estrogens is a therapeutic agent developed by Teva Pharmaceutical Industries Ltd.. It is approved for therapeutic indications via intravaginal or oral (po).
| Brand Names | Cenestin, Bijuva, Barr |
| Company | Teva Pharmaceutical Industries Ltd. |
| Molecular Target | ESR1 |
| Route | Intravaginal, Oral (PO) |
| Status | Approved |
estrogens acts on 1 molecular target:
| ESR1 | estrogen receptor 1 (ER, ESR) |
estrogens is developed for 3 unique indications across 2 therapeutic areas.
| Therapeutic Area | Condition | Phase |
|---|---|---|
| Reproductive system and breast disorders | Atrophic vulvovaginitis | ✓ Approved |
| Surgical and medical procedures | Hormone replacement therapy | ✓ Approved |
| Reproductive system and breast disorders | Menopausal symptoms | ✓ Approved |
Vijayasimha M M, Srikanth M M, Purushothama Reddy K K
Long Xihan X, Lai Liyan L, Lin Qiaomin Q, Duan Dejian D et al.
Hydroa vacciniforme-like lymphoproliferative disorder is a rare Epstein-Barr virus -associated T/NK cell proliferation predominantly. A 72-year-old female presented with persistent skin lesions and high fever. The atypical distribution of lesions, along with the spontaneous regression of some of them, and the positive Staphylococcus aureus culture, initially made the diagnostic process complicated. However, skin biopsies revealed CD3+CD8+ T-cell infiltration, partial loss of CD5 expression, a high proliferative index, and positive Epstein-Barr virus-encoded RNA in situ hybridization. Reactive lymph node hyperplasia ruled out systemic lymphoma, thus supporting the diagnosis of HVLPD. HVLPD can present in the elderly with lesions in unexposed areas. Diagnostic challenges require accounting for infectious confounders.
Szczepanik Dariusz W DW, Wieczorkiewicz Pawel A PA
Understanding the electronic structure of (anti)-aromatic poly- and macrocyclic π-conjugated systems remains a central challenge in contemporary chemistry, given their importance in materials science, molecular electronics, photophysics, and catalysis. While magnetically induced ring currents and NMR-based descriptors have long served as key indicators of (anti)-aromatic character, the extent to which such magnetic observables reflect the full ground-state π-bonding architecture becomes less transparent in large and topologically complex systems. Here we introduce a wavefunction-based analytical protocol the π-Bond Delocalization Function (BDFπ) which maps the spatial organization of localized and delocalized π-bonding directly from the ground-state one-electron density matrix. Rather than relying on predefined resonance models or orbital localization schemes, the method extracts bonding topology from the complete occupied π-space. This enables a direct comparison between the global π-electron distribution and the more selective subset of frontier-orbital excitations that dominate magnetic response phenomena. Applied to representative poly- and macrocyclic systems frequently discussed in the context of global (anti)-aromaticity, BDFπ reveals that magnetic ring currents and bonding delocalization need not coincide quantitatively in extended conjugated frameworks. Magnetic descriptors predominantly probe perturbative response channels, whereas the underlying resonance structure reflects the collective organization of the entire occupied π-manifold. By explicitly relating these two perspectives, the present framework provides a coherent and chemically transparent account of how resonance topology and experimentally observable magnetic behavior are connected and where they may diverge in large conjugated architectures.
Yuan Ni N, Wang Yi Y, Yao Dan D, Du Yanqiang Y
Green neutrophilic inclusions (GNIs) are rare cytoplasmic inclusions in peripheral blood smears, historically associated with acute liver failure and high mortality. Recent evidence suggests that GNIs may also occur in other critical illnesses; however, reports in pediatric populations remain scarce. Hemophagocytic lymphohistiocytosis (HLH) is a life-threatening hyperinflammatory syndrome, but GNIs have not been previously described in patients with HLH. We report a 9-year-and-5-month-old female with Epstein-Barr virus-related hemophagocytic lymphohistiocytosis (EBV-HLH) in whom GNIs were identified in peripheral blood neutrophils during her clinical course. The patient presented with persistent fever, progressive cytopenias, hyperferritinemia, hemophagocytosis on bone marrow aspirate, and markedly elevated cytokines. Despite intensive supportive care, including continuous renal replacement therapy and plasma exchange, her condition deteriorated rapidly. On hospital day 6, GNIs were identified in her peripheral blood neutrophils. She died of multiorgan dysfunction on hospital day 8. This is the first report of GNIs in a patient with EBV-HLH. GNIs expand the clinical spectrum of EBV-HLH and may serve as an ominous prognostic marker in pediatric patients.
Tanaka Ken K, Hasegawa Masaki M, Katsumi Akira A
Plasmablastic myeloma is an aggressive variant of plasma cell myeloma that can mimic plasmablastic lymphoma when it presents as a solitary mass. Dual kappa and lambda light-chain expression is exceptionally rare and may be missed if evaluation relies on protein-level detection alone. We report the case of a woman in her 80s who presented with left hard palate swelling and underwent resection of a solitary hard palate and maxillary tumor. Histology showed sheets of large plasmablastic cells positive for CD38, CD138, multiple myeloma oncogene 1, and immunoglobulin G, and negative for B-cell markers and Epstein-Barr virus-encoded RNA. Within weeks, she developed malaise, nausea, and pancytopenia. Laboratory studies revealed elevated lactate dehydrogenase and serum immunoglobulin G of 4,409 mg/dL with immunoparesis. Serum free light chains showed mildly elevated kappa and markedly elevated lambda, with a kappa/lambda ratio of 0.02. Positron emission tomography-computed tomography demonstrated diffuse skeletal and splenic fluorodeoxyglucose uptake without additional extramedullary lesions, confirming the hard palate tumor as the only extramedullary site. Bone marrow examination showed marked hypercellularity with extensive replacement by plasmablastic plasma cells expressing cyclin D1, while Epstein-Barr virus studies and anaplastic lymphoma kinase were negative. Light-chain immunohistochemistry showed absent kappa staining and lambda staining in only a small subset of tumor cells, whereas RNA in situ hybridization demonstrated dual light-chain messenger RNA expression in most tumor cells. Cytogenetic analysis revealed 1q21 amplification, deletion of 17p13, and immunoglobulin heavy chain/MAF rearrangement. Despite high-dose dexamethasone, sequential proteasome inhibitor-, anti-CD38 antibody-, and immunomodulatory drug-based therapies, followed by B-cell maturation antigen × CD3 bispecific antibody treatment, the disease remained refractory and the patient died 45 days after diagnosis. This case highlights that transcript-based light-chain testing can uncover exceptionally rare dual kappa and lambda expressions when protein assays are negative or misleading. In solitary plasmablastic lesions, integrated clinicopathological assessment, including cyclin D1, Epstein-Barr virus studies, and RNA in situ hybridization, is critical for accurate diagnosis and recognition of this highly aggressive subtype.
Chen Yong Y, Wang Jie J, Yao Qiuju Q, Zhong Junhui J et al.
Reactivation of Epstein-Barr virus (EBV) can lead to life-threatening complications beyond hemophagocytic lymphohistiocytosis (HLH). We report a case of severe EBV reactivation in a 24-year-old female. She had persistent high fever, severe leukopenia, hyperinflammatory shock, and myocardial injury, but lacked typical HLH features. Laboratory tests showed elevated proportions of CD3+CD8+ T cells and increased interferon-γ (IFN-γ), interleukin-6 (IL-6), interleukin-10 (IL-10), and high-sensitivity troponin. Interleukin-2 (IL-2) and tumor necrosis factor-α (TNF-α) levels were normal. The inflammatory pathway may be involved as follows: EBV infects B cells and activates specific CD8+ T cells. These T cells mainly secrete IFN-γ without concurrent IL-2 or TNF-α release, resulting in moderate macrophage activation and IL-6/IL-10-related inflammation. This mechanism differs fundamentally from the uncontrolled inflammation in HLH. With glucocorticoids and ganciclovir treatment, the patient's symptoms and laboratory markers rapidly and completely resolved. This case highlights the heterogeneity of EBV inflammatory response: clinicians should recognize its atypical manifestations, differentiate it from HLH, and provide individualized treatment based on immunophenotypic profiles.
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