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INTRODUCTION AND IMPORTANCE: Disseminated Peritoneal Leiomyomatosis (DPL) is a rare benign proliferation of solid peritoneal lesions along the abdominopelvic cavity comprised of smooth muscle and connective tissue. Though hormonal and iatrogenic causes have been theorized, the exact etiology remains unknown. Most patients with DPL are frequently premenopausal with a history of myomectomy or prior hysterectomy. These patients can present asymptomatically or with abnormal uterine bleeding and abdominal discomfort. DPL is a rare entity with less than 150 cases reported in the literature, showcasing the need of awareness of this poorly understood neoplasm. Imaging, if performed, is helpful as positron emission tomography (PET) can differentiate DPL from malignant peritoneal disease. Treatment involves medical and surgical options based on patient's clinical presentation, with medical treatment with gonadotropin-releasing hormone agonist being first line. CASE PRESENTATION: We report a case of a previously healthy female presenting for desired laparoscopic tubal ligation with incidental countless peritoneal nodules suspicious for carcinomatosis found during the operative event but proven leiomyomas after histologic examination. CLINICAL DISCUSSION: Differentiating DPL from mimickers such as leiomyosarcoma, endometriosis, and carcinomatosis remains a challenge as macroscopic appearances are similar ultimately requiring histology evaluation. CONCLUSION: Awareness of the entity is crucial to avoid misdiagnosis and unnecessary anxiety associated with a presumptive diagnosis of malignancy for a largely benign entity.
RESUMEN
The brain-derived neurotrophic factor (BDNF) and its high-affinity receptor tropomyosin-related kinase receptor B (TrkB) are widely expressed in the central nervous system. It is well documented that neurons express BDNF and full-length TrkB (TrkB.FL) as well as a lower level of truncated TrkB (TrkB.T). However, there are conflicting reports regarding the expression of BDNF and TrkB in glial cells, particularly microglia. In this study, we employed a sensitive and reliable genetic method to characterize the expression of BDNF and TrkB in glial cells in the mouse brain. We utilized three Cre mouse strains in which Cre recombinase is expressed in the same cells as BDNF, TrkB.FL, or all TrkB isoforms, and crossed them to Cre-dependent reporter mice to label BDNF- or TrkB-expressing cells with soma-localized EGFP. We performed immunohistochemistry with glial cell markers to examine the expression of BDNF and TrkB in microglia, astrocytes, and oligodendrocytes. Surprisingly, we found no BDNF- or TrkB-expressing microglia in examined CNS regions, including the somatomotor cortex, hippocampal CA1, and spinal cord. Consistent with previous studies, most astrocytes only express TrkB.T in the hippocampus of adult brains. Moreover, there are a small number of astrocytes and oligodendrocytes that express BDNF in the hippocampus, the function of which is to be determined. We also found that oligodendrocyte precursor cells, but not mature oligodendrocytes, express both TrkB.FL and TrkB.T in the hippocampus of adult mice. These results not only clarify the expression of BDNF and TrkB in glial cells but also open opportunities to investigate previously unidentified roles of BDNF and TrkB in astrocytes and oligodendrocytes.