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Increased growth of meningiomas during pregnancy as well as postpartum clinical regression of symptoms have been reported but remain poorly understood. A better understanding of the factors that contribute to these observations, including potential factors associated with pregnancy, could enable design of more effective adjuvant therapies.
We describe the presentation of a meningioma during the immediate postpartum period. Serial imaging demonstrated subsequent rapid decrease in size of the tumour prior to any intervention. The lesion was resected, and the tissue was subjected to immunostaining for gene products associated with pregnancy, including estrogen receptor (ER), progesterone receptor (PR), platelet-derived growth factor receptor B (PDGFRB), fibroblastic growth factor receptor 2 (FGFR-2), epidermal growth factor receptor (EGFR) and human placental lactogen (hPL).
The lesion proved to be an atypical fibroblastic meningioma grade II (WHO). Immunostaining demonstrated significant staining for PR, PDGFRB, and FGFR-2. No specific staining for ER, EGFR, or hPL was identified.
Although clinical regression of meningioma following pregnancy is well-recognized, imaging data are much less abundant. This report provides clear clinical and imaging documentation of a meningioma associated with pregnancy. In addition, the growth factor profile of this tumour suggests the importance of PR, PDGFRB, and FGFR-2 as potential therapeutic targets.
Geoffrey T. Manley, Department of Neurological Surgery, University of California, San Francisco, CA,
Miki Fujimura, Department of Neurosurgery, Stanford University School of Medicine, Stanford, CA,
Tonghui Ma, Departments of Medicine and Physiology, Cardiovascular Research Institute, University of California, San Francisco, CA,
Ferda Filiz, Departments of Medicine and Physiology, Cardiovascular Research Institute, University of California, San Francisco, CA,
Andrew W. Bollen, Department of Pathology, University of California, San Francisco, CA,
Pak H. Chan, Department of Neurosurgery, Stanford University School of Medicine, Stanford, CA,
Alan S. Verkman, Departments of Medicine and Physiology, Cardiovascular Research Institute, University of California, San Francisco, CA
Abnormalities in brain water balance, such as edema and increased intracranial pressure, play an important role in the pathophysiology of acute head trauma, stroke and a variety of neurological disorders. However, little is known about the molecular mechanisms responsible for these alterations in cerebral water balance. Consequently, at present the therapeutic options are limited to neurosurgical decompression, intravenous administration of hyperosmolar agents and steroids, therapies that were introduced more than 40 years ago. There is recent evidence that molecular water channels called aquaporins, which have recently been identified in mammals, may play an important role in brain edema, thus offering therapeutic alternatives.
Aquaporins are small integral membrane proteins that function primarily as bidirectional water-selective transporters in many cell types in the kidney, lung and other fluid-transporting tissues where water flow is driven by osmotic gradients and hydrostatic pressure differences. The brain expresses at least two members of the aquaporin family in areas that are known to participate in the production and absorption of brain fluid. Aquaporin-1 is selectively expressed on the ventricular surface of choroid plexus epithelium where it may play a role in cerebrospinal fluid (CSF) production. Aquaporin-4 (AQP4) is abundantly expressed throughout the brain, particularly at the blood–brain and brain–CSF interfaces. AQP4 is expressed to a much lesser extent in tissue outside of the nervous system.
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