DOCSLIB.ORG

Worsening Indurated Pink Translucent Nodules and Severe Hyperkeratosis of the Lower ExtremiEs: a Case of ElephanAsic PreBial Myxedema

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Worsening Indurated Pink Translucent Nodules and Severe Hyperkeratosis of the Lower Extremi�Es: a Case of Elephan�Asic Pre�Bial Myxedema Worsening indurated pink translucent nodules and severe hyperkeratosis of the lower extremies: A Case of Elephanasic Prebial Myxedema. Jason Solway, DO, Oben Ojong, DO, John Moesch, DO, Michael R. Heaphy, Jr, MD, Mahew Mahoney, MD. Largo Medical Center, Largo, Florida LEARNING OBJECTIVES FIGURES DISCUSSION • Recognizing elephan9asis pre9bial myxedema (PTM) • EPIDEMIOLOGY: Elephantiasic pretibial myxedema (PTM) is the 1 2 3 most severe variant of non-filarial myxedema occurring in only 1% • Understanding pathophysiology of elephan9asis PTM. of patients with Grave’s disease1. • Creang treatment plan for paent suffering from • PATHOPHYSIOLOGY: It is theorized that T-cells stimulate elephan9asis PTM. shared antigens between the thyroid and pretibial tissue and release TGF-B and IL1-alpha that stimulate fibroblasts to produce • Ddx for elephan9asis PTM. and deposit mucin-like glycosaminoglycans in tissue. The pretibial fibroblasts may be more sensitive to this stimulation2. • The Pretibial area is favored secondary to hydrostatic forces, decreased lymphatic cytokine clearance and dependent position3. • CLIINICAL: Grossly enlarged and disfigured appendage, usually CASE PRESENTATION with functional restriction and cosmetic concerns for the patient. Cutaneous changes include non-pitting edema of lower extremities that does not resolve with elevation. The initial cobblestone • A 61 year old white woman presented with bilateral appearance later becomes mossy and verrucous. Because hair HPI: follicles are prominent, it produces the characteristic peau lower extremity derma99s, swelling and skin thickening that d’orange appearance 3,6. began 5 years ago; shortly before she was diagnosed with Figures 1-3: Clinical images of indurated 1-2cm thick violaceoous plaques with • Ulceration and bacterial seeding with recurrent cellulitis or fungal Graves disease (Figures 1-3). interspersed pink translucent nodules; associated deep fissuring and non pitting edema. infections are common, with patients complaining of pain or 6 Figure 3: Active serous drainage with overlying yellow-white crust on pretibial area. pruritus . • Large amounts of mucinous deposition are seen in • Paent’s symptoms progressively worsened post PATHOLOGY: the reticular dermis. There is a lack of angioplasia and thyroidectomy and achievement of euthyroid state with hemosiderin. Sparse lymphocytic deposition in perivascular levothyroxine. Previous diagnoses included cellulis and 4 5 6 spaces and moderately increased mast cell deposition are seen3. lymphedema treated with mulple failed aempts of oral • The number of collagen fibers is reduced with increased edema, 4-5 anbiocs. No family history of related condions. No and occasional acanthosis, hyperkeratosis, and papilomatosis . • TREATMENT: Cosmesis and restoration of function are the previous biopsy was obtained. primary aims in ENV treatment3. • Therapeutic modalities like complete decompressive • PHYSICAL EXAM: Indurated, 1-2cm thick violaceous physiotherapy, topical corticosteroids with occlusive dressing, plaques with interspersed pink translucent nodules; psoriatane, octreotide and weight reduction have proven beneficial7. associated deep fissures with ac9ve serous drainage and • Tobacco cessation is imperative as it has been linked to overlying yellow-white crust on bilateral pre9bial areas, autoimmune manifestations of Grave’s disease7. ankles and dorsal feet. (Figures 1-3) Plantar surface was covered by thick scale. Figures 4-5: H&E of a 6mm punch biospy on the right shin and right dorsal foot. REFERENCES • Other physical exam findings included proptosis, Hyperkeratosis , papillomatosis, and acanthosis of the epidermis. Large quanes of mucin are exophthalmos and surgical scar on the anterior neck. deposited within the re9cular dermis, causing collagen bundles to separate and the dermis to thicken. 1. Humbert P, Dupond JL, Carbillet JP. Pretibial myxedema: an overlapping clinical manifestation of autoimmune thyroid disease. Am J Med. 1987;83:1170-1171. A grenz zone of normal collagen is also observed. 2. Korducki JM, Loftus SJ, Bahn RS. Stimulation of glycosaminoglycan production acids in localized in cultured human retroocular fibroblasts. Invest Ophthalmol Vis Sci 1992 59 (3): 409-16 • DX: Aer obtaining informed consent 2 biopsy specimens Figure 6: Colloidal iron stain demonstrating an abundance of mucin in the throughout May; 33 (6): 2037-42 were obtained for hematoxyllin-eosin and other special 3. Fatourechi V. Pretibial myxedema: pathophysiology and treatment options. American Journal of the dermis. Clinical Dermatology. 2005 6(5):295-309. stains (Figures 3-6). 4. Schwartz KM, Fatourechi V, Ahmed DD, et al. Dermopathy of Graves’ disease (pretibial myxedema): long-term outcome. J Clin Endocrinol Metab 2002 Feb; 87 (2): 438-46. 5. Sanders LJ, Slomsky JM, Burger-Caplan C. Elephantiasis nostras: an eight-year observation of progressive nonfilarial elephantiasis of the lower extremity. Cutis. 1988 Nov; 42(5):406-11. • Elephanasis pre bial myxedema was diagnosed based on 6. Ruocco E, Puca RV, Brunetti G, Schwartz RA, Ruocco V. Lymphedematous areas: privileged sites for tumors, infections, and immune disorders. Int J Dermatol. 2007 Jun; 46(6):662. these clinical and histological findings. 7. Susser WS, Heermans AG, Chapman MS, et al. Elephantiasic pretibial myxedema: a novel treatment for an uncommon disorder. J Am Acad Dermatol 2002 (May); 46 (5): 723-726. .
Load more

Recommended publications
  • 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.
    [Show full text]
  • An Unusual Course in Bullous Morphea
    Case Report An Unusual Course in Bullous Morphea İlknur Kıvanç Altunay, MD, Hilal Kaya Erdoğan*, MD, Nurhan Döner, MD, Damlanur Sakız,1 MD. Address: Dermatology and 1Pathology Departments, Şişli Etfal Training and Research Hospital, Istanbul, 34377, Turkey. * Corresponding Author: Dr. Hilal Kaya Erdoğan, Şisli Etfal Training and Research Hospital. Istanbul, 34377, Turkey. E-mail: [email protected] Published: J Turk Acad Dermatol 2010; 4 (4): 04401c This article is available from: http://www.jtad.org/2010/4/jtad04401c.pdf Key Words: bullous morphea, drug reaction Abstract Observations: We report a 75-year-old woman with bullous morphea characterized by disseminated erythemato-pigmentous plaques and a few blisters on some morphea plaques at the beginning of first visit. While she was under narrow band UV therapy, she discontinued the treatment and refused to have any more after 13 sessions. One month later, she reapplied with extensive bullae and facial edema with severe itching. We learned that she had taken naproxen sodium one a day for two days ten days ago. Bullous drug reaction was diagnosed and systemic cortisone was started. She was in remission after fifteen days. The patient had very different clinical picture on her second visit with extensive, large and cadaverous bullae, facial eryhtema and edema. It seems to be a bullous drug reaction based on bullous morphea. However, it remains a mystery whether this clinical presentation is a peculiar drug reaction or is really a mere exacerbation of existed bullous morphea. Introduction noprost eye drop and tolterodine. These medicati- ons had been used for over a year. Her family his- Bullae formation in lesions of morphea is an tory was unremarkable.
    [Show full text]
  • Oral Frictional Hyperkeratosis (FK)
    Patient information Oral frictional hyperkeratosis (FK) What is oral frictional hyperkeratosis? Hyperkeratinisation - excessive growth of stubbornly attached keratin (a fibrous protein produced by the body) - may happen for a number of reasons, and may be genetic (runs in the family), physiological e.g. due to friction from a sharp tooth, pre-malignant (pre-cancerous) and malignant (cancerous). The change may result from chemical, heat or physical irritants. Friction (the constant rubbing of two surfaces against each other) in the mouth may result in benign (non-cancerous) white patches. Various names have been used to describe particular examples of FK, including those resulting from excessive tooth-brushing force (toothbrush keratosis), the constant rubbing of the tongue against the teeth (tongue thrust keratosis), and that produced by the habit of chronic cheek or lip biting (cheek or lip bite keratosis). What are the signs and symptoms of FK? Most patients with FK are free of symptoms. A patient may notice a thickening of an area of skin in the mouth, or FK may be discovered by accident during a routine oral examination. What are the causes of FK? The white patches of FK that develop in the mouth are formed in the same way that calluses form on the skin of hands and feet. The most common causes are long term tissue chewing (biting the inside of the cheek or lips), ill-fitting dentures, jagged teeth, poorly adapted dental fillings or caps, and constant chewing on jaws that have no teeth. The constant irritation encourages the growth of keratin, giving the skin involved a different thickness and colour.
    [Show full text]
  • Investigating Biomarkers of Keloid Scarring
    Investigating Biomarkers of Keloid Scarring Zoe Drymoussi 2015 A thesis presented for the degree of Doctor of Philosophy Centre for Cutaneous Research, Blizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary, University of London 1 Declaration I, Zoe Drymoussi, declare that the work presented in this thesis is my own and has not been submitted in any form for another degree or diploma at any university or other institute of tertiary education. Information derived from the published or unpublished work of others has been acknowledged in the text and a list of references is given. Zoe Drymoussi, PhD Student 1st August 2015 2 Abstract Keloids are fibroproliferative scars that form in response to abnormal healing processes. The extracellular matrix (ECM) remodelling of the dermis in the maturation phase of normal wound healing is insufficient in keloids, leading to excessive ECM proteins being deposited in the granulation tissue. Keloid scars are unique to humans, and show increased prevalence in darker skin types. Current treatments rarely lead to permanent regression, and despite decades of study, the key molecular processes responsible for keloid scarring are still largely elusive. The research presented in this thesis aims to investigate markers of keloid scars, and to examine the impact of both the dermis and epidermis in keloid pathogenesis. Histological examination of the keloid scars showed a thickened epidermis and densely collagenous dermis, both of which demonstrated a higher level of cell proliferation and myofibroblast expression, as compared to normal skin. Differences between the central and marginal regions of the scars were also noted.
    [Show full text]
  • Fundamentals of Dermatology Describing Rashes and Lesions
    Dermatology for the Non-Dermatologist May 30 – June 3, 2018 - 1 - Fundamentals of Dermatology Describing Rashes and Lesions History remains ESSENTIAL to establish diagnosis – duration, treatments, prior history of skin conditions, drug use, systemic illness, etc., etc. Historical characteristics of lesions and rashes are also key elements of the description. Painful vs. painless? Pruritic? Burning sensation? Key descriptive elements – 1- definition and morphology of the lesion, 2- location and the extent of the disease. DEFINITIONS: Atrophy: Thinning of the epidermis and/or dermis causing a shiny appearance or fine wrinkling and/or depression of the skin (common causes: steroids, sudden weight gain, “stretch marks”) Bulla: Circumscribed superficial collection of fluid below or within the epidermis > 5mm (if <5mm vesicle), may be formed by the coalescence of vesicles (blister) Burrow: A linear, “threadlike” elevation of the skin, typically a few millimeters long. (scabies) Comedo: A plugged sebaceous follicle, such as closed (whitehead) & open comedones (blackhead) in acne Crust: Dried residue of serum, blood or pus (scab) Cyst: A circumscribed, usually slightly compressible, round, walled lesion, below the epidermis, may be filled with fluid or semi-solid material (sebaceous cyst, cystic acne) Dermatitis: nonspecific term for inflammation of the skin (many possible causes); may be a specific condition, e.g. atopic dermatitis Eczema: a generic term for acute or chronic inflammatory conditions of the skin. Typically appears erythematous,
    [Show full text]
  • “Relationship Between Smoking and Plantar Callus
    C HA PTER 3 8 RELATIONSHIP BETWEEN SMOKING AND PLANTAR CALLUS FORMATION OF THE FOOT Thomas J. Merrill, DPM Virginio Vena, DPM Luis A. Rodriguez, DPM Despite the decline in cigarette smoking in the last few smoke can remain in the body (6). The tobacco smoke years as reported by the Centers for Disease Control and components absorbed from the lungs reach the heart Prevention, and the well known health risks in cardiovascular immediately. Smoking increases the heart rate, arterial blood and pulmonary diseases, millions of Americans continue to pressure, and cardiac output. There is a 42% reduction in the smoke cigarettes. It has been proven by both experimental digital blood flow after a single cigarette (7, 8). Nicotine has and clinical observation that cigarettes impair bone and a direct cutaneous vasoconstrictive effect and is the principle wound healing. The purpose of this article is to review the vasoactive component in the gas phase of cigarette smoke. chemical components of cigarette smoke and its relationship It is an odorless, colorless, and poisonous alkaloid that when with plantar callus formation. inhaled or injected, can activate the adrenal catecholamines Increased plantar callus formation with patients who from the adrenergic nerve endings and from the adrenal smoke cigarettes seems to be a common problem. There are medulla, which cause vasoconstriction of vessels especially in approximately 46.6 million smokers in the US. There was a the extremities. Nicotine also induces the sympathetic decline during 1997-2003 in the youth population but nervous system, which results in the release of epinephrine during the last years the rates are stable (1).
    [Show full text]
  • Basal Cell Papilloma, Senile Keratosis, Seborrheic Wart)
    ATLAS OF HEAD AND NECK PATHOLOGY SEBORRHEIC KERATOSIS SEBORRHEIC KERATOSIS (BASAL CELL PAPILLOMA, SENILE KERATOSIS, SEBORRHEIC WART) These lesions, often multiple, and occurring for the most part after 50 years of age, are most common on the face and upper body. They are brownish to black, slightly greasy, slightly raised, with either a smooth or mildly verrucous surface and a “stuck-on” appearance. They measure from a few millimeters to several centimeters in diameter. Microscopically, there is variance in appearance but all types show hyperkerato- sis, acanthosis (thickening of the epidermis) and a papillary formation sharply demar- cated from the adjacent epidermis. Generally a straight line drawn from one edge of the lesion to the other will pass just under the deeper part of the tumor. Horny invaginations from the epidermis appear on cross-section as pseudo- horn cysts and there are also true horn cysts. Both of these cysts show complete keratinization, concentrically arranged, and only a thin granulosal cell layer. Melanin is prevalent in many tumors and accounts for the dark appearance as seen clinically. Both squamous and basal (“basaloid”) cells are seen in this lesion and they are ar- ranged in sheets. In some types of seborrheic keratoses there are interwoven tracts of basal cells and in others the basal cells are in nests. Intercellular bridges are common. Seborrheic keratosis, showing how the tumor tends to have a straight edge along its deep margin. Also seen are acantho- sis (large arrow), papillary projections (triangles), and hyperkeratosis (small arrows). Several cysts are present with keratin concentrically arranged. Most of the epithelial cells here are dark and, having the appearance of epidermoid basal cells, are called basaloid cells.
    [Show full text]
  • Seborrheic Keratosis
    Benign Epidermal and Dermal Tumors REAGAN ANDERSON, DO- PROGRAM DIRECTOR, COLORADO DERMATOLOGY INSTITUTE, RVU PGY3 RESIDENTS- JONATHAN BIELFIELD, GEORGE BRANT PGY2 RESIDENT- MICHELLE ELWAY Seborrheic Keratosis Common benign growth seen after third/fourth decade of life Ubiquitous among older individuals Tan to black, macular, papular, or verrucous lesion Occur everywhere except palms, soles, and mucous membranes Can simulate melanocytic neoplasms Pathogenesis: Sun exposure- Australian study found higher incidence in the head/neck Alteration in distribution of epidermal growth factors Somatic activating mutations in fibroblast growth factor receptor and phosphoinositide-3-kinase Seborrheic Keratosis Sign of Leser-Trelat: Rare cutaneous marker of internal malignancy • Gastric/colonic adenocarcinoma, breast carcinoma, and lymphoma m/c • Abrupt increase in number/size of SKs that can occur before, during, or after an internal malignancy is detected • 40% pruritus • M/C location is the back • Malignant acanthosis nigricans may also appear in 20% of patients • Should resolve when primary tumor is treated, and reappear with recurrence/mets Seborrheic Keratosis 6 Histologic types Acanthotic Hyperkeratotic Reticulated Irritated Clonal Melanoacanthoma Borst-Jadassohn phenomenon Well-demarcated nests of keratinocytes within the epidermis Seborrheic Keratoses Treatment Reassurance Irritated SKs (itching, catching on clothes, inflamed) Cryotherapy, curettage, shave excision Pulsed CO2, erbium:YAG lasers Electrodessication Flegel
    [Show full text]
  • Primary Localized Cutaneous Amyloidosis in Patients with Scleroderma
    326 Letters to the Editor Primary Localized Cutaneous Amyloidosis in Patients with Scleroderma Nobuyuki Kikuchi, Erika Sakai, Akiko Nishibu, Mikio Ohtsuka and Toshiyuki Yamamoto Department of Dermatology, Fukushima Medical University, Fukushima 960-1295, Japan. E-mail: [email protected] Accepted February 4, 2010. Primary localized cutaneous amyloidosis (PLCA) is a Case 2. A 62-year-old man was referred to our department with relatively rare condition characterized by amyloid de- skin stiffness and pigmentation of both forearms. He stated that hyperpigmentation with itching had occurred one year previously, position exclusively in the dermis without involving the and that skin sclerosis had been present for more than 6 months. internal organs. Clinically, papular, macular and tumefac- He was a builder and had been engaged in construction work, tive forms are presented. Although PLCA may sometimes tiling roofs, and had used organic solvents containing silicon ad- overlap with collagen vascular diseases, association with hesives. Physical examination revealed that his fingers were pale scleroderma is rare. We report here two cases of PLCA and oedematous (Fig. 2a), and severe sclerosis with hyperpig- mentation was observed on his forearms, the dorsa of his hands, developing in patients with scleroderma. and his fingers. Neither large nor small pinching was possible. Furthermore, multiple hyperkeratotic whitish papules were loca- lized on the lateral aspects of both forearms (Fig. 2b). Erythema CASE REPORTS and pigmentation was also seen on his abdomen and back, but Case 1. A 70-year-old Japanese woman was referred to our de- without skin sclerosis. Laboratory examination for anti-nuclear partment with swollen fingers on both hands.
    [Show full text]
  • Comparison Between Dermoscopic and Histopathological Features of Keloids and Hypertrophic Scars Before and After Different Treatment Modalities
    Original article Comparison between Dermoscopic and Histopathological Features of Keloids and Hypertrophic Scars Before and After Different Treatment Modalities Hanan H. Sabry a, Mohebat H. Gouda b, Ahmed H. Abd Elkareem a, Safaa ElBaathy a a Department of Dermatology Abstract and Andrology, Benha faculty of medicine, Benha University, Background: Keloids and hypertrophic scars (HTS) are abnormal b Egypt. Department of wound responses. Lack of knowledge about their basic biology had Pathology, Benha faculty of medicine, Benha University, prevented development of a targeted approach to the treatment of Egypt. keloids and hypertrophic scars. Aim of the work: The study aimed to Correspondence to: Mohebat evaluate the dermoscopic and histopathological features of keloids H. Gouda, Department of Pathology, Benha faculty of and hypertrophic scars before and after different treatment modalities. medicine, Benha Methods: Thirty-two patients with keloids and hypertrophic scars were included in the study for clinical, dermoscopic and Email: histopathological examination. Patients received treatment in form of [email protected] Fractional Co2 laser or 5FU or verapamil. Examination of slides Received: 21 December 2019 stained by H&E and the special stain (Masson trichrome) was Accepted: 12 June 2021 performed; also CD31 immunohistochemistry was performed in all cases. The histopathological examination of slides both HTS and keloid before and after treatment was done. The pattern of collagen fibers was determined by hematoxylin and eosin stained sections and Masson Trichrome stained sections. The pattern and extent of vascularity demonstrated by CD31 immunostaining was evaluated. Results: Vancouver scar scale showed significant improvement in all patients. histopathological improvement (the collagen fibers detected by Masson trichrome in the upper dermis of HTS cases become thinner and the MVD detected by CD31 IHC staining showed increased vascularity after treatment).
    [Show full text]
  • Morphea-Like Reaction to D-Penicillamine Therapy
    Ann Rheum Dis: first published as 10.1136/ard.40.1.42 on 1 February 1981. Downloaded from Annals of the Rheumatic Diseases, 1981, 40, 42-44 Morphea-like reaction to D-penicillamine therapy R. M. BERNSTEIN,'* M. ANN HALL,1 AND B. E. GOSTELOW2 From the 'Juvenile Rheumatism Unit, Canadian Red Cross Memorial Hospital, Taplow, and the 2Department ofHistopathology, Northwick Park Hospital, Harrow SuMMARY We report the case of a 48-year-old woman who developed morphea-like plaques after 1 year of treatment with D-penicillamine at 250 mg daily for a seronegative erosive arthritis of rheu- matoid type. The rash began as several red itchy patches on the trunk; these became thickened and shiny over about 3 months. The histological appearance was of increased dermal fibrosis with an inflammatory infiltrate round dermal capillaries. However, epidermal changes were not typical of morphea. New lesions ceased to appear within a few months of stopping penicillamine, and by 1 year all the plaques were pale and symptomless. Late skin reactions to D-penicillamine are well linear deposit of immunoglobulin in the basement known as a reason for withdrawing therapy. Some membrane. However, discoid lupus has been des- lesions such as increased friability, cutis laxa, and cribed only twice.8 elastosis perforans serpiginosa are probably dose- Here we describe a patient who developed skin related1 and may be due to the lathyrogenic effect lesions clinically suggestive of morphea (cutaneouscopyright. of D-penicillamine inhibiting the stabilisation of scleroderma), though the histology raised the cross-links in newly formed collagen.2 Indeed the question of a drug reaction.
    [Show full text]
  • Keratosis Pilaris: a Common Follicular Hyperkeratosis
    PEDIATRIC DERMATOLOGY Series Editor: Camila K. Janniger, MD Keratosis Pilaris: A Common Follicular Hyperkeratosis Sharon Hwang, MD; Robert A. Schwartz, MD, MPH Keratosis pilaris (KP) is a common inherited dis- 155 otherwise unaffected patients.2 In the adolescent order of follicular hyperkeratosis. It is character- population, its prevalence is postulated to be at least ized by small, folliculocentric keratotic papules 50%; it is more common in adolescent females than that may have surrounding erythema. The small males, seen in up to 80% of adolescent females.3 papules impart a stippled appearance to the skin The disorder is inherited in an autosomal domi- resembling gooseflesh. The disorder most com- nant fashion with variable penetrance; no specific monly affects the extensor aspects of the upper gene has been identified. In a study of 49 evaluated arms, upper legs, and buttocks. Patients with KP patients, there was a positive family history of KP in usually are asymptomatic, with complaints limited 19 patients (39%), while 27 patients (55%) had no to cosmetic appearance or mild pruritus. When family history of the disorder.4 diagnosing KP, the clinician should be aware that a number of diseases are associated with KP such Clinical Features as keratosis pilaris atrophicans, erythromelanosis The keratotic follicular papules of KP most commonly follicularis faciei et colli, and ichthyosis vulgaris. are grouped on the extensor aspects of the upper arms Treatment options vary, focusing on avoiding skin (Figure), upper legs, and buttocks.4 Other affected dryness, using emollients, and adding keratolytic locations may include the face and the trunk.5 The agents or topical steroids when necessary.
    [Show full text]