Stevens-Johnson syndrome precipitated by Moderna Inc. COVID-19 vaccine: a case-based review of literature comparing vaccine and drug-induced Stevens-Johnson syndrome/toxic epidermal necrolysis.

The Moderna COVID-19 vaccination was approved for use in the United States in December of 20201 and since that time massive public health efforts have been made to vaccinate patients against the COVID-19 infection. Adverse reactions from the vaccination are well-reported and include both local skin reactions, such as pain, swelling, and erythema at the injection site, as well as systemic reactions including fever, malaise, headache, muscle aches, drowsiness, nausea, and vomiting. While severe serious cutaneous adverse reactions, such as Stevens-Johnson syndrome (SJS) or toxic epidermal necrolysis (TEN), remain rare; two cases of SJS/TEN related to COVID-19 vaccination have been reported. We herein review the two previously reported cases of SJS/TEN and report the first case of SJS precipitated by the Moderna Inc., MRNA 1273 COVID-19 vaccination in the United States. Although we review potential adverse reactions to vaccination, the benefits of COVID-19 vaccination outweigh the risks based on current data. Cases should be reported to the Vaccine Adverse Event Reporting System (https://vaers.hhs.gov/) to help public health officials recognize and track these severe but rare adverse events.

Intravascular pseudolymphomatous angiosarcoma: A new finding potentially mistaken for intravascular lymphoma.

Pseudolymphomatous infiltrates associated with angiosarcoma are a rarely reported phenomenon. Recognition of this reactive process is critical to making an accurate diagnosis, both in diagnosing the angiosarcoma and in avoiding an incorrect diagnosis of lymphoma. Here, we present a novel histopathologic pattern, angiosarcoma with a prominently intravascular atypical lymphoid component, mimicking intravascular T-cell lymphoma. Interestingly, serial biopsies in this case revealed a progressive increase in lymphocyte density and intravascular component over time. Despite prior reports of improved progression-free survival and overall survival of patients with pseudolymphomatous angiosarcoma, this patient showed rapid disease progression.

CD4-positive T-cell recruitment in primary-provoked localized vulvodynia: potential insights into disease triggers.

OBJECTIVE: To better understand the potential disease triggers of neurogenic inflammation in provoked localized vulvodynia (PLV), our objective was to determine whether the types of infiltrating lymphocytes were different in vestibular biopsies from women with primary PLV, secondary PLV, and unaffected controls. METHODS: Secondary retrospective analysis of archived vestibular biopsies from a series of adult premenopausal women with primary PLV (n = 10), secondary PLV (n = 10), and unaffected controls (n = 4) was performed. All study patients had severe entry dyspareunia for more than 1 year. Subjects were excluded if pregnant, or they had a known infection, or history of generalized vulvodynia. Biopsies were performed during the midfollicular phase. Lymphocyte subtypes were highlighted in histologic sections using antibodies against CD3, CD4, and CD8 and scored as the mean number of T-cell subtypes per high-power field. Flow cytometry was also used to test fresh biopsies from a de novo prospective series of primary PLV (n = 4) and unaffected controls (n = 2). RESULTS: Unaffected control biopsies showed more CD8-positive than CD4-positive T cells, similar to previous reports of the gynecologic tract. In contrast, biopsies from women with primary PLV showed significantly more CD4-positive T cells than those from women with secondary PLV and unaffected controls (p = .003). This observation was further supported by flow cytometry. CONCLUSIONS: CD4-positive T cells are more numerous in vestibular biopsies from premenopausal women with primary PLV. This may be important because subtypes of CD4-positive T cells are specifically recruited by infectious, allergic, or autoimmune triggers. Future studies distinguishing these subtypes may lead to new insights into this common disease.

Features of plexiform fibrohistiocytic tumor in skin punch biopsies: a retrospective study of 6 cases.

Plexiform fibrohistiocytic tumor (PFHT) is a mesenchymal neoplasm of intermediate malignant potential, which typically presents as a dermal or subcutaneous nodule, and is therefore often sampled by skin punch biopsy where diagnostic features may be subtle or absent. We retrospectively analyzed a series of 6 cases of PFHT to highlight for dermatopathologists the features of PFHTs useful to distinguish it from the other entities in the differential diagnosis. On the basis of the proportion of spindled fibroblastic cells to histiocytoid nodules in the biopsy specimen, we divided PFHT into 3 histologic variants: cellular, fibrous, and mixed. The biopsies also were compared with the final resection specimens, in an attempt to determine which histologic features in the original biopsies were most helpful in establishing a diagnosis. Clinical follow-up and immunohistochemistry were performed on all cases. The cellular and mixed variants were a lesser diagnostic challenge inasmuch as the distinctive features were more easily identifiable in small punch biopsy specimens. The fibrous variant proved more difficult to diagnose. Features most helpful in the diagnosis of PFHT were biphasic appearance with small, cellular, histiocytoid aggregates and accompanying plump spindled cells in the deep dermis and subcutis. Negative staining for CD34, NK1/C3, factor XIIIa, and beta-catenin by immunohistochemistry proved useful in excluding some of its mimics.

KIT gene mutations and copy number in melanoma subtypes.

PURPOSE: We recently identified a KIT exon 11 mutation in an anorectal melanoma of a patient who had an excellent response to treatment with imatinib. To determine the frequency of KIT mutations across melanoma subtypes, we surveyed a large series of tumors. EXPERIMENTAL DESIGN: One hundred eighty-nine melanomas were screened for mutations in KIT exons 11, 13, and 17. KIT copy number was assessed by quantitative PCR. A subset of cases was evaluated for BRAF and NRAS mutations. Immunohistochemistry was done to assess KIT (CD117) expression. RESULTS: KIT mutations were detected in 23% (3 of 13) of acral melanomas, 15.6% (7 of 45) of mucosal melanomas, 7.7% (1 of 13) of conjunctival melanomas, 1.7% (1 of 58) of cutaneous melanomas, and 0% (0 of 60) of choroidal melanomas. Almost all the KIT mutations were of the type predicted to be imatinib sensitive. There was no overlap with NRAS mutations (11.1% of acral and 24.3% of mucosal tumors) or with BRAF mutations (absent in mucosal tumors). Increased KIT copy number was detected in 27.3% (3 of 11) of acral and 26.3% (10 of 38) of mucosal melanomas, but was less common among cutaneous (6.7%; 3 of 45), conjunctival (7.1%; 1 of 14), and choroidal melanomas (0 of 28). CD117 expression, present in 39% of 105 tumors representing all melanoma types, did not correlate with either KIT mutation status or KIT copy number. CONCLUSIONS: Our findings confirm that KIT mutations are most common in acral and mucosal melanomas but do not necessarily correlate with KIT copy number or CD117 expression. Screening for KIT mutations may open up new treatment options for melanoma patients.