Main

Sir,

Alopecia areata is thought to be mediated by an autoimmune reaction against the hair follicle or melanocytes.1 We report a case of a patient who developed alopecia areata and had successful regrowth of her eyelashes after cutaneous treatment with latanoprost.

Case report

An 11-year-old girl was referred to the ophthalmology department with a history of bilateral loss of eyelashes. An incident had occurred 2½ years previously in which she had had an exacerbation of her asthma secondary to a viral illness. During her illness, it was noted by her GP that her eyelashes had fallen out bilaterally, from the upper and lower lids. There was no loss of hair from the scalp/eyebrows or pitting of her nails. She recovered well and a follow-up was arranged with the dermatology department.

During her review, several treatments were tried (eg lid hygiene/massage), but there was no change in the amount and position of lashes present (serial photography at each three-monthly visit). There was no history of any lash growth between appointments. She was on no systemic medication. There was no past or present history or family history of any psychiatric disorders. There was no, history of any obsessive–compulsive behaviour, and interview of the child by herself did not reveal any clinical features suggestive of depression or anxiety2 or, on direct questioning, to suggest trichotillomania.

Initial slit-lamp examination revealed bilateral loss of eyelashes with no evidence of erosions, crusts, or hair follicle haemorrhage (Figure 1). There was no evidence of inflammatory lid disease or eyelid tumour. Intraocular pressure (IOP) was 10 mmHg in both eyes, and she had light blue irides. She was otherwise systemically well.

Figure 1
figure 1

Right eye at initial presentation to the eye department. No change had been noted in lashes for 2½ years.

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Both mother and child were keen on some form of treatment. After a detailed discussion, she was prescribed latanoprost to be used cutaneously, once a day, to all eyelids, to be applied by a dressed orange stick. Serial photography was done. Minimal lash growth was noted on all four lids 4 weeks after application. There was no change in IOP or iris colour. A further 8-week appointment showed pronounced lash growth of all four lids (Figure 2). There was no change in IOP or iris colour. Her treatment was altered to once a week cutaneous use. Follow-up for 6 months has shown maintenance of the number of eyelashes with no alteration in IOP or iris colour. Both mother and child are pleased with the result.

Figure 2
figure 2

Left eye 3 months after initiation of treatment.

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Comment

Alopecia areata is a condition on unknown aetiology with a possible ill-defined genetic factor. The condition may appear at any age, but is more common between the second or third decade affecting both sexes equally. An association with vitiligo, Down's syndrome, and organ-specific autoantibodies may be found. A lymphocytic infiltrate is present around the hair follicle, suggesting a T-cell-mediated autoimmune reaction. Pitting of the fingernails may also be seen. The hair follicles are stimulated into apoptotic degenerating (catagen) or resting (telogen) phase. Follicles can re-enter anagen but are prevented from progressing beyond an early stage before prematurely returning to telogen. The follicles probably undergo repeated truncated cycles until disease activity subsides. Frequently, the autoimmune reaction abates spontaneously and the hair follicle may re-enter a normal cycle or anagen. This is deemed less likely with prolongation of the disease in the telogen phase as in our case,1 or in atopic patients who have a poorer prognosis for spontaneous regrowth. However, the potential for follicular function is retained even after decades of inactivity.1

The predominant differential diagnosis is trichotillomania; diagnostic exclusion can be difficult and may require lid biopsy.3 However, unlike reports in the literature there were no episodes of spontaneous eyelash regrowth throughout the follow-up,4,5 past/present history of any psychiatric disorder,3 or direct admission of trichotillomania.3 It would also be unusual to see both upper and lower eyelashes involved in a case of trichotillomania.

Latanoprost, an analogue of prostaglandin (PG) F2∝, is a prodrug. However, it is rapidly activated to latanoprost acid (the active form) in the cornea before entering the anterior chamber.6 The activation involves hydrolysis of its ester moiety, but no further metabolism is undertaken within the eye. Only 1% of the drug applied topically penetrates the eye, the rest being absorbed systemically.6 Latanoprost-induced hypertrichosis was first documented by Johnstone7 with an average increase of 19.5% in eyelash length. However, drug-induced hypertrichosis has been seen in association with diazoxide, phenytoin, minoxidil, streptomycin, corticosteroids, pencillamine, psoralens, cyclosporin, and alpha-interferon. The mechanism of the lash growth in most cases is unclear, but eyelash follicles do express FP receptors that are target receptors for latanoprost.8 PG F2∝ has been known to stimulate the initiation of DNA synthesis in resting cells and also to act as a mitogen.9 It also evokes gene expression and prevention of apoptosis10 as well as stimulating cell receptors linked to phosphorylase C that trigger activation of protein kinases that are known to play key roles in cell growth.

In a series of 317 patients, Demitsu et al11 showed latanoprost-induced hypertrichosis in 77%. The same authors showed, in a dye distribution test, that the areas of hypertrichosis were analogous to the areas of skin discoloration. The evidence implies that cutaneous absorption may cause hypertrichosis. Since the active drug is formed in the cornea, hypertrichosis must be caused by the prodrug. Our case illustrates this theory, but also shows that the use of cutaneous cf. guttate12 application of latanoprost can stimulate hair follicle activation from telogen/catagen into anagen with minimal other ocular side effects.