Department of Dermatology

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    A case report of terbinafine-induced acute generalized exanthematous pustulosis in a striking photodistributed pattern
    (Sage, 2024-02-14) Lange, Charles D.; Madden, Laura; Rawlings Parker, Eva; Dermatology, School of Medicine
    Acute generalized exanthematous pustulosis is a rare severe cutaneous adverse reaction that classically presents in intertriginous or flexural areas and subsequently spreads diffusely across the trunk and extremities. To date, few cases of acute generalized exanthematous pustulosis arising in a photodistributed pattern are documented. Herein, we describe the second known case of photodistributed generalized exanthematous pustulosis arising in association with oral terbinafine use, providing a summary of the previously documented cases along with exploration of the potential pathophysiological mechanisms for this cutaneous reaction.
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    Abnormal Golgi morphology and decreased COPI function in cells with low levels of SMN
    (Elsevier, 2019-03) Custer, Sara K.; Foster, Joycelynn N.; Astroski, Jacob W.; Androphy, Elliot J.; Dermatology, School of Medicine
    We report here the finding of abnormal Golgi apparatus morphology in motor neuron like cells depleted of SMN as well as Golgi apparatus morphology in SMA patient fibroblasts. Rescue experiments demonstrate that this abnormality is dependent on SMN, but can also be rescued by expression of the COPI coatomer subunit alpha-COP. A motor neuron-like cell line containing an inducible alpha-COP shRNA was created to generate a parallel system to study knockdown of SMN or alpha-COP. Multiple assays of COPI-dependent intracellular trafficking in cells depleted of SMN demonstrate that alpha-COP function is suboptimal, including failed sequestration of plasma membrane proteins, altered binding of mRNA, and defective targeting and transport of Golgi-resident proteins.
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    Acute Ethanol Exposure Augments Low-Dose UVB-Mediated Systemic Immunosuppression via Enhanced Production of Platelet-Activating Factor Receptor Agonists
    (Elsevier, 2019-01-22) Travers, Jeffrey B.; Weyerbacher, Jonathan; Ocana, Jesus A.; Borchers, Christina; Rapp, Christine M.; Sahu, Ravi P.; Dermatology, School of Medicine
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    Altered mRNA Splicing in SMN-Depleted Motor Neuron-Like Cells
    (Public Library of Science (PLoS), 2016) Custer, Sara K.; Gilson, Timra D.; Li, Hongxia; Todd, A. Gary; Astroski, Jacob W.; Lin, Hai; Liu, Yunlong; Androphy, Elliot J.; Department of Dermatology, School of Medicine
    Spinal muscular atrophy (SMA) is an intractable neurodegenerative disease afflicting 1 in 6-10,000 live births. One of the key functions of the SMN protein is regulation of spliceosome assembly. Reduced levels of the SMN protein that are observed in SMA have been shown to result in aberrant mRNA splicing. SMN-dependent mis-spliced transcripts in motor neurons may cause stresses that are particularly harmful and may serve as potential targets for the treatment of motor neuron disease or as biomarkers in the SMA patient population. We performed deep RNA sequencing using motor neuron-like NSC-34 cells to screen for SMN-dependent mRNA processing changes that occur following acute depletion of SMN. We identified SMN-dependent splicing changes, including an intron retention event that results in the production of a truncated Rit1 transcript. This intron-retained transcript is stable and is mis-spliced in spinal cord from symptomatic SMA mice. Constitutively active Rit1 ameliorated the neurite outgrowth defect in SMN depleted NSC-34 cells, while expression of the truncated protein product of the mis-spliced Rit1 transcript inhibited neurite extension. These results reveal new insights into the biological consequence of SMN-dependent splicing in motor neuron-like cells.
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    An expanded population of CD8dim T cells with features of mitochondrial dysfunction and senescence is associated with persistent HIV-associated Kaposi’s sarcoma under ART
    (Frontiers, 2022-09-29) Clutton, Genevieve T.; Weideman, Ann Marie K.; Goonetilleke, Nilu P.; Maurer , Toby; Dermatology, School of Medicine
    HIV-associated Kaposi’s sarcoma (KS), which is caused by Kaposi’s sarcoma-associated herpesvirus, usually arises in the context of uncontrolled HIV replication and immunosuppression. However, disease occasionally occurs in individuals with durable HIV viral suppression and CD4 T cell recovery under antiretroviral therapy (ART). The underlying mechanisms associated with this phenomenon are unclear. Suppression of viral infections can be mediated by CD8 T cells, which detect infected cells via their T cell receptor and the CD8 coreceptor. However, CD8 T cells exhibit signs of functional exhaustion in untreated HIV infection that may not be fully reversed under ART. To investigate whether KS under ART was associated with phenotypic and functional perturbations of CD8 T cells, we performed a cross-sectional study comparing HIV-infected individuals with persistent KS under effective ART (HIV+ KS+) to HIV-infected individuals receiving effective ART with no documented history of KS (HIV+ KSneg). A subset of T cells with low cell surface expression of CD8 (“CD8dim T cells”) was expanded in HIV+ KS+ compared with HIV+ KSneg participants. Relative to CD8bright T cells, CD8dim T cells exhibited signs of senescence (CD57) and mitochondrial alterations (PGC-1α, MitoTracker) ex vivo. Mitochondrial activity (MitoTracker) was also reduced in proliferating CD8dim T cells. These findings indicate that an expanded CD8dim T cell population displaying features of senescence and mitochondrial dysfunction is associated with KS disease under ART. CD8 coreceptor down-modulation may be symptomatic of ongoing disease.
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    An expanded population of CD8dim T cells with features of mitochondrial dysfunction and senescence is associated with persistent HIV-associated Kaposi’s sarcoma under ART
    (Frontiers Media, 2022-09-29) Clutton, Genevieve T.; Weideman, Ann Marie K.; Goonetilleke, Nilu P.; Maurer, Toby; Dermatology, School of Medicine
    HIV-associated Kaposi’s sarcoma (KS), which is caused by Kaposi’s sarcoma-associated herpesvirus, usually arises in the context of uncontrolled HIV replication and immunosuppression. However, disease occasionally occurs in individuals with durable HIV viral suppression and CD4 T cell recovery under antiretroviral therapy (ART). The underlying mechanisms associated with this phenomenon are unclear. Suppression of viral infections can be mediated by CD8 T cells, which detect infected cells via their T cell receptor and the CD8 coreceptor. However, CD8 T cells exhibit signs of functional exhaustion in untreated HIV infection that may not be fully reversed under ART. To investigate whether KS under ART was associated with phenotypic and functional perturbations of CD8 T cells, we performed a cross-sectional study comparing HIV-infected individuals with persistent KS under effective ART (HIV+ KS+) to HIV-infected individuals receiving effective ART with no documented history of KS (HIV+ KSneg). A subset of T cells with low cell surface expression of CD8 (“CD8dim T cells”) was expanded in HIV+ KS+ compared with HIV+ KSneg participants. Relative to CD8bright T cells, CD8dim T cells exhibited signs of senescence (CD57) and mitochondrial alterations (PGC-1α, MitoTracker) ex vivo. Mitochondrial activity (MitoTracker) was also reduced in proliferating CD8dim T cells. These findings indicate that an expanded CD8dim T cell population displaying features of senescence and mitochondrial dysfunction is associated with KS disease under ART. CD8 coreceptor down-modulation may be symptomatic of ongoing disease.
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    An Analysis of Public Sunscreen Distribution in the United States During the COVID-19 Pandemic
    (Elsevier, 2022) Szeto, Mindy D.; Kokoska, Ryan E.; Maghfour, Jalal; Rundle, Chandler W.; Presley, Colby L.; Harp, Taylor; Hamp, Austin; Wegener, Victoria; Hugh, Jeremy; Dellavalle, Robert P.; Dermatology, School of Medicine
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    Apixaban-induced cutaneous hypersensitivity: a case series with evidence of cross-reactivity
    (University of California, 2020) Isaq, Nasro A.; Vinson, Whitney M.; Rahnama-Moghadam, Sahand; Dermatology, School of Medicine
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    Association between alopecia areata and atopic dermatitis: A nested case-control study of the All of Us database
    (Elsevier, 2023) Diaz, Michael J.; Haq, Zaim; Abdi, Parsa; Tran, Jasmine T.; Guttman-Yassky, Emma; Ungar, Benjamin; Dermatology, School of Medicine
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    Association of Demographic Factors and Infantile Hemangioma Characteristics With Risk of PHACE Syndrome
    (American Medical Association, 2021) Cotton, Colleen H.; Ahluwalia, Jusleen; Balkin, Daniel M.; Frieden, Ilona J.; Haggstrom, Anita N.; Castelo-Soccio, Leslie A.; Liy-Wong, Carmen; Pope, Elena; Steiner, Jack E.; Siegel, Dawn H.; Fernandez-Faith, Esteban; Morel, Kimberly D.; Lauren, Christine T.; Garzon, Maria C.; Mancini, Anthony J.; Chamlin, Sarah L.; Tollefson, Megha M.; Liang, Marilyn G.; Delano, Sophia; Glick, Sharon A.; Hogeling, Marcia; Barrio, Victoria R.; PHACE Retrospective Study Group; Dermatology, School of Medicine
    Importance: A 2010 prospective study of 108 infants estimated the incidence of PHACE (posterior fossa malformations, hemangioma, arterial anomalies, cardiac defects, eye anomalies) syndrome to be 31% in children with facial infantile hemangiomas (IHs) of at least 22 cm2. There is little evidence regarding the associations among IH characteristics, demographic characteristics, and risk of PHACE syndrome. Objectives: To evaluate demographic characteristics and comorbidities in a large cohort of patients at risk for PHACE syndrome and assess the clinical features of large head and neck IH that may be associated with a greater risk of a diagnosis of PHACE syndrome. Design, setting, and participants: This multicenter, retrospective cohort study assessed all patients with a facial, head, and/or neck IH who were evaluated for PHACE syndrome from August 1, 2009, to December 31, 2014, at 13 pediatric dermatology referral centers across North America. Data analysis was performed from June 15, 2017, to February 29, 2020. Main outcomes and measures: The main outcome was presence or absence of PHACE syndrome. Data included age at diagnosis, sex, patterns of IH presentation (including size, segment location, and depth), diagnostic procedures and results, and type and number of associated anomalies. Results: A total of 238 patients (mean [SD] age, 2.96 [4.71] months; 184 [77.3%] female) were included in the analysis; 106 (44.5%) met the criteria for definite (n = 98) or possible (n = 8) PHACE syndrome. A stepwise linear regression model found that a surface area of 25 cm2 or greater (odds ratio [OR] 2.99; 95% CI, 1.49-6.02) and involvement of 3 or more locations (OR, 17.96; 95% CI, 6.10-52.85) to be statistically significant risk factors for PHACE syndrome. Involvement of the parotid gland (OR, 0.39; 95% CI, 0.18-0.85) and segment S2 (OR, 0.38; 95% CI, 0.16-0.91) was associated with a lower risk. Race and ethnicity may also be associated with PHACE syndrome risk, although more studies are needed. Conclusions and relevance: This cohort study further described factors associated with both a higher and lower risk of PHACE syndrome. The presence of multiple anatomical sites and large surface area were associated with greater risk, whereas S2 or parotid IHs were associated with lower, but still potential, risk. These findings can help in counseling families and decision-making regarding evaluation of infants with large head and neck IHs.