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Can People With Ectodermal Dysplasia Get Tattoos

  • Journal List
  • Ann Dermatol
  • five.28(six); 2016 Dec
  • PMC5125970

Ann Dermatol. 2016 Dec; 28(6): 785–787.

Acquired Dermal Melanocytosis Occurring in a Patient with Hypohidrotic Ectodermal Dysplasia

Dong Ju Hyun

Department of Dermatology, CHA Bundang Medical Center, CHA Academy, Seongnam, Korea.

Dong Hyun Kim

Section of Dermatology, CHA Bundang Medical Center, CHA Academy, Seongnam, Korea.

Moon Soo Yoon

Department of Dermatology, CHA Bundang Medical Heart, CHA University, Seongnam, Korea.

Hee Jung Lee

Department of Dermatology, CHA Bundang Medical Center, CHA Academy, Seongnam, Korea.

Received 2015 Sep 9; Revised 2015 Oct 28; Accepted 2015 Nov 11.

Dear Editor:

Hypohidrotic ectodermal dysplasia (HED) is characterized past a triad of clinical features including absent or diminished eccrine sweat glands, missing teeth, and thin hair. Frequent skin manifestations of HED are xerosis and periorbital hyperpigmentation over the wrinkled pare, only there was no previous written report of acquired dermal melanocytosis (ADM) in HED patient1.

A 26-year-old man presented with bluish patches on the confront, which developed one year ago. On physical exam, an alphabet X-shaped bluish patch on the glabella and paranasal cheeks along Blaschko'southward lines and ovoid blue patches on the temples were found (Fig. 1A). Typical clinical features of HED such as the feature confront, dry out skin, periorbital hyperpigmentation over the wrinkled skin, sparse hair and teeth were presented (Fig. 1). Every bit he had sparse hair, he got a tattoo on the eyebrows. He also had a history of inability to sweat and recurrent delirious seizures since infancy and complained of high body temperature during the summer. He was diagnosed with atopic dermatitis in childhood. He had no family members showing similar manifestations.

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(A) Multiple bluish patches were observed on the glabella, both cheeks and both temples. Frontal bossing, depressed midface with a saddle nose, and everted lips were also noticed. The patient got a tattoo on the eyebrows for covering absent eyebrows. Periorbital hyperpigmentation over the wrinkled skin was also observed. (B) Hypotrichosis affecting axillary pilus. (C) Oligodontia treated with dental prosthesis.

We performed a 3-mm-punch biopsy on the left paranasal cheek, which revealed flattened epidermis, hypoplasia of skin appendages and mild superficial perivascular lymphocytic infiltrations (Fig. 2A). In the dermis, multiple elongated, slightly wavy pigmented cells reacting with melan-A and Southward-100 were seen (Fig. 2B~D). The clinicopathological findings led to the diagnosis of ADM with HED. Nosotros suggested the patient to get genetic written report merely he refused because of the high price. The pigmented lesions showed comeback after Q-switched neodymium-doped yttrium aluminium garnet (Nd:YAG) light amplification by stimulated emission of radiation treatment.

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Biopsied specimen from the left cheek. (A) Flattened epidermis and hypoplasia of peel appendages was remarkable. Balmy superficial perivascular lymphocytic infiltrations were noted (H&Due east, ×40). (B) Multiple elongated, slightly wavy pigmented cells were seen in the dermis (H&E, ×100; inset: H&E, ×400). The pigmented cells reacted with melan-A (C) and South-100 (D) (×200).

Periorbital hyperpigmentation in HED usually presents as grayish patch over fine wrinkles just like postinflmmatory hyperpigmentation in atopic dermatitisii. Because the pigmented lesion in our case presented equally X-shaped bluish patch without wrinkles, it is clinically different from previously reported cases of periorbital hyperpigmentation in HED. Although there are no biopsied cases of periorbital hyperpigmentation in HED, epidermal hypermelanosis and dermal melanophages may present in those cases similar as histopathology of postinflammatory hyperpigmentation and it would exist a differential diagnostic indicate.

The most frequent grade of ADM is acquired bilateral nevus of Ota-like macules and other unusual forms of ADM were likewise reported3. Pathogenesis of ADM is poorly understood, but the faulty activation of dormant or inactive dermal melanocytes is considered every bit the main pathogenesis4. Diverse factors, such as ultraviolet (UV) rays, excessive sex hormone, trauma, chronic inflammation, interaction of collagen and elastic fibers or genetic cistron tin trigger ADMfive. In our case, considering mild dermal inflammation seen in the pathology specimen, chronic inflammation is the most like triggering factor, but trauma from tattooing may also be involved. Furthermore, the effect of UV rays cannot be excluded.

As for about dermal pigmentary lesions, the Q-switched Nd:YAG laser is widely accepted treatment for the ADM. Our patient showed clinical improvement of the pigmentation after 8 sessions of Q-switched Nd:YAG light amplification by stimulated emission of radiation handling. Herein, we written report a rare case of ADM on the glabella, paranasal cheeks and temples in a patient with HED.

References

1. Itin PH, Fistarol SK. Ectodermal dysplasias. Am J Med Genet C Semin Med Genet. 2004;131C:45–51. [PubMed] [Google Scholar]

2. Koguchi-Yoshioka H, Wataya-Kaneda Chiliad, Yutani Grand, Murota H, Nakano H, Sawamura D, et al. Atopic diathesis in hypohidrotic/anhidrotic ectodermal dysplasia. Acta Derm Venereol. 2015;95:476–479. [PubMed] [Google Scholar]

3. Harrison-Balestra C, Gugic D, Vincek Five. Clinically distinct form of acquired dermal melanocytosis with review of published work. J Dermatol. 2007;34:178–182. [PubMed] [Google Scholar]

4. Hori Y, Takayama O. Circumscribed dermal melanoses. Classification and histologic features. Dermatol Clin. 1988;half dozen:315–326. [PubMed] [Google Scholar]

5. Fauconneau A, Beylot-Barry M, Vergier B, Robert-Barraud C, Doutre MS. Acquired dermal melanocytosis of the back in a Caucasian woman. Am J Dermatopathol. 2012;34:562–563. [PubMed] [Google Scholar]


Articles from Annals of Dermatology are provided here courtesy of Korean Dermatological Association and Korean Society for Investigative Dermatology


Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5125970/

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