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Acquired brachial cutaneous dyschromatosis

  • Author(s): Hu, Stephanie W;
  • Chu, Julie;
  • Meehan, Shane;
  • Kamino, Hideko;
  • Pomeranz, Miriam Keltz
  • et al.
Main Content

Acquired brachial cutaneous dyschromatosis
Stephanie W Hu MD, Julie Chu MD, Shane Meehan MD, Hideko Kamino MD, Miriam Keltz Pomeranz MD
Dermatology Online Journal 17 (10): 16

Department of Dermatology, New York University, New York, New York

Abstract

Acquired brachial cutaneous dyschromatosis (ABCD) is a newly described disorder of pigmentary change that occurs on the dorsal aspects of the forearms in post-menopausal women. We report a case of a 62-year-old woman who developed an asymptomatic, reticulated, gray-brown eruption on the dorsal aspects of the forearms of gradual onset that is clinically and histopathologically consistent with ABCD. Whereas the original report found an association between hypertension and/or the use of anti-hypertensive medications in the original cohort, we propose that this entity may, in fact, be associated more closely with cumulative sun damage and may be related to such acquired disorders of the skin as poikiloderma of Civatte. Treatment of these lesions may prove to be a challenge, with an emphasis on rigorous sun protection and adjunctive measures with depigmentating agents, chemical peels, and lasers.



History

A 62-year-old postmenopausal woman with a ten-year history of hypertension presented to the NYU Department of Dermatology Faculty Practice for evaluation of discoloration on the extensor aspects of the forearms. The discoloration had been present for at least four years at the time of initial presentation and developed gradually. She denied pruritus or other symptoms preceding the onset of the pigmentary change. The patient has a history of sunburns in her youth and frequent sun exposure but denied tanning bed use. A review of systems was negative.

Past medical history included hypertension, urinary tract infections, aquagenic urticaria, and angioedema. Past surgical history included cholecystectomy and laser surgery of the right eye for a retinal detachment. Current medications include lisinopril, which the patient had been taking for seven years prior to the onset of the cutaneous lesions, risedronate, calcium, vitamin D, and aspirin. The patient has smoked one-half of a pack of cigarettes daily for 40 years.

A shave biopsy was obtained from a representative patch on the left forearm. The patient was initially started on triamcinolone 0.1 percent ointment twice daily and sun protection was emphasized. However, the former has been discontinued upon confirmation of the diagnosis.


Physical examination


Figure 1

Reticulated erythema with telangiectases and hyperpigmentation is present over the dorsal aspects of the forearms. Superficial telangiectases are present over the lateral aspects of the neck and anterior portion of the chest. The patient is Fitzpatrick skin type II.


Laboratory data

None.


Histopathology


Figure 2

There is uneven epidermal pigmentation with an average number of melanocytes, which are highlighted with a Fontana Masson stain for melanin. There is focal effacement of the rete ridge pattern and a few telangiectases in the papillary dermis.


Discussion

Acquired brachial cutaneous dyschromatosis (ABCD) was described by Rongioletti and Rebora in April, 2000 [1]. A new entity in the dermatologic literature, this pigmentary disorder was first described in their report of 20 Caucasian middle-aged patients, who presented from 1995 to 1998, with asymptomatic, gray-brown patches on the dorsal aspect of the forearms. In their series, all of the patients were women except one and the age range was from 46 to 72 years (average, 53 years). On cutaneous examination, two patients were classified as having Fitzpatrick skin type II, 11 with skin type III, and 7 with skin type IV, which is a prevalence that reflects the Italian general population. In all patients, the lesions affected the dorsal aspects of the forearms and were characterized by asymptomatic, irregular, gray-brown patches with geographic borders, which were occasionally interspersed with hypopigmented, slightly atrophic macules. The lesions were bilateral in all cases except one. The distal aspect of the upper arms also was involved in two patients and the face always was spared.

The authors observed that poikiloderma of Civatte was associated with this hyperpigmentation in nine of 20 patients (45%). Pregnancy, menopause, local inflammation, and cosmetics were not found to be predisposing factors. Undue sun exposure, oral contraceptives, or estrogens were found only occasionally. Similarly to our patient, 65 percent of this population of patients had hypertension and had been taking anti-hypertensive drugs, in particular angiotensin-converting enzyme inhibitors (ACEIs), for years before the pigmentation began, in contrast with only 18 percent of controls.

Histopathologic examination showed epidermal atrophy, basal-layer hyperpigmentation, solar elastosis, and superficial telangiectases. Only one patient showed a slight, perivascular lymphocytic infiltrate. No pigmentary incontinence was observed. Fontana Masson stain confirmed that the pigment was melanin, with a homogeneous pattern of hyperpigmentation along the basal-cell layer. A direct immunofluorescence test was negative. Ultrastructural studies showed an increase in the number of the melanosome complexes in the keratinocytes of the basal cell layer in the pigmented macules.

Although Rongioletti and Rebora hypothesized that an association of ABCD with hypertension and/or anti-hypertensive medications was suggested from their analysis, the association merely may represent a consequence of the commonality of both hypertension in the general middle-aged and post-menopausal population and the current treatment regimens utilized to manage the condition. Whereas the cutaneous adverse effects of ACEIs have included angioedema, pruritus, bullous eruptions, urticaria, lichenoid eruptions, other generalized eruptions, photosensitivity, and hair loss, this class of medications previously had not been reported to induce disorders of pigmentation [2, 3]. A host of other drugs, such as antimalarials, chemotherapeutic agents, heavy metals, and antibiotics, have been associated with hyperpigmentation of various morphologies [4, 5, 6]. This association of ABCD and hypertension and/or anti-hypertensives, and in particular, ACEIs, may be coincidental.

The clinical and histopathologic findings of ABCD may link this entity more closely to a dermatosis of sun damage, such as poikiloderma of Civatte. Owing to the findings of hyperpigmentation, epidermal atrophy, and superficial telangiectases observed in both dermatoses, it is conceivable that ABCD is a related dyspigmentation disorder that is acquired from years of accumulated ultraviolet exposure, which manifests in the photodistributed site of the dorsal aspects of the forearms. Although ACEIs have not been shown to cause cutaneous pigmentary change, the possibility remains that ABCD results from the higher level of photosensitivity associated with ACEIs on occasion [2]. Our patient also had solar lentigines on the dorsal aspects of the forearms, which is a finding consistent with cumulative ultraviolet exposure.

There is currently no data on treatment of this pigmentary disorder. The natural history of pigmentary disorders is characterized by a chronic and protracted course, and treatment is often difficult, prolonged, and unsatisfactory. Our patient has thus far not pursued treatment for her asymptomatic eruption, but efforts still may be made to attenuate the dyschromia in patients who seek improvement. One potentially important consideration is to decrease, as much as possible, sun exposure; most disorders of pigmentation are aggravated by ultraviolet rays that enhance melanin synthesis and subsequent accumulation. Daily use of a broad-spectrum sunscreen is an important part of any therapeutic approach. Current treatments for other acquired skin hyperpigmentation disorders include depigmentating agents, such as hydroquinone and azelaic acid, chemical peels that physically remove melanin in the superficial layer of skin, and disruption of melanin granules by lasers, such as the Q-switched, pigment-specific lasers or resurfacing lasers (pulsed/scanned CO2 or erbium:YAG lasers) [7]. In the case of poikiloderma of Civatte, a review of the literature identified ablative fractional photothermolysis and nonablative fractional photothermolysis to be potentially effective modalities of treatment. These entities also have potential utility in melasma, postinflammatory hyperpigmentation, nevus of Ota, hypo- and hyperpigmented scars, laser-induced hypo- and hyperpigmentation, and dyschromia associated with photoaging [8]. Owing to the fact that the increased melanin pigment in ABCD is localized to the epidermis, responsiveness to treatment may be reasonably expected.

In summary, we describe a pigmentary disorder primarily of the dorsal aspects of the forearms, which occured in a post-menopausal, woman, Fitzpatrick skin type II, with a long-standing history of hypertension and ACEI usage. The clinical morphology and histopathologic findings are consistent with the newly described entity, acquired brachial cutaneous dyschromatosis. Whereas direct pigmentary induction by ACEIs or another unidentified agent remains to be investigated, ABCD tentatively may be considered to be a manifestation of chronic sun damage in this population, which either occurs on a background of cumulative UV damage or as a reaction pattern that is induced by drug-induced photosensitivity. Management options remain to be elucidated, but photoprotection may be expected to figure prominently in the treatment armamentarium.

References

1. Rongioletti F, Rebora A. Acquired brachial cutaneous dyschromatosis: a common pigmentary disorder of the arm in middle-aged women. J Am Acad Dermatol 2000;42: 680 [PubMed]

2. Steckelings UM, et al. Angiotensin-converting enzyme inhibitors as inducers of adverse cutaneous reactions. Acta Derm Venereol 2001;81:321 [PubMed]

3. Goodfield MJ, Millard LG, Severe cutaneous reactions to captopril. Br Med J 1985; 290:1111 [PubMed]

4. Hendrix JD Jr, Greer KE. Cutaneous hyperpigmentation caused by systemic drugs. Int J Dermatol 1992;31:458 [PubMed]

5. Bigby M, et al. Allergic cutaneous reactions to drugs. Primary Care. W.B. Saunders Company: Philadelphia. 1989;16:713

6. Dereure O. Drug-induced skin pigmentation: epidemiology, diagnosis and treatment. Am J Clin Dermatol 2001; 2:253 [PubMed]

7. Nikolaou V, et al. Established treatments of skin hypermelanoses. J Cosmet Dermatol 2006; 5:303 [PubMed]

8. Tierney EP, Hanke CW. Review of the literature: treatment of dyspigmentation with fractionated resurfacing. Derm Surg 2010; 6:1499 [PubMed]

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