We assessed the clinical course of patients after store and forward teledermatology in comparison with conventional consultations. Patients being referred from primary care to dermatology clinics were randomly assigned to teledermatology or a conventional consultation. A total of 392 patients were randomized; 261 patients completed the study and were included in the analysis. Their clinical course was rated on a five-point scale by a panel of three dermatologists, blinded to study assignment, who reviewed serial digital image sets. The clinical course was assessed by comparing images sets between baseline and first clinic visit (if one occurred) and between baseline and nine months. There was no evidence to suggest a difference between the two groups in either clinical course between baseline and nine months post-referral ( P = 0.88) or between baseline and the first dermatology clinic visit ( P = 0.65). Among teledermatology referrals, subsequent presentation for an in-person dermatology clinic visit was significantly correlated with clinical course ( P = 0.023). Store and forward teledermatology did not result in a significant difference in clinical course at either of two post-referral time periods.
Syphilis, a sexually transmitted disease caused by the spirochete Treponema pallidum, can affect nearly every organ system in the body. In particular, skin manifestations of secondary syphilis are common but nonspecific and can be a true masquerader of other skin disorders. Concomitant infection with HIV has been increasing and may cause even more unusual skin presentations. We present a patient with the atypical combination of palmoplantar keratoderma and ocular symptoms that closely resembled reactive arthritis (or Reiter's syndrome). When evaluating patients with HIV infection, clinicians should maintain a high level of suspicion for syphilis to accurately diagnose and treat this curable but potentially fatal disease.
Background: Although several studies have documented an undersupply of dermatologic services in the United States, little is known about the dermatopathology workforce.Objective: Objectives included the following: (1) describe the dermatopathology workforce in the United States; (2) identify characteristics associated with academic dermatopathologists; and (3) explore issues surrounding dermatopathology training.Methods: We conducted a cross-sectional survey of all Fellows of the American Society of Dermatopathology (ASDP) practicing in the United States and its territories.Results: Of 913 ASDP Fellows, 437 (48%) returned a completed questionnaire. Most were male (72%), Caucasian (85%), and had graduated from US/Canadian medical schools (88%). Approximately half (49%) had completed a dermatology residency and a quarter (24%) were in academia. As compared with those in private practice, academic dermatopathologists were more likely to be female (P = .0028), have a medical degree only (P = .0197), and earn $300,000 or less annually (P < .0001). No associations were identified for practice type with either location of medical school (United States/Canada vs other) or year of fellowship graduation (<= 1996 vs >= 1997). Although most respondents were satisfied overall with their training, the most common areas identified as inadequate included: coding/billing (47%), biostatistics (38%), pediatric clinical dermatology (27%), and electron microscopy (27%).Limitations: Moderate response rate and potential recall bias are limitations.Conclusions: This study of the US dermatopathology workforce provides benchmarks for future studies and strategies for workforce planning. (J Am Acad Dermatol 2011;65:1180-5.)
CASE REPORT A 56-year-old man with a past medical history significant for marginal zone lymphoma with plasma cell differentiation and monoclonal immunoglobulin G (IgG) k gammopathy presented after developing slowly enlarging, asymptomatic nodules on his right forearm, bilateral shoulders, and trunk over the past year. Without any attempt at treatment, the patient continued to develop new lesions, most recently on his nose. He denied any associated constitutional symptoms. Diagnosed with lymphoma 4 years earlier, he had received several rounds of chemotherapy. He was initially treated with rituximab, vincristine, cyclophosphamide, and prednisone with improvement of the bone marrow involvement but not of the gammopathy or leukopenia. A trial of etoposide, adriamycin, vincristine, cyclophosphamide, and prednisone resulted in severe toxicity. His most recent treatment had been 1 year before presentation; it consisted of 6 cycles of bortezomib that resulted in reduction of his gammopathy. At the time of his visit, he was considering a peripheral stem cell transplant. Physical examination revealed multiple firm, yellow-orange nodules with telangiectasia (Fig. 1). A 4-cm yellowish-pink nodule with a central crust was present on the right forearm (Fig. 2). A 7-mm crusted yellow nodule was observed on the nasal bridge. Laboratory tests showed pancytopenia (hemoglobin 12.4 g/dL; reference range 13.5–16.5 g/dl, white blood cells, 2.6 3 10/mL; reference range 4.5–10.03 10/mL, platelet count, 973 10/mL; reference range 150– 450 3 10/mL) with normal liver and renal function. Serum protein electrophoresis revealed a monoclonal IgG k gammopathy (monoclonal IgG k, 13.8 g/L; reference range 2.4–4.9 g/L). A skin biopsy of the lesion on the right shoulder was performed (Figs. 3 and 4).
Seelhammer, Troy BA*; Seelhammer, Todd BA*; Lilly, Kia MD*; Kaye, Valda N MD*†; Crutchfield, Charles E III MD*; Suwattee, Pitiporn MD, FRCPC*† Author Information
MICROSCOPIC FINDINGS AND CLINICAL COURSE Histopathologic evaluation revealed a granulomatous infiltrate in the dermis and subcutaneous tissue with massive necrobiosis of collagen. Multiple atypical foamy histiocytes and Touton giant cells were present. Cholesterol clefts were also found in the subcutaneous tissue (Fig. 5). No foreign body material was identified. Special stains for fungus, acid-fast bacilli, and bacteria were negative. A computed tomography of the chest, abdomen, and pelvis was obtained to evaluate for extracutaneous manifestations of necrobiotic xanthogranuloma and lymphoma progression. The study showed an upper lobe predominance of patchy reticulation in the lungs and mildly prominent iliac lymph nodes, all findings that were unchanged from computed tomographic imaging performed 2 years earlier. An ophthalmologic examination was normal. A bone marrow biopsy showed persistent marginal zone lymphoma with plasmacytic differentiation and a stable monoclonal gammopathy. Bortezomib was restarted for 2 cycles but subsequently held in anticipation of the patient’s upcoming bone marrow transplant. At his most recent follow-up with oncology, 4 months after the diagnosis of necrobiotic xanthogranuloma, it was noted that the skin lesions of the patient had stopped progressing but not resolved. The current stability of lesions cannot be attributed with any certainty to bortezomib or any other therapy.
Sweet syndrome is a reactive neutrophilic dermatosis that develops in response to various systemic illnesses. The cutaneous manifestations include an acute eruption of painful, edematous papules, plaques, pustules, or vesicles associated with fever and other constitutional symptoms. Although the etiology cannot always be determined, Sweet syndrome most commonly arises in reaction to systemic illnesses, such as infections, inflammatory bowel disease, medications, and malignancies. We report a case of chronic, recurrent Sweet syndrome lasting over 15 years in a patient with no identifiable underlying illness.
Seelhammer, Troy BA; Seelhammer, Todd BA; Lilly, Kia MD; Kaye, Valda N MD; Crutchfield, Charles E III MD; Suwattee, Pitiporn MD, FRCPC Author Information
ANSWER: FIBROUS HAMARTOMA OF INFANCY Fibrous hamartoma of infancy (FHI) is a benign but persistent mesenchymal tumor of myofibroblastic derivation originally described by Reye in 1956 as a ‘‘subdermal fibromatous tumor of infancy.’’ Although it can be present at birth, FHI occurs most frequently in the first year of life (91% of cases). A male preponderance exists at a ratio of 2.6:1. Clinically, FHI presents as a solitary, painless, slowly growing, freely mobile, subcutaneous mass with or without changes in pigmentation, hypertrichosis, and epidermal ulceration. It has a predilection for the trunk, especially the axilla and upper extremities. The inguinal region and external genital areas are also common while the head and neck are relatively less common. Multiple discrete synchronous and rapidly growing lesions have been reported. The clinical differential diagnosis of FHI may include lipoma, myofibroma, infantile myofibromatosis, fibrolipoma, cystic hygroma, calcifying aponeurotic fibroma, and the locally aggressive myofibroblastic proliferation of infantile fibromatosis. Microscopically, FHI is characterized by the presence of 3 components: (1) well-defined bundles of dense uniform fibrous tissue that branch, interweave, and project into adipose tissue; (2) immature spindled mesenchymal cells arranged in nests, whorls, or bands; and (3) mature adipose tissue admixed with other components. Individual tumors may contain varying amounts of these components; some cases may consist primarily of fibrous tissue, whereas in others, adipose tissue may predominate. Lymphocytes can be identified infiltrating mesenchymal and fibrous tissue of the tumor. Mitotic figures are rarely present. Eccrine alterations may occur including glandular hyperplasia, ductal dilation, intraluminal papillary differentiation, and squamous metaplasia of the ducts. Acid mucopolysaccharides are noted in both the primitive matrix and dense fibrous portion of the lesion. In tumors that are larger in size, the margins may become poorly demarcated and extend into nearby tissues such as muscles, nerves, and other fibroconnective tissue structures. Fine-needle aspiration is an adjuvant diagnostic modality that may be useful in arousing suspicion of FHI. On fine-needle aspiration with Papanicolaou or May–Grünwald– Giemsa stain, the tissue sample demonstrates moderate cellularity comprising an intimate admixture of mature adipose tissue with small clusters of plump spindle cells. These spindle cells have scanty to moderate amount of eosinophilic cytoplasm with monomorphic nuclei but lack prominent nucleoli. Mitotic figures or nuclear atypia are not characteristic. The cytological findings as described suggest a preoperative diagnosis of a benign mesenchymal lesion/ hamartoma, warranting subsequent diagnostic excision or biopsy for histological confirmation. Cytogenetic abnormalities reported in FHI include the reciprocal translocation t(2;3)(q31;q21) that has previously been associated with benign fibrous tissue abnormalities. More recently, a second cytogenetic anomaly involving a complex translocation of 3 regions: 6q25, 12q24.3, and 8q13. These abnormalities have been linked to a variety of benign and malignant neoplastic processes ranging from lipomas to lymphoid malignancies. The role of cytogenetic analysis in the diagnostic evaluation and treatment for FHI lesions has yet to be determined. Although FHI is histologically characterized by the triad as above, other soft tissue tumors that can mimic FHI include lipofibromatosis, myofibroma, infantile digital fibromatosis, calcifying aponeurotic fibroma, and nodular fasciitis. As the fibrous component of FHI may vary in the amount, pattern, and cellularity, it may also bear a histopathologic resemblance to granulation tissue, deep fibrous histiocytoma, or fibromatosis. Lipofibromatosis, a rare pediatric soft tissue tumor, is composed of strands of fibrocollagenous connective tissue and mature adipocytes. It, however, lacks immature cells in the myxoid matrix that is characteristic of FHI. Myofibroma is characterized by a biphasic staining pattern of the myofibroblasts resembling smooth muscle cells embedded in a fibromyxoid stroma localized to the central area with vascular channels resembling hemangiopericytomas at the periphery. The lesion usually appears as a solitary nodule located in the head, neck, and trunk in the adult population. The characteristic histologic finding of infantile digital fibromatosis is the presence of intracytoplasmic perinuclear eosinophilic inclusions that are typically lacking in FHI. Calcifying From the *Department of Dermatology, University of Minnesota, Minneapolis, MN; and †Section of Dermatology, Minneapolis Veterans Medical Center, Minneapolis, MN. Financial disclosure: none reported. The views expressed in this article are those of the authors and do not neccessarily reflect the position or policy of the Department of Veterans Affairs. Reprints: Dr. Pitiporn Suwattee, MD, FRCPC, Staff Physician, Minneapolis Veterans Affairs Medical Center, 1 Veterans Drive, 11K-Dermatology, Minneapolis, MN 55417 (e-mail: suwat001@umn.edu). Copyright 2010 by Lippincott Williams & Wilkins
Journal Article Multiple white facial papules Get access T. Seelhammer, T. Seelhammer Department of Dermatology, University of Minnesota, MN, USA Search for other works by this author on: Oxford Academic Google Scholar P. M. H. Cham, P. M. H. Cham Department of Dermatology, University of Minnesota, MN, USA Search for other works by this author on: Oxford Academic Google Scholar T. Seelhammer, T. Seelhammer Department of Dermatology, University of Minnesota, MN, USA Search for other works by this author on: Oxford Academic Google Scholar P. Suwattee P. Suwattee Department of Dermatology, University of Minnesota, MN, USASection of Dermatology, Minneapolis Veterans Affairs Medical Center, Minneapolis, MN, USA Dr Pitiporn Suwattee, Department of Dermatology, Minneapolis Veterans Affairs Medical Center – Dermatology, 1 Veterans Drive, Minneapolis, MN 55417, USA E‐mail: suwat001@umn.edu Search for other works by this author on: Oxford Academic Google Scholar Clinical and Experimental Dermatology, Volume 34, Issue 7, 1 October 2009, Pages 841–842, https://doi.org/10.1111/j.1365-2230.2008.03023.x Published: 01 October 2009 Article history Accepted: 16 May 2008 Published: 01 October 2009
Journal of Cutaneous PathologyVolume 36, Issue 2 p. 285-286 Tinea versicolor with interface dermatitis Pitiporn Suwattee MD, FRCPC, Pitiporn Suwattee MD, FRCPC Department of Dermatology, University of Minnesota, Minneapolis, MN, USA Section of Dermatology, Minneapolis Veterans Affairs Medical Center, Minneapolis, MN, USASearch for more papers by this authorPeter M. H. Cham MD, Peter M. H. Cham MD Department of Dermatology, University of Minnesota, Minneapolis, MN, USASearch for more papers by this authorRobin K. Solomon MD, Robin K. Solomon MD Department of Laboratory Medicine and Pathology, University of Minnesota, Minneapolis, MN, USA Laboratory Medicine and Pathology Service, Minneapolis Veterans Affairs Medical Center, Minneapolis, MN, USAe-mail: suwat001@umn.eduSearch for more papers by this authorValda N. Kaye MD, Valda N. Kaye MD Department of Dermatology, University of Minnesota, Minneapolis, MN, USA Section of Dermatology, Minneapolis Veterans Affairs Medical Center, Minneapolis, MN, USA Laboratory Medicine and Pathology Service, Minneapolis Veterans Affairs Medical Center, Minneapolis, MN, USAe-mail: suwat001@umn.eduSearch for more papers by this author Pitiporn Suwattee MD, FRCPC, Pitiporn Suwattee MD, FRCPC Department of Dermatology, University of Minnesota, Minneapolis, MN, USA Section of Dermatology, Minneapolis Veterans Affairs Medical Center, Minneapolis, MN, USASearch for more papers by this authorPeter M. H. Cham MD, Peter M. H. Cham MD Department of Dermatology, University of Minnesota, Minneapolis, MN, USASearch for more papers by this authorRobin K. Solomon MD, Robin K. Solomon MD Department of Laboratory Medicine and Pathology, University of Minnesota, Minneapolis, MN, USA Laboratory Medicine and Pathology Service, Minneapolis Veterans Affairs Medical Center, Minneapolis, MN, USAe-mail: suwat001@umn.eduSearch for more papers by this authorValda N. Kaye MD, Valda N. Kaye MD Department of Dermatology, University of Minnesota, Minneapolis, MN, USA Section of Dermatology, Minneapolis Veterans Affairs Medical Center, Minneapolis, MN, USA Laboratory Medicine and Pathology Service, Minneapolis Veterans Affairs Medical Center, Minneapolis, MN, USAe-mail: suwat001@umn.eduSearch for more papers by this author First published: 20 January 2009 https://doi.org/10.1111/j.1600-0560.2008.01056.xCitations: 6 The views expressed in this article are those of the authors and do not necessarily reflect the position or policy of the Department of Veterans Affairs. Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat No abstract is available for this article.Citing Literature Volume36, Issue2February 2009Pages 285-286 RelatedInformation
A 53 year old, afebrile woman presented to the dermatology clinic with a two week history of petechial rash on her lower extremities that had progressed up to her arms. In addition, she also had pain in the wrists, knees, and elbows. Approximately five months earlier, she had been diagnosed with group A streptococcal pharyngeal infection, but she had not been treated with antibiotics. She was currently taking salbutamol, famciclovir, levothyroxine, lovastatin, and varenicline. A systems review was unremarkable and she had no reported haematuria, abdominal pain, or bloody stools. A physical examination found multiple petechial macules, papules, and purpuric plaques, which were more numerous on the legs than on the arms (figure[F1]). A complete blood count and coagulation studies were normal. Urinalysis showed haematuria and proteinuria. A skin biopsy of a petechial papule revealed leucocytoclastic vasculitis, with a granular IgA reactivity around the blood vessels in the papillary dermis. ### Short answers ### Long answers #### 1 Investigations Cutaneous palpable purpura may signify small vessel vasculitis, which has many possible causes (box 1).1 2 Histological findings of leucocytoclastic vasculitis include fibrin deposition in the vessel walls, red blood cell …