A 64-year-old man with a history of celiac disease (CD), congestive heart failure, and diabetes mellitus complicated by end-stage renal disease and peripheral neuropathy, was admitted to the hospital for non-healing ulcerations of his hands with osteomyelitis from his peripheral arterial vascular disease. He reported that his CD was under good control with a strict gluten-free diet prior to admission. Physical exam revealed prominent petechiae on his bilateral palms and fingers (Fig 1). A biopsy was performed and demonstrated collections of neutrophils in the papillary dermis (Fig 2).Fig 2View Large Image Figure ViewerDownload Hi-res image Download (PPT) Question 1: What is the most likely diagnosis?A.Arterial vascular diseaseB.CapillaritisC.Dermatitis herpetiformisD.Janeway lesionsE.Rheumatoid vasculitis Answers:A.Arterial vascular disease – Incorrect. Cutaneous findings of arterial vascular occlusive disease typically include erosions, ulcers, and ischemic changes.B.Capillaritis – Incorrect. Capillaritis classically presents as copper-brown macules and petechiae on the lower extremities.C.Dermatitis herpetiformis (DH) – Correct. Palmar petechiae are a rare presentation of DH in adults and can result in delayed diagnosis when being the initial or isolated manifestation of disease. Although papules and vesicles on extensor surfaces in DH are pruritic, palmar petechiae may be pruritic, painful, or asymptomatic.1Simpson M.M. Cowen E.W. Cho S. Acral petechial eruptions without gastrointestinal symptoms: Three cases of dermatitis herpetiformis.JAAD Case Rep. 2020; 6: 935-938Abstract Full Text Full Text PDF PubMed Scopus (2) Google Scholar, 2Zaghi D. Witheiler D. Menter A.M. Petechial eruption on fingers. Dermatitis herpetiformis.JAMA Dermatol. 2014; 150: 1353-1354Crossref PubMed Scopus (7) Google Scholar, 3Heinlin J. Knoppke B. Kohl E. Landthaler M. Karrer S. Dermatitis herpetiformis presenting as digital petechiae.Pediatr Dermatol. 2012; 29: 209-212Crossref PubMed Scopus (15) Google ScholarD.Janeway lesions – Incorrect. Janeway lesions are seen in bacterial endocarditis and present as angular hemorrhage on the palms.E.Rheumatoid vasculitis – Incorrect. Rheumatoid vasculitis develops during advanced rheumatoid arthritis and can manifest as purpura, ulcerations, digital ischemia, and nodules on the hands.4Patterson J. Hosler G. Prenshaw K. Weedon’s Skin Pathology.5th ed. Elsevier, 2020Google Scholar Question 2: What would direct immunofluorescence (DIF) microscopy most likely show?A.Linear deposition of IgA along the basement membrane of perilesional skinB.Granular deposition of IgA within the dermal papillae of perilesional skinC.Linear deposition of IgG and C3 along the basement membrane of perilesional skinD.Linear and granular deposition of IgG along the basement membrane of perilesional skinE.Intercellular IgG within the epidermis of perilesional skin Answers:A.Linear deposition of IgA along the basement membrane of perilesional skin – Incorrect. While also characterized by a neutrophilic infiltrate in the papillary dermis, DIF shows linear deposition of IgA along the basement membrane in all cases of linear IgA bullous dermatosis.4Patterson J. Hosler G. Prenshaw K. Weedon’s Skin Pathology.5th ed. Elsevier, 2020Google Scholar Uncommonly, DH may demonstrate linear deposition of IgA, but granular deposition is much more typical.B.Granular deposition of IgA within the dermal papillae of perilesional skin – Correct. DIF microscopy of DH classically demonstrates granular deposition of IgA within the dermal papillae of perilesional skin.4Patterson J. Hosler G. Prenshaw K. Weedon’s Skin Pathology.5th ed. Elsevier, 2020Google Scholar Granular deposits may also be detected at the basement membrane, and C3 often co-migrates with IgA. Granular IgA deposition at the basement membrane can overlap with findings of linear IgA bullous dermatosis, but serologic testing can be utilized to confirm the correct diagnosis. Granular deposition of IgA in the dermal papillae, however, is pathognomonic for DH. While pharmacologic treatment does not clear the deposition of granular IgA deposits in the dermal papillae, a gluten-free diet results in resolution of these deposits.5Bolotin D. Petronic-Rosic V. Dermatitis herpetiformis. Part II. Diagnosis, management, and prognosis.J Am Acad Dermatol. 2011; 64: 1027-1033Abstract Full Text Full Text PDF PubMed Scopus (77) Google Scholar In this patient, DIF demonstrated granular deposition of IgA at the basement membrane zone and within the dermal papillae.C.Linear deposition of IgG and C3 along the basement membrane of perilesional skin – Incorrect. This pattern describes bullous pemphigoid. In bullous pemphigoid, the predominant inflammatory infiltrate is made up by eosinophils, which can be seen in the papillary dermis, in subepidermal blisters, and as eosinophilic spongiosis. DIF reveals linear IgG and C3 deposition along the basement membrane.4Patterson J. Hosler G. Prenshaw K. Weedon’s Skin Pathology.5th ed. Elsevier, 2020Google ScholarD.Linear and granular deposition of IgG along the basement membrane of perilesional skin – Incorrect. This pattern may be observed in bullous systemic lupus erythematosus. While bullous systemic lupus erythematosus also has neutrophilic infiltrate, DIF shows deposition of IgG, sometimes along with IgA and/or IgM, in a linear and granular pattern along the basement membrane.4Patterson J. Hosler G. Prenshaw K. Weedon’s Skin Pathology.5th ed. Elsevier, 2020Google ScholarE.Intercellular IgG within the epidermis of perilesional skin – Incorrect. This pattern describes the most common pemphigus subtypes, pemphigus vulgaris and pemphigus foliaceus.4Patterson J. Hosler G. Prenshaw K. Weedon’s Skin Pathology.5th ed. Elsevier, 2020Google Scholar Pemphigus vulgaris typically has intercellular deposition of IgG and C3, predominantly in the lower layers of the epidermis, whereas pemphigus foliaceus more commonly exhibits intercellular deposition of IgG and C3 in the upper layers of the epidermis. Question 3: What is the most specific serologic test for dermatitis herpetiformis?A.Anti-epidermal transglutaminase (eTG) antibodiesB.Anti-gliadin antibodiesC.Anti-tissue transglutaminase 2 (TTG2) antibodiesD.IgA endomysial antibodiesE.Indirect immunofluorescence on skin substrate Answers:A.Anti-epidermal transglutaminase (eTG) antibodies – Correct. High affinity and specific IgA class anti-eTG antibodies are found in patients with DH and are thought to develop through epitope spreading. While circulating anti-eTG antibodies are found in both CD and DH, deposition of these antibody-antigen complexes in the papillary dermis leads to neutrophilic infiltration and distinguishes DH from CD.4Patterson J. Hosler G. Prenshaw K. Weedon’s Skin Pathology.5th ed. Elsevier, 2020Google Scholar,6Antiga E. Maglie R. Quintarelli L. et al.Dermatitis herpetiformis: Novel perspectives.Front Immunol. 2019; 10: 1290Crossref PubMed Scopus (48) Google Scholar Additionally, anti-eTG autoantibodies correlate with disease activity in DH. The sensitivity of anti-eTG antibodies for DH ranges from 60% to just over 80% depending on the study, and specificity ranges from nearly 93% to 100%.5Bolotin D. Petronic-Rosic V. Dermatitis herpetiformis. Part II. Diagnosis, management, and prognosis.J Am Acad Dermatol. 2011; 64: 1027-1033Abstract Full Text Full Text PDF PubMed Scopus (77) Google Scholar While serologic studies were not performed for the patient presented here, he was reinitiated on a strict gluten-free diet in the hospital.B.Anti-gliadin antibodies – Incorrect. IgA antibodies to gliadin, the soluble antigenic component of gluten, are formed in the gut and contribute to small-bowel involvement in both CD and DH.4Patterson J. Hosler G. Prenshaw K. Weedon’s Skin Pathology.5th ed. Elsevier, 2020Google Scholar,6Antiga E. Maglie R. Quintarelli L. et al.Dermatitis herpetiformis: Novel perspectives.Front Immunol. 2019; 10: 1290Crossref PubMed Scopus (48) Google ScholarC.Anti-tissue transglutaminase 2 (TTG2) antibodies – Incorrect. IgA anti-TTG2 antibodies are seen in both CD and DH, and these antibodies correlate with small-bowel disease and gluten ingestion. A strict gluten-free diet is the treatment of choice for DH, with a reduction in the risk of small-bowel lymphoma, as well as clearance of skin lesions within 1-6 months. Dapsone can accelerate resolution of DH, with improvement within days upon initiating therapy.4Patterson J. Hosler G. Prenshaw K. Weedon’s Skin Pathology.5th ed. Elsevier, 2020Google Scholar,6Antiga E. Maglie R. Quintarelli L. et al.Dermatitis herpetiformis: Novel perspectives.Front Immunol. 2019; 10: 1290Crossref PubMed Scopus (48) Google ScholarD.IgA endomysial antibodies – Incorrect. IgA endomysial antibodies are formed in the gut, and these antibodies can be found in both patients with CD without cutaneous involvement, and in DH.4Patterson J. Hosler G. Prenshaw K. Weedon’s Skin Pathology.5th ed. Elsevier, 2020Google Scholar,6Antiga E. Maglie R. Quintarelli L. et al.Dermatitis herpetiformis: Novel perspectives.Front Immunol. 2019; 10: 1290Crossref PubMed Scopus (48) Google ScholarE.Indirect immunofluorescence on skin substrate – Incorrect. Indirect immunofluorescence on skin substrate is always negative in DH. Only in diseased skin do serum IgA antibodies against eTG antigen form complexes and subsequently deposit in the papillary dermis.4Patterson J. Hosler G. Prenshaw K. Weedon’s Skin Pathology.5th ed. Elsevier, 2020Google Scholar,6Antiga E. Maglie R. Quintarelli L. et al.Dermatitis herpetiformis: Novel perspectives.Front Immunol. 2019; 10: 1290Crossref PubMed Scopus (48) Google Scholar None disclosed.

Dada, Leanne DO∗; Succari, Loutfi MD∗; Vittor, Amy Y. MD, PhD†; Clapp, William L. MD‡; Zhuang, Haoyang PhD∗; Saikaly, Sami K. MD§; Auerbach, Jena DO‡; Han, Shuhong PhD∗; Mehrad, Borna MD∥; Reeves, Westley H. MD∗ Author Information

We report a case of a complex skin and soft tissue infection caused by Scedosporium apiospermum complex and Neisseria spp. following a dog bite. While Neisseria skin and soft tissue infections after dog bites have been reported, only one case of subsequent infection caused by Scedosporium spp. has been noted in the literature. To the best of our knowledge, this is the first reported case of coinfection of these particular organisms following a dog bite.

The authors declare no conflict of interest. The data that support the findings of this study are available from the corresponding author, Kiran Motaparthi, upon reasonable request.

Lichenoid granulomatous dermatitis (LGD) is a histopathologic pattern with a band-like lymphocytic infiltrate, typical of lichenoid dermatitis, combined with dermal histiocytes and granulomatous inflammation. Prior reports have described cases of LGD caused by non-tuberculous mycobacteria, with evidence of intralesional acid-fast bacilli or mycobacterial DNA. Herein, we report a patient with pulmonary and extrapulmonary Mycobacterium tuberculosis infection who developed LGD. No evidence of M. tuberculosis was detected within the cutaneous lesions, suggesting a potential delayed-type hypersensitivity reaction to tuberculosis.

To the Editor: Acute generalized exanthematous pustulosis (AGEP) and pustular psoriasis (PP) demonstrate considerable overlap in clinical and histopathologic features.1Roujeau J.C. Bioulac-Sage P. Bourseau C. et al.Acute generalized exanthematous pustulosis. Analysis of 63 cases.Arch Dermatol. 1991; 127: 1333-1338Crossref PubMed Scopus (635) Google Scholar The underlying immunologic mechanisms for AGEP and PP have not been fully characterized and thus warrant further study. Discrimination between AGEP and PP is worthwhile given the contrast in management and clinical course. The objective of this study was to identify findings to differentiate AGEP and PP. After University of Florida Institutional Review Board approval, we queried the laboratory information system at University of Florida Department of Dermatology and identified 22 patients with AGEP and 11 with PP. Defining features favoring AGEP or PP included a history of medication ingestion before onset or a history of plaque psoriasis, respectively. We reviewed the clinical and histopathologic features of each patient, and an immunohistochemistry (IHC) panel consisting of phosphohistone H3, CD3, CD4, CD8, CD161, and forkhead box P3 (FOXP3) was performed. Histopathologic variables assessed included subcorneal pustules, spongiosis (with any or all of Langerhans cell vesicles, neutrophilic spongiosis, or eosinophilic spongiosis), vacuolar interface dermatitis, perifollicular or perieccrine inflammation, dilated papillary vessels, dermal edema, and leukocytoclastic vasculitis. The number of dermal eosinophils was quantified per 1 mm2. Histopathologic and IHC variables were analyzed by a committee of 3 evaluators (K.M., D.B., and J.I.) and are listed in Table I. Clinical findings are summarized in Supplementary Table II (available via Mendeley at https://doi.org/10.17632/9fnwf5zjgv.1), including patient history, clinical morphology, final diagnosis, follow-up, mucosal involvement, Stevens-Johnson syndrome/toxic epidermal necrolysis-like features, acral purpura, and scaling plaques.Table IHistologic and immunohistochemical findings in acute generalized exanthematous pustulosis (AGEP) and pustular psoriasis (PP)Variable∗Categorical data are presented as percentages and continuous data as means ± SD or as indicated.AGEPPPP value†Bold values are statistically significant (P < .05).Histologic finding Subcorneal pustules71%91%.194 Langerhans cell vesicles43%9%.050 Neutrophilic spongiosis76%91%.311 Eosinophilic spongiosis38%0%.018 Vacuolar interface change43%0%.009 Perifollicular inflammation43%18%.153 Perieccrine inflammation24%27%.780 Dilated papillary vessels91%100%.277 Dermal edema57%27%.101 Dermal eosinophilia52%0%.014 Leukocytoclastic vasculitis19%0%.114Immunohistochemistry Intraepidermal CD3-positive cells (range)4 to >4016 to >40.052 Epidermal PHH3-positive cells (range)0 to >401-29.977 Dermal CD4:CD8 ratio2427.340 Dermal FOXP3-positive cells8.1 ± 11.8 (n = 21)9.2 ± 7.0 (n = 21).746 Dermal CD161-positive cells5.4 ± 4.5 (n = 20)11.2 ± 6.4 (n = 11).017FOXP3, Forkhead box P3; PPH3, phosphohistone H3.∗ Categorical data are presented as percentages and continuous data as means ± SD or as indicated.† Bold values are statistically significant (P < .05). Open table in a new tab FOXP3, Forkhead box P3; PPH3, phosphohistone H3. The following histopathologic findings favored AGEP (Fig 1) over PP (Supplementary Fig 2): eosinophilic spongiosis (P = .018), vacuolar interface dermatitis (P = .010), and dermal eosinophilia (>2 per mm2, P = .003). Dermal CD161 positivity with a threshold of 10 positive cells per punch biopsy specimen favored PP over AGEP (P < .001). FOXP3 was not helpful in distinguishing AGEP from PP. Clinically unique to AGEP (Supplementary Fig 3) was mucosal involvement (4 [18%]), although it lacked statistical significance (P > .05). Clinical features that favored PP were history of psoriasis (5 [45%], P < .001) and the presence of scaling plaques (6 [55%], P = .005). In summary, a combination of clinical and histopathologic findings is helpful in differentiating AGEP from PP. Additionally, IHC for CD161 and FOXP3 can be used to compare T-helper cell type 17 (Th17) cells in AGEP and PP. Th17 cells are now well described in the pathogenesis of psoriasis and psoriatic arthritis.2Zaba L.C. Fuentes-Duculan J. Eungdamrong N.J. et al.Psoriasis is characterized by accumulation of immunostimulatory and Th1/Th17 cell-polarizing myeloid dendritic cells.J Invest Dermatol. 2009; 129: 79-88Abstract Full Text Full Text PDF PubMed Scopus (351) Google Scholar CD161 is established as a marker of Th17 cell activity in psoriasis.3Antiga E. Volpi W. Chiarini C. et al.The role of etanercept on the expression of markers of T helper 17 cells and their precursors in skin lesions of patients with psoriasis vulgaris.Int J Immunopathol Pharmacol. 2010; 23: 767-774Crossref PubMed Scopus (11) Google Scholar FOXP3-positive regulatory T cells serve as progenitors of Th17 cells and thus play an important role in the production of pathogenic Th17 lines.4Komatsu N. Okamoto K. Sawa S. et al.Pathogenic conversion of Foxp3+ T cells into TH17 cells in autoimmune arthritis.Nat Med. 2014; 20: 62-68Crossref PubMed Scopus (730) Google Scholar The significantly increased CD161 expression in PP relative to AGEP is consistent with the current understanding of the Th17 pathway.3Antiga E. Volpi W. Chiarini C. et al.The role of etanercept on the expression of markers of T helper 17 cells and their precursors in skin lesions of patients with psoriasis vulgaris.Int J Immunopathol Pharmacol. 2010; 23: 767-774Crossref PubMed Scopus (11) Google Scholar FOXP3 IHC findings may be attributed to a lack of antibody specificity and concomitant increase in FOXP3-positive regulatory T cells with Th17 cells in both AGEP and PP. Elucidating the nature of the T-cell population in the dermis may permit discrimination between AGEP and PP; CD161 serves as a candidate marker in this context. Limitations of this study are its retrospective nature and small overall sample yielding low statistical power. The authors thank Mary Bohannon for assistance in Institutional Review Board preparation, Cindy Jones for query and retrieval of archived cases, and Jason Burrow for immunohistochemistry.

Infection-related glomerulonephritis (IRGN) is an immune complex-mediated glomerulonephritis (GN), often preceded by infection with subsequent recovery of renal function after the resolution of the infection. C3 deposition in the absence of immune complex deposits can be seen in patients with IRGN, but with the emergence of C3 glomerulonephritis (C3GN), the distinction is difficult as the clinical and pathological presentation may be similar. However, their treatment and clinical course vary significantly. A 64-year-old man with a history of hypertension and bioprosthetic aortic valve presented to the Emergency Department with left upper quadrant (LUQ) pain and a purpuric rash on bilateral lower extremities. The patient became septic, and further workup during the hospitalization revealed endocarditis secondary to Streptococcus viridans. On admission, the patient had acute kidney injury (AKI) with a serum creatinine of 3.79 mg/dl, which peaked at 5.72 mg/dl during the hospitalization. Renal biopsy demonstrated segmental necrotizing glomerulonephritis on light microscopy, predominant C3 deposition on immunofluorescence (IF) staining, and mesangial and paramesangial deposits on electron microscopy. This histologic picture can be seen both in IRGN and C3GN. The patient was treated with intravenous ceftriaxone for six weeks for endocarditis and the kidney injury was managed with supportive care. The patient’s renal function improved and complement levels normalized, supporting the diagnosis of IRGN retrospectively. IRGN can mimic C3GN, and evaluation for alternate pathways of the complement system may be warranted in patients with atypical presentation of IRGN.

Dermatobia hominis, also known as the human botfly, is an insect native to Central and South America that is known to parasitize both human and animal hosts through cutaneous infestation by its developing larvae. While human botfly myiasis has been commonly diagnosed through dermatologic findings, the presenting lesions and associated symptoms can be non-specific and often misconstrued as other more common cutaneous diagnoses. Here, we present a case of botfly myiasis of the scalp in which ultrasound was utilized to visualize the larvae and confirm the diagnosis prior to larval removal. In this report, we discuss our patient's presentation, ultrasound imaging, and clinical course/treatment in order to convey how ultrasound imaging, when available, is a valuable tool in establishing the diagnosis of human botfly myiasis.

Leukemia cutis (LC) is rare and can have varying clinical and histopathologic presentations.1,2 In acute lymphoblastic leukemia (ALL), LC has been reported in 1% to 3% of cases and usually after diagnosis, although it can present simultaneously, or even precede, the diagnosis of leukemia.3-5 The clinical appearance of the leukemic infiltrate in the skin typically includes papules, plaques, and nodules and infrequently has mimicked inflammatory disorders.1,3,6,7 Uncommonly, LC also mimics inflammatory disorders histopathologically, with a sparse perivascular or interstitial infiltrate instead of more dense nodular infiltrates.

ABSTRACT Objective: Gastrointestinal (GI) panels have allowed for faster and accurate detection, treatment, and control of pathogens. Because of the large number of potential pathogens included in the panel the clinical significance and manifestations of some organisms, such as Enteroaggregative Escherichia coli (EAEC) and Enteropathogenic E. coli (EPEC), remains undetermined. Methodology: We performed a single-institution retrospective chart review for 222 patients with a stool sample tested on BioFire FilmArray Gastrointestinal Panel (GI Panel) between June 1, 2016 and March 9, 2017. Results: Of the 222 patients, four had EAEC and 17 and EPEC. Patients who tested positive for EAEC and EPEC were younger (26.3 years and 33.9 years, respectively) than patients that did not test positive for a GI pathogen (47.7 years). In cases where multiple organisms were detected, EPEC was present 56.3% of the time. Analysis of symptoms showed that EPEC patients had a high prevalence of abdominal pain (p=0.0425) and vomiting (p=0.0045), but not diarrhea, when compared to the presence of these symptoms in patients with no targets detected. With only four patients positive for EAEC in this study, the results of symptoms in EAEC patients were inconclusive. Cases involving EPEC and EAEC were treated similarly to other cases of diarrhea with no significant difference in the number of imaging studies and medication changes. Conclusions: While further studies are required to determine the specific clinical significance of EAEC or EPEC, it is evident that patients positive for EPEC often experience abdominal pain and diarrhea, suggesting EPEC may be more pathogenic than previously thought.  J Microbiol Infect Dis 2019; 9(1):1-9.

The Breast JournalVolume 25, Issue 4 p. 726-727 BREAST IMAGES Intravascular nevus cell aggregate in axillary lymph node mimicking metastatic breast carcinoma Jaya Ruth Asirvatham MBBS, Corresponding Author Jaya Ruth Asirvatham MBBS ruthasirvatham@ufl.edu orcid.org/0000-0002-2266-4014 Department of Pathology, Immunology and Laboratory Medicine, College of Medicine, University of Florida, Gainesville, Florida Correspondence Jaya Ruth Asirvatham, Department of Pathology, Immunology and Laboratory Medicine, College of Medicine, University of Florida, PO Box 100275, Gainesville, FL. Email: ruthasirvatham@ufl.eduSearch for more papers by this authorAlan Siroy MD, Alan Siroy MD Department of Pathology, Immunology and Laboratory Medicine, College of Medicine, University of Florida, Gainesville, FloridaSearch for more papers by this authorJena Auerbach DO, Jena Auerbach DO Department of Pathology, Immunology and Laboratory Medicine, College of Medicine, University of Florida, Gainesville, FloridaSearch for more papers by this authorDavid Hernandez-Gonzalo MD, David Hernandez-Gonzalo MD Department of Pathology, Immunology and Laboratory Medicine, College of Medicine, University of Florida, Gainesville, FloridaSearch for more papers by this author Jaya Ruth Asirvatham MBBS, Corresponding Author Jaya Ruth Asirvatham MBBS ruthasirvatham@ufl.edu orcid.org/0000-0002-2266-4014 Department of Pathology, Immunology and Laboratory Medicine, College of Medicine, University of Florida, Gainesville, Florida Correspondence Jaya Ruth Asirvatham, Department of Pathology, Immunology and Laboratory Medicine, College of Medicine, University of Florida, PO Box 100275, Gainesville, FL. Email: ruthasirvatham@ufl.eduSearch for more papers by this authorAlan Siroy MD, Alan Siroy MD Department of Pathology, Immunology and Laboratory Medicine, College of Medicine, University of Florida, Gainesville, FloridaSearch for more papers by this authorJena Auerbach DO, Jena Auerbach DO Department of Pathology, Immunology and Laboratory Medicine, College of Medicine, University of Florida, Gainesville, FloridaSearch for more papers by this authorDavid Hernandez-Gonzalo MD, David Hernandez-Gonzalo MD Department of Pathology, Immunology and Laboratory Medicine, College of Medicine, University of Florida, Gainesville, FloridaSearch for more papers by this author First published: 13 May 2019 https://doi.org/10.1111/tbj.13310Citations: 1Read 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 onFacebookTwitterLinkedInRedditWechat No abstract is available for this article.Citing Literature Volume25, Issue4July/August 2019Pages 726-727 RelatedInformation

To the Editor: Rowell syndrome is characterized by erythema multiforme–like lesions with serologic and historical evidence of lupus erythematosus (LE).1Torchia D. Romanelli P. Kerdel F.A. Erythema multiforme and Stevens-Johnson syndrome/toxic epidermal necrolysis associated with lupus erythematosus.J Am Acad Dermatol. 2012; 67: 417-421Abstract Full Text Full Text PDF PubMed Scopus (49) Google Scholar Classification of Rowell syndrome remains controversial, given overlapping clinical features of erythema multiforme and cutaneous LE (CLE).2Rowell N.R. Beck J.S. Anderson J.R. Lupus erythematosus and erythema multiforme-like lesions. A syndrome with characteristic immunological abnormalities.Arch Dermatol. 1963; 88: 176-180Crossref PubMed Scopus (181) Google Scholar Our objective was to identify histologic and immunohistochemical findings that support classification of Rowell syndrome because current definitions lack these criteria.3Zeitouni N.C. Funaro D. Cloutier R.A. et al.Redefining Rowell's syndrome.Br J Dermatol. 2000; 142: 343-346Crossref PubMed Scopus (113) Google Scholar CD123, which labels pathogenic plasmacytoid dendritic cells in LE, might be useful in this context.4Swiecki M. Colonna M. The multifaceted biology of plasmacytoid dendritic cells.Nat Rev Immunol. 2015; 15: 471-485Crossref PubMed Scopus (659) Google Scholar, 5Vermi W. Lonardi S. Morassi M. et al.Cutaneous distribution of plasmacytoid dendritic cells in lupus erythematosus. Selective tropism at the site of epithelial apoptotic damage.Immunobiology. 2009; 214: 877-886Crossref PubMed Scopus (115) Google Scholar After institutional review board approval, the archives of the University of Florida and Inform Diagnostics were queried for diagnoses of Rowell syndrome (8 biopsies from 5 patients), subacute CLE (SCLE, 7 biopsies from 4 patients), and erythema multiforme (5 biopsies from 5 patients) rendered during November 2016-June 2018; an additional single indeterminate case was also identified. Clinical features, serology, histology, and CD123 antibody staining for plasmacytoid dendritic cells were compared between Rowell syndrome, SCLE, and erythema multiforme cases after a blinded retrospective histologic review. A Fisher's exact test was used to compare histologic variables and CD123 staining patterns among Rowell syndrome, SCLE, and erythema multiforme cases. Two-tailed P values <.05 were deemed statistically significant. Rowell syndrome and SCLE were characterized by female predominance, antecedent history of LE, lack of causative medication, absence of mucosal involvement, positivity for rheumatoid factor, and speckled antinuclear antibody pattern with anti-Ro (SS-A) positivity (Table I). Targetoid plaques were observed in Rowell syndrome (4/4) but not SCLE (0/4). Conversely, anti-La (SS-B) positivity was observed in SCLE (2/3) but not in Rowell syndrome (0/4), which might reflect variable assay sensitivity for the detection of this autoantibody.6Franceschini F. Cavazzana I. Anti-Ro/SSA and La/SSB antibodies.Autoimmunity. 2005; 38: 55-63Crossref PubMed Scopus (178) Google Scholar Direct immunofluorescence was positive in Rowell syndrome (1/1) and SCLE (1/1) but negative in erythema multiforme (0/1). Summarized in Table I, the common and unifying histologic features of Rowell syndrome (Fig 1) and SCLE (Figure 2; available at https://data.mendeley.com/datasets/bwswc4h9yb/1) include periadnexal lymphocytic infiltrates (P = 1), absence of dermal eosinophils (P = 1), and CD123 positivity of ≥10% of the inflammatory infiltrate (P = 1). Distinction of Rowell syndrome from erythema multiforme (Figure 3; available at https://data.mendeley.com/datasets/bwswc4h9yb/1) can be supported by periadnexal lymphocytic infiltrates (P = .003) and periadnexal CD123+ plasmacytoid dendritic cells (P = .049). Using these features, the indeterminate case was reclassified as Rowell syndrome. Several features did not aid classification (1 > P > .05), including interface tissue reaction subtype (lichenoid or cell poor), deep perivascular lymphocytic infiltrates, periadnexal plasmacellular aggregates, mucin deposition (by Alcian blue staining), and the predominant CD123 staining pattern (epidermal or dermal).Table IComparison of RS, SCLE, and EM by clinical, serologic, histologic and immunohistochemical findingsCharacteristic or findingRS (5 patients; 8 biopsies)SCLE (4 patients; 7 biopsies)EM (5 patients; 5 biopsies)RS and SCLE, P valueRS, SCLE, and EM, P valueAge, y, mean ± standard deviation53 ± 23.1562.8 ± 16.4452.8 ± 16.07Female sex80 (4/5)100 (4/4)80 (4/5)11History of LE∗History of systemic or cutaneous LE.100 (4/4)75 (3/4)0 (0/5)1.0047Targetoid lesions†≥2 zones of color.100 (4/4)0 (0/4)100 (5/5).0286.0028Mucosal involvement0 (0/4)0 (0/4)40 (2/5)1.2821Implicated medication0 (0/4)0 (0/4)20 (1/5)11Speckled antinuclear antibody pattern50 (2/4)67 (2/3)0 (0/2)1.5238Lesional direct immunofluorescence‡Granular deposition of IgG in the lower epidermis along the basement membrane zone, with an antinuclear antibody pattern in keratinocytes. Granular deposition of IgM, IgA, and complement C3 and C5b-9 along the basement membrane zone.100 (1/1)100 (1/1)0 (0/1)11Full-thickness epidermal necrosis50 (4/8)0 (0/7)80 (4/5).077.017Parakeratosis25 (2/8)85.7 (6/7)20 (1/5).041.034Dermal eosinophils0020 (1/5)1.250Periadnexal lymphocytic infiltrate§Perifollicular or perieccrine.87.5 (7/8)85.7 (6/7)01.003≥10% CD123+ cells¶Percentage of inflammatory cells positive for antibody staining in a single histologic section.62.5 (5/8)57.1 (4/7)20 (1/5)1.395Dermal-predominant CD123 pattern42.9 (3/7)83.3 (5/6)40 (2/5).266.292Intraepidermal CD123+ plasmacytoid DCs100 (7/7)66.7 (4/6)100 (5/5).192.163Periadnexal CD123+ plasmacytoid DCs100 (7/7)66.7 (4/6)40 (2/5).192.049Values are % (n/total) except where indicated. Significant values are in bold.DCs, Dendritic cells; EM, erythema multiforme; LE, lupus erythematosus; RS, Rowell syndrome; SCLE, subacute cutaneous lupus erythematosus.∗ History of systemic or cutaneous LE.† ≥2 zones of color.‡ Granular deposition of IgG in the lower epidermis along the basement membrane zone, with an antinuclear antibody pattern in keratinocytes. Granular deposition of IgM, IgA, and complement C3 and C5b-9 along the basement membrane zone.§ Perifollicular or perieccrine.¶ Percentage of inflammatory cells positive for antibody staining in a single histologic section. Open table in a new tab Values are % (n/total) except where indicated. Significant values are in bold. DCs, Dendritic cells; EM, erythema multiforme; LE, lupus erythematosus; RS, Rowell syndrome; SCLE, subacute cutaneous lupus erythematosus. This series is limited by its small sample size, retrospective nature, and lack of complete clinical data for all patients. Previously dependent on clinical history, serology, and nonspecific clinical morphology, diagnosis of Rowell syndrome might be improved by histologic detail and CD123 staining. Unifying features of Rowell syndrome and SCLE include antecedent history of LE, absence of mucosal involvement, serology (antinuclear antibody, anti-Ro, and rheumatoid factor), direct immunofluorescence positivity, periadnexal lymphocytic infiltrates, absence of dermal eosinophils, and CD123+ inflammatory cells only when comprising ≥10% of the inflammatory infiltrate. In the context of targetoid clinical morphology, this feature aids in the distinction of Rowell syndrome from erythema multiforme. These clinicopathologic findings support inclusion of Rowell syndrome in the spectrum of CLE and provide therapeutic or prognostic benefit to patients with diagnoses previously identified as Rowell syndrome or erythema multiforme.

Objectives: Hematopoietic stem cell transplantation (HSCT) patients are at higher risk of infection compared to their healthy counterparts.Aims were identity type and incidence of skin infections, describe the use of diagnostic tests, and identify the role of dermatology consults. Methods:In this single institution retrospective chart review, data were extracted from the medical record.A clinically diagnosed skin infection was defined as any skin pathology treated with antibiotics, antivirals, antifungals, or antiparasitics.The diagnostic tests data such as cultures, polymerase chain reactions (PCR), and direct fluorescent antibody (DFA) tests, and dermatology consultations were also collected.Results: A total of 92 patients and 143 skin infections were identified in the 5-year study period.The majority of infections occurred while the patient was not neutropenic.The infectious agents responsible for infections varied depending on a patient's age, neutropenia status, graft-versus-host disease (GVHD) diagnosis, and transplant type.Only 25 infections (17%) received a dermatology consultation.On average, infections associated with dermatology consultation received a higher number of diagnostic tests compared to those that did not receive a dermatology consultation. Conclusions:The etiologies and severities of clinically identified skin infections in HSCT patients are varied and require continuous vigilance of dermatological health.Dermatologists are not necessarily the physician's ordering more diagnostic.Therefore, earlier assessment by dermatologists might prevent excessive laboratory testing and earlier management of severe clinically identified infections.

Garcia, Dante BA*; Nielson, Colton B. MD†; Gillihan, Ryan MD†; Schoch, Jennifer MD†; Auerbach, Jena DO‡; Motaparthi, Kiran MD†Author Information

Solid organ transplant patients are well established to be at risk of herpes simplex virus and varicella zoster virus infection and reactivation. We present a case of a 41-year-old woman with a history of pancreas and renal transplant who presented with what appeared to be disseminated herpes simplex virus or varicella zoster virus induced rash, but who was ultimately diagnosed and treated as linear IgA bullous dermatosis. This case alerts physicians to other non-infectious dermatoses as a cause of vesiculobullous rash in solid organ transplant patients.

The objective of our study was to establish a detailed photomicrographing protocol for pathologists and dermatopathologists using standard overhead camera and image editing packages. Through a trial‐and‐error approach we devised a series of steps that comprise our photomicrographing protocol. Descriptive and interpretive data analyses were performed to highlight how each step improves tinctorial quality of digital photomicrographs.

Calciphylaxis is a rare syndrome of vascular calcification with thrombosis that occurs most often in patients with end‐stage renal disease, and it frequently portends a guarded prognosis. Rarely, nonuremic calciphylaxis (NUC) may occur; in this context, a strongly supportive histology is crucial in establishing the diagnosis. Herein, we describe 2 cases of NUC associated with pseudoxanthoma elasticum‐like changes, identified in both initial nondiagnostic and subsequent diagnostic biopsy specimens. This unusual but helpful histologic finding may support the early diagnosis and treatment of a potentially life‐threatening disease in the context of subtle histopathologic vascular changes or in the absence of classic clinical or laboratory findings.

CONTEXT Oncotype DX is a multigene reverse transcription-polymerase chain reaction assay used to quantify recurrence risk in patients with stage I or II estrogen receptor-positive, lymph node-negative invasive breast cancer. The results are reported as a Recurrence Score (RS). The 16 cancer genes evaluated include a proliferation set, hormone receptor set, and HER2 set. The activity of these genes is addressed by pathologic assessment of breast cancers. OBJECTIVE To determine if factors evaluated in pathologic evaluation of breast cancer could be used to predict Oncotype DX results. DESIGN We studied 138 cases of invasive breast cancer for which Oncotype DX results and pathology data were available. Grading was performed by using Nottingham grading system. For hormone receptor immunostaining, 10% nuclear staining was considered a positive result. RESULTS Oncotype DX RS was low in 81 cases, intermediate in 44 cases, and high in 13 cases. All 6 cases with both a negative progesterone receptor (PR) and a mitotic count score of 3 had a high RS. All 12 cases with both a negative PR and a mitotic count score greater than 1 had either an intermediate or high RS. Although Nottingham grade, PR status, mitotic count score, tumor size, and nuclear grade were each significantly associated with RS, in bivariate analyses the only variables that remained independently predictive of an intermediate or high RS score in a multivariate logistic regression model were negative PR and mitotic count score greater than 1. CONCLUSIONS Our study suggests that a mitotic count score greater than 1 combined with a negative PR result, as determined by pathologic assessment, could serve as a marker for an intermediate or high Oncotype DX RS.