The unpredictability of the coronavirus disease 2019 (COVID-19) pandemic has created an ongoing global healthcare crisis. Implementation of a mass vaccination program to accelerate disease control remains in progress. Although injection site soreness, fatigue, and fever are the most common adverse reactions reported after a COVID-19 vaccination, ipsilateral lymph node enlargement has increasingly been observed. In patients undergoing routine screening and surveillance for breast cancer, interpreting lymphadenopathy (LAP) is challenging in the setting of a recent COVID-19 vaccination. With a growing proportion of the population receiving the vaccine, a multifaceted approach is necessary to avoid unnecessary and costly workup. In this comprehensive review, we summarize the existing literature on COVID-19 vaccine-associated LAP in breast imaging patients.
Background Systemic therapies for refractory meningiomas are limited with no FDA approved therapeutics. Vascular endothelial growth factor (VEGF) is a signaling protein associated with neovascularization, peritumoral edema, and meningioma tumorigenesis. Methods This phase II study investigates the efficacy of bevacizumab (BEV), a VEGF binding monoclonal antibody, in patients with progressive Grade I (G1M), Grade II (G2M), Grade III (G3M) meningioma, and other non-parenchymal tumors including vestibular schwannoma (n=4) and hemangiopericytoma (HPC) (n=4) with primary endpoint of PFS-6. Non-meningiomas were included with the respective meningioma grade in analysis. Secondary endpoints include median overall survival (mOS), and response rate. Results 50 patients (26 women; median age 54 years; range 23-81), 42 with of progressive meningioma) were treated: 10 G1M, 20 G2M, and 12 G3M. Prior treatments include surgical resection (41 patients), radiosurgery (24 patients), external beam radiotherapy (28 patients) and chemotherapy (14 patients). Median infusions administered was 16 (range, 2-68). Response was graded using the Macdonald criteria. PFS-6, mPFS, and mOS were 87%, 22 months, 35 months for G1M; 77%, 23 months, 41 months for G2M, and 46%, 8 months, 12 months for G3M. Best radiographic responses include stable disease (G1M: 100%; G2M: 85%; G3M: 82%); partial response (G1M: 0%; G2M: 5%; G3M: 0%) and progressive disease (G1M: 0%; G2M: 10%; G3M:18%). The most common toxicities were hypertension (n=19, 42.2%), proteinuria (n=16, 35.6%), and fatigue (n=14, 31.1%). Conclusion This study showed BEV is well tolerated and appears to be a promising systemic treatment option for patients with recurrent and refractory meningiomas.
Background: Eosinophils are versatile reactionary cells that play a key role in the inflammatory response. Excessive proliferation and aggregation of eosinophils have been implicated in the pathogenesis of ischemic neurologic and cardiac events. We present a rare case of hypereosinophilic syndrome (HES) in a patient hospitalized for simultaneous acute cerebrovascular accident (CVA) and acute coronary syndrome. Case: A 53-year-old male with past medical history of hypertension and diabetes mellitus presented with new onset bifrontal headache, right arm numbness and apraxia, and concurrent typical angina. On physical examination, he had small non-tender raised nodules on the bilateral upper and lower limbs. MRI of the brain demonstrated multifocal infarcts in a watershed distribution. Biochemical investigation revealed rising troponins. Splenomegaly of 16.4 cm was found on CT imaging. He was admitted for management of acute CVA and non-ST segment elevation myocardial infarction (NSTEMI). Complete blood count (CBC) revealed leukocytosis (34.4 K/mcL) with an eosinophilia of 85% and an absolute eosinophil count (AEC) of 29.2 x 10 3 eosinophils/µL. Serum tryptase was 29.2 µg/L. The patient was started on a high dose steroid with subsequent resolution of his neurologic and cardiac symptoms. Due to high suspicion for HES, FISH panel and bone marrow biopsy were performed. A small focus of marrow on his biopsy showed abundant eosinophils and bland spindle cells (>15 mast cells in aggregate). FISH panel was positive for 4q12 rearrangement, consistent with a FIP1L1/PDGFRA fusion mutation. Skin biopsy of his lesions demonstrated superficial and deep inflammation with eosinophils. He was diagnosed with myeloproliferative HES with features of mastocytosis and started on imatinib. Discussion: The defining features of HES consist of eosinophilia greater than 1500/µL for greater than 6 months with evidence of eosinophil induced tissue infiltration and injury. The ability of eosinophils to induce pathologic outcomes is influenced by a variety of parameters, including the number of eosinophils present, their location, and the degree of activation. Published data suggests that neurologic and cardiac ischemic events occur in HES patients with a higher leukocyte count and AEC than what we present with in this case. Our patient meets the main lab criteria of HES and our case highlights that simultaneous clinical manifestations can occur in the absence of markedly elevated peripheral eosinophilia. As with most cases involving unexplained hypereosinophilia, a wide range of diagnostic testing was necessary. The presence of a PDGFRA fusion mutation established a clonal disorder, supporting the diagnosis of myeloproliferative HES variant. The presence of eosinophils and the lack of mast cells on skin biopsy further supports myeloproliferative HES variant rather than a true systemic mastocytosis. Despite recent advances in molecular and immunologic therapies, treatment for HES remains challenging due to the wide variety of etiological classifications necessitating targeted treatments. At the time of submission, KIT mutation analysis is pending. Identification of a KIT D816V mutation would support use of midostaurin or the recently approved avapritinib for treatment of overlap syndrome. Disclosures No relevant conflicts of interest to declare.
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