DOCSLIB.ORG

Muir-Torre Syndrome

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Muir-Torre Syndrome Muir-Torre syndrome Authors: Doctors Alexander C. Katoulis, Evangelia Bozi, Professor Nicholas G. Stavrianeas1 Creation date: May 2004 Scientific Editor: Professor Thierry Philip 1National University of Athens, 2nd Department of Dermatology and Venereology, "Attikon" General Hospital, Athens, Greece. mailto:[email protected] Abstract Keywords Disease name Definition/Diagnostic criteria Epidemiology Genetics Histogenesis Clinical description Diagnostic methods Management References Abstract Muir-Torre syndrome represents the association of multiple sebaceous tumors (i.e. hyperplasia, adenoma, epithelioma and carcinoma), or keratoacanthoma (KA) with one or more visceral carcinomas. This syndrome is very rare. Muir-Torre syndrome is dominantly inherited. It is caused by a mutation in DNA mismatch repair genes (hMLH1 at 3p21.3 or hMSH2 at 2p22-p21). Muir-Torre is therefore allelic to hereditary nonpolyposis colorectal cancer (HNPCC). Sebaceous tumors are usually multiple, with sebaceous adenomas being the commonest. KA, 3-10 in number, are usually located on the face or the trunk. Cutaneous tumors may precede or follow the first presentation of internal malignancy, which usually involves the gastrointestinal tract, the breast or the genitourinary tract. The malignancies are usually multiple, occur at an early age, but tend to be of low-grade and have a relatively low incidence of metastases. The management should be multidisciplinary including genetic counselling, regular dermatology follow-up and relevant cancer screening. Keywords Muir-Torre syndrome, sebaceous tumors, keratoacanthoma, hereditary non polyposis colon cancer, hMLH1, hMSH2 Disease name The criteria for diagnosis are: 1. At least one Muir-Torre syndrome sebaceous tumor; 2. At least one internal Definition/Diagnostic criteria malignancy. Every patient with multiple KA Muir-Torre syndrome represents the association should be evaluated for the presence of of multiple sebaceous tumors (i.e. hyperplasia, sebaceous neoplasms, the absence of which still adenoma, epithelioma and carcinoma), or requires consideration of this syndrome. keratoacanthoma (KA) (a common benign epithelial tumor of pilosebaceous origin) with one Epidemiology or more visceral carcinomas (Schwartz and Muir-Torre syndrome is very rare. Almost half of Torre, 1995). the patients have at least one KA. Katoulis A, Bozi E, Stavrianeas N. Muir-Torre syndrome. Orphanet Encyclopedia. May 2004. http://www.orpha.net/data/patho/GB/uk-MuirTorre.pdf 1 Genetics References Muir-Torre syndrome is dominantly inherited. It is Akhtar S, Oza KK, Khan SA, Wright J. Muir- caused by a mutation in DNA mismatch repair Torre syndrome: a case report of a patient with genes. Mutation may arise either in the hMSH2 concurrent jejunal and ureteral cancer and gene located on chromosome 2p22-p21 or in the review of the literature. J Am Acad Dermatol hMLH1 gene at 3p 21.3 (Mathiak et al, 2002). 1999; 41:681-6. Patients are heterozygous for the mutation. Barana D, Cetto G L, Oliani C, et al. Spectrum Normal allele inactivation results in an increased of genetic alterations in Muir-Torre syndrome is risk of malignancy. the same as in HNPCC. (Letter) Am J Med Molecular analysis in hereditary non polyposis Genet 2004;125A:318-9. colorectal cancer (HNPCC) demonstrated a Dore MX, Dieumegard B, Grandjouan S et al. common genetic basis, with the observation of Moir-Torre syndrome and colorectal cancer: two germline mutations in the hMSH2 gene in both families with molecular genetic analysis. Ann syndromes (Dore et al, 1999). Derm Venereol 1999; 126:582-6. Goudie DR, Yuille MAR, Leversha MA et al. Histogenesis Multiple self-healing epitheliomata mapped to The association of KA and sebaceous chromosome 9q22-q31 in families with common neoplasms may be explained by their common ancestry. Nat Genet 1993; 3:165-9. derivation from pilosebaceous glands. Kato N, Ito K, Kimura K, Shibata M. Ferguson Smith type multiple keratoacanthomas and a Clinical description keratoacanthoma centrifugum marginatum in a Sebaceous tumors are usually multiple, with woman from Japan. J Am Acad Dermatol 2003; sebaceous adenomas being the commonest. 49:741-6. KA, 0.5-1.0 cm in diameter, are usually located Mathiak M, Rutten A, Mangold E et al. Loss of on the face or the trunk. They vary from 3 to 10 DNA mismatch repair proteins in skin tumors in number. Cutaneous tumors may precede or from patients with Muir-Torre syndrome and follow the first presentation of internal MSH2 or MSH1 germline mutations: malignancy. Internal malignancies usually establishment of immunohistochemical analysis involve the gastrointestinal tract, such as as screening test. Am J Surg Pathol 2002; colorectal, gastric or esophageal cancer. Less 26:338-43. commonly, the breast or the genito-urinary tract Schwartz RA. Keratoacanthoma. J Am Acad may be involved. The malignancies are usually Dermatol 1994; 30:1-19. multiple, occur at an early age, but tend to be of Schwartz RA, Torre DP. The Muir-Torre low-grade and have a relatively low incidence of syndrome: a 25-year retrospect. J Am Acad metastases (Akhtar et al, 1999). Barana et al. Dermatol 1995; 33:99-104. (2004) reported the first family with Muir-Torre syndrome harboring a large deletion within the MSH2 gene. The family had 3 affected individuals in 2 generations. The father had 2 metachronous colon cancers starting at age 53 years, a daughter had a colon and ovarian cancer starting at age 42 years, and a son was affected by an adenoma with a focus of carcinoma at age 47 years. All 3 affected members presented with cutaneous lesions characteristic of Muir-Torre syndrome. Diagnostic methods Histology: typical "seboacanthoma" of Muir-Torre syndrome displays architecture of KA with well- differentiated sebaceous lobules of sebaceous adenoma (Schwartz, 1994). Management The management should be multidisciplinary including genetic counselling, regular dermatology follow-up and relevant cancer screening. For skin tumours, oral isotretinoin may be effective and might have a preventive role also for future malignancies. Katoulis A, Bozi E, Stavrianeas N. Muir-Torre syndrome. Orphanet Encyclopedia. May 2004. http://www.orpha.net/data/patho/GB/uk-MuirTorre.pdf 2 .
Load more

Recommended publications
  • Pilar Sheath Acanthoma Presenting As a Nevus
    Letter to Editor Pilar Sheath Acanthoma Presenting as a Nevus Sir, Pilar sheath acanthoma (PSA) is a rare benign follicular neoplasm, which was first described by Mehregan and Brownstein in 1978.[1] PSA usually presents as an asymptomatic, flesh colored papule with a central opening localized at the lower lip with exceptional presentations such as ear lobe, postauricular region, or cheek.[1‑3] A 42‑year‑old female referred with a solitary, slow‑growing nodular lesion at the upper lip region for 6 months. Physical exam revealed a 4 mm, pink‑brown colored nodule with a central opening [Figure 1]. Under clinical prediagnosis of melanocytic nevus, an excisional biopsy Figure 1: Physical examination of the nodule in the upper lip region was performed. In a microscopic examination, a cystic cavity that communicated with surface epidermis has been observed. The wall of the cystic cavity was composed of solid tumor islands extending in the deep dermis [Figure 2]. The cavity was lined with stratified squamous epithelium filled with keratin [Figure 3]. PSA is an uncommon, benign follicular tumor occurring in the faces of middle‑aged and elderly patients. These lesions can present at any location such as cheek, ear lobe on the head, and neck. In our case, a 42‑year‑old female was presented with a pink‑brown colored nodular lesion opening at the upper lip region. The differential diagnosis includes trichofolliculoma and dilated pore of Winer. Trichofolliculomas contain many seconder hair follicles Figure 2: A central cavity with keratin in the dermis which is continuous radiating from the wall of the primary follicle with outer with the surface epithelium (H and E, ×40) and inner root sheaths in a well‑formed stroma which are absent in PSA.
    [Show full text]
  • What Are Basal and Squamous Cell Skin Cancers?
    cancer.org | 1.800.227.2345 About Basal and Squamous Cell Skin Cancer Overview If you have been diagnosed with basal or squamous cell skin cancer or are worried about it, you likely have a lot of questions. Learning some basics is a good place to start. ● What Are Basal and Squamous Cell Skin Cancers? Research and Statistics See the latest estimates for new cases of basal and squamous cell skin cancer and deaths in the US and what research is currently being done. ● Key Statistics for Basal and Squamous Cell Skin Cancers ● What’s New in Basal and Squamous Cell Skin Cancer Research? What Are Basal and Squamous Cell Skin Cancers? Basal and squamous cell skin cancers are the most common types of skin cancer. They start in the top layer of skin (the epidermis), and are often related to sun exposure. 1 ____________________________________________________________________________________American Cancer Society cancer.org | 1.800.227.2345 Cancer starts when cells in the body begin to grow out of control. Cells in nearly any part of the body can become cancer cells. To learn more about cancer and how it starts and spreads, see What Is Cancer?1 Where do skin cancers start? Most skin cancers start in the top layer of skin, called the epidermis. There are 3 main types of cells in this layer: ● Squamous cells: These are flat cells in the upper (outer) part of the epidermis, which are constantly shed as new ones form. When these cells grow out of control, they can develop into squamous cell skin cancer (also called squamous cell carcinoma).
    [Show full text]
  • Hair Follicle Tumors
    Hair Follicle Tumors 803-808-7387 www.gracepets.com These notes are provided to help you understand the diagnosis or possible diagnosis of cancer in your pet. For general information on cancer in pets ask for our handout “What is Cancer”. Your veterinarian may suggest certain tests to help confirm or eliminate diagnosis, and to help assess treatment options and likely outcomes. Because individual situations and responses vary, and because cancers often behave unpredictably, science can only give us a guide. However, information and understanding for tumors in animals is improving all the time. We understand that this can be a very worrying time. We apologize for the need to use some technical language. If you have any questions please do not hesitate to ask us. What is this tumor? This is one of many similar tumors that arise by disordered growth of the hair follicles. These tumors are almost all benign and can be permanently cured by total surgical removal. Some occur at multiple sites within the same animal. This family of tumors grade into each other. Precise nomenclature is usually irrelevant as almost all are benign. What do we know about the cause? The reason why a particular pet may develop this, or any cancer, is not straightforward. Cancer is often seemingly the culmination of a series of circumstances that come together for the unfortunate individual. Cross Section of Skin & Hair Follicle B-catenin is required for differentiation of skin cells into hair follicles. If there is over-production of this chemical in the body, hair follicle tumors develop.
    [Show full text]
  • Just a Cutaneous (Keratotic) Horn?
    BMJ 2019;364:l595 doi: 10.1136/bmj.l595 (Published 7 March 2019) Page 1 of 2 Endgames BMJ: first published as 10.1136/bmj.l595 on 7 March 2019. Downloaded from ENDGAMES SPOT DIAGNOSIS Just a cutaneous (keratotic) horn? Jane Wilcock general practitioner, Yvonne Savage Silverdale Medical Practice, Salford, Manchester, UK A 70 year old woman attended a dermatologist with a lesion on In this case, the speed of growth made a keratoacanthoma a the dorsum of her right hand (fig 1). It had appeared over eight possibility. However, the patient also had several risk factors weeks and was painless but unsightly. She reported good health for squamous cell cancer: age, sun exposure, past lymphoma,1 and no history of warts. Fifteen years ago, she had lymphoma past chemotherapy, and no history of warts. Other invasive treated by chemotherapy; her last treatment (biological therapy) features of squamous cell cancer relevant to this case include had finished seven years ago and she had been well since. She the lesion’s arrival over eight weeks and its wide, thick, red base had holidayed in Australia for three months at a time over the with a diameter larger than the height of the horn. About 35% 2 last three years and more recently had driven frequently from of keratotic horns are invasive squamous cell cancers. http://www.bmj.com/ northern England to the south coast while a close relative was Invasive squamous cell cancer is a non-melanotic skin ill. She said she was careful to use sunscreen. malignancy with a good prognosis but may metastasise to the lymph nodes.
    [Show full text]
  • GRAND ROUNDS Department of Dermatology
    Calderm 2017 NorCal Conference Jiminy Cricket & Appropriate Use in Dermatopathology Maxwell A. Fung, MD Professor of Clinical Dermatology & Pathology University of California, Davis Sacramento, California No relevant financial relationships “Audience response (ARS)” a) Do you read your own dermpath? b) Read path for other providers? c) Mostly read path reports? +/- recut review d) More than one of the above? Objectives • Gain insight: WHEN to listen to the “little voice” in your head to “do the right thing,” improve patient care and stay out of trouble • “Appropriate Use”: a concept to improve patient care, stay out of trouble, reduce cost, and get paid Highly predictive dermpath “rule outs” • Epidermal inclusion cyst Ring CM, et al. Clinical simulators of cysts. J Am Acad Dermatol 2016; 75:1255-1257. • Lipoma • Skin tag • Pyogenic granuloma • Granuloma annulare 58/M “r/o cyst” left chest 58/M “r/o cyst” left chest 22/M “FINAL DIAGNOSIS: CYST, EXCISION” 22/M “FINAL DIAGNOSIS: CYST, EXCISION” Post-op √ “Wound is closed, no redness” 22/M “FINAL DIAGNOSIS: CYST, EXCISION” What would you do next? a) Accept diagnosis b) Additional excision c) Call pathologist d) Review pathology/2nd opinion “FINAL DIAGNOSIS: CYST, EXCISION” What is the “official” disease of California? Coccidioidomycosis (California disease, Valley fever, San Joaquin Valley fever, desert rheumatism) H&E • Coccidioides immitis • Thick walled spherule PAS containing endospores 10-80 mm “FINAL DIAGNOSIS: CYST, EXCISION” Annular plaques in a woman from SoCal • 81/WF from The OC • 4 year history annular erythematous dermal plaques • Started on left upper arm • Clinical diagnosis: GA (multiple derms) 81 yr old woman R/O GA right flank 81 yr old woman, R/O GA 81 yr old woman, R/O GA 81 yr old woman, R/O GA 81 yr old woman, R/O GA 81 yr old woman, R/O GA What is your diagnosis? a) Actinic granuloma b) Granuloma annulare c) Interstitial granulomatous dermatitis d) Other 81 yr old woman, R/O GA GA-like BT leprosy Zhu TH, Kamangar F, Silverstein M, Fung MA.
    [Show full text]
  • 7. Clear Cell Acanthoma
    Listy do Redakcji / Letters to the Editor CLEAR CELL ACANTHOMA – OPIS PRZYPADKU CASE REPORT OF CLEAR CELL ACANTHOMA Brzezi ński Piotr 6 Wojskowy Oddział Gospodarczy, Ustka, Polska 6th Military Support Unit, Ustka, Poland, [email protected] N Dermatol Online. 2010; 1(2): 29-30 Acanthoma clarocellulare (ACC) wyst ępuje Clear cell acanthoma (CCA) is characterized by jako pojedynczy, ró żowo-br ązowy guzek i zwykle pink-brown nodules and usually occurs on the legs of zlokalizowany jest na ko ńczynie dolnej u osób starszych. elderly people. ACC został po raz pierwszy opisany przez Degosa jako CCA was first described by Degos as a benign tumor of łagodny nowotwór pochodzenia nabłonkowego. ACC epidermal origin. Clear cell acanthoma are also known as wyst ępuje równie ż pod innymi nazwami: Degos Degos acanthoma, tumor Degos or acanthome à cellules acanthoma, guz Degosa czy acanthome à cellules claires. Some authors have also suggested that it is a claires. localized form of inflammatory psoriasiform dermatoses. Niektórzy autorzy sugeruj ą, że jest to forma The diagnosis is rarely made before skin biopsy. When zlokalizowanego łuszczycopodobnego zapalenia skóry. examined under the microscope, clear cell acanthoma Diagnoza jest rzadko stawiana przed otrzymaniem show a characteristic accumulation of clear glycogen- wyniku biopsji skóry. W badaniu pod mikroskopem, containing cells in the epidermis. The common wida ć jasne komórki, które wykazuj ą cechy kumulacji i dermatoscopic feature of all these articles is the presence zawieraj ą glikogen. Charakterystyczn ą cech ą w obrazie of pinpoint-like/dotted vessels, which are described as dermoskopowym jest obecno ść tzw. pinpoint-like/dotted having a homogenous/bunch-like, reticular, pearl vesseles, które s ą opisane jako homogenne, podobne do lessions.
    [Show full text]
  • Keratoacanthomas Information for Patients You Have Been Given a Diagnosis of Keratoacanthoma
    Department of Dermatology Keratoacanthomas Information for patients You have been given a diagnosis of keratoacanthoma. This leaflet has been written to give you more information about this condition and the different ways it can be treated. What are keratoacanthomas (also known as KAs)? Keratoacanthomas are relatively common skin growths. They are not cancerous but at first they look and behave like a form of skin cancer. They grow quickly over a few weeks, appearing at first as a small reddish bump which then becomes a bigger nodule, often with a central horn or plug. If left alone KAs usually go away by themselves – although this can take weeks or months to do so. They can appear anywhere on the body, but are most common in sun-exposed areas, such as the face, neck, and the back of the hands and arms. They are more likely to develop as you get older. What causes keratoacanthomas? The exact cause of KAs is not known. It is thought that sun exposure, contact with tar, smoking, some wart viral infections, injury to the skin and a suppressed immune system can lead to an increased risk of developing KAs. Are keratoacanthomas hereditary (passed from parent to child)? The majority are not hereditary, although they may be present as a feature of some rare inherited conditions. How is keratoacanthoma diagnosed? The doctor will have diagnosed your keratoacanthoma by asking you some questions and looking at its appearance. However, because it can look very similar to a skin cancer called a squamous cell carcinoma, the most common diagnosis (and treatment) is to remove it surgically and send a tissue sample to the laboratory to be tested.
    [Show full text]
  • Skin Cancer for Dental Professionals
    ARTICLE CPD: ONE HOUR Skin cancer for dental professionals ©iStockphoto/Thinkstock Visiting the dental practice is a valuable opportunity for skin cancer screening, says Ben J. Steel.1 kin cancer is the commonest Examination of the oral mucosa for signs of ad hoc screening for head and neck skin form of cancer in the UK. In of oral squamous cell carcinoma and other malignancy. Patients with suspicious lesions 2010, 112,367 skin cancers were mucosal conditions is an accepted part of could be referred to their general medical registered in the UK out of a the normal dental check-up, as is an extra- practitioner (GP) or an oral and maxillofacial total of 424,128 cancers of all oral examination to check the facial hard surgeon for further management. types.1 Three main types are and soft tissues, jaw joints and cervicofacial This article will present an overview of the Srecognised: basal cell carcinoma (BCC) lymph nodes.2 A brief look at the head three forms of skin cancer most likely to be and squamous cell carcinoma (SCC), and neck skin for suspicious lesions could seen among dental patients in the UK. which collectively comprise non-melanoma easily be incorporated into this structure. skin cancer (NMSC), and malignant In the two years leading to September 2012, BASAL CELL CARCINOMA melanoma (MM). 29.6 million people in the UK attended a Epidemiology dentist, representing some 52.1% of the This is the commonest type of skin cancer, 1Medical student, Hull York Medical adult population.3 With such a considerable and indeed any cancer, in the UK, with at School; general dental practitioner, proportion of the population passing through, least 48,000 cases registered in England each Hull Royal Infirmary there exists a valuable opportunity for a form year between 2004 and 2006.4 This is believed 09 BDJ Team www.nature.com/BDJTeam © 2014 Macmillan Publishers Limited.
    [Show full text]
  • Keratoacanthoma Centrifugum Marginatum: a Diagnostic and Therapeutic Challenge
    CONTINUING MEDICAL EDUCATION Keratoacanthoma Centrifugum Marginatum: A Diagnostic and Therapeutic Challenge Allison K. Divers, MD; Dana Correale, MD; Jason B. Lee, MD GOAL To recognize and explain keratoacanthoma centrifugum marginatum (KACM) OBJECTIVES Upon completion of this activity, dermatologists and general practitioners should be able to: 1. Describe the clinical presentation of KACM. 2. Differentiate KACM from similar presenting lesions. 3. Discuss the therapeutic options for KACM. CME Test on page 263. This article has been peer reviewed and is accredited by the ACCME to provide continuing approved by Michael Fisher, MD, Professor of medical education for physicians. Medicine, Albert Einstein College of Medicine. Albert Einstein College of Medicine designates Review date: March 2004. this educational activity for a maximum of 1 This activity has been planned and implemented category 1 credit toward the AMA Physician’s in accordance with the Essential Areas and Policies Recognition Award. Each physician should claim of the Accreditation Council for Continuing Medical only that hour of credit that he/she actually spent Education through the joint sponsorship of Albert in the activity. Einstein College of Medicine and Quadrant This activity has been planned and produced in HealthCom, Inc. Albert Einstein College of Medicine accordance with ACCME Essentials. Drs. Divers, Correale, and Lee report no conflict of interest. The authors report discussion of off-label use for imiquimod, intralesional methotrexate, isotretinoin, and 5-fluorouracil cream. Dr. Fisher reports no conflict of interest. A keratoacanthoma centrifugum marginatum because the lesion can expand to a great size. (KACM) may pose a diagnostic and therapeutic We report on a patient with multiple lesions of challenge.
    [Show full text]
  • University of Illinois at Chicago, December 2009
    Chicago Dermatological Society December 2009 Monthly Educational Conference Program Information Continuing Medical Education Certification and Case Presentations Wednesday, December 9, 2009 Conference Host: Department of Dermatology University of Illinois at Chicago Chicago, Illinois Program Venue Information See site map on following pages UIC DERMATOLOGY DEPARTMENT CLINIC 1801 W. Taylor, Suite 3E • Registration for practicing members & guests (8 - 10 a.m. only) • Patient viewing STUDENT CENTER WEST (SCW) 828 S. Wolcott, 2nd Floor • Registration • Committee meetings • Slide viewing • Lectures, business meeting & case discussions • Lunch • Exhibitors Committee Meetings 8:00 a.m. CDS Plans & Policies Committee - SCW Room 213 A/B 9:00 a.m. IDS Board of Directors - SCW Room 216 A/B Program Activities 9:00 a.m. - 10:00 a.m. Registration for Members & Guests Dermatology Clinic (moves to SCW 2nd floor foyer at 10 a.m.) 10:00 a.m. - 2:30 p.m. Registration for Members & Guests SCW - 2nd Floor Foyer 8:00 a.m. - 2:30 p.m. Registration for Residents/Fellows SCW - 2nd Floor Foyer 9:00 a.m. - 10:00 a.m. RESIDENT LECTURE – SCW Chicago Room A-C “Dermatitis Herpetiformis: A Model for Cutaneous Manifestations of Gastrointestinal Disease” – Russell P. Hall, III, MD 9:30 a.m. - 10:45 a.m. CLINICAL ROUNDS Patient viewing – Dermatology Clinic Slide viewing – SCW Room 206 A/B 11:00 a.m. - 12:00 p.m. GENERAL SESSION - SCW Chicago Room A-C David Fretzin Lecture: “Dapsone: Uses and Abuses” – Russell P. Hall, III, MD 12:00 p.m. - 12:30 p.m. Box lunches & visit with exhibitors 12:30 p.m.
    [Show full text]
  • Keratoacanthoma
    KERATOACANTHOMA What are the aims of this leaflet? This leaflet has been written to help you understand more about keratoacanthomas (KAs). It tells you what they are, what causes them, what can be done about them, and where you can find out more about them. What are keratoacanthomas? KAs are relatively common benign skin growths from the cells surrounding the hair unit that usually appear in sun exposed skin. Clinically they can’t be easily differentiated from a more serious skin cancer, a squamous cell carcinoma (SCC). KAs grow quickly over the first few weeks but do not spread to other parts of the body. If left alone, they will usually go away by themselves in 4 to 6 months. What causes keratoacanthomas? Their precise cause is not known. Factors that may play a part include heavy sun exposure, contact with some chemicals, smoking, infection with some strains of wart virus, a suppressed immune system, and minor injuries to the skin. KAs are more common in fair than in dark-skinned individuals, and more so in men than in women. They are rare under the age of 20 and become more common with age. Are keratoacanthomas hereditary? Usually not, although multiple KAs are a part of a few rare inherited conditions. 4 Fitzroy Square, London W1T 5HQ Tel: 020 7383 0266 Fax: 020 7388 5263 e-mail: [email protected] Registered Charity No. 258474 What are the symptoms of a keratoacanthoma? Usually there are none apart from their cosmetic appearance, as they tend to be on exposed skin. What does a keratoacanthoma look like? KAs occur more frequently on the face, and less often on the backs of the hands and forearms.
    [Show full text]
  • Keratoacanthoma As a Postoperative Complication of Skin Cancer Excision
    DERMATOLOGIC SURGERY Keratoacanthoma as a postoperative complication of skin cancer excision Leonard H. Goldberg, MD, FRCP,a,b Sirunya Silapunt, MD,a Kathleen K. Beyrau, MD,c S. Ray Peterson, MD,a Paul M. Friedman, MD,a and Murad Alam, MDd Houston, Texas, Portage, Wisconsin; and Chicago, Illinois Background: Keratoacanthomas usually occur spontaneously as a single rapidly growing tumor on sun-exposed skin. Multiple keratoacanthomas are rarely seen. Keratoacanthomas may also develop after trauma, laser resurfacing, radiation therapy, and at the donor site after skin grafting. Objective: We report 6 cases of keratoacanthomas that developed in and around healing and healed surgical sites after treatment of skin cancer. These tumors developed 1 to 3 months after surgery and were sometimes multiple. Methods: We performed follow-up examinations of patients’ wounds after the treatment of skin cancer. Histological examination of nodules developing in the margins of healing wound sites and in the scars of healed wound sites after Mohs micrographic surgery revealed keratoacanthomas. Results: The tumors presented as a rapidly growing nodule or nodules, with the typical morphology and pathology of keratoacanthoma. One patient developed multiple keratoacanthomas at surgical and nonsur- gical sites. These nodules were treated by a combination of excision, curettage and electrodesiccation, and oral isotretinoin, 4 mg/d. Conclusion: Keratoacanthoma must be considered in the differential diagnosis of a rapidly growing nodule within or around the surgical site after skin cancer surgery. (J Am Acad Dermatol 2004;50:753-8.) eratoacanthoma (KA) usually occurs spon- of KA that developed in wounds healing by second taneously as a single rapidly growing tumor intention and in scars within 3 months after Mohs K with characteristic morphology on the sun- micrographic surgery (MMS) for squamous cell car- exposed regions of middle-aged or older persons.
    [Show full text]