Postpartum Telogen Effluvium Unmasking Traction Alopecia

Abstract

Introduction

Telogen effluvium (TE) is a type of diffuse hair shedding that occurs 2–3 months after an exposure or trigger. The excessive hair loss may “unmask” underlying hair loss disorders such as female pattern hair loss.

Case Presentation

This is a case series of 3 patients with postpartum TE in which an underlying traction alopecia (TA) was revealed.

Conclusion

TE can unmask underlying TA. Awareness of this phenomenon is critical to appropriate diagnosis and treatment.

Established Facts

• Traction alopecia is a nonscarring alopecia caused by chronic use of hairstyles that cause prolonged tension on the hair follicle.

• Telogen effluvium (TE) is a diffuse hair shedding that occurs 2–3 months after an exposure or trigger. In most cases, TE resolves on its own.

Novel Insights

• Telogen effluvium can unmask the presence of an underlying traction alopecia.

• Awareness of this phenomenon is important for accurate diagnosis and treatment.

Introduction/Literature Review

Telogen effluvium (TE) is diffuse hair shedding that begins 2–3 months after an exposure or trigger and stops 4–6 months after the exposure or trigger has been eliminated [1]. Typical triggers include trauma, chronic illness, autoimmune diseases, hypo- and hyperthyroidism, medications, and childbirth [1]. On a normal scalp, 85–90% of hair follicles are in anagen (hair growth stage), 1–2% are in catagen (involution stage), and 10–15% are in telogen (resting stage) [2, 3]. Anagen typically lasts 2–5 years, while catagen and telogen are much shorter, 3–6 weeks and 3–5 months, respectively [1]. In TE almost 30% of hair follicles shift to telogen which results in massive, diffuse hair shedding. Clinically, patients present with diffuse hair loss and short frontal hairs. Hair thinning is sometimes accentuated at the temporal scalp. Pain and burning are not infrequent symptoms.

In contrast to TE, traction alopecia (TA) is a type of alopecia characterized by localized patchy hair loss, most commonly at the frontal or temporal scalp [4]. TA is caused by the chronic wearing of tight hairstyles. It typically presents months to years after prolonged tension on the hair follicles [4, 5, 6, 7, 8]. TE has been known to cause an unmasking of underlying androgenic alopecia or female pattern hair loss [9, 10]. In a recent study, 12 of 16 patients with postpartum TE were diagnosed with female pattern hair loss 1 year later [9]. Here, we report a case series of postpartum TE unmasking TA.

Case Presentations

Patient 1: is a 32-year-old black female with a history of hair loss along the margins of her scalp. She has 8-month-old twins and first noticed her hair loss about 2 months after giving birth. Initially, she described diffuse hair thinning but over time her thinning was confined to the frontal and temporal scalp. She reported a history of wearing braids when she was younger and then weaves later in life. The weaves were admittedly tight. On examination, she had short, type 4b hair. Hair loss was pronounced at the temporal and frontal scalp (Fig. 1a). A fringe of spared hair was also present (Fig. 1b). There was some loss of follicular markings. On trichoscopy, follicular markings were diminished, and no evidence of scalp inflammation was noted (Fig. 1c). Hair shafts were of variable thickness. A 4-mm scalp biopsy was performed and was consistent with a diagnosis of TA showing a decreased terminal hair count, retention of vellus hairs, and presence of follicular streamers. No significant fibrosis or loss of sebaceous glands was present. Laboratory workup revealed a normal CBC, TSH, and ferritin.

Fig. 1.

Patient 1. a Hair loss at the frontal and temporal scalp. b A fringe of spared hair is present at the anterior hairline. Inflammation is absent and follicular markings appear diminished. c Dermoscopy revealed loss of follicular markings without inflammation.

Patient 2: is a 43-year-old Hispanic female with a 20-year history of hair loss at her temples. She recalled that hair thinning began as a diffuse shedding shortly after giving birth and then progressed to hair loss localized at the temples. She denied pain or itching of the scalp. Upon further questioning, she reported a history of pulling her hair back in tight hairstyles. On exam, she had long, thick, type 1 hair. There were large bare patches of alopecia at the temporal scalp and a fringe of spared hair at the anterior hairline (Fig. 2a, b). There was some loss of follicular markings but no inflammation of the scalp. Her referring physician suspected alopecia areata because of the patchy hair loss. However, she received 2 intralesional Kenalog injections (10 mg/mL) 6 weeks apart and applied minoxidil 2% solution twice a day without improvement. A 4-mm scalp biopsy was then performed and showed few follicular streamers, some perifollicular fibrosis, and few miniaturized hairs. There was partial loss of sebaceous glands without perifollicular inflammation.

Fig. 2.

Patient 2. a, b Hair loss confined to the temporal scalp with a fringe of spared hair at the anterior hairline. Inflammation is absent.

Patient 3: is a 33-year-old female of Hawaiian/Pacific Island descent with a 13-year history of hair loss that began after childbirth. The diffuse postpartum shedding eventually resolved and involved only her temporal scalp. She reported mild scalp pain and no itching. She had long, thick, type 2b hair, and admitted to wearing it in ponytails or tight buns. On examination, she had 2 temporal bare patches and a fringe of spared hair at the anterior hairline (Fig. 3a, b). There was no loss of follicular markings and no inflammation of the scalp. Alopecia areata was suspected by her referring physician due to the presentation of hair loss in patches. She received multiple intralesional Kenalog injections (5 and 10 mg/mL) and applied minoxidil 5% foam once a day without improvement. After seeing no response, a 4-mm scalp biopsy was done which showed increased miniaturized hairs and follicular dropout. Inflammation was absent. Laboratory workup revealed a normal TSH, ferritin, and CBC.

Fig. 3.

Patient 3. a, b Patches of hair loss at the temporal scalp with marked sparing of hairs at the hairline margin.

Discussion

The 3 patients presented here illustrate that a postpartum TE can “unmask” TA. It is important for clinicians to be aware of this phenomenon to make the correct diagnosis and provide appropriate treatment. While TA is typically slow and gradual in onset, patients who present after a postpartum TE may report “sudden onset” patchy hair loss and this history may lead to a mistaken diagnosis of alopecia areata. Prior reports of TA masquerading as AA highlight the need for having a high index of suspicion and taking a comprehensive hair care history [11].

Hormonal changes during pregnancy and the postpartum period are known to impact the hair follicle and hair cycling [3]. During pregnancy, anagen is prolonged due to the hormonal effects of progesterone [3]. Prolongation of anagen increases hair shaft diameter. High levels of progesterone in pregnancy also inhibit secretion of luteinizing hormone thereby suppressing androgen secretion from ovarian theca cells [3, 12]. This inhibition of androgens during pregnancy helps maintain anagen.

Postpartum, progesterone levels decrease resulting in a return to baseline levels of androgen production. At the same time, prolactin levels increase. Prolactin is a hormone that has been shown to inhibit hair shaft elongation and prematurely induce catagen [3]. These hormonal variations result in shorter, finer hairs after childbirth. It is plausible that a pre-existing population of intermediate or miniaturized hairs is disproportionately affected by these hormonal fluctuations. Thus, as demonstrated in this case series, the postpartum TE might “unmask” TA which shows increased miniaturization clinically and histologically [13, 14, 15]. Another potential mechanism of hair loss is that the shorter finer hairs caused by postpartum hormonal variations are more susceptible to tension from tight hairstyles resulting in more noticeable TA.

It is estimated that postpartum TE (telogen gravidarum) affects one-third to one-half of women [2]. Physical exam findings in TE include shorter regrowing frontal hair, diffuse hair thinning, and a positive hair pull test. Patients may report trichodynia, pain, and/or paresthesia of the scalp. Trichoscopy shows empty follicles, numerous short regrowing hairs, and less than 20% hair diameter variability [10, 16]. Diminished hair shaft variability is a key to the diagnosis of chronic TE. Histopathology reveals an increase in telogen hair follicles but a normal ratio of telogen to vellus follicles and a normal number of hair follicles overall [17, 18].

Patients with TA present with patchy hair loss, commonly at the frontal and/or temporal scalp. A fringe of spared fine or miniaturized hair at the anterior hairline may also be present [13]. Trichoscopy can reveal hair casts around the shafts at the periphery of patches, increased vellus hairs, and diminished follicular markings [14, 16, 19]. In early TA, histopathology reveals a normal number of hair follicles, an increased number of catagen and telogen hairs, and trichomalacia [15, 17, 18]. In chronic TA, several follicles may be replaced by fibrous tracts [16, 17]. Miniaturized or vellus hairs are also increased. Inflammation is mild to absent.

We present 3 patients in whom postpartum TE unmasked an underlying TA. Patient 1 initially reported diffuse hair loss, but with time there were more focal areas of loss suggesting that there may have been an evolution from TE to an “unmasking” of TA. Thus, the timing and location of the scalp biopsy may be a critical component for accurate diagnosis. In a patient who presents with “persistent” or “new onset” hair loss after a postpartum TE, the differential diagnosis should include other types of hair loss such as TA that have been “unmasked.” Our patients all presented with hair loss one to several years after postpartum TE. History, examination, and histopathology were all consistent with TA in our patients. This case series highlights a novel and important association between postpartum TE and TA. Awareness of this phenomenon is important for accurate diagnosis and treatment.

Statement of Ethics

The study was exempt from ethical approval according to the Institutional Review Board of the Kaiser-Permanente Division of Research. Subjects have given their written informed consent to publish photos and details of the case.

Conflict of Interest Statement

The authors have no conflicts of interest to declare.

Funding Sources

This manuscript did not receive funding.

Author Contributions

Paradi Mirmirani, MD contributed to the study design and drafting of the manuscript. Aman Samrao, MD contributed to drafting of the manuscript.

Data Availability Statement

All data generated or analyzed during this study are included in this article. Further inquiries can be directed to the corresponding author.