Elastosis colloidalis conglomerata (adult colloid milium, paracolloid of the skin): a maximal manifestation of actinic elastosis?

ARTICLE

Auteur(s) : Reinhard Dummer¹, Barbara Laetsch¹, Sylvia Stutz², Leo Schärer¹

¹University Hospital of Zurich, Department of Dermatology, Gloriastrasse 31, 8091 Zurich
²Praxis Dr. med. Sylvia Stutz, Parkstrasse 1, 6440 Brunnen SZ

accepté le 23 Novembre 2005

Case report

The patient did not present any type I or type IV sensitization and there were no accompanying internal medical problems. The patient had a normal blood count and serum chemistry, and there was no paraproteinemia nor detectable anti-nuclear antibodies.

Previous treatments included topical corticosteroids and oral therapy with minocycline and metronidazole. Neither led to any improvement.

A 4 mm punch biopsy of one of these papules was taken. It showed nodular masses of homogenous, weakly eosinophilic material. These masses extended from the papillary dermis into the adjacent mid dermis. This amorphic material showed cleft formation. The overlying epidermis was atrophic and a thin layer of papillary dermis lay between the homogenous masses and the epidermis. In the periphery of the lesion there was marked solar elastosis, clearly visible with elastic stains. The lesion itself stained PAS positive but was negative for elastic stains. Alcian blue and pagoda/congored (amyloid stainings) were negative (( figures 3A and 3B )).

The patient was treated with topical tretinoin 0.025% (Retin A) for a period of twelve months, once daily in the evening combined with UV protection using a lotion with a UVB protection factor of 60 and a high UVA protection(Anthelios 60 XL) in the morning. This treatment showed both subjective and objective improvement and was continued (( figure 2 )).

Discussion

Most of the cases reported in the literature concern chronic UV-exposed skin of the face or the dorsum of the hands (( figures 4A and 4B )). Its distribution suggests that the disorder is dependent on chronic and intensive UV-exposure. Our patient reported intensive UV-exposure in her childhood and adolescence. Her solar elastosis was more severe than expected for her age.

There are few publications dealing with treatment of these diseases.

In 1978 Apfelberg and co-workers reported the successful treatment of colloid milium on the dorsum of the hands with dermabrasion [4]. A successful treatment of colloid milium of both hands and face with dermabrasion was reported by Netscher and co-workers. Clinical and histological follow up at 10 months post-treatment showed no recurrence [5].

There are further publications showing that dermabrasion is a successful treatment. However, there are no detailed descriptions concerning the long term cosmetic consequences.

In 2002, there was a report of the successful treatment of colloid milium using a Erbium:YAG Laser emitting at a wavelength of 2,940 nm [6]. The treatment was successful with no evidence of recurrence or hypopigmentation within a follow-up period of 13 months.

We discussed this therapeutic option with our patient. However, there were doubts concerning the risks and there were problems with financing the procedure.

Therefore, considering colloid milium as being analogous to other UV damaged skin conditions, such as solar elastosis, we used local retinoids for treatment.

Retinoids are vitamin A derivatives that act through nuclear receptor- and non-receptor-mediated mechanisms. Retinoic acid receptors are transcription factors that activate genes only when bound with the appropriate ligand [7]. Retinoids bind to both the retinoic acid receptor (RAR) and retinoid X receptor (RXR) families of receptors, each of which is comprised of alpha, beta and gamma forms, and form homodimers with themselves or heterodimers with corresponding RXR receptors [8, 9]. The RXR receptors/transcription factors also form heterodimers with a wide variety of other nuclear receptors/transcription factors, which explains their pleiotropic effects.

Regulation of the critical processes of cellular replication, differentiation and death occurs through a complex network of interlinked signaling pathways. Large numbers of genes possess retinoid-responsive elements regulating their expression levels. Many of these are elements of the cellular network, such as steroid receptors and cell-surface receptors, as well as internal control elements of the cell cycle. Clearly, much of the complexity of this network is involved with ensuring cellular and tissue specificity. We used a broad-spectrum retinoid (tretinoin) topically, as broad-spectrum retinoids show a high affinity for most of the receptors.

The positive effects of tretinoin on sun damaged skin was serendipitously noticed in patients who used the medication for acne and experienced a reduction of wrinkling [10, 11]. Since this finding, the effects of tretinoin against actinic damage have been extensively investigated and discussed. In numerous clinical trials the positive impact of tretinoin on UV-damaged skin has been proven. A diminishing of wrinkling, roughness and pigmentation are the most obvious effects [12, 13]. The improvement of tretinoin-treated skin is not only clinically visible, but also presents histologically, where extensive changes in the epidermis and dermis occur during treatment [14, 15]. Kligman and co-workers analyzed samples of skin that were treated with tretinoin and compared them with control samples. They could demonstrate a histological correlation with various well known clinical effects like the replacement of atrophic epidermis by hyperplasia, elimination of dysplasia and atypia, eradication of microscopic actinic keratoses, dispersion of melanin granules, new collagen formation, angiogenesis and exfoliation of retained horn in the follicles [16]. The effects of tretinoin are time-dependent, as the first improvements are noticed clinically and histologically in the first 6 to 12 months. Dermal collagen synthesis is only seen after prolonged application (12 to 24 months) and does not have a clinical correlative [17].

Other drugs that are used for the treatment of photoaged skin are antioxidants or alpha-hydroxy acids, but their potency for repair of skin damage is not as well documented as for retinoids [18].

Topical tretinoin has also shown potential for the treatment and clearance of premalignant skin tumors. Its antineoplastic effects make an important impact on the reduced prevalence of basal cell carcinoma, squamous cell carcinoma and perhaps even lentigo maligna [19].

The most common adverse event of topical tretinoin is mild to moderate dermatitis. Erythema and peeling are experienced within a few days of initiating topical tretinoin therapy. This condition is dependent on the tretinoin concentration, usually persists no longer than 3 months and seldom leads to a discontinuation of the therapy [20].

In our patient this treatment was well tolerated, however improvement after six months of therapy was only minor. We decided to continue with this approach for an additional six months and after this a further improvement of the patient’s skin condition was recorded (( figure 2 )).

References

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