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Open Access Publications from the University of California

Scholarly Works (6 results)

  • Article
  • Peer Reviewed
Dermatology Online Journal, Volume 20, Issue 9 (2014)

Background: Lichen planus is an inflammatory disease that affects the skin, the oral mucosa, or both.  Generalized cutaneous lichen planus may pose a therapeutic challenge for clinicians if the condition persists or flares after topical or systemic corticosteroid therapy.

Purpose: Acitretin, a systemic retinoid, can be considered a potential second-line treatment for patients with generalized cutaneous lichen planus.  Herein, we describe a postmenopausal woman with generalized cutaneous lichen planus who was successfully treated with acitretin.

Methods: A 58-year-old woman presented with generalized cutaneous lichen planus involving her upper and lower extremities as well as her lower back.  After failing corticosteroid therapy, she was started on acitretin 20 mg/day, which was later increased to 30 mg/day.  To review the literature on the use of acitretin in cutaneous lichen planus, we used the PubMed search engine and searched for the terms “acitretin” and “cutaneous lichen planus.”

Results: Our patient had complete resolution of pruritus within one week of initiating acitretin 20 mg/day.  After an increase in dose to 30 mg/day, the cutaneous lesions completely resolved over a 3-month period.  There was no recurrence of disease as acitretin was tapered and discontinued.

Conclusion: Generalized cutaneous lichen planus may pose a therapeutic challenge for the symptomatic relief of skin lesions.  Topical and systemic corticosteroids are first-line treatments.  In patients who fail corticosteroids, relapse after corticosteroid therapy, or have contraindications to corticosteroids, acitretin may be considered a potential second-line therapy.

    Cover page: Acitretin for the management of generalized cutaneous lichen planusCreative Commons 'BY-NC-ND' version 4.0 license
    • Article
    • Peer Reviewed
    Dermatology Online Journal, Volume 23, Issue 5 (2017)
    Purpose: As established by the AccreditationCouncil for Graduate Medical Education (ACGME),dermatology residents in the United States mustparticipate in continuity clinic. This requirementmay be achieved through multiple means, allowingfor program variation. To better assess continuityclinic’s role in resident learning, more data onthis component of graduate medical education isneeded. Methods: An anonymous online survey wasdistributed via the American Board of Dermatologylistserv to all U.S. dermatology residents. Continuityclinic organization, setting, frequency, and patientand preceptor characteristics were assessed; residentsatisfaction and learning were compared. Results:Of 231 responses, 7.8% reported continuity clinicdaily, 77.1% weekly, 9.1% every other week, 3.0%monthly, 0.4% once every several months, and 2.2%only during certain blocks. Of the clinics reported,80.1% were “resident-run with attending” and 11.3%were attending-run. The rest were “resident-run withno attending” (0.9%), both resident and attendingrun(3.0%), or “other” (4.8%). Trainees in resident-runclinics (with attendings) reported greater continuityof care than those in attending-run clinics (p<0.001).Residents reported better teaching with attendingpresence during patient encounters than whenattendings were present only if concerns were raised(p<0.01).
      Cover page: Continuity of care in dermatology residency programs in the United StatesCreative Commons 'BY-NC-ND' version 4.0 license
      • Article
      • Peer Reviewed
      Dermatology Online Journal, Volume 24, Issue 3 (2018)

      Genitogluteal porokeratosis is a disorder of keratinization that may present in men in their fourth decade of life. We describe a 52-year-old human immunodeficiency virus (HIV)-positive man with history of anal squamous cell carcinoma who developed verrucous lesions on the buttocks and genitals. The buttock lesions presented shortly after radiotherapy for anal carcinoma a decade prior, whereas the genital lesions presented three months prior in areas treated with injectable medication for erectile dysfunction. Skin biopsy revealed a cornoid lamella, leading to the diagnosis of genitogluteal porokeratosis. The buttock lesions were treated with shave excision and the genital lesions were treated with topical agents. Using the PubMed database, a literature search was performed with combinations of the following key words: acuminata, condyloma, cornoid lamella, genital, genitogluteal, HIV, penile, porokeratosis, verrucous, vulvar. The generated papers and their references were reviewed. To the best of our knowledge, we present the first reported case of genitogluteal porokeratosis in an HIV-positive man. Notably, these lesions developed in sites of prior radiation or injection. This condition should be included in the differential diagnosis of chronic lesions of the genitals and buttocks in patients with HIV and/or history of radiation treatment and/or trauma to the genitogluteal region.

        Cover page: Genitogluteal porokeratosis in an HIV-positive man: a case report and review of the literature on genital porokeratosisCreative Commons 'BY-NC-ND' version 4.0 license
        • Article
        • Peer Reviewed
        UC San Diego Previously Published Works (2014)

        Objectives

        Black patients with head and neck cancer (HNC) have poorer survival and disease control compared to non-black patients, but disparities in death from non-cancer causes (i.e., competing mortality) are less well-studied.

        Materials and methods

        We conducted an analysis of 538 patients (169 black, 369 non-black) with stage III-IV HNC treated on one of six multi-institutional protocols between 1993 and 2004 involving multi-agent chemoradiotherapy with or without surgery. Competing mortality was defined as death due to intercurrent comorbid disease, treatment-related morbidity, or unknown cause in the absence of disease recurrence, progression, or second malignancy. Cox proportional hazards and competing risks regression were used to estimate the effect of black race on competing mortality.

        Results

        Black race was associated with increased rates of comorbidity, smoking, heavy alcohol use, advanced tumor stage, and poorer performance status (p<.001 for all). Compared to non-black patients, black HNC patients had a higher 5 year cumulative incidence of disease progression (31.4%; 95% CI, 24.4-38.5% vs 23.4%; 95% CI, 19.1-28.1%) and competing mortality (28.1%; 95% CI, 21.2-35.3% vs 14.5%; 95% CI, 11.0-18.5%). When adjusting for age, male sex, body mass index, distance traveled, smoking and alcohol use, performance status, comorbidity, and tumor stage, the black race was associated with death from comorbid disease (Cox hazard ratio 2.13; 95% CI, 1.06-4.28, p=0.033).

        Conclusions

        Black patients with advanced HNC are at increased risk of both disease progression and death from competing non-cancer mortality, particularly death from comorbid disease. Improved strategies to manage comorbid disease may increase the benefit of treatment intensification in black patients.
          Cover page: Race and competing mortality in advanced head and neck cancer
          • Article
          • Peer Reviewed
          UCLA Previously Published Works (2009)
          Antimicrobial effector mechanisms are central to the function of the innate immune response in host defense against microbial pathogens. In humans, activation of Toll-like receptor 2/1 (TLR2/1) on monocytes induces a vitamin D dependent antimicrobial activity against intracellular mycobacteria. Here, we report that TLR activation of monocytes triggers induction of the defensin beta 4 gene (DEFB4), requiring convergence of the IL-1beta and vitamin D receptor (VDR) pathways. TLR2/1 activation triggered IL-1beta activity, involving the upregulation of both IL-1beta and IL-1 receptor, and downregulation of the IL-1 receptor antagonist. TLR2/1L induction of IL-1beta was required for upregulation of DEFB4, but not cathelicidin, whereas VDR activation was required for expression of both antimicrobial genes. The differential requirements for induction of DEFB4 and cathelicidin were reflected by differences in their respective promoter regions; the DEFB4 promoter had one vitamin D response element (VDRE) and two NF-kappaB sites, whereas the cathelicidin promoter had three VDREs and no NF-kappaB sites. Transfection of NF-kappaB into primary monocytes synergized with 1,25D3 in the induction of DEFB4 expression. Knockdown of either DEFB4 or cathelicidin in primary monocytes resulted in the loss of TLR2/1-mediated antimicrobial activity against intracellular mycobacteria. Therefore, these data identify a novel mechanism of host defense requiring the induction of IL-1beta in synergy with vitamin D activation, for the TLR-induced antimicrobial pathway against an intracellular pathogen.
            Cover page: Convergence of IL-1β and VDR Activation Pathways in Human TLR2/1-Induced Antimicrobial Responses
            • Article
            • Peer Reviewed
            UCLA Previously Published Works (2012)
            Leprosy provides a model to investigate mechanisms of immune regulation in humans, given that the disease forms a spectrum of clinical presentations that correlate with host immune responses. Here we identified 13 miRNAs that were differentially expressed in the lesions of subjects with progressive lepromatous (L-lep) versus the self-limited tuberculoid (T-lep) disease. Bioinformatic analysis revealed a significant enrichment of L-lep-specific miRNAs that preferentially target key immune genes downregulated in L-lep versus T-lep lesions. The most differentially expressed miRNA in L-lep lesions, hsa-mir-21, was upregulated in Mycobacterium leprae-infected monocytes. By directly downregulating Toll-like receptor 2/1 heterodimer (TLR2/1)-induced CYP27B1 and IL1B expression as well as indirectly upregulating interleukin-10 (IL-10), hsa-mir-21 inhibited expression of the genes encoding two vitamin D-dependent antimicrobial peptides, CAMP and DEFB4A. Conversely, knockdown of hsa-mir-21 in M. leprae-infected monocytes enhanced expression of CAMP and DEFB4A and restored TLR2/1-mediated antimicrobial activity against M. leprae. Therefore, the ability of M. leprae to upregulate hsa-mir-21 targets multiple genes associated with the immunologically localized disease form, providing an effective mechanism to escape from the vitamin D-dependent antimicrobial pathway.
              Cover page: MicroRNA-21 targets the vitamin D–dependent antimicrobial pathway in leprosy
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