Search

Background: Acute febrile neutrophilic dermatosis, or Sweet's Syndrome (SS), was first characterized by Dr. Robert Sweet in 1964 with eight cases of fever, neutrophilic polymorphonuclear leukocytosis, dermatological lesions, and histological evidence of dense dermal infiltration by mature neutrophils. SS presents in three settings: idiopathic, malignancy-associated, and drug-induced. In 1996, Walker and Cohen outlined the current diagnostic criteria for drug-induced SS with abrupt onset of painful lesions, dermal histology showing dense neutrophilic infiltrate, pyrexia > 38 °C, temporal relationship of drug administration to clinical presentation, and symptom resolution following drug withdrawal or systemic corticosteroid treatment. SS has rarely been reported in association with gynecologic malignancies., Method: Case Report., Case: A 41-year-old female receiving neoadjuvant chemotherapy for advanced high-grade serous ovarian carcinoma presented for evaluation of cyclic fevers with dermatologic lesions following treatment with Carboplatin and Taxol, with Pegfilgrastim. On days 11-17 of treatment she reported fevers ranging from 101°F-104°F (38 °C- 40 °C) with subsequent eruption of truncal erythematous, pustular, and painful coalescing plaques. Lesion biopsies confirmed histologic presence of dense neutrophilic infiltration. The patient was initiated on oral corticosteroid therapy with symptom improvement., Discussion: This case represents an example of SS in a patient receiving therapy with the most commonly implicated medication class, granulocyte colony-stimulating factor (GCSF). In drug-induced SS, there's often a temporal relationship between medication administration and symptom development. In this case, all criteria for drug-induced SS were met with a GCS-F as the likely causative agent. This case illustrates a rare diagnosis in the context of gynecologic cancer treatment and will expand available reports of SS in the Gynecologic Oncology literature. We hope to elicit more prompt recognition and diagnosis of SS from practitioners to minimize patient morbidity and long-term sequelae., Competing Interests: The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (© 2022 The Authors.)

Objective: Our objective was to determine the rate of BRCA1/2 deficiency in platinum-sensitive and platinum-resistant tumors from a cohort of unselect patients with advanced epithelial ovarian cancer (EOH)., Methods: BRCA1/2 mutation analysis was performed in 29 patients with platinum-sensitive EOC and 24 patients with platinum-resistant disease. Germline DNA was analyzed in mutation carriers when normal tissue was available. BRCA expression was ascertained by quantitative rt-PCR. Associations between BRCA mutation status and expression levels and parameters of platinum response were analyzed., Results: Fifteen of 53 (28.3%) EOC tumors had BRCA1/2 mutations. Twelve mutations were in BRCA1, while 3 involved BRCA2. Of the 12 mutation-carriers with normal tissue available for DNA analyses, 33.3% of the mutations were found to be somatic. Three mutations were novel. The majority of BRCA mutations (73%) were identified in patients with platinum-sensitive disease. In total, 38% of platinum-sensitive tumors were found to have a BRCA mutation, compared to 17% of the platinum-resistant patients. A statistical trend toward platinum-sensitive disease was seen in BRCA mutation carriers (p=0.079). Nineteen (36%) study patients had some form of BRCA deficiency, and these patients were less likely to have platinum-resistant tumors (OR=0.29; p value=0.048)., Conclusions: BRCA mutations occurred more frequently in platinum-sensitive EOC than platinum-resistant disease. The high overall frequency of BRCA deficiency in EOC underscores the importance of tumor profiling as therapies targeting the DNA repair pathway are being investigated., (Copyright © 2012 Elsevier Inc. All rights reserved.)

Women who have documented BRCA1 or BRCA2 mutations have a significantly increased lifetime risk of ovarian and breast malignancies. Many women, however, have a perceived personal risk of ovarian cancer despite a calculated low risk, and some seek ways to reduce the risk for ovarian cancer. Given the low prevalence of ovarian cancer in the general population, no screening test has achieved satisfactory levels of disease prediction. This article discusses the efficacy of available screening modalities and reviews current risk-reduction strategies and their effectiveness for preventing ovarian cancer.