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Gheorghita V.,Dr Carol Davila Central Universitary Emergency Military Hospital | Gheorghita V.,National Institute For Infectious Diseases Prof Dr Matei Bals | Barbu A.E.,National Institute For Infectious Diseases Prof Dr Matei Bals | Gheorghiu M.L.,Carol Davila University of Medicine and Pharmacy | And 3 more authors.
GERMS | Year: 2015

Sepsis is a systemic, deleterious inflammatory host response triggered by an infective agent leading to severe sepsis, septic shock and multi-organ failure. The host response to infection involves a complex, organized and coherent interaction between immune, autonomic, neuroendocrine and behavioral systems. Recent data have confirmed that disturbances of the autonomic nervous and neuroendocrine systems could contribute to sepsis-induced organ dysfunction. Through this review, we aimed to summarize the current knowledge about the endocrine dysfunction as response to sepsis, specifically addressed to vasopressin, copeptin, cortisol, insulin and leptin. We searched the following readily accessible, clinically relevant databases: PubMed, UpToDate, BioMed Central. The immune system could be regarded as a “diffuse sensory organ” that signals the presence of pathogens to the brain through different pathways, such as the vagus nerve, endothelial activation/dysfunction, cytokines and neurotoxic mediators and the circumventricular organs, especially the neurohypophysis. The hormonal profile changes substantially as a consequence of inflammatory mediators and microorganism products leading to inappropriately low levels of vasopressin, sick euthyroid syndrome, reduced adrenal responsiveness to ACTH, insulin resistance, hyperglycemia as well as hyperleptinemia. In conclusion, clinical diagnosis of this “pan-endocrine illness” is frequently challenging due to the many limiting factors. The most important benefits of endocrine markers in the management of sepsis may be reflected by their potential to be used as biomarkers in different scoring systems to estimate the severity of the disease and the risk of death. © GERMS 2015.


PubMed | Parhon National Institute of Endocrinology
Type: Journal Article | Journal: Journal of ovarian research | Year: 2013

This study aimed to investigate an unusual case of immature ovarian teratoma with onset of mature glial cells implanted on the contralateral ovary, a challenge in the diagnosis of the second ovarian tumor. We report the case of a 31- yr-old woman, who developed at the age of 16 an immature teratoma in the right ovary that was surgically removed. Six years later mature glial implants were present on the left ovary and six months later at the level of peritoneum that relapsed after other six months. The patient suffered three surgical resections after the initial one. Paraffin sections and immunohistochemical examinations using antibodies against glial and neuronal antigens were performed. In the teratoma, the neuroectodermal tissue expressed Glial fibrillary acidic protein (GFAP), S100 protein, Epithelial membrane antigen (EMA) and Cytokeratin 34 beta E12 (Ck34beta E12), wheares the implants expressed only GFAP and S100 protein. The immature teratoma is the rarest type of ovarian teratomas. Gliomatosis peritonei is an exceptional finding, expecially with onset on the contralaterally ovary. The implant of the mature glial cells has a high risk of relapse, as seen in our case, thus close follow-up of the patient is necessary.

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