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SHORT COMMUNICATION
A Case of Aplasia Cutis Congenita with Widespread Multifocal Skin Defects Without Extracutaneous
Abnormalities
Jemin KIM 1 , Jihee KIM 1 , Myeongseob LEE 2 , Eui Ra HUH 2 , Joohee LIM 2 , Kook In PARK 2 and Sang Ho OH 1 *
1
Department of Dermatology, Severance Hospital, Cutaneous Biology Research Institute, Yonsei University College of Medicine, 50 Yonsei-
ro, Seodaemun-gu, Seoul 03722, and 2 Department of Pediatrics, Severance Children’s Hospital, Seoul, Korea. *E-mail: [email protected]
Accepted Nov 20, 2018; E-published Nov 21, 2018
Aplasia cutis congenita (ACC) is a rare congenital disor-
der characterized by focal, localized absence of skin or
defects of the skin in neonates. The estimated incidence
of ACC is approximately 0.5–1 in 10,000 newborns (1).
The clinical appearance of ACC is heterogeneous and
it can be associated with various systemic congenital
anomalies. However, the causative gene mutation is un-
clear. Frieden (2) proposed a classification of ACC based
on clinical characteristics, such as involved body area,
associated anomalies, and inheritance patterns. Most
cases of ACC manifest as a solitary lesion involving the
scalp, especially at the vertex. However, ACC is also
associated with underlying malformations, such as limb
or skull defects, or organ involvements, including central
nervous, cardiovascular, and gastrointestinal systems
(1–4). ACC treatment is controversial, but most cases
heal spontaneously within a few weeks with conservative
treatment (1, 3, 4).
We report here a rare presentation of ACC with multifo-
cal, symmetrical, discrete skin lesions over the entire body,
including the scalp and extremities, in a newborn male.
CASE REPORTS
A full-term male infant born at 39 weeks of gestation (birthweight
2,560 g) was transferred to the neonatal intensive care unit (NICU)
with multifocal full-thickness skin defects over the entire body:
scalp, trunk, and extremities. His parents denied any family history
of congenital skin disease, and there was no history of infectious
disease, trauma, and maternal intake of drugs in the prenatal period.
The mother had a history of one previous pregnancy, resulting in
a normal child. During prenatal evaluation, no signs of systemic
or macroscopic placental anomaly were detected.
Fig. 1. (a) Full-thickness skin defects immediately after birth. (b) Within
a few hours, several lesions covered with thin yellowish crusts with signs
of spontaneous healing (arrowhead).
At delivery, more than 30 individually demarcated, well-defined,
coin-sized, full-thickness skin defects were noted on the entire
body, including the scalp and extremities (Fig. 1). However, there
was no sign of blister formation or mucosal erosions, and the distal
ends of the patient’s digits were intact with no dystrophy of the
nail units. The patient underwent a thorough evaluation, including
skull and whole-spine radiography, brain ultrasonography, and
echocardiography, to detect possible anomalies, and there were
no additional systemic abnormalities apart from the skin manifes-
tations. A genetic assay panel for possible dysmorphisms (ARX,
FOXC2, PLEC, LAD1, etc.) was performed using next-generation
sequencing combined with direct sequencing. No genetic muta-
tions associated with congenital bullous disease were noted.
Since no newly formed lesions were observed during the first few
days after birth and several lesions showed signs of spontaneous
healing, it was decided to provide conservative treatment with
no additional surgical treatment. The infant was placed in incu-
bator care with a humidity of more than 80%, in order to prevent
excessive trans-epidermal water loss and desiccation of healing
lesions. He was treated with semi-occlusive dressings twice a
day for the first week after birth. To prevent maceration due to
wound exudates, a combination mixture of petrolatum ointment,
paraffin emollient and mupirocin ointment was used, covered
with antibacterial dressing material (Sorbact ® Compress, ABIGO
Medical AB, Sweden). The dressing protocol was continued for
the following weeks with occasional wound swabs to detect any
possible infection. Prophylactic antibiotics (ampicillin/sulbactam,
cefotaxime) were initiated, but were discontinued after 10 days
when subsequent swab culture results showed no bacterial growth.
After 3 weeks, the patient was discharged from the NICU when
more than 70% of the lesions showed re-epithelization. Some
lesions, especially on the flanks where the defects were most
extensive at birth, presented with peripheral cicatrization, but the
surrounding skin did not show contracture.
Until the age of 12 months, no medical problems were apparent,
and the infant showed completely normal development on routine
paediatric examination. No new lesions developed, most lesions
were fully epithelized, and visible hair follicles were observed
from healed lesions on the scalp (Fig. 2).
Fig. 2. (a) Well-healed skin defect leaving whitish scars without contracture
at the age of 9 months. (b) Hair regrowth on healed scalp lesions (circle).
This is an open access article under the CC BY-NC license. www.medicaljournals.se/acta
Journal Compilation © 2019 Acta Dermato-Venereologica.
doi: 10.2340/00015555-3088
Acta Derm Venereol 2019; 99: 343–344