The Effective Management of Hyperkeratosis
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Idiopathic Spiny Keratoderma: a Report of Two Cases and Literature Review
Idiopathic Spiny Keratoderma: A Report of Two Cases and Literature Review Jessica Schweitzer, DO,* Matthew Koehler, DO,** David Horowitz, DO*** *Intern, Largo Medical Center, Largo, FL **Dermatology Resident, Third Year, College Medical Center/Western University, Long Beach, CA ***Dermatology Residency Program Director, College Medical Center/Western University, Long Beach, CA Abstract Spiny keratoderma is a rare and likely underreported condition that presents with punctate hyperkeratotic growths localized to the palms and soles. We present two cases of clinically diagnosed spiny keratoderma. Although the lesions were asymptomatic, patients are at risk of an underlying internal malignancy with this condition, so diagnosis is crucial. Neither men were seeking treatment for the lesions when they were discovered, suggesting that this condition may be much more common than reported. Patients with histories of manual labor, increased UV exposure, and non-melanoma skin cancer (NMSC) may also be at higher risk for developing spiny keratoderma.1 The epidemiology, histopathologic features, differential diagnosis, and current treatments for spiny keratoderma are reviewed. Introduction Case 2 enthusiast for his entire life, spending significant Spiny keratoderma is a rare palmoplantar A 67-year-old Caucasian male presented with a time using his hands to maintain and fire his keratoderma that presents with keratotic, pinpoint one-year history of insidiously growing, pinpoint weapons and many hours outside without sun papules on the palms and soles. There are both hyperkeratotic papules projecting from his palms protection. The patient was referred back to his hereditary and acquired forms. When found, bilaterally (Figures 4-5). He presented to the clinic primary care physician for internal evaluation. -
Skin Lesions in Diabetic Patients
Rev Saúde Pública 2005;39(4) 1 www.fsp.usp.br/rsp Skin lesions in diabetic patients N T Foss, D P Polon, M H Takada, M C Foss-Freitas and M C Foss Departamento de Clínica Médica. Faculdade de Medicina de Ribeirão Preto. Universidade de São Paulo. Ribeirão Preto, SP, Brasil Keywords Abstract Skin diseases. Dermatomycoses. Diabetes mellitus. Metabolic control. Objective It is yet unknown the relationship between diabetes and determinants or triggering factors of skin lesions in diabetic patients. The purpose of the present study was to investigate the presence of unreported skin lesions in diabetic patients and their relationship with metabolic control of diabetes. Methods A total of 403 diabetic patients, 31% type 1 and 69% type 2, underwent dermatological examination in an outpatient clinic of a university hospital. The endocrine-metabolic evaluation was carried out by an endocrinologist followed by the dermatological evaluation by a dermatologist. The metabolic control of 136 patients was evaluated using glycated hemoglobin. Results High number of dermophytosis (82.6%) followed by different types of skin lesions such as acne and actinic degeneration (66.7%), pyoderma (5%), cutaneous tumors (3%) and necrobiosis lipoidic (1%) were found. Among the most common skin lesions in diabetic patients, confirmed by histopathology, there were seen necrobiosis lipoidic (2 cases, 0.4%), diabetic dermopathy (5 cases, 1.2%) and foot ulcerations (3 cases, 0.7%). Glycated hemoglobin was 7.2% in both type 1 and 2 patients with adequate metabolic control and 11.9% and 12.7% in type 1 and 2 diabetic patients, respectively, with inadequate metabolic controls. -
Palmoplantar Keratoderma with Progressive Gingivitis and Recurrent Pyodermas
Palmoplantar Keratoderma With Progressive Gingivitis and Recurrent Pyodermas Tyler A. Moss, DO; Anne P. Spillane, MD; Sam F. Almquist, MD; Patrick E. McCleskey, MD; Oliver J. Wisco, DO Practice Points Papillon-Lefèvre syndrome (PLS) is an autosomal-recessive inherited transgredient palmoplantar kerato- derma (PPK) that is associated with gingivitis and recurrent pyodermas. The symptoms associated with PLS are thought to be due to cathepsin C gene, CTSC, mutations. CTSC is expressed in epithelial regions commonly affected by PLS and also plays a role in the activation of immune and inflammatory responses. Papillon-Lefèvre syndrome must be differentiated from other conditions causing PPK, such as Haim-Munk syndrome, Greither syndrome, mal de Meleda, Clouston syndrome, Vohwinkel syndrome, and Olmsted syndrome. Treatment of PLS includesCUTIS keratolytics such as urea and/or salicylic acid comb ined with oral retinoids. Active gingivitis may be treated with combined use of amoxicillin and metronidazole. Papillon-Lefèvre syndrome (PLS) is a rare inher- Case Report ited palmoplantar keratoderma (PPK) that is asso- A 30-year-old woman presented to the dermatology ciated with progressive gingivitis and recurrent clinic with erythematous hyperkeratotic plaques on pyodermas.Do We present a caseNot exhibiting classic the palmsCopy and soles. The plaques extended onto features of this autosomal-recessive condition the dorsal aspects of the fingers, toes, hands, and and review the current understanding of its patho- feet (Figures 1 and 2). The patient had psoriasiform physiology, diagnosis, and treatment. Addition- plaques on the extensor surfaces of the knees and ally, a review of pertinent transgredient PPKs is elbows (Figure 3) along with a history of slow- undertaken, with key and distinguishing features progressing gingivitis and periodontal disease that of each syndrome highlighted. -
The Prevalence of Cutaneous Manifestations in Young Patients with Type 1 Diabetes
Clinical Care/Education/Nutrition/Psychosocial Research ORIGINAL ARTICLE The Prevalence of Cutaneous Manifestations in Young Patients With Type 1 Diabetes 1 2 MILOSˇ D. PAVLOVIC´, MD, PHD SLAANA TODOROVIC´, MD tions, such as neuropathic foot ulcers; 2 4 TATJANA MILENKOVIC´, MD ZORANA ÐAKOVIC´, MD and 4) skin reactions to diabetes treat- 1 1 MIROSLAV DINIC´, MD RADOSˇ D. ZECEVIˇ , MD, PHD ment (1). 1 5 MILAN MISOVIˇ C´, MD RADOJE DODER, MD, PHD 3 To understand the development of DRAGANA DAKOVIC´, DS skin lesions and their relationship to dia- betes complications, a useful approach would be a long-term follow-up of type 1 OBJECTIVE — The aim of the study was to assess the prevalence of cutaneous disorders and diabetic patients and/or surveys of cuta- their relation to disease duration, metabolic control, and microvascular complications in chil- neous disorders in younger type 1 dia- dren and adolescents with type 1 diabetes. betic subjects. Available data suggest that skin dryness and scleroderma-like RESEARCH DESIGN AND METHODS — The presence and frequency of skin mani- festations were examined and compared in 212 unselected type 1 diabetic patients (aged 2–22 changes of the hand represent the most years, diabetes duration 1–15 years) and 196 healthy sex- and age-matched control subjects. common cutaneous manifestations of Logistic regression was used to analyze the relation of cutaneous disorders with diabetes dura- type 1 diabetes seen in up to 49% of the tion, glycemic control, and microvascular complications. patients (3). They are interrelated and also related to diabetes duration. Timing RESULTS — One hundred forty-two (68%) type 1 diabetic patients had at least one cutaneous of appearance of various cutaneous le- disorder vs. -
Pediatric and Adolescent Dermatology
Pediatric and adolescent dermatology Management and referral guidelines ICD-10 guide • Acne: L70.0 acne vulgaris; L70.1 acne conglobata; • Molluscum contagiosum: B08.1 L70.4 infantile acne; L70.5 acne excoriae; L70.8 • Nevi (moles): Start with D22 and rest depends other acne; or L70.9 acne unspecified on site • Alopecia areata: L63 alopecia; L63.0 alopecia • Onychomycosis (nail fungus): B35.1 (capitis) totalis; L63.1 alopecia universalis; L63.8 other alopecia areata; or L63.9 alopecia areata • Psoriasis: L40.0 plaque; L40.1 generalized unspecified pustular psoriasis; L40.3 palmoplantar pustulosis; L40.4 guttate; L40.54 psoriatic juvenile • Atopic dermatitis (eczema): L20.82 flexural; arthropathy; L40.8 other psoriasis; or L40.9 L20.83 infantile; L20.89 other atopic dermatitis; or psoriasis unspecified L20.9 atopic dermatitis unspecified • Scabies: B86 • Hemangioma of infancy: D18 hemangioma and lymphangioma any site; D18.0 hemangioma; • Seborrheic dermatitis: L21.0 capitis; L21.1 infantile; D18.00 hemangioma unspecified site; D18.01 L21.8 other seborrheic dermatitis; or L21.9 hemangioma of skin and subcutaneous tissue; seborrheic dermatitis unspecified D18.02 hemangioma of intracranial structures; • Tinea capitis: B35.0 D18.03 hemangioma of intraabdominal structures; or D18.09 hemangioma of other sites • Tinea versicolor: B36.0 • Hyperhidrosis: R61 generalized hyperhidrosis; • Vitiligo: L80 L74.5 focal hyperhidrosis; L74.51 primary focal • Warts: B07.0 verruca plantaris; B07.8 verruca hyperhidrosis, rest depends on site; L74.52 vulgaris (common warts); B07.9 viral wart secondary focal hyperhidrosis unspecified; or A63.0 anogenital warts • Keratosis pilaris: L85.8 other specified epidermal thickening 1 Acne Treatment basics • Tretinoin 0.025% or 0.05% cream • Education: Medications often take weeks to work AND and the patient’s skin may get “worse” (dry and red) • Clindamycin-benzoyl peroxide 1%-5% gel in the before it gets better. -
EXTENDED CARRIER SCREENING Peace of Mind for Planned Pregnancies
Focusing on Personalised Medicine EXTENDED CARRIER SCREENING Peace of Mind for Planned Pregnancies Extended carrier screening is an important tool for prospective parents to help them determine their risk of having a child affected with a heritable disease. In many cases, parents aren’t aware they are carriers and have no family history due to the rarity of some diseases in the general population. What is covered by the screening? Genomics For Life offers a comprehensive Extended Carrier Screening test, providing prospective parents with the information they require when planning their pregnancy. Extended Carrier Screening has been shown to detect carriers who would not have been considered candidates for traditional risk- based screening. With a simple mouth swab collection, we are able to test for over 419 genes associated with inherited diseases, including Fragile X Syndrome, Cystic Fibrosis and Spinal Muscular Atrophy. The assay has been developed in conjunction with clinical molecular geneticists, and includes genes listed in the NIH Genetic Test Registry. For a list of genes and disorders covered, please see the reverse of this brochure. If your gene of interest is not covered on our Extended Carrier Screening panel, please contact our friendly team to assist you in finding a gene test panel that suits your needs. Why have Extended Carrier Screening? Extended Carrier Screening prior to pregnancy enables couples to learn about their reproductive risk and consider a complete range of reproductive options, including whether or not to become pregnant, whether to use advanced reproductive technologies, such as preimplantation genetic diagnosis, or to use donor gametes. -
White Lesions of the Oral Cavity and Derive a Differential Diagnosis Four for Various White Lesions
2014 self-study course four course The Ohio State University College of Dentistry is a recognized provider for ADA, CERP, and AGD Fellowship, Mastership and Maintenance credit. ADA CERP is a service of the American Dental Association to assist dental professionals in identifying quality providers of continuing dental education. ADA CERP does not approve or endorse individual courses or instructors, nor does it imply acceptance of credit hours by boards of dentistry. Concerns or complaints about a CE provider may be directed to the provider or to ADA CERP at www.ada.org/goto/cerp. The Ohio State University College of Dentistry is approved by the Ohio State Dental Board as a permanent sponsor of continuing dental education ABOUT this FREQUENTLY asked COURSE… QUESTIONS… Q: Who can earn FREE CE credits? . READ the MATERIALS. Read and review the course materials. A: EVERYONE - All dental professionals in your office may earn free CE contact . COMPLETE the TEST. Answer the credits. Each person must read the eight question test. A total of 6/8 course materials and submit an questions must be answered correctly online answer form independently. for credit. us . SUBMIT the ANSWER FORM Q: What if I did not receive a ONLINE. You MUST submit your confirmation ID? answers ONLINE at: A: Once you have fully completed your p h o n e http://dent.osu.edu/sterilization/ce answer form and click “submit” you will be directed to a page with a . RECORD or PRINT THE 614-292-6737 unique confirmation ID. CONFIRMATION ID This unique ID is displayed upon successful submission Q: Where can I find my SMS number? of your answer form. -
Download PDF (Inglês)
Revista6Vol89ingles_Layout 1 10/10/14 11:08 AM Página 1003 WHAT IS YOUR DIAGNOSIS? 1003 s Case for diagnosis* João Roberto Antonio1 Larissa Cannizza Pacheco de Lucca1 Mariana Perez Borim1 Natália Cristina Pires Rossi1 Guilherme Bueno de Oliveira1 DOI: http://dx.doi.org/10.1590/abd1806-4841.20143156 CASE REPORT A 60-year-old woman reports a 5-year history of violaceous and intensely pruritic lesions on the dorsum and scalp, associated with a 2-year history of hair loss. She also reports decreased hair growth in the axillary and inguinal regions in the same period. Dermatological examination shows small, scaly, erythematous-violaceous, flat papules on the dorsal region; multifocal scarring alopecia areas, with smooth, bright and atrophic surface; discrete hair rarefaction in the axillary and inguinal regions; presence of longitu- FIGURE 2: dinal grooves and some depressions on the surface of Perifollicular the nail plate; no oral lesions (Figures 1 and 2). The erythema with desquamation at histopathology of the dorsal lesion is shown in figure the vertex of the 3A and that of the scalp is shown in figure 3B. scalp; cicatricial The treatment was performed using high- alopecia and potency corticoids and resulted, after three months, in smooth, bright and atrophic surface an improvement of pruritus and a slight lightening of the lesions. A FIGURE 1: B Cutaneous, erythematous- FIGURE 3: A. HE 200x. Interface dermatitis with lichenoid pattern purpuric lesions associated with dermo-epidermic detachment and lymphocytic on the infiltrate in band-like pattern in the upper dermis. B. HE 200x. dorsal region Detail of partially destroyed follicle, with perifollicular fibrosis and perivascular lymphocytic infiltrate Received on 19.09.2013. -
How to Deal with Distressingly Dry Skin? — by Melissa Raue, PA-C How to Deal with Distressingly Dry Skin?
How To Deal With Distressingly Dry Skin? — By Melissa Raue, PA-C How To Deal With Distressingly Dry Skin? During the winter, some people’s skin often gets so dry that it flakes, cracks, or even bleeds. What can they do? Should they wash more or less often? Apply more moisturizer? Here are several preventive measures that will keep you comfortable and out of the doctor’s office. 1 Bathe daily. A 5-10 minute warm bath or shower adds moisture to the skin. Longer or hotter showers remove moisture and wash away natural protective oils. Close the 2 bathroom door. When taking that bath or shower, keep the door to the bathroom shut. This keeps the much-needed humidity in the room. Use a mild cleanser. 3 Deodorant bars, fragrance in soaps, and products containing alcohol strip natural oils from the skin, which dries the skin. Gently pat the skin dry. 4 Rubbing hard removes moisture and irritates sensitive dry skin. 5 Apply moisturizer within 3 minutes of getting out of the bath or shower. Many people think that moisturizer adds moisture to the skin. This is incorrect! Moisturizer traps existing water in the skin, preventing the water from evaporating. Moisturize 6 again if you need to! If skin is noticeably dry and uncomfortable, moisturizing more frequently throughout the day can help the skin heal. And will help prevent dry skin from returning. Ointments and creams will be more effective than lotions. Choose your moisturizer 7 by ingredients, not price. Moisturizer does not need to be expensive to be effective. -
Harlequin Ichthyosis
orphananesthesia Anaesthesia recommendations for patients suffering from Harlequin ichthyosis Disease name: Harlequin ichthyosis ICD 10: Q80.4 Synonyms: Harlequin baby, ichthyosis congenita, Ichthyosis fetalis, keratosis diffusa fetalis, Harlequin fetus, Ichthyosis congenita gravior Disease summary: Harlequin ichthyosis (HI) is an autosomal recessive congenital ichthyosis. HI is an extremely rare and most severe form of ichthyosis. The condition is caused by mutation of the ABCA12 gene resulting in impaired lipid transport in the outermost layer of the skin, the epidermis. During the neontatal period, harlequin ichthyosis manifests phenotypically as dramatic large polygonal plate-like scaling of the skin that cracks and can slough, revealing the underlying diffusely bright red skin. These thick skin plates can pull and distort facial features. The tightness of the skin can also pull on the eyes and mouth resulting in difficulties with closing these structures. The tightness also causes the eyes and the mouth to turn inside out resulting in ectropion and eclabium. Other features include hypoplasia of the fingers, malformation of the ears and nose, and alopecia. Affected neonates often do not survive and mortality is commonly attributed to respiratory failure and/or sepsis. Clinical data obtained from 45 HI patients revealed 25 survivors and 20 deaths with an overall survival rate of only 56%. The ages of survivors ranged from 10 months to 25 years and death usually occurred in the first 3 months. HI infants need to be cared for in a neonatal intensive care unit immediately after birth. Several harlequin neonates have survived. They tend to have severe erythroderma and fine scaling, even with optimal management. -
In Dermatology Visit with Me to Discuss
From time to time new treatments surface for any medical field, and the last couple of years have seen new treatments emerge, or new applications for familiar treatments. I wanted to summarize some of these New Therapies widely available remedies and encourage you to schedule a in Dermatology visit with me to discuss. Written by Board Certified Dermatologist James W. Young, DO, FAOCD Nicotinamide a significant reduction in melanoma in Antioxidants Nicotinamide (niacinamide) is a form high risk skin cancer patients at doses Green tea, pomegranate, delphinidin of vitamin B3. The deficiency of vitamin more than 600 and less than 4,000 IU and fisetin are all under current study for daily. B3 causes pellagra, a condition marked either oral or topical use in the reduction by 4D’s – (photo) Dermatitis, Dementia, Polypodium Leucotomos of the incidence of skin cancer, psoriasis Diarrhea and (if left untreated) Death. and other inflammatory disorders. I’ll be Polypodium leucotomos is a Central This deficiency is rare in developed sure to keep patients updated. countries, but is occasionally seen America fern that is available in several in alcoholism, dieting restrictions, or forms, most widely as Fernblock What Are My Own Thoughts? malabsorption syndromes. Nicotinamide (Amazon) or Heliocare (Walgreen’s and I take Vitamin D 1,000 IU and Heliocare does not cause the adverse effects of Amazon) and others. It is an antioxidant personally. Based on new research, I Nicotinic acid and is safe at doses up to that reduces free oxygen radicals and have also added Nicotinamide which 3,000mg daily. may reduce inflammation in eczema, dementia, sunburn, psoriasis, and vitiligo. -
A Review of the Evidence for and Against a Role for Mast Cells in Cutaneous Scarring and Fibrosis
International Journal of Molecular Sciences Review A Review of the Evidence for and against a Role for Mast Cells in Cutaneous Scarring and Fibrosis Traci A. Wilgus 1,*, Sara Ud-Din 2 and Ardeshir Bayat 2,3 1 Department of Pathology, Ohio State University, Columbus, OH 43210, USA 2 Centre for Dermatology Research, NIHR Manchester Biomedical Research Centre, Plastic and Reconstructive Surgery Research, University of Manchester, Manchester M13 9PT, UK; [email protected] (S.U.-D.); [email protected] (A.B.) 3 MRC-SA Wound Healing Unit, Division of Dermatology, University of Cape Town, Observatory, Cape Town 7945, South Africa * Correspondence: [email protected]; Tel.: +1-614-366-8526 Received: 1 October 2020; Accepted: 12 December 2020; Published: 18 December 2020 Abstract: Scars are generated in mature skin as a result of the normal repair process, but the replacement of normal tissue with scar tissue can lead to biomechanical and functional deficiencies in the skin as well as psychological and social issues for patients that negatively affect quality of life. Abnormal scars, such as hypertrophic scars and keloids, and cutaneous fibrosis that develops in diseases such as systemic sclerosis and graft-versus-host disease can be even more challenging for patients. There is a large body of literature suggesting that inflammation promotes the deposition of scar tissue by fibroblasts. Mast cells represent one inflammatory cell type in particular that has been implicated in skin scarring and fibrosis. Most published studies in this area support a pro-fibrotic role for mast cells in the skin, as many mast cell-derived mediators stimulate fibroblast activity and studies generally indicate higher numbers of mast cells and/or mast cell activation in scars and fibrotic skin.