycle. This type of hair shedding usually occurs 2–8 weeks, following therapy with topical minoxidil [16]. As the exogen hair at resting is released, this

Hair follicles do not shed or recycle into anagen, but remain in prolonged telogen. When teloptosis defined as the termination of telogen phase with hair shedding occurs, the main clinical manifestion of increased shedding of the club hair presents. In such cases, the major

Idiopathic shortening of anagen duration results in persistent telogen shedding. The condition is not associated with the hair shaft fragility or hair unruliness. It leads to resistant and chronic TE. It is common in hereditary hypotrichosis and ectodermal dysplasia and as an

#### **6.1. Acute telogen effluvium**

Women with acute TE are usually admitted with complaints of increased hair loss while washing hair and combing or brushing hair. These patients often have a concern of baldness. Despite excessive hair shedding, the density of the hair is visible [14]. If the main triggering cause of TE is eliminated, hair loss lasts for up to 6 months [1].

In the absence of a concomitant hair or scalp disorder, the scalp and hair shafts seem normal without any symptoms. In TE, the distribution of the scalp hair loss is diffuse; however, the bitemporal area may be the most affected area [10, 11]. In general, patients do not relate these events to their recent illness and have a concern of baldness [7]. In addition, no scarring or inflammation is present [2, 13].

To date, several factors have been suggested to be associated with the induction of TE, depending on clinical observations. However, there is no data to confirm and define the level of risk for TE related to these factors. It is estimated that an inciting factor is unable to be detected in about one-third of patients with acute TE [10].

In postpartum TE, time to hair loss often takes 2 or 3 months after delivery, although it can be delayed up to 6 months, depending on the length of the telogen phase. More interestingly, TE can be more pronounced, if delivery occurs in the fall, as the time of postpartum TE coincides with an increased seasonal hair shedding during the winter. In addition, breastfeeding may partially reduce TE with the effects of prolactin, since lactating women have an increased anagen-to-telogen ratio at 4 months in the postpartum period, compared to the nonlactating women. The condition often resolves by 12 months after delivery, even if breastfeeding continues [14, 17].

#### **6.2. Chronic telogen effluvium**

Women with chronic TE usually suffer from a prolonged, fluctuating course of TE for more than 6 months. In general, there is no trigger factor; however, some patients may have a continuation of acute TE with a shortened anagen phase, underlying a complaint of shortened hair as well as hair shedding seen in all patients with TE [13, 14].

In some cases, this type of hair loss may last for several years. Prolonged TE may be caused by multiple sequential triggers, although no trigger is identified in certain cases [1, 12].

In primary chronic TE, there is no specific triggering agent. Chronic TE can be induced by an acute TE [16]. Both hypothyroidism and hyperthyroidism are associated with chronic diffuse telogen hair loss (CDTHL). This is usually reversible upon reestablishment of the euthyroid state, although at times, longstanding hypothyroidism may cause hair follicle atrophy [18].

Iron deficiency anemia is also a causative factor of CDTHL, since follicles need iron to stimulate the anagen phase of the hair cycle [19]. The hair loss can be reversed with the iron supplementation. Iron deficiency without anemia is more controversial, as it has a potential relationship with CDTHL [20]. In the majority of cases, drug-induced CDTHL occurs mechanistically via the immediate anagen release [19]. It typically occurs within 6–12 weeks of treatment and progresses while on the medication. It, then, begins to resolve after the discontinuation of the drug [21]. To the best of our knowledge, no controlled trials showing a causal relationship for specific medications have been conducted; however, if a medication is suspected, it should be discontinued for a period of at least 3 months to examine its possible link to the hair loss [4, 14].

Moreover, diet is associated with the hair condition. Therefore, each patient should be questioned for the protein intake. Eating disorders can also lead to hair loss. In a study, 67% of the patients with TE had bulimia, while 61% had anorexia nervosa [22].
