Importance Solar ultraviolet (UV) irradiation causes photoaging, characterized by fragmentation and reduced production of type I collagen fibrils that provide strength to skin. UVB irradiation (280–320 nm) causes these changes by inducing matrix metalloproteinase (MMP)-1 and suppressing type I collagen synthesis. The role of UVA irradiation (320–400 nm) in promoting similar molecular alterations is less clear, yet important to consider, since it is 10–100 times more abundant in natural sunlight than UVB irradiation and penetrates deeper into the dermis than UVB irradiation. The majority (~75%) of solar UVA irradiation is comprised of UVA1 irradiation (340–400 nm), which is also the primary component of tanning beds. Objective To evaluate the effects of low levels of UVA1 irradiation, as might be encountered in daily life, on expression of MMP-1 and type I procollagen (the precursor of type I collagen). Design In vivo biochemical analyses after UVA1 irradiation of normal human skin. Setting Academic referral center. Participants Healthy human volunteers without skin disease. Main Outcome(s) and Measure(s) Skin pigmentation was measured by a color meter (chromameter) under the L* variable (luminescence), which ranges from 0 (black) to 100 (white). Gene expression in skin samples was assessed by real-time polymerase chain reaction. Results Lightly pigmented human skin (L*>65) was exposed up to four times (one exposure/day) to UVA1 irradiation at a low-dose (20 J/cm2), mimicking UVA levels from strong sun exposure lasting approximately two hours. A single exposure to low-dose UVA1 irradiation darkened skin slightly, and did not alter MMP-1 or type I procollagen gene expression. With repeated low-dose UVA1 irradiation, skin darkened incrementally with each exposure. Despite this darkening, two or more exposures to low-dose UVA1 irradiation significantly induced MMP-1 gene expression, which increased progressively with successive exposures. Repeated UVA1 exposures did not suppress type I procollagen expression. Conclusions and Relevance A limited number of low-dose UVA1 exposures, as commonly experienced in daily life, potentially promotes photoaging by affecting breakdown, rather than synthesis, of collagen. Progressive skin darkening in response to repeated low-dose UVA1 exposures in lightly pigmented individuals does not prevent UVA1-induced collagenolytic changes. Therefore, for optimal protection against skin damage, sunscreen formulations should filter all UV wavelengths, including UVA1 irradiation.

A 6‐year‐old girl with a history of chronic immunosuppression following small bowel and colon transplantation for tufting enteropathy presented with a diffuse, facial‐predominant eruption composed of pink‐to‐skin‐colored papules with central white dystrophic spicules. Histology from a punch biopsy and polymerase chain reaction (PCR) from plucked spicules confirmed a diagnosis of trichodysplasia spinulosa (TS). Additional molecular studies identified several strains of the trichodysplasia spinulosa–associated polyomavirus infecting multiple tissues of the patient, confirming the systemic nature of trichodysplasia spinulosa infections.

The findings reveal no difference in complication rates following abdominal body contouring procedures attributable to method of weight loss. Rather, there was a proportional rise in complication rates in patients with a higher body mass index at the time of surgery. Surgeons and patients should be aware of this trend, and it should be part of any discussion of abdominal body contouring procedures and informing patients of their risk profile.

No abstract

Segmental neurofibromatosis is a rare condition that most commonly affects women and presents as neurofibromas, café au lait spots, and freckling. The neurofibromas usually occur in a dermatomal pattern, whereas the café au lait spots may follow Blaschko’s lines. There is often no family history. The etiology is due to a postzygotic mutation in the gene encoding neurofibromin. Histopathology reveals a tumor with haphazardly arranged spindle cells and a pale myxoid stroma from mucin deposition and fibroplasia. There have been few reported cases of segmental neurofibromatosis. In this case report, we will discuss the clinical features, histopathology, differential diagnosis, and management of segmental neurofibromatosis.