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Abstracts
ROLE OF CELL VOLUME DISREGULATION IN CLINICAL PATHOPHYSIOLOGY OF ENDOCRINE DISORDERS
Churilov, L.P. and Stroev, Yu.I.
Department of Pathology, Faculty of Medicine, St. Petersburg State University, St. Petersburg, Russian Federation
Cell volume changes may cause some manifestations of the endocrinopathiae or push to their misdiagnosis. Our clinical experience shows that abdominal viscera cell swelling in exacerbation of Addison's disease (Addisonian crises) is regularly displayed with liver enlargement, right side subcostal pain and even imitate acute abdomen. Acute pain in abdominal and liver areas is often accompanied by vomiting, diarrhea and fever. This is di-agnostically misleading for physicians not aware of cell volume disorders. Our observation of an Addisonian crisis case is described and discussed. Case was misdiagnosed as acute abdomen and lead to laparotomy with fatal outcome due to lack of glucocorticoid protection [1]. False acute abdomen signs were caused by sodium loss and relative decrease of extracellular fluid tonicity with cell swelling and painful distension of abdominal organs' capsules. Differential signs of Addisonian crises and acute abdomen are discussed. In sub-compensated diabetes mellitus (DM) cell volume of red blood cells (RBC) may vary due to sharp
changes of extracellular glucose level and shifts of extracellular fluid tonicity. When RBC loaded with glucose are diluted with isotonic media for electronic counter mean corpuscular volume (MCV) and hematocrit (Ht) check, it may produce false enlargement of MCV and Ht. We checked these parameters with K-800 cell counter in 337 patients with DM type I and 211 patients with DM type II (megaloblastic anemiae were excluded). MCV in DM I appeared to be greater than in DM II (94,5 ± 0,7 vs 90,5 ± 0,7; p < 0,02). This data correlated to greater Ht and blood glucose level elevated [2]. Similar data also reported by Strauchen, J.A., et al. [3].
References
1. Stroev, Yu.I. First aid and pre-hospital care in common emergencies. Ed. Valenkevich L.N. Leningrad, LPMI Publ., 1985. Pp. 51-76.
2. Stroev, Yu.I., et al. IVAll-Russ. Congr. in Endocrinol. SPb., 2001. P. 196.
3. Strauchen, J.A., et al. Blood., 1981, v. 57, no. 6, pp. 1065-1067.
SIGNALING PATHWAYS ASSOCIATED WITH APOPTOTIC RESISTANCE AND REGULATORY VOLUME MECHANISMS IN OSMOTICALLY STRESSED LYMPHOID CELLS
Cidlowski, J.A., Scoltock, A.B., and Bortner, C.D.
Laboratory of Signal Transduction, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709
Apoptosis is a stochastic, physiological mode of cell death characterized by a distinct set of morphological and biochemical properties. The loss of cell volume, termed Apoptotic Volume Decrease (AVD) has been a defining feature of this programmed cell death process. Most cells have inherent volume regulatory mechanisms to combat a change in cell size, however T-cells are devoid of a regulatory volume increase (RVI) response when challenged in a hyperosmotic environment. We have developed a T-cell line, designed S49 (OS) that has gained an inherent RVI response upon acute hyperosmotic exposure. Interestingly, these S49 (OS) cells are resistant to cell death agents that
induce the intrinsic apoptotic pathway, while remaining sensitive to extrinsic apoptotic stimuli. We have explored the signaling properties that impact this apoptotic resistance and RVI response in S49 (OS) cells. We show that S49 (OS) cells show a constitutive phosphorylation of AKT upon acute osmotic stress that is absent in the parent cells, and inhibition of this phosphorylation results in sensitivity to apoptosis. Additionally, inhibition of upstream signaling molecules, such as PI3 kinase, also sensitizes S49 (OS) cells to undergo apoptosis. We will present our latest data on the signaling networks that influence not only apoptotic resistance, but also cell volume regulation in lymphoid cells.
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Бюллетень сибирской медицины, 2013, том 12, № 4, с. 24-68
