DOCSLIB.ORG

The Summer Skin Check

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
The Summer Skin Check Pictorial essay • CLINICAL PRACTICE The summer skin check Belinda Welsh, MBBS, MMed, FACD, is consultant dermatologist, St Vincent’s Hospital, Melbourne, Skin and Cancer Foundation, Carlton, and is in private practice, Sunbury, Victoria. BACKGROUND Skin cancer is a major public health problem in Australia and represents a substantial health cost. General practitioners provide the majority of care to patients with skin cancer, so becoming familiar with the clinical features and management of these tumours is important. OBJECTIVE To provide a pictorial essay on the common types of benign and malignant skin lesions encountered in general of suspicion is necessary in this population in women, the neck, shoulders and outer practice, and briefly describe key clinical • exposure to arsenic is a known risk factor arms are also sites of predilection4 features, differential diagnosis and for the development of basal cell carci- • scars should be checked for evidence of management options. noma (BCC)2 and Bowen disease3 recurrence of previously excised lesions - •a history of change or symptomatology in BCCs may develop within longstanding DISCUSSION any lesion – skin cancers are changing scars and ulcers5,6 Examination for skin cancer should be lesions and the time course for this change • lymph nodes should be assessed for the considered in the general practice setting is generally evident over a period of months. early detection of metastatic disease if for all patients over the age of 40 years, there is a history of melanoma or squa- particularly the elderly. A proper skin check Examination mous cell carcinomas (SCCs). requires a systematic approach and ideally The following factors are important in examination: an entire consultation should be set aside • good lighting, preferably natural light Management for this purpose. However, clinical • magnification – a dermatoscope can be Biopsy of a lesion (punch or shave) is advisable examination conducted for other purposes helpful in diagnosis of both melanocytic when a firm clinical diagnosis cannot be made or provides an opportunity for screening and and nonmelanocytic lesions when the treatment choice may be dictated by early detection of skin cancer. • positioning – patients should be the tumour type or pattern of growth. Multiple 2 undressed to their underwear, so a warm mm punch biopsies may be necessary to define History taking room or blanket for comfort is desirable. poorly demarcated tumours. Tailor each manage- Having the patient lie on the examination ment decision to the particular lesion in the The following points in history taking can help couch can be useful so the soles of the individual patient. In general, simple surgical exci- identify high risk patients: feet are not missed sion with primary closure is the treatment of • blistering sunburns • look closely – gently stretching the skin choice for most skin cancers, although some • occupational and recreational exposure to can often make BCCs more obvious. anatomical areas require particular care (Table 1) solar radiation • palpate – dermatofibromas for example and specialist referral may be desirable for tech- • family or personal history of melanoma or have a characteristic feel on palpation nically difficult excisions. Prevention should be multiple atypical (dysplastic) naevi • concentrate on high risk areas – the emphasised (Table 2) and changes to look for in • family or personal history of non- highest rates for NMSC are found on the suspicious lesions discussed. Follow up is rec- melanoma skin cancer (NMSC) face, especially the nasolabial fold, eyelid ommended for three reasons: detection of •immunosuppression – higher rates and and the nonmucosal skin of the lip fol- further primary tumours, detecting local persis- earlier onset of skin cancer is present in lowed by the ears, nose and cheek. In tence of previously treated tumours, and early transplant patients,1 therefore a high index men, the neck, back and shoulders, and detection of metastatic disease. Reprinted from Australian Family Physician Vol. 33, No. 1/2, January/February 2004 37 Clinical practice: The summer skin check Recurrence after excision is not Table 1. Problem areas uncommon as clinical margins are often requiring care in management underestimated Face – for cosmetic reasons and the possibility of nerve damage Eyelids – scarring can cause entropion Lips and helix of the ear – because of malignant potential Neck – where the accessory nerve is Figure 2. Seborrhoeic keratosis superficial Fingers – function is a major consideration later thickening to become brownish-black. Lower limb – healing can be very slow The surface is irregular and shows minute pits. Management Figure 4. Porokeratosis Table 2. Recommendations for When flat and pigmented, seborrhoeic ker- prevention of skin cancer atoses may require biopsy to differentiate Porokeratoses them from lentigo maligna melanoma. These can be removed with a number of destructive Clinical features Where possible use clothing as the techniques such as cryotherapy, curettage, primary means of photoprotection – electrosurgery or shave excision. Porokeratoses (Figure 4) are uncommon, dis- preferably closely woven fabrics that aren’t transparent when held up to tinctive, benign lesions due to clones of the light Multiple eruptive seborrhoeic epidermal cells that show varying degrees of Wear hats and sunglasses keratoses are rare but may be a sign of dysplasia. They develop as annular dry internal malignancy (Leser-Trelat sign) plaques surrounded by a raised fine keratotic Seek shade. Avoid the sun in the middle of the day wall. Porokeratoses may be isolated or multi- ple and most often appear on the limbs. Use sunscreen – broad spectrum SPF15 or greater should be applied to Management all exposed areas of the skin as a last line of defence. Reapply every 2 hours None usually needed. If lesions are hyperkera- Advise against the use of sunbeds, totic or multiple, cryotherapy may be performed. tanning booths and tanning lamps The rare giant forms may be premalignant Figure 3. Dermatofibroma Dermatofibroma Clinical features Dermatofibroma (Figure 3) are benign tumours of fibroblasts that are firm, solitary Figure 1. Seborrhoeic keratosis dermal nodules usually found on the limbs of Figure 5. Solar keratosis younger people. They have an ‘iceberg’ effect Seborrhoeic keratoses in that they feel larger than they look. The Clinical features overlying epidermis is often lightly pigmented Solar keratoses and dimples when the nodule is squeezed. Seborrhoeic keratoses (Figure 1, 2) are very Management Solar keratoses (Figure 5) are common common benign tumours usually found on the lesions associated with dysplasia, particularly face and trunk. They develop gradually as No treatment is usually necessary, although within basal keratinocytes. They represent a slightly elevated, ovoid yellow-brown, well biopsy may be performed if the diagnosis potential precursor of SCC, although only a defined papules with a greasy appearance, is uncertain. small percentage evolve into invasive SCCs. 38 Reprinted from Australian Family Physician Vol. 33, No. 1/2, January/February 2004 Clinical practice: The summer skin check Clinical features to invasive SCC has not been established, Differential diagnosis but appears to be low.7 Solar keratoses are found on the chronically Differential diagnosis • SCC sun exposed sites of the head and neck, • Atypical fibroxanthoma dorsa of the hands, and the forearms, and • Superficial BCC • Merkel cell carcinoma present as erythematous macule with super- • Psoriasis • Amelanotic melanoma. imposed hyperkeratosis. Solar keratoses are • SCC Management options generally multiple and may be confluent. • If pigmented, may mimic superficial Differential diagnosis spreading melanoma. • Partial biopsy will almost always be Management options reported as a well differentiated SCC as Bowen disease, SCC, solar lentigo or lentigo pathology requires the entire architecture maligna if pigmented. • Surgical excision to suggest the possibility of keratoacan- Management options • Cryotherapy thoma. If in doubt, treat as a SCC • Imiquimod • Curettage +/- cryotherapy •No treatment • 5-flurouracil • Shave excision • Cryotherapy • Curettage and diathermy • Surgical excision • 5-flurouracil • Photodynamic therapy • Intralesional methotrexate • Imiquimod • Superficial radiotherapy • Superficial radiotherapy. • Curettage • Laser ablation. • Laser resurfacing. Extra caution is required in Due to extension of keratinocyte atypia, immunosuppressed patients as keratoa- Thickening and tenderness on down hair follicles recurrence after canthomas may progressively grow lateral palpation are indicators of possible treatment with superficial modalities rather than involute10 transformation into invasive SCC (eg. cryotherapy) can occur, particularly on the face Figure 8. Squamous cell carcinoma Figure 6. Bowen disease Figure 7. Keratoacanthoma Bowen disease Bowen disease (intraepidermal SCC) (Figure Keratoacanthoma 6) is associated with full thickness epidermal dysplasia with follicular involvement and is Keratoacanthoma (Figure 7) are lesions that classified as an intraepidermal SCC. Despite can be thought of as a well differentiated this, they tend to have a prolonged in-situ forms of SCC characterised by spontaneous Figure 9. Squamous cell carcinoma phase that may last many years. resolution. Clinical features Clinical features Squamous cell carcinoma Longstanding, slowly enlarging lesions that Keratoacanthoma are most common
Load more

Recommended publications
  • Dermatology DDX Deck, 2Nd Edition 65
    63. Herpes simplex (cold sores, fever blisters) PREMALIGNANT AND MALIGNANT NON- 64. Varicella (chicken pox) MELANOMA SKIN TUMORS Dermatology DDX Deck, 2nd Edition 65. Herpes zoster (shingles) 126. Basal cell carcinoma 66. Hand, foot, and mouth disease 127. Actinic keratosis TOPICAL THERAPY 128. Squamous cell carcinoma 1. Basic principles of treatment FUNGAL INFECTIONS 129. Bowen disease 2. Topical corticosteroids 67. Candidiasis (moniliasis) 130. Leukoplakia 68. Candidal balanitis 131. Cutaneous T-cell lymphoma ECZEMA 69. Candidiasis (diaper dermatitis) 132. Paget disease of the breast 3. Acute eczematous inflammation 70. Candidiasis of large skin folds (candidal 133. Extramammary Paget disease 4. Rhus dermatitis (poison ivy, poison oak, intertrigo) 134. Cutaneous metastasis poison sumac) 71. Tinea versicolor 5. Subacute eczematous inflammation 72. Tinea of the nails NEVI AND MALIGNANT MELANOMA 6. Chronic eczematous inflammation 73. Angular cheilitis 135. Nevi, melanocytic nevi, moles 7. Lichen simplex chronicus 74. Cutaneous fungal infections (tinea) 136. Atypical mole syndrome (dysplastic nevus 8. Hand eczema 75. Tinea of the foot syndrome) 9. Asteatotic eczema 76. Tinea of the groin 137. Malignant melanoma, lentigo maligna 10. Chapped, fissured feet 77. Tinea of the body 138. Melanoma mimics 11. Allergic contact dermatitis 78. Tinea of the hand 139. Congenital melanocytic nevi 12. Irritant contact dermatitis 79. Tinea incognito 13. Fingertip eczema 80. Tinea of the scalp VASCULAR TUMORS AND MALFORMATIONS 14. Keratolysis exfoliativa 81. Tinea of the beard 140. Hemangiomas of infancy 15. Nummular eczema 141. Vascular malformations 16. Pompholyx EXANTHEMS AND DRUG REACTIONS 142. Cherry angioma 17. Prurigo nodularis 82. Non-specific viral rash 143. Angiokeratoma 18. Stasis dermatitis 83.
    [Show full text]
  • Diagnostic Pitfall of Localized Lentigo Accompanied by Post-Inflammatory
    Letter to the Editor Diagnostic pitfall of localized lentigo accompanied by post-inflammatory pigmentation on the palm with a several-month history Keisuke Imafuku, Hiroo Hata, Shinya Kitamura, Toshifumi Nomura, Hiroshi Shimizu Department of Dermatology, Hokkaido University Graduate School of MedicineNorth 15, West 7, Kita-ku, Sapporo 060- 8638, Japan Corresponding author: Dr. Hiroo Hata, MD, PhD, E-mail: [email protected] Sir, When dermatologists see acquired and well- circumscribed pigmented macules on the palm, dorsal hand or forearm of the elderly, they tend to consider blue nevus, hematoma, nevus cell nevus and malignant melanoma as differential diagnoses [1]. We a b herein described the very rare case of localized lentigo Figure 1: Clinical manifestations. a. The macule is brown to dark black, accompanied by post-inflammatory pigmentation well-demarcated, flat, round and 3 x 4 mm in size. b. Dermoscopy of the macule shows homogenous brownish pigmentation without the in a patient who has been treated for palmoplanter parallel ridge or furrow pattern that is commonly observed in acral pustulosis for a long time. This eruption mimicked lentiginous lesion some kinds of lentiginous lesion and it was difficult to diagnose clinically. A 59-year-old female was referred to our hospital with a pigmented macule on her left palm. She had been to the family doctor for treatment of palmoplanter pustulosis by topical steroid ointment application for several years. According to the a history-taking interview, she said that the lesion had b appeared 5 months before referral to our hospital as a tiny pigmented macule and had gradually enlarged during those 5 months (Fig.
    [Show full text]
  • Hutchinson's Melanotic Freckle
    Hutchiso’s elaotic freckle Also known as Lentigo maligna What is lentigo maligna? Lentigo maligna is an early form of melanoma. In lentigo maligna the cancer cells are confined to the upper layer of the skin (epidermis). When the cancer cells spread deeper into the skin (to dermis) it is called lentigo maligna melanoma. Lentigo maligna occurs most commonly in sun damaged areas such as the face and neck in fair skinned people over the age of 60. The lesion grows slowly in size over a number of years. Melanoma is a potentially lethal disease and lentigo maligna should be diagnosed and excised as soon as possible. What causes lentigo maligna? The cause of lentigo maligna is sun exposure or solarium use. Factors that predispose a person to developing lentigo maligna or associated condition include: . chronic sun damaged/solar-induced skin damage . fair skin complexion . male gender . a personal history of non melanoma skin cancer and precancerous lesions . older individuals (those between 60 to 80 years are most commonly affected) What does lentigo maligna look like? Lentigo maligna commonly looks like a freckle, age spot, sun spot or brown patch that slowly changes shape and grows in size. The spot may be large in size, irregularly shaped with a smooth surface, and of multiple shades of brown and sometimes other colours. Thickening of part of the lesion, increasing number of colours, ulceration or bleeding can be markers that the lesion is changing into a lentigo maligna melanoma. How is lentigo maligna diagnosed? Lentigo maligna is diagnosed clinically by a dermatologist, sometimes with the help of a dermatoscope (a tool used to magnify and look closely at skin moles).
    [Show full text]
  • Pigmented Contact Dermatitis and Chemical Depigmentation
    18_319_334* 05.11.2005 10:30 Uhr Seite 319 Chapter 18 Pigmented Contact Dermatitis 18 and Chemical Depigmentation Hideo Nakayama Contents ca, often occurs without showing any positive mani- 18.1 Hyperpigmentation Associated festations of dermatitis such as marked erythema, with Contact Dermatitis . 319 vesiculation, swelling, papules, rough skin or scaling. 18.1.1 Classification . 319 Therefore, patients may complain only of a pigmen- 18.1.2 Pigmented Contact Dermatitis . 320 tary disorder, even though the disease is entirely the 18.1.2.1 History and Causative Agents . 320 result of allergic contact dermatitis. Hyperpigmenta- 18.1.2.2 Differential Diagnosis . 323 tion caused by incontinentia pigmenti histologica 18.1.2.3 Prevention and Treatment . 323 has often been called a lichenoid reaction, since the 18.1.3 Pigmented Cosmetic Dermatitis . 324 presence of basal liquefaction degeneration, the ac- 18.1.3.1 Signs . 324 cumulation of melanin pigment, and the mononucle- 18.1.3.2 Causative Allergens . 325 ar cell infiltrate in the upper dermis are very similar 18.1.3.3 Treatment . 326 to the histopathological manifestations of lichen pla- 18.1.4 Purpuric Dermatitis . 328 nus. However, compared with typical lichen planus, 18.1.5 “Dirty Neck” of Atopic Eczema . 329 hyperkeratosis is usually milder, hypergranulosis 18.2 Depigmentation from Contact and saw-tooth-shape acanthosis are lacking, hyaline with Chemicals . 330 bodies are hardly seen, and the band-like massive in- 18.2.1 Mechanism of Leukoderma filtration with lymphocytes and histiocytes is lack- due to Chemicals . 330 ing. 18.2.2 Contact Leukoderma Caused Mainly by Contact Sensitization .
    [Show full text]
  • Unilateral Nevus of Ota with Palatal and Optic Disc
    Case Report DOI: 10.7860/JCDR/2020/44666.13951 Unilateral Nevus of Ota with Palatal and Optic Section Ophthalmology Disc Pigmentation with Coincidental Preauricular Tag- A Case Report PRASANNA NAREDDY1, AMBATI DIVYA2 ABSTRACT Nevus of Ota also known as oculodermal melanosis presents as hyperpigmentation of face involving ophthalmic and maxillary branches of trigeminal nerve associated with ocular hyperpigmentation. It is due to confinement of melanocytes in the dermis. Most commonly it is unilateral but sometimes it may have bilateral presentation. Typically, it presents at birth but can also be an acquired condition. Frequently seen in Japanese and rarely in Indian subcontinent. It has more predilection towards females. Less frequently, hyperpigmentation is seen in other sites like oral mucosa, tympanum and nasal mucosa. These patients are at high risk of developing glaucoma and malignancy. The author reported a case of 12-year-old male child with unilateral pigmentation of left side face involving forehead, periorbital and cheek, along with ocular pigmentation. Hyperpigmentation of conjunctiva, iris and angles is present in left eye with intraocular pressure being normal in both eyes. Fundus showing optic disc pigmentation in the left eye with cup disc asymmetry in both eyes. Child has coexistent preauricular tag on the left side. Keywords: Congenital, Heterochromia iridis, Ocular pigmentation CASE REPORT in right eye and 14 mm of Hg in left eye. Gonioscopy revealed open A 12-year-old male child presented with complaints of abdominal angles in both eyes with hyperpigmentation of angles in the left eye. pain since 3 days to Paediatric Department where the child was admitted and further evaluation was done.
    [Show full text]
  • Vitiligo-Like Primary Cutaneous Melanoma One of the Winning Presentations Given by Dermatology Residents at the Cosmetic Surgery Forum in December 2013
    RESIDENT REPORTS Vitiligo-like Primary Cutaneous Melanoma One of the winning presentations given by dermatology residents at the Cosmetic Surgery Forum in December 2013. BY HADAS SKUPSKY, MD, JENNIFER K. CHEN, MD, AND KENNETH G. LINDEN, MD melanotic melanomas comprise two percent of all melanomas. The clinical presentation is varied and may include erythematous patches, papules, or plaques.1,2 Depigmented macules and patches Ahave been described in association with both primary and metastatic melanomas. This phenomenon often represents regression of a melanoma or a side effect of melanoma- targeted immunochemotherapy. In addition, vitiligo may present at sites remotely from a melanoma.3-5 However, primary melanoma presenting as a vitiligo-like patch with- out histopathologic evidence of regression is an exceedingly rare phenomenon. To our knowledge, there is only a single Figure 1 Figure 2 report of two cases of vitiligo-like primary melanoma in situ in the literature to date.6 We herein report a case of invasive inferior shoulder with no subcutaneous nodules. She had no lentigo maligna melanoma presenting as a vitiliginous patch cervical, axillary, or supraclavicular lymphadenopathy. Biopsy of and review the possible immunopathogenesis of this lesion. the erythematous macule at the center of the patch revealed a proliferation of typical melanocytes, solitary and in irregular CASE REPORT nests, throughout the lower aspect of the epidermis and focal A 70-year-old female presented with a five-year history of an dermal invasion consistent with a lentigo maligna melanoma asymptomatic hypopigmented patch on her left upper arm. 0.2mm in depth. Biopsy of the superior aspect revealed lentigo Although the patch had initially grown slowly, the patient had maligna melanoma in situ (Figure 3).
    [Show full text]
  • Differential Diagnosis in Dermatology
    Differential Diagnosis in Dermatology ZohrehTehranchi Dermatologist COMMON ACNE AND CYSTIC ACNE Rosacea Rosacea PERIORAL DERMATITIS ECZEMA/DERMATITIS Chronic irritant dermatitis Dyshidrotic eczematous dermatitis Childood atopic dermatitis Autosensitization dermatitis (“id” reaction): dermatophytid Seborrheic dermatitis PSORIASIS VULGARIS Pemphigus vulgaris BULLOUS PEMPHIGOID (BP) Pityriasis rosea small-plaque parapsoriasis Large-plaque parapsoriasis (parapsoriasis en plaques) LICHEN PLANUS (LP) GRANULOMA ANNULARE (GA) Erythema multiforme ERYTHEMA NODOSUM Actinic keratoses Bowen disease (Squamous cell carcinoma in situ) Bowen disease and invasive SCC Squamous cell carcinoma: invasive on the lip Squamous cell carcinoma, well differentiated Squamous cell carcinoma, undifferentiated Squamous cell carcinoma, advanced, well differentiated, on the hand Keratoacanthoma showing different stages of evolution BASAL CELL CARCINOMA (BCC) Basal cell carcinoma, ulcerated: Rodent ulcer A large rodent ulcer in the nuchal and Bas cell calarcinoma: sclerosing type retroauricular area extending to the temple Basal cell carcinoma, sclerosing, nodular, Superficial basal cell carcinoma: solitary lesion and multiple lesions Superficial basal cell carcinoma, invasive Basal cell carcinoma, pigmented Dysplastic nevi Superficial spreading melanoma: arising within a dysplastic nevus Congenital nevomelanocytic nevus Melanoma: arising in small CNMN Melanoma in situ: lentigo maligna Melanoma in situ, superficial spreading type Superficial spreading melanoma, vertical
    [Show full text]
  • Joseph Butterfield, MD Mayo Clinic Melody Carter, MD National Institutes of Health 90 80 70 T
    Joseph Butterfield, MD Mayo Clinic Melody Carter, MD National Institutes of Health Percent 50 60 70 80 90 10 20 30 40 0 Clinical o Historical • Mast cell-mediator symptoms • Less atopic disease than general population o Cutaneous • Permanent pigmented lesions with a general distribution or diffuse thickening “peau d’ orange” appearance o Other organ systems-mainly systemic disease Laboratory o Tryptase-reflects overall mast cell burden • May trend down over time and elevates with mast cell activation o Urinary metabolites-correlates with serum tryptase o Hematologic-Usually WNL; may see lymphs, PT/PTT, Plts Sonographic-Hepatosplenomegaly with systemic disease, rare lymphadenopathy Most Likely Diffuse or localized hyper-pigmented macules o Café au lait spots o Neurofibromatosis o Albright syndrome Bullous Lesions o Chronic bullous disease of childhood o Linear IgA dermatosis Solitary or multiple nodules o Congenital nevus o Juvenile Xanthogranuloma Consider No lesions o Idiopathic flushing Diffuse or localized hyper-pigmented macules o Post-inflammatory hyperpigmentation o Secondary syphilis o Chronic urticaria o Atopic dermatitis Bullous Lesions o Staphylococcus infection o Drug eruption o Incontinentia pigmenti o Bullous pemphigoid Solitary or multiple nodules Always Rule Out No lesions o Identifiable causes of anaphylaxis o Idiopathic anaphylaxis Diffuse or localized hyper-pigmented macules or papules o Secondary Syphilis o Addison’s disease o Lentigo Bullous Lesions o Bullous impetigo of infancy o Incongenta pigmenta Solitary or multiple nodules o Leukemia o Lymphoma Hypertensive spells Symptoms that improve with medications not targeting mast cell mediators or their effects: Ex: medications for anxiety or depression Seizure activity; incontinence (Delayed) problems with memory Dementia Arthritic complaints involving small joints or involving muscles.
    [Show full text]
  • Dermatoscopic Findings of Pigmented Purpuric Dermatosis*
    584 INVESTIGATION s Dermatoscopic findings of pigmented purpuric dermatosis* Dilek Biyik Ozkaya1 Nazan Emiroglu1 Ozlem Su1 Fatma Pelin Cengiz1 Anil Gulsel Bahali1 Pelin Yildiz1 Cuyan Demirkesen2 Nahide Onsun1 DOI: http://dx.doi.org/10.1590/abd1806-4841.20165124 Abstract: BACKGROUND: Pigmented purpuric dermatosis is a chronic skin disorder of unknown aetiology characterised by sym- metrical petechial and pigmented macules, often confined to the lower limbs. The aetiology of pigmented purpuric dermatosis is unknown. Dermatoscopy is a non-invasive diagnostic technique that allows the visualisation of morphological features invisible to the naked eye; it combines a method that renders the corneal layer of the skin translucent with an optical system that magnifies the image projected onto the retina. OBJECTIVES: The aim of this study is to investigate the dermatoscopic findings of pigmented purpuric dermatosis. METHODS: This study enrolled patients diagnosed histopathologically with pigmented purpuric dermatosis who had derma- toscopic records. We reviewed the dermatoscopic images of PPD patients who attended the outpatient clinic in the Istanbul Dermatovenereology Department at the Bezmialem Vakıf University Medical Faculty. RESULTS: Dermatoscopy showed: coppery-red pigmentation (97%, n = 31) in the background, a brown network (34%, n = 11), linear vessels (22%, n = 7), round to oval red dots, globules, and patches (69%, n = 22; 75%, n = 24; 34%, n = 11; respectively), brown globules (26%, n = 8) and dots (53%, n = 17), linear brown lines (22%, n = 7), and follicular openings (13%, n = 4). CONCLUSION: To our knowledge, this is the first study to report the dermatoscopy of pigmented purpuric dermatosis. In our opinion, dermatoscopy can be useful in the diagnosis of pigmented purpuric dermatosis.
    [Show full text]
  • A Rash of Information - It's Dermatology Day
    INTENSIVE UPDATE AUGUST 24 - 26, 2018 & BOARD REVIEW Loews Chicago O’Hare Hotel Rosemont, IL INNOVATIVE • COMPREHENSIVE • HANDS-ON A Rash of Information - It's Dermatology Day Rob Danoff, DO, MS, FACOFP, FAAFP The American College of Osteopathic Family Physicians is accredited by the American Osteopathic Association Council to sponsor continuing medical education for osteopathic physicians. The American College of Osteopathic Family Physicians designates the lectures and workshops for Category 1-A credits on an hour-for-hour basis, pending approval by the AOA CCME, ACOFP is not responsible for the content. + A Rash of Information – It’s Dermatology Day ACOFP Intensive Review Update 8-25-18 Rob Danoff, DO, MS, FACOFP, FAAFP + Disclosure No conflicts of interest to disclose The presentation will not involve discussion of products for investigational use 1 + What’s the Diagnosis? + Pityriasis Alba Mainly affects children and adolescents – prevalence about 5% A type of eczema – unknown cause - often seen in those with dry skin and atopic dermatitis – sun exposure may trigger Most common locations are face: cheeks and chin May also be seen on neck, shoulders and upper arm Hypopigmentation more noticeable in summer, especially on darker skin tones Dry skin and scale more noticeable in dry winter weather Lesions go through stages – scaly pink plaque to hypo- pigmented plaque with fine scale to post-inflammatory macule with no scale and then eventual resolution in a few months or a few years 2 + Key Points – Pityriasis Alba Does NOT enhance
    [Show full text]
  • Boards Fodder Disorders of Dyschromia (Hypo- and Hyperpigmentation) by Parin Pearl Rimtepathip, MD, and Janna Mieko Vassantachart, MD
    boards fodder Disorders of dyschromia (hypo- and hyperpigmentation) by Parin Pearl Rimtepathip, MD, and Janna Mieko Vassantachart, MD Genetic conditions Gene Disorder Pathophysiology Clinical Features (Unique Features) Mutation Dyskeratosis XLR (MC): Reduced telomerase activ- Male > Female. Bone marrow failure up to Congenita DKC 1 ity and abnormally short- 90% (increase risk of hematopoietic malig- (Zinsser-Engman- ened telomeres chro- nancies) + triad of abnormal skin pigmenta- Cole syndrome) AD: TERT, mosomal instability/cellu- tion (poikilodermatous patches of face/neck/ TERC lar replication dysfunction upper torso), onychodystrophy, premalignant oral leukoplakia (vs benign oral leukoplakia in Pachyonychia Congenita type I) Dyschromatosis AD: ADAR Heterozygous mutations in Presents by 6-years-old with hyper/hypopig- Symmetrica (SDAR the gene encodes an RNA mented macules restricted to sun-exposed Hereditaria gene) specific adenosine deami- skin on the dorsal aspects of bilateral (Reticulate nase extremities and face Acropigmentation of Dohi) Naegeli- AD: Location of expression of Allelic to DPR. Brown gray reticulated hyper- Franceschetti- Keratin keratin 14 - Basal kerati- pigmentation typically localized to abdomen, Jadassohn 14 nocytes develops around age 2 and improves after Syndrome (NFJS) puberty. Other findings: PPK + adermato- glyphia (no finger prints) + dental anomalies including early loss of teeth (not seen in DPR) + hypohidrosis + onychodystrophy Dermatopathia AD: Location of expression of Allelic to NFJS. Unique features: diffuse non- Pigmentosa Keratin keratin 14 - Basal kerati- scarring alopecia (not seen in NFJS) + ony- Reticularis (DPR) 14 nocytes chodystrophy + adermatoglyphia + persistent reticulated hyperpigmentation of torso and proximal UE + No dental anomalies Dyschromatosis AD/AR: Mutation in ATP bind- Japanese. Torso predominant with mottled Universalis ABCB6 ing cassette subfamily B, appearance, nail dystrophy, and pterygium.
    [Show full text]
  • Malignant Skin Tumors in Patients with Oculocutaneous Albinism
    igmentar f P y D l o i a so n r r d u e r o J s Journal of Pigmentary Disorders Yasumizu et al., Pigmentary Disorders 2015, 2:10 DOI: 10.4172/2376-0427.1000218 ISSN: 2376-0427 Research Open Access Malignant Skin Tumors in Patients with Oculocutaneous Albinism Makiko Yasumizu1, Chikako Nishigori2, Masakazu Kawaguchi3, Tomoya Takata4, Naoki Oiso5, Tamio Suzuki3, Ayano Umekoji1, Daisuke Tsuruta1 and Kazuyoshi Fukai*1 1Department of Dermatology, Graduate School of Medicine, Osaka City University, Osaka, Japan 2Division of Dermatology, Department of Internal Related, Kobe University Graduate School of Medicine, Kobe, Japan 3Department of Dermatology, Faculty of Medicine, Yamagata University, Yamagata, Osaka-Sayama, Japan 4Department of Dermatology, Kochi University, Kochi, Japan 5Department of Dermatology, Faculty of Medicine, Kinki University, Osaka-Sayama, Japan *Corresponding author: Kazuyoshi Fukai, Department of Dermatology, Graduate School of Medicine, Osaka City University, Osaka, Japan, Tel: +81-6-6645-3826; Fax: +81-6-6645-3828; E-mail: [email protected] Rec date: September 25, 2015; Acc date: October 01, 2015; Pub date: October 5, 2015 Copyright: © 2015 Yasumizu M et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Abstract Background: Patients with oculocutaneous albinism (OCA) are prone to develop skin cancers. Aim and Objectives: To analyze reports of skin cancers in albinos published in the English and the Japanese literature in order to prepare guidelines for the successful management of skin cancer in albinos.
    [Show full text]