Dermatosis papulosa nigra (DPN) is a condition of many small, benign skin lesions on the face, a condition generally presenting on dark-skinned individuals. : 638–9  DPN is extremely common, affecting up to 30% of Black people in the US. From a histological perspective, DPN resembles seborrheic keratoses. The condition may be cosmetically undesirable to some. They should not be confused for Leser-Trélat sign, a sudden explosion of lesions due to a growing tumor. Pathophysiology
The pathophysiology of DPN is unknown. Evidence of family history may suggest a genetic propensity. Treatment
DPN lesions are benign and no treatment generally is indicated unless lesions are cosmetically undesirable. Surgical options including curettage, cryotherapy and laser therapy are options. Scarring, postoperative skin discoloration or keloid formation are potential complications. Therefore, conservative DPN treatment is advisable. Prognosis
DPN is not a pre-malignant condition nor is it associated with any underlying systemic disease. DPN lesions show no tendency to regress spontaneously, and often increase in size and number as an individual ages. Epidemiology
DPN affects up to 35% of the African American population in the USA. Insufficient data is available on the international frequency of DPN. Lesions generally emerge during puberty, increasing steadily in number and size as an individual ages. The incidence of DPN lesions increases with age. Black people with a fair complexion have the lowest frequency of involvement. DPN also occurs among Asians and Polynesians, although the exact incidence is unknown. Females are affected more frequently than males.
Signs and symptoms
Signs and symptoms of Angelman syndrome and their relative frequency in affected individuals are:

Consistent (100%)
Developmental delay, functionally severe
Speech impairment, no or minimal use of words; receptive and non-verbal communication skills higher than verbal ones
Movement or balance disorder, usually ataxia of gait and/or tremulous movement of limbs
Behavioral characteristics of the following types: any combination of atypical frequent laughter/smiling; atypically happy demeanor; easily excitable personality, often with hand flapping movements; hypermotoric behavior; short attention span

Frequent (more than 80%)
Delayed, disproportionate growth in head circumference, usually resulting in microcephaly (absolute or relative) by age 2
Seizures, onset usually less than 3 years of age
Abnormal EEG, characteristic pattern with large amplitude slow-spike waves

Associated (20–80%)
Cause
Angelman syndrome is caused by the lack of expression of a gene known as UBE3A during development. This gene is located within a region of chromosome 15 known as 15q11-q13 and is part of the ubiquitin pathway. In fact, UBE3A codes for a very selective E6-AP ubiquitin ligase for which MAPK1, PRMT5, CDK1, CDK4, β-catenin, and UBXD8 have been identified as ubiquitination targetsTypically, a fetus inherits a maternal copy of UBE3A and a paternal copy of UBE3A. In certain areas of the developing brain, the paternal copy of UBE3A is inactivated through a process known as imprinting and the fetus relies on the functioning maternal copy of UBE3A in order to develop normally. In an individual with AS, however, the maternal UBE3A gene is absent or not functioning normally.