Dermatology faculty are responsible for the undergraduate education of all medical students, most of whom will not become dermatologists but will encounter skin disease throughout their careers, and are also responsible for the intensive, specialized graduate education of dermatology residents. Over the past 75 years, dermatology faculty have grappled with defining the fundamental curriculum, grumbled about time limitations, and debated the fundamental role of dermatology in general medical education. Although dermatology trainee education continues to evolve, fundamentals still focus on observational skills developed through clinical and nonclinical experiences. We highlight major trends and turning points in undergraduate and graduate dermatology education that have occurred during the career of Dr Irwin M. Braverman, many of which Dr Braverman himself influenced, and reflect on the current state of dermatology education at our institution. (c) 2024 Elsevier Inc. All rights are reserved, including those for text and data mining, AI training, and similar technologies.

A 48-year-old woman was being evaluated for enlarging lower extremity ulcers, starting as small pustules 7 months earlier. She was afebrile but hypotensive despite broad-spectrum antibiotics. Physical examination revealed a circumferential ulcer on the left shin, with exposed bone and a tender and violaceous border (Fig 1, A), and similar ulcers on the right shin (Fig 1, B), groin, and axillae. Laboratory findings were notable for an elevated white blood cell count and creatinine; skin biopsy was performed (Fig 2). Testing for antineutrophil cytoplasmic antibodies (ANCA), antineutrophil antibodies, cryoglobulins, coagulation panel, serum immunofixation, and microbial cultures was negative. The patient partially responded to oral prednisone (1 mg/kg), but ultimately died of refractory shock.Fig 2Figure Nelson Ugwu, BS; Nour Kibbi, MD; Earl J. Glusac, MD; Sugura Imaeda, MDView Large Image Figure ViewerDownload Hi-res image Download (PPT) What is the diagnosis? Part 1: Vignette/Question A.Nonuremic calciphylaxisB.Antiphospholipid syndromeC.Pyoderma gangrenosumD.Necrotizing fasciitisE.ANCA-negative medium vessel vasculitis Click here to view disclosures, take the quiz, and claim CME credit.

IgA vasculitis, also called Henoch-Schönlein purpura (HSP), is a form of cutaneous small-vessel vasculitis characterized by palpable purpura favoring the lower extremities, arthritis, nephritis, and IgA deposition within postcapillary venules of the skin and mesangium. In children, respiratory infections are well known to precede HSP. In adults, infectious endocarditis is a rare but potentially fatal trigger for HSP. We report the subtle presentations of subacute endocarditis in 2 adults with cutaneous IgA vasculitis.

Ustekinumab (UST) is an effective treatment for Crohn’s disease (CD). Here we present two cases of leukocytoclastic vasculitis (LCV) in CD patients after UST induction therapy with a review of the literature. Patient #1: A 26 year old woman with a 14 year history of Crohn’s ileocolitis. She was previously treated with 6-mercaptopurine, infliximab, and vedolizumab without durable response. She ultimately underwent a left hemicolectomy due to development of a sigmoid stricture and was started on UST postoperatively. Thirty-six days after her initial UST intravenous (IV) infusion of 390 milligrams (mg) she developed new partially blanching, erythematous, non-tender, non-pruritic macules and papules over the right medial thigh, which later evolved into palpable purpura involving both lower extremities (Figure 1A). She reported no gastrointestinal (GI) or other symptoms. White blood cell (WBC) count and metabolic panel were normal. Antinuclear antibody (ANA) titer was 1:80. Perinuclear pattern antineutrophil cytoplasmic antibodies (p-ANCA) were positive. C-reactive protein (CRP) was elevated to 41.5 mg/liter (L). One lesion was biopsied, and pathology findings were consistent with LCV (Figure 1B). She was started on colchicine 0.6 mg daily with improvement in her rash and has received her second dose of UST without further complications. Patient #2: A 29 year old woman with a 6 year history of Crohn’s ileocolitis. Her prior treatments include budesonide, mesalamine, and infliximab. While on infliximab, she developed jejunal and ileal ulcers on video capsule endoscopy. Infliximab was discontinued, and UST was started. Three months following initial IV induction therapy of UST, she developed pink purpuric papules and hemorrhagic vesicles involving her bilateral shins, dorsal feet, calves, and bilateral extensor forearms. The appearance of the rash was consistent with LCV (Figure 2). She was started on prednisone at 60 mg daily for 1 week with taper resulting in complete resolution of her rash. UST was continued with no recurrence. WBC count and metabolic panel were normal. ANCA was negative, and ANA titer was 1:80. CRP was elevated to 13.2 mg/L. Literature review revealed only one prior published case report of a patient with inflammatory bowel disease developing LCV after administration of UST. In this case, UST was discontinued since re-administration caused the rash to return. Here we have two patients who developed LCV soon after initiating UST therapy, although after treatment with prednisone/colchicine, there was no recurrence with continuing UST. It is possible to develop LCV in association with CD alone; however, these patients had longstanding disease without occurrence of LCV until being started on UST. Moreover, patient #1, was in remission from a Crohn’s disease standpoint at the time of UST initiation and onset of the rash.

A man in his forties presented with multiple cutaneous nodules on his left flank that had been present for more than 20 years. Family history was notable for neurofibromatosis 1 (NF1) in his 21-year-old daughter who has caf e au lait macules (CALM) and axillary freckling. There are no other affected family members, including his wife and two other children. Physical examination revealed approximately 20 soft, flesh-colored papulonodules on the left flank (Fig. 1). There were no axillary or inguinal freckles, CALM, or Lisch nodules. The patient did not have any neurological deficits or symptoms. Previous biopsy of the patient’s papulonodules showed a diffuse proliferation of spindle cells and scattered mast cells within a fibrillary matrix consistent with neurofibroma (Fig. 2). Given the constellation of findings, he was diagnosed with segmental NF1 (SNF1), which is characterized by cutaneous features of NF1 (CALM and/or neurofibromas), limited to one body segment. He had no evidence of plexiform disease or systemic complications, and was scheduled for follow-up with dermatology and ophthalmology for surveillance. The occurrence of one daughter with classical NF1 and two unaffected children in this patient with SNF1 is consistent with gonosomal mosaicism. Genetic counseling was offered and deferred as the patient and his spouse have no future plans to conceive. NF1 is an autosomal dominant disorder resulting from germline mutations in neurofibromin, NF1. SNF1 is a rare form of NF1 that is regionally limited and can present with CALM and/or neurofibromas, or plexiform neurofibromas alone. The distribution is usually unilateral but can be bilateral. SNF1 is generally thought to occur due to postzygotic mutations in NF1, resulting in somatic mosaicism, without affecting the germline. By contrast, mutations arising during very early stages of embryonic development can cause mosaicism in both somatic cells and germ cells (gonosomal mosaicism). Gonosomal mosaicism, while rare, has been previously reported with SNF1 and is important to recognize as NF1 is among the most common tumor-prone autosomal dominant diseases. Moreover, though NF1 can arise from de novo sporadic mutations, almost half of the cases arise from inherited germline mutations. Therefore, clinicians should be aware in order to facilitate genetic counseling in individuals with SNF1 about the risk of NF1 in their offspring. Lastly, genetic counseling should extend to instances of eggor sperm-donor pregnancies, where gonosomal mosaicism in donor cells has been reported to result in offspring affected by classical NF1.

WWW.MDEDGE.COM/CUTIS A 75-year-old man presented for evaluation of lesions on the umbilicus and lower abdomen that had developed over the past 4 weeks and were asymptomatic. His medical history was notable for plasma cell myeloma (stage III, IgA λ light chain restricted), deep vein thrombosis, and a 30-year history of smoking (20 packs per year). On physical examination, violaceous plaques and papulonodules were noted on the umbilicus. The lesions had a firm consistency and smooth surface without epidermal change. Violaceous papulonodules and subcutaneous plaques were noted on the lower abdomen. The lesions were nontender to palpation. Bilateral edema of the legs also was noted. The remainder of the skin was normal and there was no cervical, axillary, or inguinal lymphadenopathy.

Metastatic basal cell carcinoma (mBCC) is exceedingly rare, with an estimated incidence of 0.0028% to 0.55%.1Wysong A. Aasi S. Tang J.Y. Update on metastatic basal cell carcinoma: a summary of published cases from 1981 through 2011.JAMA Derm. 2013; 149: 615-616Crossref PubMed Scopus (81) Google Scholar Although the behavior of mBCC is poorly understood, the primary tumor typically exhibits aggressive histopathology, such as morpheaform, infiltrating, or basosquamous features. Basal cell carcinoma (BCC) usually metastasizes to regional lymph nodes (53%), lungs (33%), and bone (20%). Until a few years ago, the median survival after diagnosis was only 8 to 10 months. After the demonstration that more than 90% of BCC expressed abnormal Hedgehog signaling, 2 Hedgehog pathway inhibitors, vismodegib and sonidegib, were approved for advanced BCC.2Sekulic A. Migden M.R. Lewis K. Hainsworth J. Solomon J.A. et al.Pivotal ERIVANCE basal cell carcinoma (BCC) study: 12-month update of efficacy and safety of vismodegib in advanced BCC.J Am Acad Dermatol. 2015; 72: 1021-1026Abstract Full Text Full Text PDF PubMed Scopus (164) Google Scholar, 3Basset-Seguin N. Hauschild A. Kunstfeld R. Grob J. Dreno B. et al.Vismodegib in patients with advanced basal cell carcinoma: primary analysis of STEVIE, an international, open-label trial.Eur J Cancer. 2017; 86: 334-348Abstract Full Text Full Text PDF PubMed Scopus (173) Google Scholar, 4Dummer R. Guminski A. Gutzmer R. Dirix L. Lewis K.D. et al.The 12-month analysis from basal cell carcinoma outcomes with LDE225 treatment (BOLT): a phase II, randomized, double-blind study of sonidegib in patients with advanced basal cell carcinoma.J Am Acad Dermatol. 2016; 75: 113-125Abstract Full Text Full Text PDF PubMed Scopus (103) Google Scholar We describe a patient with a chronic burn in whom mBCC with diffuse skeletal and possibly lung metastases developed. The patient was started on vismodegib but ultimately died of his disease. A 65-year-old man lost to medical care for more than 3 decades presented with a nonhealing ulcer on the posterior neck, tachycardia, and left hip pain. The lesion, present for at least 15 years, was the site of a fireplace burn during childhood. The patient reported a 20-pound weight loss over a few months but denied other constitutional symptoms. On examination, he appeared cachectic. On the posterior neck was an 8- x 10-centimeter pearly ulcer with raised borders (Fig 1, A). He had no lymphadenopathy. Biopsy of the ulcer border found infiltrating BCC (Fig 1, B). Given his tachycardia and hip pain, chest computed tomography angiogram and abdominal computed tomography found multiple sub 4-mm pulmonary nodules as well as numerous lytic and osteoblastic lesions throughout the ribs, the lumbar spine, and pelvis (Fig 1,C). A core biopsy from the iliac crest showed an infiltrative basaloid neoplasm, consistent with mBCC (Fig 1, D). After ulcer debulking and skin grafting, he was started on vismodegib, 150 mg/d, and received 2 doses of radiation therapy for the left hip, with improvement in symptoms. He suffered from severe nausea, vomiting, and malaise on vismodegib, and, ultimately, given lack of tumor response, he was switched to comfort care and died only 2 months after his diagnosis. This case adds to the sparse literature on metastatic BCC. Intriguingly, the history of prior fireplace burn in our patient may have represented a contributing factor. Trauma has long been proposed to be an inciting factor for the development of BCC.5Ozyazgan I. Kontaş O. Previous injuries or scars as risk factors for the development of basal cell carcinoma.Scand J Plast Reconstr Surg Hand Surg. 2004; 38: 11-15Crossref PubMed Scopus (54) Google Scholar, 6Noodleman F.R. Pollack S.V. Trauma as a possible etiologic factor in basal cell carcinoma.J Dermatol Surg Oncol. 1986; 12: 841-846Crossref PubMed Scopus (109) Google Scholar Most frequently, such carcinomas have reportedly been encountered in men; their histology is not particularly aggressive, and although they may be deceptive clinically, surgical excision is often curative.6Noodleman F.R. Pollack S.V. Trauma as a possible etiologic factor in basal cell carcinoma.J Dermatol Surg Oncol. 1986; 12: 841-846Crossref PubMed Scopus (109) Google Scholar Various different types of trauma have been reported, including sharp or blunt injury,7Rahimizadeh A. Shelton R. Weinberg H. Sadick N. The development of a Marjolin's cancer in a human immunodeficiency virus–positive hemophilic man and review of the literature.Dermatol Surg. 1997; 23: 560-563Crossref PubMed Scopus (11) Google Scholar surgical incisions,8Ozyazgan I. Kontaçs O. Basal cell carcinoma arising from surgical scars: a case and review of the literature.Derm Surg. 1999; 25: 965-968Crossref PubMed Scopus (49) Google Scholar vaccination sites,9Rich J.D. Shesol B.F. Horne D.W. Basal cell carcinoma arising in a smallpox vaccination site.J Clin Pathol. 1980; 33: 134-135Crossref PubMed Scopus (24) Google Scholar piercings,10Lee J. Russell M.A. Basal cell carcinoma arising at the site of a lip piercing.Derm Surg. 2018; ([Epub ahead of print])https://doi.org/10.1097/DSS.0000000000001508Crossref Scopus (2) Google Scholar abscesses,11Ghalig H.S. Karthik K. Rathod S.S. Bojen N. Devi S.R. Pigmented basal cell carcinoma in Marjolin's ulcer.J Clin Diagn Res. 2013; 7: 2990-2991PubMed Google Scholar or fistulas.12Kim N.G. Kim J.O. Park Y.J. Kim J.S. Lee Y.J. Lee K.S. Cutaneous basal cell carcinoma arising in odontogenic cutaneous fistula.Arch Craniofac Surg. 2017; 18: 141-144Crossref Google Scholar Thermal or chemical burns are a common type of trauma associated with carcinoma. In fact, certain cultural practices of using thermal injury to the skin lead to burn scars with subsequent carcinomas that have been given eponyms such as Kangri and Kang cancers.13Suryanarayan C.R. Kangri cancer in Kashmir Valley: preliminary study.J Surg Oncol. 1973; 5: 327-333Crossref PubMed Scopus (11) Google Scholar, 14Laycock H.T. The Kang cancer of Northwest China.Br Med J. 1948; 1: 982Crossref PubMed Scopus (18) Google Scholar A meta-analysis in 2005 by Kowal-Vern and Criswell15Kowal-Vern A. Criswell B.K. Burn scar neoplasms: a literature review and statistical analysis.Burns. 2005; 31: 403-413Abstract Full Text Full Text PDF PubMed Scopus (196) Google Scholar reviewed more than 1000 cases of skin cancers arising from chronic burns. Twelve percent of cases were BCC, whereas 71% were squamous cell carcinoma (SCC). Surprisingly, they found that BCC had a shorter latency period to malignancy (from the time of burn injury) compared with SCC, although that period ranged widely. To try to get at the association between burns and carcinoma, a recent Danish populationwide registry study examined 16,903 patients who were admitted from 1973 to 1993 for a thermal or chemical burn. The cohort was followed up for the development of cancer through the Danish Cancer Registry until 2002.16Mellemkjaer L. Holmich L.R. Gridley G. Rabkin C. Olsen J.H. Risks for skin and other cancers up to 25 years after burn injuries.Epidemiology. 2006; 17: 668-673Crossref PubMed Scopus (28) Google Scholar This study failed to show an increased incidence of skin cancer (BCC, SCC, and melanoma) arising within burns compared with that of the general population. However, it did not include information on tumor size, histology, locoregional spread, or distant metastasis, factors that may have been significantly different in burn carcinomas. That said, Kowal-Vern and Criswell,s15Kowal-Vern A. Criswell B.K. Burn scar neoplasms: a literature review and statistical analysis.Burns. 2005; 31: 403-413Abstract Full Text Full Text PDF PubMed Scopus (196) Google Scholar meta-analysis did not have any cases of locoregional or metastatic spread. Moreover, in our review of the 6 most recent cases (since 2005) of BCC arising within burn scars, none had locoregional or metastatic spread,17Martín J.M. Monteagudo C. Alonso V. Llombart B. de la Fuente C. et al.Basal cell carcinomas arising on a skin graft secondary to a thermal burn scar.Burns. 2005; 31: 789-791Abstract Full Text Full Text PDF PubMed Scopus (6) Google Scholar, 18Combemale P. Bousquet M. Kanitakis J. Bernard P. Malignant transformation of leg ulcers: a retrospective study of 85 cases.J Eur Acad Dermatol Venereol. 2007; 21: 935-941Crossref PubMed Scopus (54) Google Scholar, 19Ng D. Gilbert P.M. Dheansa B.S. Basal cell carcinoma concealed by a burn wound.Burns. 2007; 33: 935-936Abstract Full Text Full Text PDF PubMed Scopus (1) Google Scholar, 20Bagazgoitia L. Bea S. Santiago J.L. Cuevas J. Juarranz A. Jaén P. Multiple basal cell carcinomas arising on a thermal-burn scar. Successful treatment with photodynamic therapy.J Eur Acad Dermatol Venereol. 2009 Apr; 23: 459-461Crossref PubMed Scopus (6) Google Scholar, 21Kannan R.Y. Rauf G.K. Acute burn scar basal cell carcinoma.Ann Plast Surg. 2010; 64: 321-322Crossref PubMed Scopus (7) Google Scholar and among the 4 cases that reported histology of the tumor, only 2 had an aggressive histology (infiltrative pattern).17Martín J.M. Monteagudo C. Alonso V. Llombart B. de la Fuente C. et al.Basal cell carcinomas arising on a skin graft secondary to a thermal burn scar.Burns. 2005; 31: 789-791Abstract Full Text Full Text PDF PubMed Scopus (6) Google Scholar, 21Kannan R.Y. Rauf G.K. Acute burn scar basal cell carcinoma.Ann Plast Surg. 2010; 64: 321-322Crossref PubMed Scopus (7) Google Scholar All were reportedly cured. To our knowledge, our case is the first to describe metastatic BCC arising within a chronic burn. One issue with the current literature is that case reports and retrospective studies, by nature of design, are replete with recall bias. Moreover, ascertaining that BCC evolved from a traumatic ulcer is difficult in these cases without a prior biopsy showing the absence of preexisting carcinoma. A prospective cross-sectional study of 154 chronic, mostly venous, leg ulcers tried to address that issue.22Senet P. Combemale P. Debure C. et al.Malignancy and chronic leg ulcers.Arch Dermatol. 2012; 148: 704-708Crossref PubMed Scopus (70) Google Scholar After obtaining baseline biopsies to rule out carcinoma, the ulcers were followed up for 1 year and evaluated for the development of carcinoma. Of the 16 carcinomas that developed, 5 were BCC; the rest were SCC. Although the relationship between chronic ulcers and carcinoma is better characterized in SCC as Marjolin ulcer, there is likely an unrecognized relation with BCC. Our patient's overall poor response to vismodegib highlights the unfortunate gap that remains in treatment options for mBCC, with hedgehog signaling inhibitors constituting the main therapeutic class. The 3 pivotal phase II trials of vismodegib2Sekulic A. Migden M.R. Lewis K. Hainsworth J. Solomon J.A. et al.Pivotal ERIVANCE basal cell carcinoma (BCC) study: 12-month update of efficacy and safety of vismodegib in advanced BCC.J Am Acad Dermatol. 2015; 72: 1021-1026Abstract Full Text Full Text PDF PubMed Scopus (164) Google Scholar, 3Basset-Seguin N. Hauschild A. Kunstfeld R. Grob J. Dreno B. et al.Vismodegib in patients with advanced basal cell carcinoma: primary analysis of STEVIE, an international, open-label trial.Eur J Cancer. 2017; 86: 334-348Abstract Full Text Full Text PDF PubMed Scopus (173) Google Scholar and sonidegib4Dummer R. Guminski A. Gutzmer R. Dirix L. Lewis K.D. et al.The 12-month analysis from basal cell carcinoma outcomes with LDE225 treatment (BOLT): a phase II, randomized, double-blind study of sonidegib in patients with advanced basal cell carcinoma.J Am Acad Dermatol. 2016; 75: 113-125Abstract Full Text Full Text PDF PubMed Scopus (103) Google Scholar are described in Table I. Response rates in the mBCC subgroups ranged widely from 23% to 48%, with complete responses seen in only 3.8% to 8.7%. These responses, albeit low, are promising, and longer follow-up periods are needed to ensure that they are sustained. Unfortunately, grade 3 to 4 adverse event rates were reported as high as 59% and were typically worse in the first year of treatment and in some cases warranted treatment discontinuation, as with our patient.Table IThree phase II clinical trials showing the response to vismodegib and sonidegib in locally advanced and metastatic BCCInterventionERIVANCE, 20152Sekulic A. Migden M.R. Lewis K. Hainsworth J. Solomon J.A. et al.Pivotal ERIVANCE basal cell carcinoma (BCC) study: 12-month update of efficacy and safety of vismodegib in advanced BCC.J Am Acad Dermatol. 2015; 72: 1021-1026Abstract Full Text Full Text PDF PubMed Scopus (164) Google ScholarBOLT, 20164Dummer R. Guminski A. Gutzmer R. Dirix L. Lewis K.D. et al.The 12-month analysis from basal cell carcinoma outcomes with LDE225 treatment (BOLT): a phase II, randomized, double-blind study of sonidegib in patients with advanced basal cell carcinoma.J Am Acad Dermatol. 2016; 75: 113-125Abstract Full Text Full Text PDF PubMed Scopus (103) Google ScholarSTEVIE, 20173Basset-Seguin N. Hauschild A. Kunstfeld R. Grob J. Dreno B. et al.Vismodegib in patients with advanced basal cell carcinoma: primary analysis of STEVIE, an international, open-label trial.Eur J Cancer. 2017; 86: 334-348Abstract Full Text Full Text PDF PubMed Scopus (173) Google ScholarVismodegib 150 mg/dSonidegib 1:2 randomizationVismodegib 150 mg/d200 mg/d800 mg/dMedian follow up (mo)22.420.017.917.9No. mBCC from total33/10413/7923/15196/1119Overall response rate (%, IA), (% CR, % PR)48.5(0, 48.5)23.1(0, 23.1)34.8(8.7, 26.1)36.9(4.8, 32.1)Median duration of treatment, mo (95% CI)13.3 (0.7-24.8)8.9 (1.3-21.4)11.0 (1.3-27.8)8.6 (0-44)∗Responses for the entire population of locally advanced and metastatic BCC.Median duration of response, mo (95% CI)14.7 (5.6-NE)17.7 (NE)10.2 (NE)13.9 (9.2-NE)Median PFS (mo)9.3 (7.4-16.16)13.1 (9.2-18.6)14.3 (11.1-20.2)13.1 (12.0-17.7)Survival rateMedian OS: 24.1 mo (14.3-NE)31.6%, 12 mo23.8%, 12 moUnknownAdverse events, % (% ≥ grade 3)100 (51.9)97.5 (38)100 (59.3)97 (10)∗Responses for the entire population of locally advanced and metastatic BCC.Note. Results are shown for the mBCC subgroup.CI, Confidence interval; CR, complete response; IA, investigator-assessed; NE, not estimable; OS, overall survival; PFS, progression-free survival; PR, partial response.∗ Responses for the entire population of locally advanced and metastatic BCC. Open table in a new tab Note. Results are shown for the mBCC subgroup. CI, Confidence interval; CR, complete response; IA, investigator-assessed; NE, not estimable; OS, overall survival; PFS, progression-free survival; PR, partial response.

Chronic actinic dermatitis (CAD) is an uncommon inflammatory dermatosis characterized by dermatitis involving ultraviolet (UV) light–exposed skin with notable sparing of sun-protected areas. Rarely, spread of the exanthema to UV-protected areas of skin and even erythroderma with palmoplantar hyperkeratosis occurs.1 CAD typically afflicts men in the fifth decade of life or older. Although the pathophysiology remains unknown, it is thought that lymphocyte recognition of UV-induced neoantigens in the skin underlies this process.

The treatment of in-transit and satellite melanoma metastases is challenging. Treatment options for these cutaneous and subcutaneous lesions include surgical excision, radiotherapy, isolated limb infusion/perfusion, electrochemotherapy, cryotherapy, laser therapy (pulsed dye or carbon dioxide), systemic treatment with interferon-α or interleukin-2 (IL-2), topical imiquimod, dinitrochlorobenzene, and intralesional immunotherapy with bacillus Calmette-Guérin vaccine, granulocyte macrophage colony-stimulating factor, IL-2, or talimogene laherparepvec.

Maintaining clear skin markings after preparation before a skin procedure was the challenge.

Acute generalized exanthematous pustulosis (AGEP) is an acute sterile pustular eruption most commonly induced by medications. We present a case of AGEP with erythroderma following use of midodrine in a 58-year-old man. Although antibiotics are most commonly implicated in AGEP, we emphasize that nonantibiotic agents also may cause AGEP, which often manifests after a longer time interval compared to antibiotic-associated AGEP.

Subcutaneous histiocytoid Sweet's syndrome is a rare variant of histiocytoid Sweet's syndrome (SS). We present a 68-year-old woman with subcutaneous histiocytoid SS in association with refractory myelodysplastic syndrome transformed to acute myeloblastic leukemia (AML), status post induction chemotherapy and with persistent blasts (50%) in the bone marrow and blood, accompanied with neutropenia. The patient presented to the emergency room with fever and altered mental status. Clinical examination revealed approximately 20 scattered 0.5-2cm, pink to pink-purple non-tender firm nodules on the legs and left arm. The differential diagnosis included Sweet's syndrome (deep), leukemia cutis, infection, polyarteritis nodosa and erythema nodosum. Histopathologic examination of a biopsy from the left arm revealed a nodular infiltrate of neutrophils and histiocytoid mononuclear cells solely in the lobular compartment of the subcutaneous fat with focal areas of necrosis. Most cells in the infiltrate labeled with myeloperoxidase (MPO) including the histiocytoid cells. The cells were negative for CD34 and CD117. All special stains for microorganisms were negative. A diagnosis of subcutaneous histiocytoid SS was made. A subcutaneous histiocytoid SS should be suspected when a neutrophilic/histiocytoid panniculitis, occurring in the setting of myeloid disorders, is encountered and after exclusion of an infectious process and leukemia cutis.

Post-vaccinial non-viral folliculitis has been recognized in the past decade as a new adverse cutaneous reaction to smallpox vaccination. Contrary to more serious smallpox vaccine reactions, post-vaccinial non-viral folliculitis has a benign course and resolves spontaneously within approximately 7 days. We describe additional histopathologic findings associated with post-vaccinial non-viral folliculitis, which has only been described once previously. New findings include the presence of a neutrophilic or lymphohistiocytic infiltrate that is concentrated around the hair follicles. We compare our findings to the follicular nature of varicella and herpes zoster infections, generating the hypothesis of deposition of vaccinia protein within folliculosebaceous units as a potential pathophysiologic mechanism behind post-vaccinial non-viral folliculitis.

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A 78-year-old man presented for his yearly skin exam and was noted to have an oval-shaped, green-black eschar on his midback. A pink, atrophic scar was located nearby, in addition to a medicated patch of similar size.

A 78-year-old man presented for his yearly skin exam and was noted to have an oval-shaped, green-black eschar on his midback. A pink, atrophic scar was located nearby, in addition to a medicated patch of similar size.