After observing 2 cases of acute telogen effluvium induced by allergic contact dermatitis to hair dyes, we decided to evaluate the effects of acute contact dermatitis of the scalp on the hair cycle.
Single-center, 6-month study of consecutive patients affected by acute scalp dermatitis.
Department of Dermatology, University of Bologna, Bologna, Italy.
Diagnosis of allergic contact dermatitis of the scalp was confirmed by patch testing. Eight women presenting with acute contact dermatitis of the scalp entered the study. Hair shedding was evaluated monthly for 6 months by pull test and wash test. Increased hair loss was detected in 4 of the 7 patients who completed the study. Hair loss was mild to moderate and appeared 2 to 4 months after the episode of scalp dermatitis. A scalp biopsy specimen from 2 patients confirmed the diagnosis of telogen effluvium.
Allergic contact dermatitis of the scalp should be included among the possible causes of telogen effluvium. The pathogenesis of telogen effluvium caused by contact dermatitis is unknown but may be related to cytokine release during the inflammatory process.
ACUTE TELOGEN effluvium (TE) is a very common and distressing condition. The most commonly reported causes of acute TE include drugs, crash diets, childbirth, emotional stress, iron deficiency, and systemic illnesses.1- 4 Scalp exposure to UV radiation has also been implicated.5,6
Allergic contact dermatitis of the scalp is not common and is most frequently caused by hair dyes or topical drugs. Although the occurrence of TE after acute scalp dermatitis is occasionally observed in clinical practice (A.T., 1997, and D.J.J.N., 1999, unpublished observations), textbooks on hair rarely include contact dermatitis among possible causes of TE.7 The possibility of extensively irreversible follicular damage after repeated use of hair dyes in allergic subjects has, however, been reported.8
The observation of 2 cases of acute and severe TE after scalp dermatitis from hair dyes prompted us to evaluate the effect of acute contact dermatitis of the scalp on telogen hair count.
Since January 1999, all patients who consulted our patch test clinic because of acute contact dermatitis of the face and scalp after hair dyeing were asked to participate in a follow-up study on hair loss. Eight patients, all women, ranging in age from 25 to 51 years (mean age, 35.2 years), agreed to be included. All these patients had an acute contact dermatitis at the time of our first examination. They were otherwise healthy and not affected by autoimmune or thyroid diseases. Clinical examination of the scalp showed mild erythema in 5 patients, mild erythema and scaling in 2, and moderate erythema and scaling with scalp erosions caused by scratching in 1. Blistering was never observed. Scalp itching was present in all cases. In addition to the scalp, the dermatitis involved the forehead in all patients, the retroauricular region in 3, and the neck in 1. The skin lesions were always more severe than the scalp lesions, with evident erythema and vesicles.
The contact dermatitis had developed 12 hours to 3 days after hair dyeing, and the time between onset of the dermatitis and our examination ranged from 1 to 5 days. Five patients had had their hair dyed by a hairdresser, whereas 3 patients had performed the procedure by themselves at home.
All patients were scheduled for patch testing 1 month later. No treatment was given except in 1 patient, who complained of very severe itching and received oral loratadine (Claritin; Schering Corp, Kenilworth, NJ), 10 mg/d for 5 days.
At the time of diagnosis, each patient was subjected to a pull test. The test was performed in 5 different areas of the scalp (frontal, right parietal, left parietal, vertex, and occipital) by gently pulling a tuft of about 100 hairs and counting the extracted hairs. The patients were then asked to come back every month for 6 months. They were instructed to wash their hair 5 days before each visit. They were also asked to shampoo their hair the evening after our examination and were given a special labeled envelope to collect all the hair shed and mail it to us. The hairs obtained from the pull tests and the wash tests were counted blindly at the end of the 6-month period by a physician not involved in the clinical study.
Patch tests were performed with the standard series and the hairdresser series (Trolab; Hermal Kurt Herrmann, Hamburg, Germany) (Table 1). Readings were carried out at 48 and 72 hours and after 7 days. A positive reaction to paraphenylendiamine was documented in all cases. Two patients also had positive results to nickel sulfate, and 1 patient showed positive reactions to several dyes, including resorcinol and p-phenyltoluenediamine.
A 50-year-old woman was seen for examination of diffuse hair loss. The patient had no particular history related to hair problems or general health. When she was first seen, more than 70% of the hair was lost, based on clinical examination and in comparison with recent photographs taken before the hair loss developed.
According to the patient and the general practitioner, hair loss had occurred after an acute scalp eruption initiated within 2 weeks after application at home of a hair dye. Following the manufacturer's instructions, the patient performed a single open application test (small amount of product applied to the back of the ear) and observed no reaction within 72 hours. The patient then applied the hair dye to the scalp at home 7 days later.
An acute and severe eczematous dermatitis developed 5 days after application of the hair dye to the scalp, ie, about 2 weeks after the first open patch test procedure. The erythematous and edematous eruption extended to the surrounding skin, including forehead, helix, and back of the ears and neck. Neither oozing nor crusting was reported. Treatment with topical and oral corticosteroids was prescribed and helped resolve the acute-phase reaction.
Within 6 weeks after the initial application, the patient reported a sudden increase of hair shedding. According to the patient, the estimated increase was 5 to 10 times more than the usual rate of shedding during daily combing and shampooing. Six months after the initial episode, hair shedding subsided and massive hair regrowth was evident. However, 11 months after the initial episode, scalp skin was still reported as itchy, and mild desquamation was noticed. Patch tests showed an intense delayed erythematous and bullous response to the hair dye containing paraphenylendiamine under occlusion, while the open test was erythematous and edematous at 48 hours. No further patch testing was allowed.
A 32-year-old woman, who had normal density of scalp hair, had a history of an episode of hair loss at the age of 19 years after a restrictive diet with weight loss of 7 kg. The patient had no history of allergies. She had first dyed her hair at the age of 28 years, in 1994, and had never experienced any problem before January 1998, when she developed an acute contact dermatitis after her usual dyeing procedure performed by her hairdresser.
She consulted us with acute TE in March 1998. She was very distressed because of hair loss and complained of noticeable hair shedding on her clothes and pillow. She also complained of scalp paresthesia and a burning sensation. The pull test performed 24 hours after shampooing was positive, with extraction of 25 hairs. Moderate hair thinning was evident in the crown region (Figure 1). The symptoms persisted for 6 months, when hair loss abruptly subsided.
Case 2. Evident hair thinning of the crown region caused by telogen effluvium after acute contact dermatitis of the scalp.
Figure 2 reports the total number of hairs obtained from the pull test and collected by the wash test during the 6-month period for each patient.
Variations in hair shedding by pull test and wash test during 6 months. Each patient is represented by a different line pattern.
Four of the 8 patients showed increased hair shedding 2 to 4 months after the episode of scalp dermatitis. Three of them also complained of hair loss when attending the follow-up visits. Mean increase in the pull test count at month 3 in these 4 patients was 13 hairs (range, 7-23). Mean increase in the wash test count was 218.7 hairs (range, 39-389). In these 4 patients, the increase in the hair count demonstrated by the pull test and wash test persisted at month 6. In 3 patients, the values of the pull test and wash test did not change considerably during the study period. One patient did not complete the study for personal reasons, and her data were not evaluated. Development of TE was not related to severity of the scalp contact dermatitis. Routine hematologic evaluation, including blood cell count and ferritin and iron levels, were within the reference range in all patients. Two of the patients with increased hair loss agreed to undergo a 4-mm punch biopsy of the parietal scalp. The pathological findings of transverse sections in both cases showed a terminal-vellus ratio greater than 4:1 and a reduced anagen-telogen ratio (69:31 and 75:25) (Figure 3 and Figure 4). No inflammatory infiltration was present. These findings were consistent with a pathological diagnosis of TE.
Scalp biopsy specimen of a 45-year-old woman taken during telogen effluvium, 3 months after the acute scalp contact dermatitis. Transverse section shows 2 telogen and 4 terminal anagen follicles. No inflammation is present (hematoxylin-eosin, original magnification ×70).
Scalp biopsy specimen of a 37-year-old woman taken during telogen effluvium, 3 months after the acute scalp contact dermatitis. Transverse section shows 3 telogen and 2 terminal anagen follicles. No inflammation is present (hematoxylin-eosin, original magnification ×50).
The clinical observation of 2 patients with diffuse alopecia that developed with telogen hair shedding a few months after an episode of acute scalp contact dermatitis prompted us to specifically monitor variations of telogen shedding in the 6 months after acute scalp contact dermatitis in a group of 8 patients. Methods to evaluate hair loss are not completely standardized and vary considerably in the published literature.9- 11 In all our patients, hair loss was evaluated by means of the pull test and the wash test (both performed 5 days after shampooing) every month for 6 months. This method permitted us to monitor for each of our patients possible differences in telogen shedding compared with baseline.
The results of our study showed that contact dermatitis of the scalp should be included among possible causes of acute TE. A mild to moderate TE was documented in 4 of the 7 patients with allergic scalp contact dermatitis who completed the follow-up. In all these patients, TE persisted for more than 3 months and was still present at 6 months. The diagnosis of TE was confirmed by the pathological findings in the scalp, which showed a normal terminal-vellus ratio and a reduced anagen-telogen ratio in the absence of inflammatory infiltration.4
The pathogenesis of TE caused by contact dermatitis may be related to cytokines released during the inflammatory process.12 The 2- to 3-month delay between the contact dermatitis and the onset of TE explains why inflammation was not present in the scalp biopsy specimens. A number of cytokines and adhesion molecules are known to be released during the efferent phase of acute contact dermatitis, including some molecules that are implicated in the premature termination of anagen, such as interleukin 1 and tumor necrosis factor α.13,14 As with other possible causes of TE, hair loss does not occur in all the exposed patients, and severity of alopecia also may vary considerably between individuals. In 2 of our patients, who actually consulted our hair clinic, TE produced a diffuse alopecia that clinically mimicked alopecia areata incognita or acute drug-induced alopecia.15 The microscopic examination of the hairs extracted by pull test, however, excluded these diagnoses. In all the other patients, who were recruited from our patch test clinic, TE produced only minimal hair thinning. This suggests that severe alopecia is a rare complication of scalp dermatitis and that most patients experience hair shedding but not alopecia. This may be because susceptibility of anagen follicles to noxious events depends on their mitotic activity and therefore on their anagen subphases. According to Rebora,3,13 in fact, TE develops only when the noxious event affects a patient in whom a large number of hair follicles are in the same anagen subphase. This type of TE corresponds to the "acute anagen release" described by Headington.2 During our longitudinal study, however, the latency between the noxious event and the onset of hair shedding was longer than 3 to 5 weeks. Although it may be difficult to distinguish mild TE from normal shedding because of the high variability in quantitative hair loss by pull and wash test in the different individuals, our 4 patients experienced an increased shedding of hair compared with their baseline values.
The possibility that allergic contact dermatitis from hair dyes may be responsible for TE should therefore always be considered in a female patient with increased hair loss. A careful clinical history should be obtained, focusing on types and times of dyeing procedures and on episodes of scalp reddening or itching after hair dyeing. Consumers, dermatologists, and cosmetics manufacturers should be aware of the possible occurrence of massive hair loss after anallergic reaction to hair dyes.
Accepted for publication September 19, 2000.
Corresponding author and reprints: Antonella Tosti, MD, Department of Dermatology, University of Bologna, Via Massarenti, 1 I-40138 Bologna, Italy (e-mail: firstname.lastname@example.org).
Tosti A, Piraccini BM, van Neste DJJ. Telogen Effluvium After Allergic Contact Dermatitis of the Scalp. Arch Dermatol. 2001;137(2):187-190. doi:10-1001/pubs.Arch Dermatol.-ISSN-0003-987x-137-2-dob00019