Telogen and Anagen Effluvium

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Background

Understanding the pathophysiology of telogen effluvium requires knowledge of the hair growth cycle. All hair has a growth phase, termed anagen; a transitional phase, termed catagen; and a resting phase, termed telogen. On the scalp, anagen lasts approximately 3 years and telogen roughly 3 months, though these times can vary widely from one individual to another. During telogen, the resting hair remains in the follicle until it is pushed out by growth of a new anagen hair.

Telogen effluvium is a form of nonscarring alopecia characterized by diffuse hair shedding, often with an acute onset.[1, 2]  It can affect hair on all parts of the body, but in general, only loss of scalp hair is symptomatic. A chronic form of telogen effluvium with a more insidious onset and a longer duration also exists,[3]  though it has been suggested that this may not be a truly distinct condition.[4] Telogen effluvium is a reactive process caused by a metabolic or hormonal stress or by medications. Generally, recovery is spontaneous and occurs within 6 months, unless a background of pattern alopecia is present.[5]  

Anagen effluvium is a nonscarring alopecia that leaves the follicular ostia intact. Most hair follicles are in the anagen stage at any given time; consequently, anagen alopecia affects a large percentage of the scalp. Some chemotherapeutic agents can also induce telogen effluvium. The combination of telogen effluvium and anagen effluvium can result in complete baldness.

Pathophysiology

Normal human hairs can be classified according to the three phases of their growth cycle: anagen, catagen, and telogen. Anagen hairs are in a growing phase, during which the matrix cells of the hair follicle undergo vigorous mitotic activity. These hairs have long, indented roots covered with intact inner and outer root sheaths, and they are fully pigmented.

Toward the end of the anagen phase, the amount of pigment decreases at the base of the follicle, which expands to form a keratinized club. Then, the hair enters the catagen phase, a transitional phase in which mitotic activity decreases. The follicle separates from the dermal papilla and the capillary plexus and moves upward within its connective tissue sheath toward the epidermis. The resulting telogen hairs, or club hairs, are in a resting phase. These hairs have short, club-shaped roots that anchor them in the follicle. They lack root sheaths and show depigmentation of the proximal part of the shaft.

The hairs continue in this resting state until the follicle spontaneously reenters the anagen phase. At this point, the club hairs are forced out by growing hairs underneath them, and the cycle begins anew. The cycle is not synchronous throughout the scalp. The length of each phase of the cycle, as well as the length of the entire cycle, varies with the site and the age of the patient. In the scalp, for example, the average length of the anagen phase is 1000 days; the catagen phase lasts only a few days; and the telogen phase lasts 100 days.

Telogen effluvium

In most people, 5-15% of the hair on the scalp is in telogen at any given time. Telogen effluvium is triggered when a physiologic stress or hormonal change causes a large number of hairs to enter telogen at one time. Shedding does not occur until the new anagen hairs begin to grow. The emerging hairs help to force the resting hairs out of the follicle. Evidence has suggested that the mechanism by which a telogen hair is shed is an active process that may occur independent of the emerging anagen hair. The interval between the inciting event in telogen effluvium and the onset of shedding corresponds to the length of the telogen phase, 1-6 months (average, 3 mo).

In 1993, Headington described the following five functional subtypes of telogen effluvium, defined according to which portion of the hair cycle is abnormally shortened or lengthened[6] :

These subtypes represent variations on the principles discussed above. It is rarely possible to distinguish these subtypes clinically.

Anagen effluvium

Anagen effluvium occurs after any insult to the hair follicle that impairs its mitotic or metabolic activity. The hair loss is usually the result of an exposure to chemotherapeutic agents such as antimetabolites, alkylating agents, and mitotic inhibitors that are used to treat cancer, though it is not the only type of chemotherapy induced-hair loss that can occur in these patients.[7]

The inhibition or arrest of cell division in the hair matrix can lead to a narrow weakened segment of the hair shaft that is susceptible to fracture with minimal trauma. It can also result in complete failure of hair formation. The hair bulb itself may be damaged, and the hairs may separate at the bulb and fall out. Only actively growing anagen follicles are subject to these processes. This form of alopecia is more common and severe with combination chemotherapy than with the use of a single drug, and the severity is generally dose-dependent. Anagen effluvium also occurs in persons with alopecia areata as the result of the inflammatory insult to the matrix.

The characteristic finding in anagen effluvium is the tapered fracture of the hair shafts. The hair shaft narrows as a result of damage to the matrix. Eventually, the shaft fractures at the site of narrowing.

Anagen effluvium is an uncommon symptom of pemphigus vulgaris.[8]  The hair follicle is a preferential target for pemphigus autoantibodies because the desmosomal proteins are overexpressed in the follicular epithelium. The ensuing intercellular cleavage causes the anagen hairs in lesional and perilesional areas to fall out.

Etiology

Telogen effluvium

Physiologic stress is the cause of telogen effluvium. These inciting factors can be organized into several categories (see below). Evidence from murine studies has indicated that psychological stress can induce catagen (the transition phase from anagen to telogen), mainly by exerting effects on neurotransmitters and hormones.[9] In humans, however, the role these effects play in hair loss remains to be determined. Although substance P has been extensively studied in human hair follicles in vitro, in-vivo studies have not been performed.[10] In HIV disease,[11] apoptosis may be related to HIV-1 viral protein R.[12]

The following have been identified as inciting factors for telogen effluvium:



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Telogen effluvium secondary to hypothyroidism.

Several studies have reported increased rates of telogen effluvium associated with COVID-19 infection.[24, 25]  A multicenter study from South Korea supported this association but did not find a significant association between COVID-19 vaccination and telogen effluvium.[26]

Anagen effluvium

Chemotherapeutics used to treat cancer are the most common causes of anagen effluvium.[27, 28, 29, 30]  A study of 384 patients with chemotherapy reactions showed that by far the most common reaction was anagen effluvium (78.6%).[31]  The most severe alopecia is caused by doxorubicin, the nitrosoureas, and cyclophosphamide. Other causative agents include bleomycin, dactinomycin, daunorubicin, fluorouracil, methotrexate, and azathioprine.[32, 33]  

Additional medications that can cause anagen effluvium include bismuth, levodopa, colchicine, albendazole, cyclosporine, and, possibly, strontium ranelate and pegylated interferon alfa-2a/ribavirin therapy.[34, 35, 36, 37, 38]  Anagen effluvium with permanent alopecia has been described in patients treated with taxanes.[39]

Exposure to chemicals such as thallium, boron, and arsenic can precipitate anagen effluvium.[40]

Causes of anagen arrest also include radiation therapy, endocrine diseases, alopecia areata, cicatrizing disease, and trauma or pressure.[41]

Pemphigus vulgaris is reported to be a cause of anagen effluvium.

Acute vesiculobullous hand dermatitis and anagen effluvium can occur in Ganoderma lucidum–induced aplastic crisis.[42]

COVID-19-related anagen effluvium has been described.[43]

Epidemiology

Telogen effluvium is quite common, but its exact prevalence remains to be defined. A large percentage of adults have experienced an episode of telogen effluvium at some point in their lives.

Telogen effluvium can occur at any age. It is not uncommon for infants in the first months of life to experience an episode of telogen effluvium.

Acute telogen effluvium can occur in either sex if the proper inciting conditions are present. Because hormonal changes in the postpartum period are a common cause of telogen effluvium, women may be more likely to experience this condition. In addition, women tend to find the hair shedding more troublesome than men do and thus are more likely to seek medical attention for it. Chronic telogen effluvium has been reported mainly in women.[44]

No racial predilection has been recognized.

Prognosis

Mortality has not been reported with telogen effluvium. Morbidity is limited to mild cosmetic changes. However, telogen effluvium can have substantial impact on those affected.[45, 46]  In acute telogen effluvium, the prognosis is good for recovery of normal hair density. In chronic telogen effluvium, a good cosmetic outcome can be expected, even if hair shedding continues.

Anagen effluvium is entirely reversible, with hair regrowth typically occurring after a delay of 3-6 months.[7]  Upon cessation of drug therapy, the follicle resumes its normal activity within a few weeks. Mitotic inhibition apparently stops the reproduction of matrix cells, but it does not permanently destroy the hair. In some cases, hair regrows despite continued or maintenance therapy. On occasion, the color and texture of the hair that regrows after chemotherapy-induced alopecia are different from those of the original hair.

Patient Education

Drug-induced alopecia can be psychologically devastating to a patient. Patients have even refused possibly palliative or life-saving treatments because they could not accept the temporary or prolonged baldness.

Patients must be warned of the potential for hair loss when they undergo treatment with any of the medications responsible for anagen effluvium. They should also be reassured that the hair loss is temporary. Normal hair growth resumes a few weeks after the termination of treatment, although the color or texture of the regrowing hair may differ from those of the original hair.

History

Telogen effluvium

The symptom of both acute and chronic telogen effluvium is increased hair shedding. Usually, patients' only complaint is that that their hair is falling out at an increased rate; occasionally, they note that the remaining hair feels less dense. In both forms of telogen effluvium, hair is lost diffusely from the entire scalp. Complete alopecia is not seen. Some patients experience trichodynia, but this occurs in multiple forms of alopecia and is not specific to telogen effluvium.[47]

Acute telogen effluvium is defined as hair shedding lasting less than 6 months. Patients typically report relatively sudden onset of hair loss. Careful questioning usually reveals some form of metabolic or physiologic stress occurring 1-6 months before the hair shedding started. Physiologic stresses that can induce telogen effluvium include febrile illness, major injury, change in diet, pregnancy and delivery, and starting a new medication. Immunizations also have been reported to cause acute hair shedding. Papulosquamous diseases of the scalp, such as psoriasis and seborrheic dermatitis, can produce telogen effluvium.

Chronic telogen effluvium is defined as hair shedding lasting longer than 6 months. The onset of hair loss is often insidious, and it can be difficult to identify an inciting event. Because of the duration of the hair shedding, patients are more likely to complain of decreased scalp hair density or of hair that appears thin and lifeless. A visual analogue scale (VAS) can be used to help patients assess the severity of hair shedding.[48]

Anagen effluvium

Patients with anagen effluvium present with diffuse hair loss after an exposure to drugs or toxic chemicals. Chemotherapeutic agents are most commonly responsible for hair loss. The most severe hair loss occurs in association with doxorubicin, the nitrosoureas, and cyclophosphamide. Hair loss usually begins 7-14 days after a single pulse of chemotherapy.[49]  The hair loss is clinically most apparent after 1-2 months.

The patient's full dermatologic, systemic, and family histories should be obtained to rule out other causes of hair loss, including malnutrition, iron deficiency, endocrine and metabolic disorders, collagen disease, infections (eg, syphilis), and widespread skin disease.

Anagen effluvium may be an uncommon symptom in a patient with pemphigus vulgaris.

A variety of medications may cause hair loss, stimulate hair growth, or induce changes in hair shape and color. Drug-induced hair loss is usually a consequence of a toxic effect of the drug on the hair matrix. Although many drugs have been occasionally described as producing hair loss, the relation between drug intake and hair loss has been proved for only a few agents. The type of hair loss (ie, anagen effluvium, telogen effluvium, or both) depends on the medication, its dosage, and patient susceptibility.

Tamoxifen is associated with anagen effluvium, producing diffuse hair loss that starts shortly after initiation of therapy and becomes most prominent after 6 weeks, with the hair growth rate returning to baseline within 3 months after tamoxifen is stopped.[50]

Physical Examination

Telogen effluvium

The physical examination is the same in both acute and chronic telogen effluvium. Physical findings are sparse. Usually, the physician does not appreciate a decrease in hair density. However, if the patient's hair has been falling out for several months, the hair may appear thin when its current appearance is compared with old photographs.

Depending on the duration of hair loss, close examination of the scalp may reveal a higher than expected number of short new hairs growing. Because hair grows at a nearly constant rate (~1 cm/mo), the duration of the hair shedding can be estimated by measuring the length of the short hairs. Trichoscopy can be helpful in visualizing the hairs.[51]

In active telogen effluvium, the gentle hair-pull test yields at least two hairs with each pull.[52] If the patient's active shedding has ceased, the hair pull will be normal. Forced extraction of 10-20 hairs will yield a large percentage of telogen hairs. If more than 25% of extracted hairs are in telogen, the diagnosis of telogen effluvium is confirmed.

There is one caveat to strict reliance on physical findings or numerical criteria in the diagnosis of telogen effluvium—namely, that each patient's scalp hair has an individual characteristic growth cycle. There are patients who have a very long anagen phase and thus a small proportion of hair in telogen at any given time. These patients may experience an episode of telogen effluvium but have completely normal physical findings. History alone must guide the physician to the correct diagnosis in these cases.

There should be no areas of total alopecia in a patient with telogen effluvium. No scarring is present. There also should be no sign of an inflammatory scalp dermatitis. Usually, there are no complaints of body hair loss.

Anagen effluvium

The diffuse alopecia of anagen effluvium (see the image below) can be distinguished from androgenetic alopecia, which is characterized by frontotemporal thinning followed by hair loss in the crown.



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Anagen effluvium. Image from DermNet New Zealand (https://www.dermnetnz.org/assets/Uploads/hair-nails-sweat/anagen-effluvium-01.jpg).

The hair and scalp should be thoroughly inspected to rule out local disease. Any erythema, scale, pustules, bogginess, sinus tract formation, or obliteration of the follicular openings should be noted. Any of these findings may indicate another cause of the alopecia.

Laboratory Studies

Telogen effluvium

Laboratory studies are of little use in the diagnosis of telogen effluvium if there is clear history of an inciting event (see Presentation).

Chronic telogen effluvium may have a metabolic cause. Testing should be directed toward causes that are common and correctable. If any sign or symptom of hypothyroidism is present, a thyrotropin test is warranted. Iron deficiency is common in premenopausal women. Evaluation of the complete blood count (CBC), serum iron, iron saturation, and ferritin may be warranted.

It should be noted that the CBC may be completely normal in women with mild iron deficiency and hair loss, particularly in women older than 40 years. Blood is more essential than hair, and the body will shed hair before red blood cell (RBC) indices become microcytic. It should also be noted that ferritin behaves as an acute-phase reactant. Inflammation can produce normal ferritin levels in an individual who is iron-deficient. Although a low ferritin level is proof of iron deficiency, a normal ferritin level does not exclude iron deficiency. Some experts in the field regard iron saturation as the most sensitive indicator of iron deficiency.

In a study assessing biochemical status in women (>18 y) with chronic telogen effluvium (n = 90) as compared with control subjects (n = 90), Turkoglu et al found that hemoglobin, ferritin, vitamin B12, vitamin D, copper, and serum and urine biotin levels, as well as thyroid function test results, did not differ significantly between the two groups.[57]  However, zinc level, selenium level, and copper-to-zinc ratio were significant predictors of the diagnosis of chronic telogen effluvium.

Occasionally, screening for renal and hepatic enzymes may detect a systemic cause of hair shedding. If syphilis is considered a possible cause of the hair loss, a rapid plasma reagin (RPOR) or Venereal Disease Research Laboratory (VDRL) test should be performed.

Anagen effluvium

A few select laboratory studies may be performed, as indicated by features of the history or physical findings. Serologic tests may include the following:

Serum and urine amino acid levels may be determined.

If tinea capitis is a concern in the differential diagnosis, microscopic examination for fungal elements and culture for fungi may be performed.[60]

Other Tests

Telogen effluvium

If a patient is unwilling to undergo a scalp biopsy (see Procedures) but would like confirmation of the diagnosis, serial hair collections may be obtained. This process can educate the patient in the normal hair cycle and can confirm the spontaneous resolution of the process.

The patient should be instructed to collect all hairs shed in a 24-hour period. The patient should not shampoo the hair during the day of collection. This process should be repeated every week or every other week, for a total of three or four collections.

Collections totaling 100 hairs or more in a given 24-hour period are indicative of ongoing telogen effluvium. If the collections are performed over several weeks while the telogen effluvium is resolving, the number of hairs collected each time should decrease. This finding can be very comforting to the patient.

An alternate method of hair collection was proposed[61]  in which the patient collects hair during shampooing, and the physician both counts and measures the length of these hairs. The advantage of this method is that it can detect and differentiate between telogen effluvium and androgenetic alopecia, even when the two conditions occur in the same individual; the disadvantage is that it cannot be used in patients who have short hair (< 3 cm). In addition, the process of counting and measuring the hairs is highly labor-intensive, which limits its practicality in normal clinical practice.

Successful use of videodermoscopy to diagnose hair and scalp disorders has been described.[62] The color-transition sign has been used to differentiate alopecia areata from telogen effluvium on trichoscopy.[63]

Anagen effluvium

Anagen effluvium can be distinguished from telogen effluvium by means of the pull test. This test is performed by firmly grasping 40 hairs between the thumb and forefinger and slowly pulling on them to remove them, causing only mild discomfort to the patient. Then, a trichogram is used to quantify the ratio of terminal anagen hairs to telogen hairs.

Anagen and telogen hairs can often be identified with the naked eye, but any doubts can be resolved by means of light microscopy. Anagen hairs have long indented roots covered with intact inner and outer root sheaths, and they are fully pigmented. Telogen hairs have short, club-shaped roots without root sheaths, and they show depigmentation of the proximal part of the shaft. Typically, fewer than 4-6 telogen hairs are present; a greater number of telogen hairs indicates a shift toward the telogen phase and suggests a probable diagnosis of telogen effluvium.

An alternative to a gentle pull test is to examine hairs removed by combing. The presence of tapered fractures is diagnostic of anagen effluvium.

Phototrichography, trichoscanning, trichoscopy, and reflectance confocal microscopy may be used to evaluate hair loss from anagen effluvium.[64, 65]

Procedures

Telogen effluvium

Scalp biopsy is the most useful test for confirming the diagnosis of telogen effluvium, though it is seldom necessary if the history is characteristic and a gentle hair pull produces numerous telogen hairs. Telogen hairs are identified by a white bulb and the lack of a gelatinous hair sheath.

If a biopsy is performed, some authors have advocated taking three 4-mm punch biopsy specimens, all embedded horizontally.[66]  This method provides a generous sample for determining anagen-to-telogen and terminal-to-vellus ratios and leads to greater diagnostic accuracy.

Anagen effluvium

Anagen effluvium can be distinguished from other forms of alopecia on the basis of the histologic changes on horizontal sections. A 4-mm punch biopsy sample of the scalp contains 25-50 follicles for inspection. Normally, fewer than 15% of the follicles are in the telogen phase at a given time. A normal anagen-to-telogen ratio in a patient with hair loss is characteristic of anagen effluvium. A finding of more than 15% of follicles in the telogen phase indicates a significant shift toward telogen in most individuals and is suggestive of telogen effluvium.

The follicles should show no signs of inflammation, dystrophic changes of the inner sheath, or traction. These features permit the distinction of anagen effluvium from alopecia areata, androgenetic alopecia, and traction alopecia.

Histologic Findings

Histologic findings in telogen effluvium are subtle and are most easily seen on transverse sections of a punch biopsy. The number and density of hair follicles are normal, but an increased percentage of the hair follicles are in the telogen phase or the catagen phase (the transition phase between anagen and telogen). If more than 25% of the follicles are in telogen phase, the diagnosis is confirmed. The percentage of telogen hairs generally should not be higher than 50%.

Anagen hairs have long, indented roots covered with intact inner and outer root sheaths. These hairs are fully pigmented. Telogen hairs have short, club-shaped roots. These hairs lack root sheaths and show depigmentation of the proximal parts of the shaft.

Medical Care

Telogen effluvium

Because acute telogen effluvium is a reactive process that resolves spontaneously, treatment usually is limited to reassurance. Any reversible cause of hair shedding (eg, poor diet, iron deficiency, hypothyroidism, or medication use) should be corrected.

Although chronic telogen effluvium is less likely to resolve rapidly, reassurance is still appropriate in such cases. Often, the knowledge that the hair loss will not progress to baldness proves comforting to the patient. The patient should be encouraged to style the hair in a way that masks any perceived defects in hair density.

Topical minoxidil has not been definitively proved to promote recovery of hair in telogen effluvium, but it has a theoretical benefit and is well tolerated. Low-dose oral minoxidil may also be considered as an option.[67, 68]

Some have found vitamin D supplementation to be promising[69] ; others have not found a clear association between vitamin D deficiency and telogen effluvium.[70]

A prospective single-arm open-label study found that a commercial product combination of shampoo and lotion containing anti-inflammatory and antioxidant agents was safe and effective for attenuating hair loss in telogen effluvium.[71]

Low-level laser/LED therapy (LLLT) has been studied as a treatment option for various types of alopecia but has not been demonstrated to be beneficial for telogen effluvium.[72]

Anagen effluvium

Although topical minoxidil is not effective in preventing chemotherapy-induced alopecia, it shortens the period of baldness by about 50 days.[73]

Vitamin D supplementation and monitoring for vitamin D deficiency may be beneficial.[74]

Scalp cooling may be used, accomplished either with cooling agents applied via a cooling cap that is changed several times or by continuous cooling of the scalp with cold air or liquid.[7]

The application of a pressure cuff around the scalp and local hypothermia can retard—though not prevent—anagen arrest if these measures are implemented during the infusion of medication. The pressure cuff and local hypothermia presumably decrease blood flow in the scalp and hinder the delivery of medication to this site. However, because the scalp may act as a sanctuary for circulating malignant cells, patients with leukemia, lymphoma, and other hematologic malignancies are generally not suitable candidates for these procedures.

A medical corrective preparation makeup can be applied to camouflage eyebrow alopecia induced by chemotherapy and to improve self-esteem.[75]

Surgical Care

Hair transplantation is not an effective treatment for telogen effluvium.

Diet

If an unbalanced diet is believed to be a contributing factor to telogen effluvium, especially in a case of chronic telogen effluvium, consultation with a dietitian may be extremely helpful. The dietary consultation should focus on ensuring adequate protein intake, replenishing low iron stores, and obtaining essential nutrients. If the patient takes large doses of vitamin A, this practice should be stopped.

Prevention

The application of a pressure cuff around the scalp and local hypothermia retard anagen arrest, if these measures are implemented during the infusion of the causative medication (see Medical Care).

Discontinuance or avoidance of the causative drug reverses anagen effluvium.

A randomized controlled trial of the possible prophylactic effects of pretreatment with calcipotriol before chemotherapy did not find this approach to be successful in preventing telogen effluvium.[76]

Long-Term Monitoring

In most cases, the patient is satisfied with an explanation of the cause and expected course of the condition. If a patient is distraught about hair loss, intermittent office visits for reassurance may be necessary.

Minoxidil (Loniten, Minodyl, Minoxidil HTN)

Clinical Context: 

Minoxidil topical (Rogaine, Women's Rogaine)

Clinical Context: 

What is telogen effluvium?What is the pathophysiology of telogen effluvium?What are the causes of telogen effluvium?What is the prevalence of telogen effluvium?What are the racial predilections of telogen effluvium?How does the prevalence of telogen effluvium vary by sex?In which age groups is telogen effluvium most common?What is the prognosis of telogen effluvium?Which history is characteristic of telogen effluvium?Which physical findings suggest telogen effluvium?What are the differential diagnoses for Telogen and Anagen Effluvium?Which tests are performed in the workup of telogen effluvium?What is the role of hair collection in the workup of telogen effluvium?Which histologic findings are characteristic of telogen effluvium?What are the treatment options for telogen effluvium?What is the role of surgery in the treatment of telogen effluvium?Which dietary modifications are used in the treatment of telogen effluvium?What is included in long-term monitoring of patients with telogen effluvium?What are the goals of drug treatment for telogen effluvium?Which medications in the drug class Vasodilators are used in the treatment of Telogen and Anagen Effluvium?

Author

Elizabeth CW Hughes, MD, Dermatologist, Group Health Cooperative

Disclosure: Nothing to disclose.

Coauthor(s)

Pere Gascon, MD, PhD, Professor and Senior Consultant, Division of Medical Oncology, Institute of Hematology and Medical Oncology, Hospital Clinic; Director, Laboratory of Molecular and Translational Oncology, University of Barcelona Faculty of Biology, Spain

Disclosure: Nothing to disclose.

Robert A Schwartz, MD, MPH, Professor and Head of Dermatology, Professor of Pathology, Professor of Pediatrics, Professor of Medicine, Rutgers New Jersey Medical School

Disclosure: Nothing to disclose.

Specialty Editors

David F Butler, MD, Former Section Chief of Dermatology, Central Texas Veterans Healthcare System; Professor of Dermatology, Texas A&M University College of Medicine; Founding Chair, Department of Dermatology, Scott and White Clinic

Disclosure: Nothing to disclose.

Edward F Chan, MD, Clinical Assistant Professor, Department of Dermatology, University of Pennsylvania School of Medicine

Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD, Professor and Chairman, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina College of Medicine

Disclosure: Nothing to disclose.

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Telogen effluvium secondary to hypothyroidism.

Anagen effluvium. Image from DermNet New Zealand (https://www.dermnetnz.org/assets/Uploads/hair-nails-sweat/anagen-effluvium-01.jpg).

Telogen effluvium secondary to hypothyroidism.

Anagen effluvium. Image from DermNet New Zealand (https://www.dermnetnz.org/assets/Uploads/hair-nails-sweat/anagen-effluvium-01.jpg).