Telogen effluvium

INTRODUCTION — Telogen effluvium is a form of diffuse, nonscarring hair loss that presents as a transient or chronic loss of hair (picture 1A-C). Hair loss in telogen effluvium occurs as a result of an abnormal shift in follicular cycling that leads to the premature shedding of hair. (See "Evaluation and diagnosis of hair loss", section on 'Hair cycle'.)

A wide variety of endogenous and exogenous factors have been linked to the induction of telogen effluvium. Examples include major surgery, serious illness, childbirth, protein or caloric malnutrition, drugs, and severe emotional distress. In some cases, the inciting cause is unclear or multiple inciting triggers are identified.

The clinical features, diagnosis, and management of telogen effluvium will be reviewed here. An overview of the evaluation of patients with scalp hair loss is provided separately. (See "Evaluation and diagnosis of hair loss".)

EPIDEMIOLOGY — Data on the epidemiology of telogen effluvium are limited. The disorder is one of the most common forms of nonscarring hair loss for which patients present for clinical evaluation [1]. Telogen effluvium does not appear to have a predilection for particular racial or ethnic groups.

Most experts divide telogen effluvium into acute and chronic variants:

●Acute telogen effluvium – Acute telogen effluvium may occur at any age, including infants and children [2,3]. For unclear reasons, women are more likely to present for evaluation of acute telogen effluvium than men [4]. (See 'Clinical features' below.)

●Chronic telogen effluvium – Chronic telogen effluvium is much less common than the acute variant and is most frequently diagnosed in women between the ages of 30 and 60 years [5,6]. Chronic telogen effluvium can be further subdivided into chronic and chronic-repetitive clinical presentations. (See 'Clinical features' below.)

PATHOGENESIS — The excessive hair shedding that characterizes telogen effluvium occurs as a result of altered regulation of the hair follicle growth cycle:

●Normal hair cycle – Normally, each follicle on the human scalp cycles independently through three major phases: anagen (growth), catagen (transformation), and telogen (rest). The end of the three-month telogen phase is marked by the shedding of hair from the follicle [4]. (See "Evaluation and diagnosis of hair loss", section on 'Hair cycle'.)

The asynchronous cycling of scalp hair follicles in humans prevents periodic episodes of mass shedding of hair. Rather, shedding of hair occurs on a continuous basis. In the absence of scalp or hair disorders, 50 to 150 hairs are typically shed each day [7].

●Hair cycle changes in telogen effluvium – Telogen effluvium occurs when the proportion of hair follicles in the telogen phase increases significantly, resulting in subsequent prominent shedding of hair. On the normal human scalp, only approximately 10 percent of follicles are in the telogen phase at any given time, while anagen and catagen follicles account for approximately 90 and <1 percent of follicles, respectively [8]. In telogen effluvium, it is estimated that 7 to 35 percent of the follicles that normally would have remained in the anagen phase shift into the telogen phase [9].

●Proposed mechanisms for telogen hair loss – The mechanism of hair loss in telogen effluvium is not completely understood. It is generally accepted that an identifiable or occult, physiologic event stimulates a change in follicular cycling due to an insult to the anagen bulb (one of the two hair growth centers).

Several theories of the mechanism of hair loss have been proposed, some of which have been associated with specific stimuli for telogen effluvium [10]. Immediate anagen release and delayed anagen release are the most commonly cited theories:

•Immediate anagen release – Immediate anagen release may be a common mechanism for telogen effluvium. According to this theory, a significant proportion of anagen follicles are stimulated to enter telogen prematurely. Immediate anagen release may be the primary mechanism for telogen effluvium related to physiologic stress (eg, high fever) or drugs [10].

•Delayed anagen release – The theory of delayed anagen release describes prolongation of the duration of anagen, thereby delaying the onset of telogen. Hair loss is noted once the stimulus for sustaining anagen ends and the affected follicles enter telogen and, subsequently, shed. Delayed anagen release may be the primary mechanism for postpartum telogen effluvium [10,11].

Additional theories for the mechanism of telogen effluvium have been proposed [10,12]. Abnormal shortening of the anagen phase could contribute to an increase in hair shedding by augmenting the proportion of follicles in the telogen phase. In addition, shortening of the telogen phase could lead to the simultaneous release of hair from a large proportion of telogen follicles (immediate telogen release). Reduced variance in the duration of anagen has been proposed as a mechanism of chronic telogen effluvium [12]. Last, a delay in telogen release could lead to an increase in hair shedding due to the sudden release of hairs from follicles that were stimulated to remain in the telogen phase for an extended period. Delayed telogen release may account for seasonal fur shedding in mammals.

INCITING FACTORS — A wide variety of factors have been associated with the induction of telogen effluvium based upon clinical observations. However, data to confirm and define the level of risk for telogen effluvium related to these factors are lacking.

It is estimated that in approximately one-third of patients with acute telogen effluvium, an inciting factor cannot be identified [4]. The cause of chronic telogen effluvium is usually more difficult to identify, but careful history taking can be helpful. (See 'Diagnosis' below.)

Potential inciting factors for telogen effluvium include:

●Acute or chronic major illness (eg, systemic rheumatic disease [collagen vascular disease] [13], febrile illness, major surgery)

●Childbirth (telogen gravidarum)

●Significant emotional stress

●Nutritional changes:

•Rapid weight loss

•Protein or caloric dietary restriction

•Nutritional deficiencies (eg, iron deficiency anemia, congenital or acquired zinc deficiency, vitamin D)

●Endocrine disorders (eg, hypothyroidism, hyperthyroidism, androgen excess)

●Drugs, supplements, or toxins (eg, heavy metals [14]) (table 1)

●Inflammatory conditions of the scalp (eg, seborrheic dermatitis, psoriasis)

●Infectious conditions that affect the scalp (eg, fungal, bacterial, viral, or spirochetal)

Lower serum vitamin D and serum ferritin (iron storage) levels have been proposed as contributors to telogen effluvium; however, data are insufficient to confirm a causative relationship. Observational studies have suggested a correlation between low serum levels of vitamin D and telogen effluvium [15-18]. Vitamin D receptors are found in epidermal keratinocytes and mesodermal dermal papilla cells and are postulated to play an important role in hair follicle cycling [19]. Studies evaluating the relationship between serum ferritin levels and telogen effluvium have yielded conflicting results [15,16,20-28].

CLINICAL FEATURES — The major clinical finding in telogen effluvium is an acute or chronic reduction in scalp hair density (picture 1A-C). Less than 50 percent of scalp hair is typically lost. Therefore, progression to complete balding does not occur [5].

Because only a portion of the hair is lost, the severity of hair loss may not be readily apparent in patients with a history of voluminous hair prior to the onset of telogen effluvium. In such cases, the patient history and viewing of prior photographs may provide the clinician with a clearer idea of the change in hair density.

The progression of telogen effluvium typically follows one of two courses (figure 1):

●Acute telogen effluvium – Telogen hair loss develops within two to three months after the inciting factor and reverses once the inciting factor is eliminated. The time for clinically relevant hair regrowth is between 6 to 12 months since length of hair is important for the perception of regrowth.

●Chronic telogen effluvium – An idiopathic condition in which telogen hair loss persists for more than four to six months. Some patients develop a chronic-repetitive pattern of telogen effluvium that is punctuated by serial episodes of acute hair loss as a result of multiple intermittent triggers.

The distribution of scalp hair loss in telogen effluvium is typically diffuse; however, hair loss may be most noticeable in the bitemporal (picture 1B, 1D), frontal, and vertex areas [5]. A patchy or "moth-eaten" pattern of hair loss is often evident in syphilis-related telogen effluvium (picture 2A-B).

In the absence of a concomitant hair or scalp disorder, the scalp and hair shafts appear normal, with normal variation in hair shaft diameters, and symptoms are absent. In addition to the scalp, telogen effluvium may affect other hair-bearing areas [9,29].

Hair loss due to telogen effluvium may lead to the recognition of a pre-existing hair loss disorder that was not as obvious previously. For example, this may occur in patients with early-stage male or female androgenetic alopecia or central centrifugal cicatricial alopecia. (See "Male pattern hair loss (androgenetic alopecia in males): Pathogenesis, clinical features, and diagnosis" and "Female pattern hair loss (androgenetic alopecia in females): Pathogenesis, clinical features, and diagnosis" and "Central centrifugal cicatricial alopecia".)

HISTOPATHOLOGY — An increased proportion of telogen follicles is the key histopathologic finding [30]. Unlike androgenetic alopecia, the proportion of vellus or indeterminate hair follicles is not increased [6]. Therefore, variation in hair shaft diameters is much less than that observed in androgenetic alopecia.

In the absence of co-occurring inflammatory disorder of the scalp, scalp biopsies from patients with telogen effluvium do not demonstrate inflammation. Biopsies taken from patients with telogen effluvium induced by inflammation in the scalp will demonstrate an increased proportion of telogen follicles as well as histopathologic findings consistent with the inciting inflammatory disorder. As an example, biopsies of syphilitic alopecia usually demonstrate characteristic lymphoplasmacytic, perivascular, and perifollicular infiltrates [31]. (See "Seborrheic dermatitis in adolescents and adults", section on 'Histopathology'.)

DIAGNOSIS — The recognition of diffuse, noninflammatory, nonscarring hair loss should raise clinical suspicion for telogen effluvium, particularly when it occurs acutely and is preceded by a physiologic or psychologic stressor.

A diagnosis of acute telogen effluvium can usually be made based upon the patient history, physical examination, and a hair pull test. Scalp biopsies are helpful for evaluating patients in whom the diagnosis is unclear and as a component of the diagnostic evaluation of hair loss in patients with findings suggestive of chronic telogen effluvium. (See 'Clinical features' above.)

Patient history — The patient history is of great value in the evaluation of the patient with suspected telogen effluvium. A thorough patient history confirms a course of hair loss consistent with telogen effluvium, may reveal the underlying cause(s) of telogen effluvium, and is useful for ruling out other causes of hair loss. In older adult patients or other patients with multiple medical disorders, the cause of telogen effluvium may be multifactorial. (See 'Inciting factors' above and "Evaluation and diagnosis of hair loss".)

Key inquiries include:

●Course of hair loss (date of onset, duration, apparent triggers)

●Characteristics of hair loss (estimated amount of hair lost daily, appearance of lost hair shafts [intact versus broken hairs])

●Medical history (see 'Inciting factors' above):

•Recent or chronic medical illness

•Major surgeries

•Rapid weight loss

•Restricted diets

•Recent childbirth, miscarriage, or abortion

•Iron deficiency anemia

•Nutritional deficiency (ie, zinc, protein, iron, ferritin, vitamin D)

•Thyroid disorder

•Review of systems to identify unknown underlying disorders

●Psychologic stressors

●Drug and nutritional supplement history

●History of toxic exposure

●Family history of hair disease(s)

In addition, the patient history may provide clues that a different (or concomitant) hair loss disorder is present. Inquiring about the menstrual and reproductive history of women may lead to consideration of the possibility of androgenetic alopecia due to androgen excess or conditions such as polycystic ovarian syndrome (PCOS). Similarly, a careful family history may elucidate information that raises suspicion for a heritable hair loss disorder, such as androgenetic alopecia, which may lead to increased shedding associated with shortening of the anagen phase. (See "Evaluation and diagnosis of hair loss", section on 'Inherited and acquired structural hair disorders'.)

Physical examination — Patients should receive a careful examination of the scalp skin, scalp hair, and nails (see "Evaluation and diagnosis of hair loss", section on 'Physical examination'):

●Scalp – The entire skin surface of the scalp should be examined to identify the extent of hair loss and to detect features of other hair or scalp disorders. Scale, inflammation, pustules, and scarring (evidenced by loss of follicular ostia or a bound-down appearance of skin) are not features of isolated telogen effluvium. The detection of such findings suggests the presence of a different (or concomitant) scalp disorder. As an example, greasy scale and erythema on the scalp suggests the possibility of seborrheic dermatitis, a common disorder associated with telogen effluvium and androgenetic alopecia. (See 'Inciting factors' above.)

●Hair shafts – Abnormalities of the hair shaft are also not features of telogen effluvium. If many broken hairs are visualized in a patient with a complaint of hair loss, the clinician should consider the possibility of heat- or chemical-related damage to the hair shaft, trichotillomania, or a structural hair disorder. (See "Evaluation and diagnosis of hair loss", section on 'Scalp and hair examination'.)

●Nails – Examination of the nails should be performed and may offer clues to the cause of telogen effluvium. As examples, Beau lines in the nails suggest the recent occurrence of a significant medical illness (picture 3A-B), and patients with iron deficiency anemia may demonstrate koilonychia (nail "spooning" (picture 4)). (See "Overview of nail disorders", section on 'Nail signs of systemic diseases'.)

Hair pull test — A hair pull test should be performed on multiple sites of the scalp as part of the physical examination in patients who present with clinical findings suggestive of telogen effluvium. The test aids in the recognition of active hair shedding and the identification of telogen hair loss. A hair pull test will be negative in patients in whom hair shedding secondary to telogen effluvium has ceased.

The procedure is as follows:

●Grasp 50 to 60 hair fibers close to the skin surface.

●Gently tug the hairs from the proximal to distal ends.

●Repeat the hair pull in several areas of the scalp (eg, right parietal, left parietal, and frontal scalp).

●Examine the hair shafts with a light microscope to confirm that the loose hairs are telogen hairs (picture 5). Examination of the proximal portion of the hair can identify a telogen bulb. Other features, such as dystrophic anagen bulb or trichorrhexis nodosum, suggest the presence of other hair disorders. (See "Evaluation and diagnosis of hair loss", section on 'Microscopic examination' and "Hair shaft disorders".)

The extraction of five or more telogen hair fibers in a single pull or more than 15 telogen hairs in three pulls is consistent with active telogen effluvium.

Of note, a false-negative hair pull test can occur if the patient has shampooed or vigorously groomed the hair on the day of examination. The test is best performed two to three days after shampooing. Conversely, a false-positive hair pull test may be noted if the patient has not shampooed or combed the hair for several days.

Dermoscopy — Data on dermoscopic findings in telogen effluvium are limited. Acute telogen effluvium may demonstrate empty follicles and many upright regrowing hairs of normal thickness (>0.06 to 0.09 mm) (picture 6).

Dermoscopic findings may help to distinguish chronic telogen effluvium from female pattern hair loss (female androgenetic alopecia). The latter exhibits greater hair diameter variability [32].

Wood's light examination — Examination with a Wood's light (a source of ultraviolet A light) can be helpful for detecting findings of seborrheic dermatitis, a condition that has been associated with telogen effluvium. A Wood's lamp can also facilitate detection of hyperpigmentation, a finding more strongly associated with chronic cicatricial (scarring) alopecias than telogen effluvium. (See "Evaluation and diagnosis of hair loss", section on 'Cicatricial alopecia'.)

In seborrheic dermatitis, the Wood's lamp can highlight the presence of scale that is not easily seen with visible light. In addition, Malassezia yeasts, which are thought to play a role in seborrheic dermatitis, fluoresce orange upon exposure to ultraviolet light [33].

Scalp biopsy — Scalp biopsies are primarily reserved for patients in whom the diagnosis is uncertain or who exhibit features suggestive of chronic telogen effluvium (eg, persistence of shedding for at least four to six months) because it can be difficult to clinically distinguish chronic telogen effluvium from diffuse presentations of alopecia areata and female pattern hair loss. (See 'Differential diagnosis' below and "Female pattern hair loss (androgenetic alopecia in females): Pathogenesis, clinical features, and diagnosis", section on 'Scalp biopsy' and "Alopecia areata: Clinical manifestations and diagnosis", section on 'Histopathology'.)

Scalp biopsies are typically performed as 4 mm punch biopsies that extend into the subcutaneous fat. Many dermatopathologists prefer to receive two punch biopsies (one sectioned horizontally, one sectioned vertically) rather than a single biopsy because this allows for the evaluation of the tissue in both vertical and horizontal sections. (See "Skin biopsy techniques", section on 'Punch biopsy'.)

The preferred site for biopsy is an area outside sites of predilection for androgenetic alopecia to reduce the possibility of diagnostic confusion; thus, when feasible, it is helpful to avoid the bitemporal, frontal, and vertex areas of the scalp. The preferred site is the leading edge of an affected area of hair thinning (but not a bald area) on the scalp. If there is no obvious leading edge of hair thinning, biopsies may be taken from the parietal scalp. Examination of the biopsy specimens by a dermatopathologist experienced in the evaluation of hair and scalp disorders is ideal. (See 'Histopathology' above and "Evaluation and diagnosis of hair loss", section on 'Scalp biopsies' and "Skin biopsy techniques", section on 'Punch biopsy'.)

Additional tests — Less common methods for evaluating telogen effluvium primarily utilized in specialized hair centers and research studies include trichograms, phototrichograms, and hair collections:

●Trichograms and phototrichograms – Trichograms and phototrichograms are evaluation techniques that provide an assessment of the proportion of telogen and anagen hair follicles/hairs on the scalp. These procedures are described in greater detail separately. (See "Evaluation and diagnosis of hair loss", section on 'Trichograms and phototrichograms'.)

●Hair collections – Hair collections can be useful for quantifying the amount of hair that is being lost as well as following the course of telogen effluvium. To perform a hair collection, the patient is instructed to collect hair that sheds during morning hair grooming each day for two weeks. These collections are packaged in separate envelopes or other containers and labeled with the date and an "S" for the shampoo days. Hair loss of greater than 100 to 150 hairs per day is consistent with an effluvium. The collected hairs can be examined under a microscope to confirm that they are telogen hairs. This collection can be repeated at intervals to determine improvement or worsening of the telogen effluvium.

EVALUATION FOR CAUSE — When the patient history and physical examination fail to identify a clear trigger for telogen effluvium, testing to search for a contributing factor is typically performed. There are no laboratory tests that definitively diagnose telogen effluvium. (See 'Inciting factors' above.)

The author typically obtains the following tests:

●Complete blood count with red blood cell indices (to assess for anemia)

●Complete metabolic panel (to assess for signs of underlying disease)

●Thyroid-stimulating hormone (to assess for a thyroid disorder) (see "Laboratory assessment of thyroid function", section on 'Evaluating for thyroid dysfunction')

●Ferritin (to assess iron storage) (see "Causes and diagnosis of iron deficiency and iron deficiency anemia in adults", section on 'Iron studies (list of available tests)')

●25-hydroxyvitamin D levels (to assess for vitamin D deficiency) [17,34]

The selection of additional laboratory studies is guided by the need to rule out disorders in the differential diagnosis or to further investigate patients with signs or symptoms suggestive of a particular underlying disease, nutritional deficiency, heavy metal or other toxin exposure, or other causes of hair loss. As examples, a hormonal work-up to rule out hair loss related to hyperandrogenemia would be appropriate in women with signs of virilization, acne, and obesity, and further evaluation with antinuclear antibodies (ANAs) or other studies would be appropriate for a patient with signs or symptoms of an underlying autoimmune disease. In addition, dietary history may reveal nutritional deficiencies that should be evaluated.

DIFFERENTIAL DIAGNOSIS — A variety of nonscarring hair and scalp disorders share clinical features with telogen effluvium:

●Anagen effluvium – Anagen effluvium is an acute loss of anagen hair fibers secondary to chemotherapy or toxin exposure and represents acute loss of greater than 80 percent of the scalp hair. Exclamation point hairs (short, 1 to 3 mm hairs with a tapered base) that result from dystrophic hair growth are a common finding. Microscopic evaluation of the proximal ends of hairs dislodged during a hair pull test demonstrates normal or dystrophic anagen hairs rather than telogen hairs. (See "Alopecia related to systemic cancer therapy".)

●Androgenetic alopecia (male or female pattern hair loss) – Features of androgenetic alopecia that are useful for distinguishing this condition from telogen effluvium include a clinical examination that demonstrates a characteristic pattern of hair loss and miniaturized hairs (picture 7A-C). A biopsy can be useful for differentiating between these diagnoses in difficult cases. Of note, the two conditions may coexist, and telogen hair shedding can occur early in the course of androgenetic alopecia. (See "Male pattern hair loss (androgenetic alopecia in males): Pathogenesis, clinical features, and diagnosis" and "Female pattern hair loss (androgenetic alopecia in females): Pathogenesis, clinical features, and diagnosis".)

●Diffuse alopecia areata – Diffuse alopecia areata is an uncommon form of alopecia areata that is characterized by the diffuse loss of scalp hair, resulting in the appearance of generalized hair thinning (picture 8). Similar to anagen effluvium, exclamation point hairs may be present, and performance of the hair pull test may reveal dystrophic anagen hairs. A biopsy revealing an inflammatory infiltrate consistent with alopecia areata differentiates this condition from telogen effluvium. (See "Alopecia areata: Clinical manifestations and diagnosis".)

●Loose anagen syndrome – Loose anagen syndrome is a rare, nonscarring hair loss disorder that manifests with easily extracted anagen hairs from the scalp (picture 9). Young children are typically affected, particularly females with blond hair. Characteristically, examination of shed hairs reveals anagen hairs with ruffled cuticles (picture 10).

●Structural hair disorders – A variety of structural hair disorders causes weakening of the hair shaft that results in easily fractured hair. Unlike telogen effluvium, in which hair is shed from the follicle, these conditions result in increased breakage of hair. Close examination and 2x magnification of the loose hair will reveal broken hairs and may also reveal characteristic findings of a particular structural hair disorder. (See "Hair shaft disorders".)

MANAGEMENT — Telogen effluvium is usually a reactive and reversible disorder but may be the heralding event of underlying medical disorders or an adverse effect of treatments. Therefore, identifying and correcting the underlying cause is the most important component of patient management. Psychologic support, techniques for camouflaging hair loss, and clinical follow-up are useful adjuncts for managing the psychosocial effects of hair loss. (See 'Psychologic support' below and 'Cosmetic measures' below and 'Follow-up' below.)

Removal or treatment of underlying cause — Although spontaneous improvement is expected for patients with telogen effluvium related to an isolated event (eg, childbirth), patients with telogen effluvium related to a persisting insult should have the cause eliminated or treated when feasible.

Examples of interventions include:

●Treatment for associated illness

●Rectification for dietary deficiency

●Discontinuation of suspect drug (cease suspected drug for at least three months prior to reassessment of shedding)

●Treatment of concomitant hair or scalp disorders (eg, seborrheic dermatitis)

Psychologic support — Hair loss can have a profound psychosocial impact, which may seem out of proportion to the degree of hair loss [35,36]. Thus, consideration of the patient's emotional well-being is an important component of patient management.

Measures that may be helpful include:

●Addressing the patient's concerns in a sensitive manner.

●Providing a basic explanation of the hair growth cycle and its relationship to telogen effluvium, such as communication of the following points:

•Normally, individual scalp hairs are in different phases of the hair cycle (growing, resting, or shedding). The growing phase is the longest (three to seven years). The resting and shedding phase is shorter (approximately three to four months). In the normal scalp, the majority of hairs are in the growing phase.

•In telogen effluvium, something triggers many hair follicles that are in the growing phase to prematurely enter the resting phase, which results in shedding up to 30 percent of the scalp hair. The amount of hair lost depends upon the impact of the inciting cause of telogen effluvium on the hair follicles.

•If the cause of hair loss is discovered and either eliminated or treated, the hair loss resolves and regrowth becomes noticeable over 6 to 12 months.

•Complete loss of scalp hair is not expected.

●Providing a follow-up visit. Follow-up evaluations can be helpful for reassuring patients as well as for identifying patients who require further evaluation because of persistent telogen effluvium. (See 'Follow-up' below.)

Cosmetic measures — Consultation with a cosmetologist can help patients identify measures that minimize the cosmetic effects of hair loss. Hair styling techniques, hair coloring, scalp camouflage, and hair prostheses can be useful for camouflaging hair loss. Hair transplantation is not indicated for patients with telogen effluvium.

Interventions with uncertain efficacy — The efficacy of treatments, such as topical minoxidil and nutritional supplementation in the absence of nutrient deficiency, on telogen effluvium is unclear.

Our approach to supplementation involves correction of diagnosed nutrient deficiencies and iron supplementation for patients with ferritin levels beneath a certain threshold. (See 'Iron supplementation in the absence of iron deficiency anemia' below.)

Topical minoxidil — Some clinicians utilize topical minoxidil, a drug primarily used for the treatment of male and female androgenetic alopecia, for chronic telogen effluvium, despite insufficient evidence to confirm efficacy. The drug is prescribed in an attempt to maintain hair density and stimulate regrowth of hair. Most experts believe that minoxidil is not helpful for telogen effluvium that is expected to resolve spontaneously or has an inciting cause that can be eliminated [37]. Others, including the author, opt to start minoxidil when shedding begins in an attempt to support hair regrowth.

In androgenetic alopecia, minoxidil promotes hair growth by prolonging anagen, shortening telogen and kenogen, and enlarging miniaturized hair follicles. The efficacy of topical minoxidil in telogen effluvium has not been evaluated in clinical studies. (See "Male pattern hair loss (androgenetic alopecia in males): Management", section on 'Topical minoxidil'.)

A typical regimen involves the application of topical 5% minoxidil once daily to the entire scalp. Twice-daily application of minoxidil 2% is an alternative.

Beneficial effects of minoxidil on hair maintenance and growth are not expected to be evident immediately; a full year of use is considered necessary to assess efficacy. In patients with chronic telogen effluvium, clinical experience suggests that continued use may be necessary to maintain benefit.

Of note, occasionally, increased hair shedding can occur within the first two to eight weeks of treatment in patients treated with topical minoxidil for androgenetic alopecia. This is thought to result from the release of hairs from telogen follicles as they are stimulated by minoxidil to transition from telogen to anagen [1,38]. A telogen effluvium frequently follows the cessation of topical minoxidil in patients with androgenetic alopecia [39].

Oral minoxidil — Although small, retrospective studies have suggested improvement in telogen effluvium during treatment with low-dose oral minoxidil, additional study is necessary to determine whether oral minoxidil is an effective treatment [40-42]. In one retrospective study of 36 female patients with chronic telogen effluvium (increased telogen hair shedding for >6 months), treatment with oral minoxidil (0.25 to 2.5 mg per day) was associated with a reduction in hair shedding scores [40]. Additional study is necessary to determine whether oral minoxidil is an effective treatment.

Examples of potential adverse effects of oral minoxidil include hypertrichosis, postural hypotension, and edema [43].

Iron supplementation in the absence of iron deficiency anemia — Although it is accepted that patients with iron deficiency anemia should receive iron supplementation, iron supplementation for the treatment of telogen effluvium in the absence of iron deficiency or iron storage anemia is controversial. Additional studies are necessary to clarify whether iron supplementation is beneficial for nonanemic patients with telogen effluvium.

Supplementing iron intake to reach ferritin levels greater than 30, 40, or 70 mcg/L in patients with hair loss has been recommended by some experts based upon a belief that treatment for hair loss is optimized at greater serum ferritin levels [1,22,26,44]. In one small, placebo-controlled, randomized trial of 12 women with chronic telogen effluvium who were treated with iron and lysine supplements (n = 5) or placebo (n = 7) for six months, a 31 percent reduction in the proportion of hairs in the telogen phase was detected in the treatment group compared with a 9 percent increase in the proportion of telogen hairs in the placebo group [26]. (See "Treatment of iron deficiency anemia in adults".)

The uncertainty regarding the impact of iron supplementation on telogen effluvium has contributed to disagreement among experts about the need for iron supplementation and the target for the ferritin level when iron therapy is given. Based upon personal clinical experience that suggests benefit, the author routinely prescribes dietary modification or oral iron supplementation for patients with telogen effluvium to obtain and maintain serum levels of ferritin well within the reference range of the assay used at her institution (at least 70 mcg/L). Of note, ferritin reference ranges are assay specific.

Other supplements — The impact of supplements such as zinc (in the absence of symptomatic zinc deficiency), biotin, and vitamin D on telogen effluvium is unclear. Although correction of identified nutritional deficiencies is advised, the effects of correction on the course of telogen effluvium are unconfirmed. Benefit of these supplements in the absence of nutritional deficiency is also unconfirmed.

FOLLOW-UP — Arranging clinical follow-up six months after the initial visit is useful. This visit provides helpful reassurance for patients with acute telogen effluvium that improves and allows for the identification of patients who require additional evaluation due to persistent or worsening telogen effluvium. (See 'Prognosis' below and 'Evaluation for cause' above.)

Photographs are less helpful in telogen effluvium than in androgenetic hair loss, alopecia areata, or primary scarring alopecia. However, standardized photographs of midline part, central, and occipital scalp at the time of diagnosis provide a baseline assessment and a frame of reference for future visits. Since hair grows 0.5 to 1 cm a month, photographic follow-up will also allow for assessment of regrowth [45].

PROGNOSIS — The prognosis of telogen effluvium is dependent on the ability to remove or treat the inciting factor. If the underlying cause spontaneously resolves or can be eliminated, the course of telogen effluvium is self-limited.

Patients typically exhibit active shedding that persists for two to three months followed by stabilization and regrowth of hair. Cosmetically significant improvement is usually noted within 6 to 12 months. Telogen effluvium in which the underlying cause cannot be identified or removed may persist for years [46]. Complete baldness does not occur in acute or chronic telogen effluvium [6].

SUMMARY AND RECOMMENDATIONS

●Epidemiology – Telogen effluvium is one of the most common forms of nonscarring hair loss for which patients present for clinical evaluation. Both children and adults may develop telogen effluvium. (See 'Epidemiology' above.)

●Pathogenesis – Telogen effluvium results from an alteration in follicular cycling that leads to the excessive shedding of telogen hairs. A wide variety of endogenous and exogenous factors have been linked to induction of telogen effluvium. Examples include serious illness, major surgery, childbirth, rapid weight loss, nutritional deficiency, profound emotional stress, and drug exposure. The cause of telogen effluvium may be multifactorial in patients who have multiple medical problems or who are taking multiple drugs. In some cases, an inciting factor cannot be identified. (See 'Pathogenesis' above.)

●Clinical features – Hair loss in telogen effluvium manifests as a diffuse reduction in hair density (picture 1A-C). Less than 50 percent of the normal hair density is usually lost in telogen effluvium. Progression to complete balding does not occur (see 'Clinical features' above and 'Prognosis' above):

•Acute telogen effluvium – In most cases of telogen effluvium, the course is self-limited, with hair loss beginning two to three months after the inciting factor and reversing once the inciting factor resolves or is eliminated (figure 1). (See 'Clinical features' above.)

•Chronic telogen effluvium – Chronic telogen effluvium is a less common, idiopathic presentation of telogen effluvium that most commonly occurs in women between the ages of 30 and 60 years. Chronic telogen effluvium may persist for years (figure 1). (See 'Clinical features' above.)

●Diagnosis – The diagnosis of telogen effluvium can usually be made based upon the patient history and physical examination. Laboratory testing may be helpful for identifying an etiology when the inciting factor for telogen effluvium is unknown. Scalp biopsies are typically reserved for patients in whom the diagnosis is uncertain and for patients with findings suggestive of chronic telogen effluvium (hair loss persisting for more than four to six months). (See 'Diagnosis' above.)

●Management – The most important component of the management of patients with telogen effluvium is the identification and removal of the underlying cause. Data are insufficient to determine whether iron supplementation is beneficial in the absence of iron deficiency or iron storage anemia. (See 'Management' above.)