The Clonal Nature of Pityriasis Lichenoides

Total Page:16

File Type:pdf, Size:1020Kb

The Clonal Nature of Pityriasis Lichenoides STUDY The Clonal Nature of Pityriasis Lichenoides Jeffrey M. Weinberg, MD; Leonard Kristal, MD; Lillian Chooback, PhD; Paul J. Honig, MD; E. Michael Kramer, MD; Stuart R. Lessin, MD Background: Pityriasis lichenoides et varioliformis acuta PLC. These samples were analyzed by PCR/DGGE. (PLEVA) and pityriasis lichenoides chronica (PLC) are be- nign lymphocytic infiltrates of the skin that classically pre- Main Outcome Measure: The presence or absence sent as either a recurrent papulonecrotic eruption (PLEVA) of T-cell receptor gene rearrangements on PCR/DGGE or a persistent, scaling, papular eruption (PLC). Obser- analysis corresponding to a clonal population of T vations of both types of lesions present on individual pa- cells. tients have led to speculation that both entities are re- lated. Previous studies evaluating the DNA of biopsy Results: Of 14 PLEVA specimens, 8 (57%) demon- specimens from patients with PLEVA and PLC revealed strated monoclonal T-cell receptor gene rearrange- clonal T-cell receptor ␤ gene rearrangements. ments; 1 (8%) of 13 PLC specimens showed a gene re- arrangement (P=.008, Fisher exact test). Objective: To analyze and compare the T-cell popula- tions between lesions of PLEVA and PLC. Conclusions: Our results demonstrate the polyclonal na- ture of the lymphocytic infiltrate found in almost all of Design: Retrospective and prospective analysis of pa- the PLC specimens, which contrasts with the mono- tient tissue samples, classified by histologic analysis. Ex- clonal nature found in most of the PLEVA specimens. tracted DNA from 13 skin biopsy specimens with the di- These differences may represent different stages of the agnosis of PLC and 14 skin biopsy specimens with the clinical evolution of a single entity that results from vary- diagnosis of PLEVA was analyzed by polymerase chain ing host immune responses to pathogenic factors. Spe- reaction/denaturing gradient gel electrophoresis cifically, we propose that PLEVA is a benign clonal T- (PCR/DGGE). cell disorder in which the clone arises from a subset of T cells in lesions of PLC. The host immune response to this Setting: Molecular diagnostic laboratory at an aca- clone determines the clinical and histologic findings in demic medical center. PLEVA. Patients: Twenty-seven tissue samples were obtained from patients with a histologic diagnosis of PLEVA or Arch Dermatol. 2002;138:1063-1067 ITYRIASIS LICHENOIDES is char- (PLC). Brocq6 later included PLC in his acterized by papulosqua- classification of parapsoriasis as guttate mous to papulonecrotic le- parapsoriasis. In 1916, Mucha7 re- sional morphology, a chronic described the acute form of pityriasis li- and recurrent clinical course, chenoides, distinguishing it from both PLC and, as demonstrated by histopathologic and other diseases. This entity was termed From the Department of P Dermatology, University of analysis, a lichenoid infiltrate with vari- pityriasis lichenoides et varioliformis acuta 8 Pennsylvania (Drs Weinberg, able dermal hemorrhage and keratinocyte (PLEVA) by Habermann in 1925. Accord- Chooback, and Lessin), the necrosis. Pityriasis lichenoides and its prin- ingly, PLEVA is also known as Mucha- Children’s Hospital of cipal variants were identified and re- Habermann disease. Philadelphia (Drs Kristal and ported in a series of articles published in Honig), and Thomas Jefferson the late 19th and early 20th centuries.1 It For editorial comment Medical College (Dr Kramer), was first described by Neisser2 and Jadas- see page 1089 Philadelphia, Pa. Dr Weinberg sohn3 in separate reports in 1894; both in- is now with the Department cluded cases of what would now be con- Observations of both acute and of Dermatology, sidered acute and chronic variants of the chronic lesions present on the same indi- St Luke’s–Roosevelt Hospital 4 5 Center, New York, NY, disease. Juliusberg redescribed the chronic vidual have led to speculation that both and Dr Lessin is now with form of pityriasis lichenoides in 1899 and entities are related to and may be a part the Fox Chase Cancer Center, designated it as a separate entity, introduc- of a continuous disease spectrum.9 The Philadelphia. ing the term pityriasis lichenoides chronica term pityriasis lichenoides can be used to (REPRINTED) ARCH DERMATOL / VOL 138, AUG 2002 WWW.ARCHDERMATOL.COM 1063 ©2002 American Medical Association. All rights reserved. Downloaded From: https://jamanetwork.com/ on 09/28/2021 MATERIALS AND METHODS DNA from formalin-fixed paraffin-embedded blocks (21 ret- rospective cases) was extracted in the following manner. Ten PATIENT SAMPLES 10-mm sections were cut from each block, deparaffinized in xylene, rinsed with 95% ethanol, dried, resuspended in In the present study, 27 biopsy specimens were analyzed: tris-EDTA (10mM Tris–hydrochloric acid and 1mM EDTA, 13 from patients with PLC and 14 from patients with PLEVA. pH 7.8) and incubated with proteinase K (Sigma-Aldrich Of the 27 cases, 6 (4 PLC and 2 PLEVA) were analyzed pro- Corp, St Louis, Mo) at 37°C overnight. Samples were heated spectively, and 21 (9 PLC and 12 PLEVA) were studied ret- for 10 minutes at 95°C (inactivate proteinase K), spun, and rospectively from archived tissue specimens. Informed con- supernatants were phenol-chloroform extracted and etha- sent and approval by the institutional review board of the nol precipitated. Dried DNA was resuspended in sterile wa- University of Pennsylvania, Philadelphia, was obtained to ter and used for PCR. study unused portions of diagnostic samples. In the retro- spective arm of the study, questionnaires were mailed to the patients’ primary dermatologists to obtain the follow- PCR/DDGE ANALYSIS OF TCR␥ GENE ing information: patient age at biopsy, duration of erup- REARRANGEMENTS AND STATISTICAL ANALYSIS tion prior to biopsy, location of eruption, and follow-up. We used the method of Wood et al17 to perform PCR/ HISTOPATHOLOGIC ANALYSIS DGGE analysis of TCRγ gene rearrangements. Genomic ␥ All hematoxylin- eosin–stained skin biopsy specimens were DNA was PCR-amplified using 2 sets of TCR-V and ␥ reviewed by one of us (E.M.K.) in a blinded fashion to es- TCR-J consensus oligonucleotide primers (primers ␥ ␥ ␥ ␥ tablish uniform diagnosis. All 27 skin biopsy specimens in- V 1-8 and J 1-2; primers V 9 and J 1-2) in 2 separate cluded in this study were assigned a diagnosis of either PLEVA PCR reactions. To detect clonality, PCR products were or PLC. Histologic diagnosis was based on the following 4 analyzed by DGGE using a DGGE System (CBS Scientific criteria: (1) density of the lymphocytic infiltrate, (2) degree Company Inc, Del Mar, Calif) according to manufactur- ␥ of epidermal necrosis, (3) number of extravasated erythro- er’s specifications. Our detection sensitivity of TCR PCR/ 18 cytes, and (4) number of necrotic keratinocytes. DGGE analysis of skin biopsy specimens is at the 1% level and comparable with others reports.17 Two-by-two DNA EXTRACTION comparisons were made between cases of PLEVA and PLC with and without detection of T-cell clonality by the Genomic DNA was extracted from snap frozen samples Fisher exact test using StatView II software (Abacus Con- (6 prospective cases) as previously described.16 Genomic cepts Inc, Berkeley, Calif). encompass both acute and chronic presentations that are cell clonality in PLEVA using PCR of TCR gene rear- characterized by papulosquamous lesions located pri- rangements. An analysis of 13 of 20 PLEVA biopsy speci- marily on the trunk or extremities. The papules in PLEVA mens revealed the presence of a dominant T-cell clone. develop immediately and heal spontaneously with cen- Despite its lymphoproliferative nature, PLEVA is a clini- tral necrosis. The acute episodes are recurrent and per- cally benign entity with no significantly documented as- sistent. The maculopapular lesions of PLC develop less sociation with malignant lymphoma,9 except for a few, quickly with an adherent scale and resolves spontane- poorly documented case reports.14 ously with residual pigmentary changes. Both lesions his- Another recent study evaluated clonality in cases of tologically show similarities. The lesions of PLEVA re- PLC15: 6 cases of PLC were analyzed using a frozen sec- veal a superficial and deep perivascular lymphocytic tion–immunoperoxidase technique and PCR/ infiltrate accompanied by lymphocytes that obscure the denaturing gradient gel electrophoresis (PCR/DGGE). Of dermoepidermal interface, where there are also extrava- these, 3 demonstrated a monoclonal gene rearrange- sated erythrocytes and necrotic keratinocytes. The le- ment. The purpose of the present study was to analyze sions of PLC have a bandlike lymphocytic infiltrate with and compare the T-cell populations, by TCR gene rear- a few extravasated erythrocytes in the papillary dermis rangement analysis, in lesions of PLC and PLEVA in an and vacuoles and necrotic keratinocytes at the dermo- attempt to develop a model of the clonal relationship be- epidermal interface. tween the 2 disorders. To our knowledge, our study is The etiology of these disorders remains unknown. the first to directly compare both entities. Immunohistochemical analysis has found similarities in 10 both entities. Molecular characterization of the infil- RESULTS trating cells in a small series of patients with PLEVA in- dicated that the lymphocytic infiltrate is lymphoprolif- CLINICOPATHOLOGIC CORRELATION erative in nature11 and demonstrated a monoclonal population of T cells by Southern blot analysis of T-cell Of the 27 specimens analyzed, 13 were classified as PLC receptor(TCR) ␤ gene rearrangement. In addition, Pan- and 14 as PLEVA based on the histologic criteria outlined hans et al12 described the case of a 7-year-old boy with in the “Materials and Methods” section. Figure 1 illus- atypical CD30-positive cells and a clonal TCR gene re- trates the histologic findings of PLC: a sparse, superficial arrangement by polymerase chain reaction (PCR) of TCRγ perivascular lymphocytic infiltrate associated with a few genes. Recently, Dereure et al13 reported a study of T- extravasated erythrocytes in the papillary dermis and some (REPRINTED) ARCH DERMATOL / VOL 138, AUG 2002 WWW.ARCHDERMATOL.COM 1064 ©2002 American Medical Association.
Recommended publications
  • Pityriasis Rosea DANIEL L
    CARING FOR COMMON SKIN CONDITIONS Pityriasis Rosea DANIEL L. STULBERG, M.D., Utah Valley Regional Medical Center, Provo, Utah JEFF WOLFREY, M.D., Good Samaritan Regional Medical Center, Phoenix, Arizona Pityriasis rosea is a common, acute exanthem of uncertain etiology. Viral and bacterial causes have been sought, but convincing answers have not yet been found. Pityriasis O A patient informa- rosea typically affects children and young adults. It is characterized by an initial herald tion handout on pityriasis rosea, written patch, followed by the development of a diffuse papulosquamous rash. The herald by the authors of this patch often is misdiagnosed as eczema. Pityriasis rosea is difficult to identify until the article, is provided on appearance of characteristic smaller secondary lesions that follow Langer’s lines (cleav- page 94. age lines). Several medications can cause a rash similar to pityriasis rosea, and several diseases, including secondary syphilis, are included in the differential diagnosis. One small controlled trial reported faster clearing of the exanthem with the use of ery- thromycin, but the mechanism of effect is unknown. Resolution of the rash may be has- tened by ultraviolet light therapy but not without the risk of hyperpigmentation. Top- ical or systemic steroids and antihistamines often are used to relieve itching. (Am Fam Physician 2004;69:87-92,94. Copyright© 2004 American Academy of Family Physicians.) This article is one in a ityriasis rosea is a common skin cytes, a decrease in T lymphocytes, and an ele- series coordinated by condition characterized by a her- vated sedimentation rate.6 Daniel L. Stulberg, M.D., director of der- ald patch and the later appear- Unfortunately, even though electron matology curriculum at ance of lesions arrayed along microscopy shows some viral changes and the Utah Valley Family Langer’s lines (cleavage lines).
    [Show full text]
  • History of Psoriasis and Parapsoriasis
    History of Psoriasis and Parapsoriasis By Karl Holubar Summary Parapsoriasis is «oï a disease entity. Jt is an auxiliary term introduced in J 902 to group several dermatoses w>itk a/aint similarity to psoriasis. Tlie liistorical development leading to tlie creation o/ t/ie term parapsoriasis is outlined and t/te Itistory o/psoriasis is 6rie/ly reviewed. Semantic and terminological considerations Obviously, para-psoriasis as a term has been created in analogy to psoriasis. We should remember similar neologisms in medical language, e. g. protein and para-protein; typhoid and para-typhoid, thyroid and para-thyroid, phimosis and para-phimosis, eventually, pemphigus and para-pemphigus (the latter in 1955 this term was to be employed instead of pemphigoid but was not accepted by the dermatological world). Literally, para is a Greek preposition, (with the genitive, dative and accusative), meaning: by the side of, next to something, alongside something. In medicine, para is used often as a prefix to another term, which designates a condition somewhat similar to the one under consideration. The same holds for psoriasis and parapsoria- sis. In detail, though, it is a bit more complicated. Parapsoriasis has more than one "/at/ier", three in fact: ideiurick /Iu.spitz f 1835—1886,), Paul Gerson Luna (A850—1929j and Louis Procç fI856—I928J. Auspitz, in 1881, had published a new system of skin diseases the seventh class of which was called epidermidoses, subdivided into liypcrlcfiratose.s, parakeratoses, kerato/y- ses, the characteristics of which were excessive keratinization, abnormal keratinization and insufficent keratinization. When Unna, in 1890®, pub- lished his two reports on what he called parakeratosis variegata, he referred to Auspitz' system and term when coining his own.
    [Show full text]
  • Errata to the 7/1/2016 Prioritized List
    Errata to the 7/1/2016 Prioritized List 1) On 6/29/2017, the following corrections were made: a. Website addresses were corrected for the new Oregon Health Authority Web site in all guideline notes referencing a Coverage Guidance. In addition, a web address in the Multisector Interventions section on Tobacco Use was updated. b. M67.0 (Short Achilles tendon (acquired)) was moved to line 297 NEUROLOGICAL DYSFUNCTION IN POSTURE AND MOVEMENT CAUSED BY CHRONIC CONDITIONS from line 382 DYSFUNCTION RESULTING IN LOSS OF ABILITY TO MAXIMIZE LEVEL OF INDEPENDENCE IN SELF- DIRECTED CARE CAUSED BY CHRONIC CONDITIONS THAT CAUSE NEUROLOGICAL DYSFUNCTION c. Psoriasis corrections: i. Add psoriasis, parapsoriasis and similar ICD-10 codes to line 544 MILD PSORIASIS; DERMATOPHYTOSIS: SCALP, HAND, BODY, DEEP-SEATED 1. L40.0 Psoriasis vulgaris 2. L40.1 Generalized pustular psoriasis 3. L40.2 Acrodermatitis continua 4. L40.3 Pustulosis palmaris et plantaris 5. L40.4 Guttate psoriasis 6. L40.8 Other psoriasis 7. L40.9 Psoriasis, unspecified 8. L41.0 Pityriasis lichenoides et varioliformis acuta ii. Add psoriatic arthropathy ICD-10 codes to line 50 RHEUMATOID ARTHRITIS AND OTHER INFLAMMATORY POLYARTHROPATHIES) and remove from line SEVERE INFLAMMATORY SKIN DISEASE 1. L40.51 Distal interphalangeal psoriatic arthropathy 2. L40.52 Psoriatic arthritis mutilans 3. L40.53 Psoriatic spondylitis 4. L40.54 Psoriatic juvenile arthropathy 5. L40.59 Other psoriatic arthropathy d. Add line 544 to Guideline Note 21 SEVERE INFLAMMATORY SKIN DISEASE, and append “See Guideline Note 57 for the definition of mild psoriasis included on line 544.” e. Add line 430 to Guideline Note 57 MILD PSORIASIS and append “See Guideline Note 21 for the definition of moderate/severe psoriasis included on line 430.” f.
    [Show full text]
  • The Prevalence of Paediatric Skin Conditions at a Dermatology Clinic
    RESEARCH The prevalence of paediatric skin conditions at a dermatology clinic in KwaZulu-Natal Province over a 3-month period O S Katibi,1,2 MBBS, FMCPaed, MMedSci; N C Dlova,2 MB ChB, FCDerm, PhD; A V Chateau,2 BSc, MB ChB, DCH, FCDerm, MMedSci; A Mosam,2 MB ChB, FCDerm, MMed, PhD 1 Dermatology Unit, Department of Paediatrics and Child Health, University of Ilorin, Kwara State, Nigeria 2 Department of Dermatology, Nelson R Mandela School of Medicine, University of KwaZulu-Natal, Durban, South Africa Corresponding author: O S Katibi ([email protected]) Background. Skin conditions are common in children, and studying their spectrum in a tertiary dermatology clinic will assist in quantifying skin diseases associated with greatest burden. Objective. To investigate the spectrum and characteristics of paediatric skin disorders referred to a tertiary dermatology clinic in Durban, KwaZulu-Natal (KZN) Province, South Africa. Methods. A cross-sectional study of children attending the dermatology clinic at King Edward VIII Hospital, KZN, was carried out over 3 months. Relevant demographic information and clinical history pertaining to the skin conditions were recorded and diagnoses were made by specialist dermatologists. Data were analysed with EPI Info 2007 (USA). Results. There were 419 children included in the study; 222 (53%) were males and 197 (47%) were females. A total of 64 diagnosed skin conditions were classified into 16 categories. The most prevalent conditions by category were dermatitis (67.8%), infections (16.7%) and pigmentary disorders (5.5%). For the specific skin diseases, 60.1% were atopic dermatitis (AD), 7.2% were viral warts, 6% seborrhoeic dermatitis and 4.1% vitiligo.
    [Show full text]
  • A Deep Learning System for Differential Diagnosis of Skin Diseases
    A deep learning system for differential diagnosis of skin diseases 1 1 1 1 1 1,2 † Yuan Liu ,​ Ayush Jain ,​ Clara Eng ,​ David H. Way ,​ Kang Lee ,​ Peggy Bui ,​ Kimberly Kanada ,​ ​ ​ ‡ ​ 1​ ​ 1 ​ 1 ​ Guilherme de Oliveira Marinho ,​ Jessica Gallegos ,​ Sara Gabriele ,​ Vishakha Gupta ,​ Nalini 1,3,§ 1 ​ ​ 4 ​ 1 ​ ​ 1 Singh ,​ Vivek Natarajan ,​ Rainer Hofmann-Wellenhof ,​ Greg S. Corrado ,​ Lily H. Peng ,​ Dale ​ ​ 1 1 ​ † 1, ​ 1, ​ 1, ​ R. Webster ,​ Dennis Ai ,​ Susan Huang ,​ Yun Liu *​ , R. Carter Dunn *​ *, David Coz *​ * ​ ​ ​ ​ ​ ​ Affiliations: 1 G​ oogle Health, Palo Alto, CA, USA 2 U​ niversity of California, San Francisco, CA, USA 3 M​ assachusetts Institute of Technology, Cambridge, MA, USA 4 M​ edical University of Graz, Graz, Austria † W​ ork done at Google Health via Advanced Clinical. ‡ W​ ork done at Google Health via Adecco Staffing. § W​ ork done at Google Health. *Corresponding author: [email protected] **These authors contributed equally to this work. Abstract Skin and subcutaneous conditions affect an estimated 1.9 billion people at any given time and remain the fourth leading cause of non-fatal disease burden worldwide. Access to dermatology care is limited due to a shortage of dermatologists, causing long wait times and leading patients to seek dermatologic care from general practitioners. However, the diagnostic accuracy of general practitioners has been reported to be only 0.24-0.70 (compared to 0.77-0.96 for dermatologists), resulting in over- and ​ ​ ​ ​ ​ ​ ​ under-referrals, delays in care, and errors in diagnosis and treatment. In this paper, we developed a deep learning system (DLS) to provide a differential diagnosis of skin conditions for clinical cases (skin photographs and associated medical histories).
    [Show full text]
  • PWO for Home Phototherapy
    Physician’s Written Order For Office Use Only : Daavlin PO Box 626 Bryan, OH 43506 For Home Phototherapy Fax To: 419-636-7916 Other__________________________ Rx Prescriber Instructions: This form is a Prescription and Statement of Medical Necessity for Billing Entity ___________________________________ Daavlin home phototherapy products. (For Levia orders, please use the Levia version of ___________________________________ this form.) All fields are required for insurance approval. Call 800-322-8546 for assistance. First Name _______________________ Last Name _________________________ Middle Initial ____ DOB ____/____/____ Address _________________________________________ City_________________________ State_______ Zip___________ Patient: Gender: M F Phone #________________________________ Alt Phone #_________________________________ Physician Name _________________________________ ICD-10 : Description ICD-10 Code L40 . _____ Psoriasis Must Be Practice ________________________________________ Indicated L80 Vitiligo NPI# ____________________________________________ ______ . ____ Other: ____________________ (See back for ICD -10 Code Quick Referrence Guide) Address _______________________________________ Estimated Duration of Need: ___ Months ( 99 = Lifetime ) City ____________________ State ____ Zip _________ Body Area Affected (Check all that apply) Prescribing Physician: Prescribing Phone (____)_____________*Fax (____)_____________ 3 % - 10 % (Moderate) Hands (2 %) * IMPORTANT: We will use this fax number to fax the Prescriber’s Dosing
    [Show full text]
  • Pediatric Psoriasis
    Pediatric Papulosquamous and Eczematous Disorders St. John’s Episcopal Hospital Program Director- Dr. Suzanne Sirota-Rozenberg Dr. Brett Dolgin, DO Dr. Asma Ahmed, DO Dr. Anna Slobodskya, DO Dr. Stephanie Lasky, DO Dr. Louis Siegel, DO Dr. Evelyn Gordon, DO Dr. Vanita Chand, DO Pediatric Psoriasis Epidemiology • Psoriasis can first appear at any age, from infancy to the eighth decade of life • The prevalence of psoriasis in children ages 0 to 18 years old is 1% with an incidence of 40.8 per 100,000 ppl • ~ 75% have onset before 40 years of age What causes psoriasis? • Multifactorial • Genetics – HLA associations (Cw6, B13, B17, B57, B27, DR7) • Abnormal T cell activation – Th1, Th17 with increased cytokines IL 1, 2, 12, 17, 23, IFN-gamma, TNF-alpha • External triggers: – Injury (Koebner phenomenon) – medications (lithium, IFNs, β-blockers, antimalarials, rapid taper of systemic corticosteroids) – infections (particularly streptococcal tonsillitis). Pediatric Psoriasis Types: • Acute Guttate Psoriasis – Small erythematous plaques occurring after infection (MOST common in children) • 40% of patients with guttate psoriasis will progress to develop plaque type psoriasis • Chronic plaque Psoriasis – erythematous plaques with scaling • Flexural Psoriasis – Erythematous areas between skin folds • Scalp Psoriasis – Thick scale found on scalp • Nail Psoriasis – Nail dystrophy • Erythrodermic Psoriasis– Severe erythema covering all or most of the body • Pustular Psoriasis – Acutely arising pustules • Photosensitive Psoriasis – Seen in areas of sun
    [Show full text]
  • The Conundrum of Parapsoriasis Versus Patch Stage of Mycosis Fungoides
    View TThehe cconundrumonundrum ofof parapsoriasisparapsoriasis versusversus patchpatch stagestage Point ooff mmycosisycosis ffungoidesungoides KK.. NN.. SSarveswari,arveswari, PPatrickatrick YYesudianesudian Sundaram Medical Foundation, ABSTRACT Dr. Rangarajan Memorial Hospital, Chennai, Tamilnadu, Terminological confusion with benign dermatosis, such as parapsoriasis en plaques, makes India it difÞ cult to diagnose mycosis fungoides in the early patch stage. Early diagnosis of mycosis fungoides (MF) is important for deciding on type of therapy, prognosis and for further follow-up. Address for correspondence: Dr. K. N. Sarveswari, However, until recently, there has been no consensus on criteria that would help in diagnosing Sundaram Medical the disease early. Some believe that large plaque parapsoriasis (LPP) should be classiÞ ed Foundation, Dr. Rangarajan with early patch stage of MF and should be treated aggressively. However, there is no Þ rm Memorial Hospital, Shanthi clinical or laboratory criteria to predict which LPP will progress to MF and we can only discuss Colony - IV Avenue, Anna about statistical probability. Moreover, long-term outcome analysis of even patch stage of MF Nagar, Chennai - 600 040, Tamilnadu, India. is similar to that of control population. We therefore believe that LPP should be considered E-mail: sarveswari@ as a separate entity at least to prevent the patient from being given a frightening diagnosis. smfhospital.org We also feel that patients need not be treated with aggressive therapy for LPP and will need
    [Show full text]
  • Pityriasis Lichenoides Devang G
    pediatric dermatology Pityriasis Lichenoides Devang G. Patel, MD George Kihiczak, MD Robert A. Schwartz, MD, MPH Camila K. Janniger, MD W. Clark Lambert, MD, PhD Pityriasis lichenoides (PL) is a skin disorder of un- PL from small and large plaque parapsoriasis, includ- known etiology that mainly affects children and young ing digitate dermatosis, xanthoerythrodermia perstans, adults. Pityriasis lichenoides is perhaps best considered and the rare entity, retiform parapsoriasis. a disease spectrum with acute and chronic types: pityr- iasis lichenoides et varioliformis acuta (PLEVA) and Incidence pityriasis lichenoides chronica (PLC). Pityriasis Pityriasis lichenoides most commonly occurs in chil- lichenoides et varioliformis acuta, the acute variant, is dren and young adults; however, its precise incidence characterized by the onset of papulovesicular eruptions is unknown. Both PLC and PLEVA appear to be that evolve into necrotic lesions over the trunk and about as common in males as in females, with PLC extremities, and hence the name “varioliformis,” occurring more frequently. Pityriasis lichenoides et which means “like variola” (like smallpox). Pityriasis varioliformis acuta most often occurs during the sec- lichenoides chronica, the chronic form, involves re- ond or third decade of life. However, the disease may current crops of papules that may last from several also arise in children and the elderly, and may even months to several years. Both types are further char- be evident at birth.10 There is no apparent racial or acterized by independent evolution of each lesion, so geographic predisposition.1,2 that lesions in all different states of progression are found next to each other in a random array.
    [Show full text]
  • Pityriasis Lichenoides-Like Drug Reaction
    Volume 23 Number 11 | November 2017 Dermatology Online Journal || Case Report 23 (11): 2 Pityriasis lichenoides-like drug reaction: A clinical histopathologic study of 10 cases Cynthia Magro1 MD, Ruifeng Guo2 MD PhD, Giang Huong Nguyen3 MD PhD, Hamilton Tsang4 MD, Shabnam Momtahen5 MD Affiliations: 1Department of Pathology and Laboratory Medicine, Weill Cornell Medicine, New York, New York, 2University of Florida Health Pathology Laboratories, Gainesville, Florida, 3Department of Dermatology, University of Colorado, Aurora, Colorado, 4Department of Laboratory Medicine, University of Washington, Seattle, Washington, 5Department of Pathology, Dartmouth- Hitchcock Medical Center, Lebanon, New Hampshire Corresponding Author: Cynthia M. Magro M.D., Professor of Pathology and Laboratory Medicine, Professor of Dermatopathology in Dermatology, Director of Dermatopathology, Weill Cornell Medicine, Department of Pathology & Laboratory Medicine, 1300 York Avenue, F-309, New York, NY 10065, Tel: 212-746-6434, Fax: 212-746-8570, Email: [email protected] Abstract Introduction Cutaneous drug eruptions define a common Background: Lymphomatoid drug reactions can mimic adverse effect of drug therapy [1-5]. Although most endogenous T and B cell lymphoproliferative diseases. drug eruptions are mild, life-threatening reactions Objectives: We present a novel form of cutaneous are common. These include Stevens-Johnson drug reaction with features of pityriasis lichenoides syndrome, toxic epidermal necrolysis, erythroderma, (PL), a recognized form of T cell dyscrasia. Methods: and angioedema [6-9]. Most drug eruptions Ten cases were studied where a cutaneous eruption are immunologically mediated, although non- exhibiting semblance to PL within a few weeks to immunological drug eruptions are known to occur months after starting a particular drug. Results: The [10].
    [Show full text]
  • Infantile Psoriasis
    PEDIATRIC DERMATOLOGY Series Editor: Camila K. Janniger, MD Infantile Psoriasis Camila K. Janniger, MD; Robert A. Schwartz, MD, MPH; Maria Letizia Musumeci, MD, PhD; Aurora Tedeschi, MD; Barbara Mirona, MD; Giuseppe Micali, MD Psoriasis is a common inherited papulosqua- several chromosomes at which putative psoriasis mous dermatosis that may be a diagnostic genes may be located. Disease susceptibility genes dilemma, particularly in infants and children. The are thought to be present on chromosomes 4q, 6p, treatment of children with psoriasis should be 16q, and 20p. Moreover, on chromosome 1q, genes handled with caution and tailored according to regulating epidermal differentiation have been iden- the child’s age, as well as to the extent, distribu- tified. Linkage to this area has been proposed. tion, and type of psoriasis. Furthermore, psoriasis gene loci on chromosomes 2, Cutis. 2005;76:173-177. 8, and 20 have been suggested.12 Physical injury to the skin (Köbner phe- soriasis is a common inherited papulosquamous nomenon), low humidity,5 cold weather, and stress dermatosis that often represents a diagnostic may represent important triggering factors.9 Worsen- P dilemma in infants.1-3 The diagnosis may be ing of psoriasis following stress was observed in 50% challenging if the disease is mild or if the presenta- of 223 pediatric patients in one survey and in 90% tion is atypical.4 of 245 children in another.9,13 In addition, in young children, viral or bacterial infection (particularly Pathogenesis due to Streptococcus) may be a common initiating Both genetic and environmental factors interact to and maintaining factor, especially for the develop- precipitate the development of psoriasis.5 A family ment of acute guttate psoriasis.14,15 history of psoriasis is seen in 25% to 71% of patients In childhood, psoriasis may be induced by some with the disease.2,6-9 Generally, an earlier onset of medications, the most common being antimalarials the disease correlates with familial frequency7; the and systemic corticosteroids.
    [Show full text]
  • A Dissertation on a CLINICAL STUDY of NAIL CHANGES in PAPULOSQUAMOUS DISORDER
    A Dissertation on A CLINICAL STUDY OF NAIL CHANGES IN PAPULOSQUAMOUS DISORDER Dissertation Submitted to THE TAMILNADU Dr.M.G.R. MEDICAL UNIVERSITY CHENNAI - 600 032 With partial fulfillment of the regulations for the award of M.D. DEGREE IN DERMATOLOGY , VENEREOLOGY AND LEPROLOGY (BRANCH – XII) COIMBATORE MEDICAL COLLEGE, COIMBATORE MAY 2018 DECLARATION I Dr. A. AMUTHA solemnly declare that the dissertation entitled “A CLINICALSTUDY OF NAIL CHANGES IN PAPULOSQUAMOUS DISORDER ” is a bonafide work done by me at Coimbatore Medical College Hospital during the year JUNE 2016- JUNE 2017 under the guidance & supervision of Dr.M .REVATHY M.D.,D.D., Professor & Head of Department, Department of Dermatology, Coimbatore Medical College & Hospital. The dissertation is submitted to Dr.MGR Medical University toward partial fulfilment of requirement for the award of MD degree branch XII Dermatology, Venereology and Leprology. PLACE: Dr A. AMUTHA DATE : COPYRIGHT DECLARATION BY THE CANDIDATE I hereby declare that The Tamilnadu Dr. M.G.R Medical University, Chennai shall have the rights to preserve, use and disseminate thisdissertation / thesis in print or electronic format for academic / researchpurpose. PLACE: COIMBATORE Dr.A.AMUTHA DATE: CERTIFICATE This is to certify that the dissertation entitled “A CLINICAL STUDY OF NAIL CHANGES IN PAPULOSQUAMOUS DISORDER” is a bonafide original work done by Dr. A. AMUTHA post graduate student in the Department of Dermatology, Venereology and Leprology, Coimbatore Medical College Hospital during the year JUNE 2016- JUNE 2017 under the guidance & supervision of Dr.M.REVATHYM.D (Derm)., Professor & Head of Department, Department of Dermatology, Coimbatore Medical College & Hospital. The dissertation is submitted to Dr.MGR Medical University toward partial fulfilment of requirement for the award of MD degree branch XII Dermatology, Venereology and Leprology.
    [Show full text]