Dermatology In General Medicine Research Articles

H14 ‘Reflection for the day’

Abstract Thomas B. Fitzpatrick had a tremendous influence on the specialty of dermatology, including seminal scientific contributions, a legendary ability to teach and train, and remarkable innovations in clinical dermatology. Born in Wisconsin in 1919, he received his medical degree from Harvard, followed by a PhD in pathology. He served 2 years at an Army Chemical Centre, where his interest in skin pigmentation led to the discovery of human tyrosinase. Further innovation in basic sciences followed, with the discovery of the melanosome and epidermal melanin unit. He added to his academic accolades by completing a fellowship in chemistry at Oxford, then returned to the USA to pursue clinical dermatology training at Mayo Clinic. At the age of 32 years, following substantial success in his early career, he was appointed Professor and Chair of Dermatology at the University of Oregon. By 39 years of age, he was Chair of the Harvard Medical School Dermatology Department, Harvard’s youngest Professor and Chair, while serving as Chief of Dermatology at Massachusetts General Hospital. He was a master at motivating students and sharing his passion for dermatology. He often said ‘Practicing dermatologists are like the woodwind section of the orchestra—small in number, when they play they must play well’. In 1971, he wrote the first multiauthor medical textbook in the field entitled Fitzpatrick’s Dermatology in General Medicine, now in its eighth edition. Dr Fitzpatrick contributed heavily to the clinical advances in dermatology in the latter half of the 20th century. Alongside dermatopathologist Wallace Clark, he established the very first pigmented lesion clinic in 1966. From that clinic, studies enabled Dr Clark to devise the Clark level staging system for melanoma. Fitzpatrick described early diagnostic signs in melanoma, and the concept of sunlight as a factor in its aetiology. In 1975, he devised the Fitzpatrick scale of skin phototypes, which described a person’s skin type in terms of response to ultraviolet (UV) radiation exposure. To huge success, he experimented with psoralen and UVA to treat psoriasis, coining the term photochemotherapy, or PUVA. Fitzpatrick was a highly productive medical scholar, while having many other notable qualities and interests. He was an avid lover of music, a skilled pianist and a Johannes Brahms enthusiast. The Boston Globe called him a ‘dermatologist with an infectious enthusiasm for his specialty and philosopher’s love of a good quote’. For 20 years, he co-edited the Globe’s popular ‘Reflection for the Day’, alongside his loving wife Beatrice. Thomas Fitzpatrick was admired by many until his passing in 2003, leaving us with so much to remember him by.

Cutaneous Signs in Dermatological Diseases; An Overview.

Cutaneous signs in dermatology are pathognomonic or diagnostic for certain conditions. A knowledge of these signs is a useful skill, which must not be forgotten in the recent trend towards relying on molecular biology and other investigative tools including histological findings to make a diagnosis. The aim of this review is to summarize all cutaneous signs in dermatology in a systematic way that would benefit dermatologists, trainee or experienced, in identifying diseases and sharpening their clinical skills. A keyword search for the terms “cutaneous signs,” “sign” AND “dermatology” was conducted through PUBMED, Google, and the major textbooks in dermatology (i.e., Rooks Textbook of Dermatology; Fitzpatrick's Dermatology in General Medicine and Dermatology). References were searched thoroughly for all cutaneous signs described. One hundred and nineteen signs were noted and summarized under the following categories: autoimmune, infective, inflammatory, neoplastic, genetic, trauma/miscellaneous. This review would serve as a good reference for those wanting to improve their clinical acumen in diagnosing dermatological disease.

Efficacy and safety of secukinumab in moderate to severe palmoplantar pustular psoriasis over 148 weeks: Extension of the 2PRECISE study

To the Editor: Palmoplantar pustular psoriasis is a debilitating inflammatory disease confined to the palms and/or soles and resistant to treatment.1Mrowietz U. Pustular eruptions of palms and soles.in: Goldsmith LA Fitzpatrick's Dermatology in General Medicine. McGraw-Hill, New York, NY2012: 252-259Google Scholar Secukinumab, a fully human monoclonal antibody selectively targeting interleukin 17A, is efficacious in the treatment of moderate to severe psoriasis, with a sustained effect and favorable safety profile.2Langley R.G. Elewski B.E. Lebwohl M. et al.Secukinumab in plaque psoriasis—results of two phase 3 trials.N Engl J Med. 2014; 371: 326-338Crossref PubMed Scopus (1297) Google Scholar 2PRECISE was a phase 3b multicenter, randomized, double-blind, placebo-controlled, parallel-group study comparing secukinumab 300 mg (n = 79) and 150 mg (n = 80) to placebo (n = 78) in individuals with moderate to severe palmoplantar pustular psoriasis over 52 weeks. The primary objective was a response of at least a 75% reduction in Palmoplantar Pustular Psoriasis Area Severity Index (ppPASI75) with secukinumab at week 16 versus placebo.3Mrowietz U. Bachelez H. Burden A.D. et al.Secukinumab for moderate-to-severe palmoplantar pustular psoriasis: results of the 2PRECISE study.J Am Acad Dermatol. 2019; 80: 1344-1352Abstract Full Text Full Text PDF PubMed Scopus (37) Google Scholar Baseline patient characteristics, study design, and primary endpoint were previously reported.3Mrowietz U. Bachelez H. Burden A.D. et al.Secukinumab for moderate-to-severe palmoplantar pustular psoriasis: results of the 2PRECISE study.J Am Acad Dermatol. 2019; 80: 1344-1352Abstract Full Text Full Text PDF PubMed Scopus (37) Google Scholar Extension of treatment after week 52 was possible to up to 148 weeks, with patients who achieved meaningful clinical response in the investigator's judgment either maintained on secukinumab 300 mg (n = 36) or secukinumab 150 mg (n = 31) and placebo nonresponder patients who had switched to secukinumab 300 mg (n = 17) or 150 mg (n = 10) at week 16 of the core study.3Mrowietz U. Bachelez H. Burden A.D. et al.Secukinumab for moderate-to-severe palmoplantar pustular psoriasis: results of the 2PRECISE study.J Am Acad Dermatol. 2019; 80: 1344-1352Abstract Full Text Full Text PDF PubMed Scopus (37) Google Scholar Missing values were imputed using the last observation carried forward (LOCF). The mean ppPASI at study baseline was 22.7 (standard deviation, 9.5) in patients who entered the extension period. The ppPASI75 response rates increased during the extension period in all groups (Fig 1). At week 148, the percentages of patients with ppPASI75 response had increased in all groups, with similar levels in the placebo/secukinumab 150 mg group (75.0%), placebo/secukinumab 300 mg group (77.8%), and initial secukinumab 300 mg group (78.3%), and 100% responders in the initial secukinumab 150 mg group. At the end of the extension treatment period at week 148, the mean ppPASI in the placebo/secukinumab 150 mg group remained at the same level, at 9.75, whereas it had decreased in all other groups (initial secukinumab 150 mg, 1.01; initial secukinumab 300 mg, 3.43; and placebo/secukinumab 300 mg, 4.19) (Fig 2). The overall incidence of adverse events in the extension treatment period was slightly lower under secukinumab 150 mg (61.0%) than under secukinumab 300 mg (69.8%), and no new or unexpected adverse events were observed. During the extension period, there were 5 discontinuations in the secukinumab 150 mg group (16.1%), 5 in the secukinumab 300 mg group (13.9%), 4 in the placebo/secukinumab 150 mg group (40.0%), and 4 in the placebo/secukinumab 300 mg group (23.5%).Fig 2Time course of mean absolute ppPASI score during extension treatment period (full analysis set, last observation carried forward). ppPASI, Palmoplantar Pustular Psoriasis Area Severity Index; Pts, patients; Sec, secukinumab.View Large Image Figure ViewerDownload Hi-res image Download (PPT) The low numbers of patients in each group warrant caution in interpreting these results and render unfeasible any further analysis of efficacy by patient characteristics on entering the extension study. The apparently greater benefit observed for the 150-mg dose compared to the 300-mg dose may also be due to small group numbers and discontinuations. However, these data suggest a sustained clinical benefit and an acceptable safety and tolerability profile of extended treatment with secukinumab 300 mg or 150 mg in patients with palmoplantar pustular psoriasis who had achieved a meaningful clinical response at weeks 16 and 52 when continuing secukinumab up to week 148.

Representation of dark skin images of common dermatologic conditions in educational resources: A cross-sectional analysis

Representation of dark skin images of common dermatologic conditions in educational resources: A cross-sectional analysis

Dermoscopy predicts outcome in hemoporfin-mediated photodynamic therapy of port-wine stains: A prospective observational study

To the Editor: Port-wine stain (PWS) is defined as ectasia of the vessels in the dermis, affecting the dermal papillae capillary loops, the horizontal plexus at the dermal-subcutaneous junction, or a combination of these.1Anderson R.R. Levins P.C. Grevelink J.M. Lasers in dermatology.in: Fitzpatrick T.B. Eisen A.Z. Wolff K. Freedberg I.M. Austen K.F. Dermatology in General Medicine. 4th ed. McGraw-Hill, New York1971: 1755-1766Google Scholar Recent studies have identified 2 main dermoscopic patterns of PWS. Type 1 is a superficial pattern composed of red globules and dots that correspond to dilated capillary loops in the papillary dermis. Type 2 is a deep pattern that features red ring structures corresponding to dilated ectatic vessels located deep in the horizontal vascular plexus.2Piccolo V. Russo T. Moscarella E. et al.Dermatoscopy of vascular lesions.Dermatol Clin. 2018; 36: 389-395Abstract Full Text Full Text PDF PubMed Scopus (22) Google Scholar Histopathologic examination is the standard approach to determine the depth of the vascular lesion, but it is invasive. Dermoscopy can preoperatively predict the outcome of treatment and the minimal effective fluence in pulsed dye laser treatment.3Eubanks L.E. McBurney E.I. Videomicroscopy of port-wine stains: correlation of location and depth of lesion.J Am Acad Dermatol. 2001; 44: 948-951Abstract Full Text Full Text PDF PubMed Scopus (50) Google Scholar,4Shirakawa M. Ozawa T. Wakami S. et al.Utility of dermoscopy before and after laser irradiation in port wine stains.Ann Dermatol. 2012; 24: 7-10Crossref PubMed Scopus (17) Google Scholar PWS in areas that typically respond well to laser treatment were more likely to have a superficial type 1 but those that have a poorer response were more likely to have a deeper type 2. The immediate vessel disappearance after pulsed dye laser treatment observed by dermoscopy can predict the minimal effective fluence and prevent adverse effects. Hemoporfin-mediated photodynamic therapy (HMME-PDT) is considered to be a successful and well-tolerated treatment option for PWS.5Zhao Y. Tu P. Zhou G. et al.Hemoporfin photodynamic therapy for port-wine stain: a randomized controlled trial.PLoS One. 2016; 11: e0156219Crossref PubMed Scopus (38) Google Scholar The response of different depth vessels to HMME-PDT and the relationship between dermoscopic features and the efficacy of HMME-PDT have not been reported to our knowledge. We present a prospective observational study of 16 patients with PWS who received HMME-PDT. The Ethics Committee of Tongji Medical College, Huazhong University of Science and Technology (2019S1170) approved this study. All of the detailed methods are in the Supplemental file available on Mendeley at https://doi.org/10.17632/b968gsy7bp.1. Group A consisted of 8 patients with the type 1 pattern, and group B consisted 8 patients with the type 2 pattern (Table I). Dermoscopic images of PWS lesions were taken from each patient using the hand-held dermoscope with 50× polarized light (CH-DSIS-2000 Plus; Guangzhou Chuanghong Medical Technology Co, Ltd, Guangzhou, China). Clinical efficacy was observed after 1 treatment of HMME-PDT.Table IProfile of the patients in the studyPatient No.Age, ySexPWS locationResponse∗No improvement (NI): <20%; some improvement (SI): 20%-59%; great improvement (GI): 60%-89%; nearly completely resolved (CR): 90%.Group A 110FemaleRight cheekCR 231MaleMandible and neckGI 34FemaleMandibleCR 48MaleRight chinGI 56MaleLeft cheekGI 611MaleLeft cheekGI 74FemaleLeft cheek and orbitCR 84FemaleLeft temporalCRGroup B 18MaleRight cheekNI 240FemaleMandible and neckSI 36FemaleRight cheekNI 47MaleRight cheekNI 518MaleLeft cheekNI 69MaleLeft cheekNI 78MaleRight cheekNI 819MaleRight cheekNIPWS, Port wine stain.∗ No improvement (NI): <20%; some improvement (SI): 20%-59%; great improvement (GI): 60%-89%; nearly completely resolved (CR): 90%. Open table in a new tab PWS, Port wine stain. Patients in the 2 groups had markedly different responses after 1 treatment with HMME-PDT. Patients in group A (type 1 pattern) had an excellent response to HMME-PDT, whereas those in group B (type 2 pattern) had a poor response (Fig 1). In HMME-PDT treatment, the 532-nm laser can activate the photosensitizer injected into the blood vessels to produce highly reactive singlet oxygen, which can destroy the endothelial cells.5Zhao Y. Tu P. Zhou G. et al.Hemoporfin photodynamic therapy for port-wine stain: a randomized controlled trial.PLoS One. 2016; 11: e0156219Crossref PubMed Scopus (38) Google Scholar HMME-PDT can more easily destroy or remove deformed vessels that are superficial because of the limited range of wavelength penetration. It is still difficult to penetrate PWS lesions with thicker vessel walls, deeper locations, and larger diameters. Possibility of the need for multiple treatments should be discussed in the initial consultation. Dermoscopy is a simple, noninvasive technique that allows the microvascular patterns in PWS to be assessed and recorded. We have observed that the type 1 pattern is readily treated with HMME-PDT and an excellent response can be expected, whereas the type 2 pattern resists treatment. Further studies will increase the sample size, refine the dermoscopic patterns, and study the relationship between different patterns and HMME-PDT results.

Uremic Frost

A 58-year-old man presented to the emergency department with acute urinary retention and abdominal pain. Laboratory tests revealed a serum creatinine level of 20 mg/dL and blood urea nitrogen of 263 mg/dL. A urinary catheter was placed and drained 2 L of urine. On examination, his skin was covered diffusely with a fine white powder known as “uremic frost” (Figure). These skin findings rapidly resolved over the next 48 hours with improvement of his severe uremia. Uremic frost is a manifestation of severe azotemia where tiny, yellow-white urea crystals deposit on the skin, resulting in a frosted appearance as sweat evaporates.1Johnston G.A. Graham-Brown R.C. Chapter 150. The skin and disorders of the alimentary tract, the hepatobiliary system, the kidney, and the cardiopulmonary system.in: Goldsmith L.A. Katz S.I. Gilchrest B.A. Paller A.S. Leffell D.J. Wolff K. Fitzpatrick's Dermatology in General Medicine. 8th ed. McGraw-Hill, New York, NY2012http://accessmedicine.mhmedical.com.ucsf.idm.oclc.org/content.aspx?bookid=392&sectionid= 41138873Date accessed: August 1, 2018Google Scholar It is most frequently observed on areas of skin with eccrine glands and hair such as the scalp, neck, face, forearms, and chest and can be easily wiped away.2Saardi K.M. Schwartz R.A. Uremic frost: a harbinger of impending renal failure.Int J Dermatol. 2016; 55: 17-20Crossref PubMed Scopus (9) Google Scholar Uremic frost was first described by Hirschsprung in 18653Kuo C.C. Hung J.B. Tsai C.W. Chen Y.M. Uremic frost.CMAJ. 2010; 182: E800Crossref PubMed Scopus (8) Google Scholar but is now a rarely observed physical examination finding in settings in which hemodialysis is readily available. Among 9 cases of uremic frost published in the literature, the mean blood urea nitrogen was 199 mg/dL and the mean serum creatinine level was 17.5 mg/dL.2Saardi K.M. Schwartz R.A. Uremic frost: a harbinger of impending renal failure.Int J Dermatol. 2016; 55: 17-20Crossref PubMed Scopus (9) Google Scholar Although a rare finding, uremic frost remains an important sign of severe renal failure, particularly in clinical settings with limited resources.

Neurofibromatosis With Recurrent Spontaneous Pneumothorax

SESSION TITLE: Disorders of the Pleura Global Case Reports SESSION TYPE: Global Case Report Poster PRESENTED ON: Tuesday, October 27, 2015 at 01:30 PM - 02:30 PM INTRODUCTION: Neurofibromatosis(NF); is a genetic heterogeneous disease of nervous system, skin, eyes, lungs and skeletal system. NF is classified in two groups of NF1 and 2. NF-1 is the most common form and affects 1 in about 4000 births in the world (1) CASE PRESENTATION: We present a patient from our clinic who is diagnosed with Neurofibromatosis and recurrent spontaneous pneumothorax. Our patient was 28 years old male who had received the diagnosis of pneumothorax for two times. He is an active smoker and suffering from chest pain, shortness of breath and trembling hands. His first degree family history revealed malignancies. His mother and sister have the similar skin lesions. Physical examination findings are decreased breath sounds, bilateral axillary freckling, café au lait spots from 6 to 15 mm and multiple neurofibromas. We performed Computed Tomography(CT) and revealed multiple air cysts measuring up to 25x13 mm in the upper lobes. Cranial CT revealed subcutaneous nodules on the right parietal and left frontal region. After the EMG VEP (visuel evoked potential), P100 latency in the study was normal. On the eye examination, bilateral Lisch nodules of the iris and congenital subcapsular cataracts were detected. Also he has a slight mix-type hearing loss in the right ear detected by audiometric evaluation. So we recommend smoking cessation and control chest CT scannings at regular intervals. DISCUSSION: Neurofibromatosis is a rare but important disease. Thoracic manifestations of the disease include intrathoracic neurogenic tumors, meningoceles, kyphoscoliosis and pulmonary fibrosis. Chest radiographic findings of these patients are large apical asymmetric thin-walled bullae (73%) and subpleural reticular abnormality (61%). There is a relationship between neurofibromatosis and interstitial lung disease. Honeycombing may be seen in neurofibromatosis rarely. Some investigators suggest that the pulmonary parenchymal disease of neurofibromatosis is attributed to a mesenchymal defect, resulting in primary deposition of collagen. Also, it has been suggested that neurofibromatosis may increase the sensitivity of the lungs to cigarette smoke which cause the early development of emphysema-like changes. So smoking is a risk factor for the development and severity of diffuse lung diseases in neurofibromatosis. CONCLUSIONS: As a result, because neurofibromatosis is a rare disease and may predispose to the tumor growth of the nervous system or other organs (2); careful long-term follow up after dignosis is therefore required (3). Reference #1: Pivnick EK, Riccardi VM. The neurofibromatosis. In: Freedberg IM, Eisen AZ, Wolff K, Austen KF, Goldsmith LA, Katz SI, Fitzpatrick TB, eds. Fitzpatrick's Dermatology in General Medicine. 5 th ed. New York: Mc Graw-Hill; 1999. p.2152-8. Reference #2: Hirsch NP, Murphy A, Radcliffe JJ. Neurofibromatosis: Clinical presentations and anaesthetic implications. Br J Anaesth 2001; 86: 555-64 Reference #3: Gawlewicz-Mroczka A, Mastalerz L, Nizankowska-Mogilnicka E. Neurofibromatosis type 1 in an adult diagnosed by a pulmonologist. Pneumonol Alergol Pol 2009;77:474-8 DISCLOSURE: The following authors have nothing to disclose: Seher Satar, Aysenaz Ozcan, Tugba Kara, Sema Canbakan No Product/Research Disclosure Information

TNF-α and Th2 Cytokines Induce Atopic Dermatitis–Like Features on Epidermal Differentiation Proteins and Stratum Corneum Lipids in Human Skin Equivalents

Atopic dermatitis (AD) is a chronic inflammatory skin disease in which the skin barrier function is disrupted. In this inflammatory AD environment, cytokines are upregulated, but the cytokine effect on the AD skin barrier is not fully understood. We aimed to investigate the influence of Th2 (IL-4, IL-13, IL-31) and pro-inflammatory (tumor necrosis factor alpha (TNF-α)) cytokines on epidermal morphogenesis, proliferation, differentiation, and stratum corneum lipid properties. For this purpose, we used the Leiden epidermal model (LEM) in which the medium was supplemented with these cytokines. Our results show that IL-4, IL-13, IL-31, and TNF-α induce spongiosis, augment TSLP secretion by keratinocytes, and alter early and terminal differentiation-protein expression in LEMs. TNF-α alone or in combination with Th2 cytokines decreases the level of long chain free fatty acids (FFAs) and ester linked ω-hydroxy (EO) ceramides, consequently affecting the lipid organization. IL-31 increases long chain FFAs in LEMs but decreases relative abundance of EO ceramides. These findings clearly show that supplementation with TNF-α and Th2 cytokines influence epidermal morphogenesis and barrier function. As a result, these LEMs show similar characteristics as found in AD skin and can be used as an excellent tool for screening formulations and drugs for the treatment of AD.

Cutaneous Pigmentation in Health and Disease: Novel and Well-Established Players

Cutaneous pigment formation and aberration in disease are addressed. Dynoodt et al. (this issue) present data on a specific micro RNA that downregulates proteins involved in melanogenesis and melanosome movement. Kim et al. (this issue) present data showing that Wnt signaling is involved in the pathogenesis of melasma. Both articles enhance our understanding of cutaneous pigmentation and point to targets in the development of novel therapeutic modalities.

Fitzpatrickʼs Dermatology in General Medicine

Fitzpatrickʼs Dermatology in General Medicine

Fitzpatrick's Dermatology in General Medicine, 7th edition

Fitzpatrick's Dermatology in General Medicine, 7th edition

Fitzpatrick’s Dermatology in General Medicine, 2 Volumes, 7th Ed

Fitzpatrick’s Dermatology in General Medicine, 2 Volumes, 7th Ed

Fitzpatrick's Dermatology in General Medicine by KLAUS WOLFF, LOWELL A. GOLDSMITH, STEPHEN I. KATZ, BARBARA A. GILCHREST, AMY S. PALLER, AND DAVID J. LEFFELL, EDITORS

Fitzpatrick's Dermatology in General Medicine by KLAUS WOLFF, LOWELL A. GOLDSMITH, STEPHEN I. KATZ, BARBARA A. GILCHREST, AMY S. PALLER, AND DAVID J. LEFFELL, EDITORS

P131: Bone-Anchored Hearing Aid Abutment Skin Overgrowth Reduction

P131: Bone-Anchored Hearing Aid Abutment Skin Overgrowth Reduction

Serotonin Activates Human Monocytes and Prevents Apoptosis

Monocytes play a critical role in chronic atopic dermatitis (AD) and are the primary leukocytes that interact with activated platelets. Although activated platelets release a variety of mediators, the role of platelets in cutaneous allergic inflammation remains unclear. Serotonin (5-hydroxytryptamine, 5-HT) is one of the prototypic mediators produced by activated platelets. We examined the effect of 5-HT on the function and lifespan of human monocytes. Normal human monocytes treated with 5-HT exhibited upregulated expression of costimulatory molecules, enhanced capacity to produce cytokines following lipopolysaccharide treatment, and to stimulate allogeneic CD4+ T cells. 5-HT also attenuated the apoptosis in normal human monocytes in a dose-dependent manner. The plasma levels of 5-HT were increased in patients with AD compared with controls and correlated with the SCORAD index. 5-HT also inhibited monocyte apoptosis in these patients. 5-HT upregulated Bcl-2 and Mcl-1, and inhibited the activation of caspase-3. The effects of 5-HT on monocyte apoptosis were mediated by the 5-HT1 and/or 5-HT7 receptors. 5-HT and a 5-HT(1/6/7)-receptor agonist induced phosphorylation of extracellular signal-regulated kinase1/2 and activation of nuclear transcription factor-kappaB. These findings support that 5-HT activates monocytes and inhibits apoptosis, allowing them to remain in the tissue and contribute to chronic inflammation.

Bone Morphogenetic Protein-4, a Novel Modulator of Melanogenesis

Bone morphogenetic proteins (BMPs), members of the transforming growth factor-beta family, signal in many cells including neural precursors. Two receptors, types 1 and 2, coordinately mediate BMP signaling, and type 1 receptor has two forms: A and B. Using RT-PCR we found that neural crest-derived human melanocytes express BMP receptor-1A, -1B, and -2. Furthermore, melanocytes and the surrounding keratinocytes express BMP-4, suggesting both autocrine and paracrine effects of this molecule. Moreover, BMP-4 supplementation of cultured human melanocytes decreases melanin synthesis, tyrosinase mRNA, and protein. The mechanism of this BMP-4 effect on tyrosinase and ultimately on melanogenesis involves modest decreases of tyrosinase transcription rate and mRNA stability. Moreover, ultraviolet irradiation, the best recognized environmental stimulator of melanogenesis, down-regulated the mRNA of BMP receptor-1B in melanocytes. Our data provide evidence of a novel regulatory pathway for melanogenesis in human skin.

Irwin Freedberg, Editor Extraordinaire of Fitzpatrick's DIGM

This is a thank you to Irwin M. Freedberg, MD, the exceptional senior editor of the two most recent editions of Fitzpatrick's Dermatology in General Medicine (DIGM). He was the captain who steered the ship through smooth and also sometimes rough waters, expanding the book's already stellar reputation. Dr Thomas B. Fitzpatrick, the founding editor, asked Irwin to join the second (1979) edition of DIGM as a Young Turk to bring fresh blood to a textbook already recognized eight years after the first edition as one of the classics. Irwin served as senior editor of the fifth and sixth editions, published in 1999 and 2003, respectively. As he had done for the Journal of Investigative Dermatology in his role as editor (1972–1977), he brought DIGM to new heights.

Misnomers in Dermatology

Background: Dermatology lexicon is rich with descriptive terminology. However, for a variety of reasons, it also includes a number of misnomers. ObjectiveTo review the more commonly encountered and critically appraised misnomers in dermatology. Methods: A search of MEDLINE (1966 – 2004), eMedicine dermatology text and electronic versions of two standard dermatology texts, Fitzpatrick's Dermatology in General Medicine and Dermatology, was performed using the permutations of the terms: dermatology, skin, cutaneous, and misnomer. Results: Greater than 40 misnomers were identified. Conclusions: Misnomers in dermatology stem largely from lack of appreciation of underlying etiology or histopathological features of certain skin conditions, imprecise historical observations and erroneous eponymous credit. Historical, clinical, or histopathological explanations are used to clarify the nature of the misnomers, and in some cases suggestions for improved terminology are provided.

Misnomers in Dermatology

Dermatology lexicon is rich with descriptive terminology. However, for a variety of reasons, it also includes a number of misnomers. To review the more commonly encountered and critically appraised misnomers in dermatology. A search of MEDLINE (1966 - 2004), eMedicine dermatology text and electronic versions of two standard dermatology texts, Fitzpatrick's Dermatology in General Medicine and Dermatology, was performed using the permutations of the terms: dermatology, skin, cutaneous, and misnomer. Greater than 40 misnomers were identified. Misnomers in dermatology stem largely from lack of appreciation of underlying etiology or histopathological features of certain skin conditions, imprecise historical observations and erroneous eponymous credit. Historical, clinical, or histopathological explanations are used to clarify the nature of the misnomers, and in some cases suggestions for improved terminology are provided.

Expression and regulation of 1-acyl-sn-glycerol- 3-phosphate acyltransferases in the epidermis

Phospholipids are a major class of lipids in epidermis, where they serve as a source of free fatty acids that are important for the maintenance of epidermal permeability barrier function. The phospholipid biosynthetic enzyme, 1-acyl-sn-glycerol-3-phosphate acyltransferase (AGPAT), catalyzes the acylation of lysophosphatidic acid to form phosphatidic acid, the major precursor of all glycerolipids. We identified an expression pattern of AGPAT isoforms that is unique to epidermis, with relatively high constitutive expression of mouse AGPAT (mAGPAT) 3, 4, and 5 but low constitutive expression of mAGPAT 1 and 2. Localization studies indicate that all five isoforms of AGPAT were expressed in all nucleated layers of epidermis. Furthermore, rat AGPAT 2 and 5 mRNAs increased in parallel with both an increase in enzyme activity and permeability barrier formation late in rat epidermal development. Moreover, after two methods of acute permeability barrier disruption, mAGPAT 1, 2, and 3 mRNA levels increased rapidly and were sustained for at least 24 h. In parallel with the increase in mRNA levels, an increase in AGPAT activity also occurred. Because upregulation of mAGPAT mRNAs after tape-stripping could be partially reversed by artificial barrier restoration by occlusion, these studies suggest that an increase in the expression of AGPATs is linked to barrier requirements.