The EAACI/GA 2 LEN/EDF/ WAO guideline for the definition, classification, diagnosis and management of urticaria. Allergy 2018; 73:1393-414. 2 B erard F, Ferrierle Bou€ edec MC, Bouillet L et al. Omalizumab in chronic spontaneous urticaria patients nonresponsive to H1-antihistamine treatment: results of the phase IV open-label SUNRISE study.

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The purpose of this study was to give dermatologists important information on the association of isotretinoin with aplastic anemia and therefore change their approach for monitoring patients taking isotretinoin. We reviewed FDA reports and most recent literature on the association of isotretinoin with bone marrow suppression. We then applied this information to the clinical course of a patient who had been on isotretinoin for a year and then presented six months later in septic shock with AA and ultimately died of multiorgan failure. Retinoic acid induces stem cells to further differentiate into mature cells by upregulating FoxO transcription factors. These factors are involved in multiple cellular functions including cell proliferation, apoptosis, reactive oxygene homeostasis and stem cell homeostasis. Retinoic acid at pharmacological doses also suppresses the growth and differentiation of mesenchymal stem cells in the human bone marrow by the up regulation of CDK inhibitors, down regulation of CDK 2 activity and pRB phosphorylation. Hematopoeitic stem cells have a high expression of retinaldehyde dehydrogenase, and inhibition of retinoic acid signaling causes the stem cells to remain primitive in phenotype and function which provides a definitive role for retinoic acid in the maturation process. There are 19 FDA reports of aplastic anemia associated with isotretinoin. It is a possibility that isotretinoin exposure caused the terminal differentiation of our patient's marrow stem cells, leading to aplastic anemia. We propose that more frequent (quarterly) monitoring with a CBC could potentially give providers the opportunity for early intervention when a patient demonstrates down trending cell lines.

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Chronic exposure to sUVR and, more recently, exposure to PM have been reported to be associated with more facial lentigines. In most urban environments, human skin is exposed to both environmental factors. In this epidemiological study we therefore assessed their combined effect on lentigines formation. We studied facial lentigines in 799 elderly Caucasian women (mean age 73.5 years) of the SALIA cohort using the SCINEXA TM skin aging score. Long-term exposure to PM was estimated with land use regression models. Based on satellite data and data from the German Climate Center 5-year mean exposure to sUVR was calculated either as (i) daily UVB (290-315 nm) exposure based on the whole daylight period or as (ii) UV index based on the hour per day with maximal UV (290-400 nm). Associations between PM or sUVR with lentigines formation and the interactions PM*sUVR were estimated in single and multi-pollutant models. As expected sUVR exposure was associated with more lentigines on the cheeks (7.6% higher score on average; p¼0.008) and this effect was only slightly attenuated when adjusting for PM. We also confirmed that PM was associated with more facial lentigines, and this association was still visible after adjusting for sUVR. We next observed that the association between sUVR and lentigines is affected by the level of PM. The sUVR effect was increasing at lower PM levels (e.g. UVBxPM 10 p(interaction)¼0.007), likely because sUVR was less shielded by PM in the troposphere. Of note, we also found that the association between PM and lentigines is modulated by the level of sUVR. At lower sUVR exposure, the PM effect on lentigines was stronger. All of these interactions indicated linear dose-responses. Thus, facial lentigines are the consequence of an interplay of at least two ubiquitous, environmental factors. It might take place in the troposphere and/or in the skin, where sUVR exposure might alter the response to PM.