Relevant bibliographies by topics / Diabetes Insipidus

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Diabetes Insipidus'

Author: Grafiati
Published: 4 June 2021
Last updated: 30 July 2024

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Journal articles on the topic "Diabetes Insipidus"

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Astapenko, D., and V. Černý. "Perioperative diabetes insipidus." Anesteziologie a intenzivní medicína 32, no. 2 (April 29, 2021): 111–12. http://dx.doi.org/10.36290/aim.2021.028.

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Islam, KMT, S. Alam, R. Amin, M. Haque, HD Nath, M. Hossain, AH Khan, MATM Hossain, and KK Barua. "Incidence of central diabetes insipid us among the patients undergoing pituitary tumor surgery 06 through trans-sphenoidal approach." Journal of Surgical Sciences 21, no. 1 (November 17, 2019): 6–10. http://dx.doi.org/10.3329/jss.v21i1.43831.

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Background: Diabetes insipidus (DI) is a common complication following pituitary surgery. Thiscondition can be transient or permanent and the signs and symptoms of this disorder can bemimicked by the normal postoperative course. Objective: This study was carried out to find out the incidence of central diabetes insipidus (DI)among the patients undergoing pituitary tumor surgery through trans-sphenoidal approach eitherendoscopic or microsurgical for the first time.Study Design: Cross sectional observational study Methods: Patients with central (Neurogenic) diabetes insipidus prior to surgery, co-morbiditieslike diabetes mellitus, kidney diseases, electrolyte imbalance, recurrent cases were excludedfrom this study. Patients were followed up to 7th postoperative day by recording and analyzingfindings of postoperative serum electrolytes, urinary specific gravity, hourly urinary volume forestablishing diabetes insipid us. Results: 76.9% of patients developed diabetes insipidus and 70.0% of patients did not developdiabetes insipid us those who underwent pituitary tumour surgery by trans-sphenoidal endoscopicapproach; 23.1% of patients developed diabetes insipid us and 30.0% of patients did not developdiabetes insipid us those who underwent pituitary tumour surgery by trans-sphenoidal mlcrosurgicalapproach. Conclusion: Prediction of DI help us in pre-operative counseling and post-operative managementof the patients as well as to reduce complications related morbidity after pituitary tumor surgery. Journal of Surgical Sciences (2017) Vol. 21 (1) :6-10
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Weiner, Alyson, and Patricia Vuguin. "Diabetes Insipidus." Pediatrics in Review 41, no. 2 (January 31, 2020): 96–99. http://dx.doi.org/10.1542/pir.2018-0337.

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Saborio, P., G. A. Tipton, and J. C. M. Chan. "Diabetes Insipidus." Pediatrics in Review 21, no. 4 (April 1, 2000): 122–29. http://dx.doi.org/10.1542/pir.21-4-122.

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Seckl, Jonathan R., and David B. Dunger. "Diabetes Insipidus." Drugs 44, no. 2 (August 1992): 216–24. http://dx.doi.org/10.2165/00003495-199244020-00006.

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Christ-Crain, Mirjam, and Odile Gaisl. "Diabetes insipidus." La Presse Médicale 50, no. 4 (December 2021): 104093. http://dx.doi.org/10.1016/j.lpm.2021.104093.

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Saborio, Pablo, Gary A. Tipton, and James C. M. Chan. "Diabetes Insipidus." Pediatrics In Review 21, no. 4 (April 1, 2000): 122–29. http://dx.doi.org/10.1542/pir.21.4.122.

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Elisaus, Panchami, and Stephen Ball. "Diabetes insipidus." Medicine 49, no. 8 (August 2021): 495–97. http://dx.doi.org/10.1016/j.mpmed.2021.05.009.

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Cagno, JM. "Diabetes insipidus." Critical Care Nurse 9, no. 6 (July 1, 1989): 86–93. http://dx.doi.org/10.4037/ccn1989.9.6.86.

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Maghnie, Mohamad. "Diabetes insipidus." Hormone Research in Paediatrics 59, no. 1 (2003): 42–54. http://dx.doi.org/10.1159/000067844.

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Dissertations / Theses on the topic "Diabetes Insipidus"

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Hedrich, Christian Michael, Agnieszka Zachurzok-Buczynska, Aneta Gawlik, Susanne Russ, Gabriele Hahn, Katrin Köhler, Ewa Malecka-Tendera, and Angela Hübner. "Autosomal Dominant Neurohypophyseal Diabetes Insipidus in Two Families." Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2014. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-134493.

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Background: Autosomal dominant familial neurohypophyseal diabetes insipidus (adFNDI) is a rare disease with symptoms of polydipsia, polyuria and dehydration caused by arginine vasopressin deficiency. Disease onset is within infancy or adolescence. A variety of disease-causing mutations of the arginine vasopressin neurophysin II gene (AVP) on chromosome 20p13 have been described. Methods: Two Polish families with adFNDI were screened for mutations. Processing of wild-type (WT) and mutant AVP was monitored using immunocytochemical methods in stably transfected Neuro2A cells. AVP secretion into the cell culture supernatant was investigated with an enzyme immunoassay. Results: In the first family a heterozygous p.G96D mutation was identified. Some patients additionally carried a novel heterozygous mutation p.A159T. The second family presented with a heterozygous mutation p.C98G. Confocal laser microscopy unveiled accumulation of p.G96D and p.C98G prohormones in the cellular bodies, whereas WT and p.A159T prohormones and/or processed products were located in the tips of cellular processes. Reduced levels of AVP in supernatant culture medium of p.G96D and p.C98G transfected cells in comparison to p.A159T and WT cells were found. Conclusions: We conclude that the p.G96D and p.C98G mutations cause adFNDI in the two reported families. The sequence variant p.A159T does not seem to have disease-causing effects
Dieser Beitrag ist mit Zustimmung des Rechteinhabers aufgrund einer (DFG-geförderten) Allianz- bzw. Nationallizenz frei zugänglich
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Ho, Tsun-bond Horace. "Aldose reductase deficient mice develop nephrogenic diabetes insipidus /." Hong Kong : University of Hong Kong, 2000. http://sunzi.lib.hku.hk/hkuto/record.jsp?B21949074.

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Davies, Janet Elizabeth. "Towards a transgenic rat model of Familial Neurohypophysial Diabetes Insipidus." Thesis, University of Bristol, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.247860.

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Zaarouri, Kamel. "Closed-loop control of plasma osmolality in patients with central diabetes insipidus." Thesis, McGill University, 2010. http://digitool.Library.McGill.CA:8881/R/?func=dbin-jump-full&object_id=92300.

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Sanches, Talita Rojas Cunha. "Vias intracelulares da ação do Sildenafil no diabetes insipidus induzido pelo lítio." Universidade de São Paulo, 2012. http://www.teses.usp.br/teses/disponiveis/5/5148/tde-27082012-163342/.

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Os pacientes que usam lítio (Li) para tratamento do transtorno bipolar frequentemente apresentam poliúria e deficiência de concentração urinária, sintomas do Diabetes Insipidus Nefrogênico (DIN). Animais tratados com Li apresentam baixos níveis de produção de adenosina monofosfato cíclico (AMPc) em resposta ao hormônio antidiurético (HAD). O Sildenafil (Sil), um inibidor da fosfodiesterase 5 (PDE5), eleva os níveis intracelulares de guanosina monofosfato cíclico (GMPc), levando a inserção de aquaporina 2 (AQP2) na membrana plasmática das células do ducto coletor. Portanto, inibidores de PDE podem promover a inserção de AQP2 na membrana plasmática mesmo sem a ativação do receptor de HAD, indicando a participação de uma via alternativa mediada pelo GMPc. Nós investigamos as vias de ação do Sil no tratamento da DIN induzida pelo Li. Ratos Wistar foram divididos nos seguintes grupos: grupo controle, recebendo dieta alimentar normal durante quatro semanas; grupo Li, recebendo dieta alimentar normal com 40 mmol Li por quilo de dieta durante quatro semanas; grupo Li + Sil, recebendo dieta alimentar normal com 40 mmol Li por quilo de dieta durante quatro semanas e 200 mg por quilo de dieta de Sil a partir da segunda semana; grupo Sil, recebendo dieta alimentar normal durante a primeira semana e a partir da segunda semana recebendo dieta normal com 200 mg de Sil por quilo de dieta. Os animais do grupo Li desenvolveram poliúria, diminuição da osmolalidade urinária e diminuição da expressão da AQP2 tanto na fração citoplasmática como de membrana celular e o Sil reverteu essas alterações. Demonstramos ainda que a concentração de GMPc intracelular estava aumentada nos túbulos papilares tratados com Sil. Observamos que a provável via de fosforilação da AQP2 induzida pelo GMPc é pela PKA. Além disso, o tratamento com Sil aumenta a expressão de pCreb, fator de transcrição para ativação do gene da AQP2. Observamos ainda que o Li diminui a expressão de eNOS e o tratamento com Sil normaliza essa diminuição. Assim, concluímos que o tratamento com Sil em ratos com DIN melhora a poliúria aumentando a produção e a inserção de AQP2. O tratamento com Sil pode ser benéfico para pacientes que sofrem com DIN induzido pelo Li
Patients taking lithium to treat bipolar disorder often present polyuria and urinary concentrating defect. In addition, lithium-treated animals present lower cyclic adenosine monophosphate production in response to vasopressin. Sildenafil (Sil), a phosphodiesterase 5 (PDE5) inhibitor, elevates intracellular cyclic guanosine monophosphate (cGMP) levels, leading to plasma membrane accumulation of aquaporin 2 (AQP2). Therefore, PDE inhibitors might induce AQP2 membrane insertion even without vasopressin receptor activation by activating a parallel cGMP-mediated signal transduction pathway. We investigated Sil pathways of action in rats with lithium-induced nephrogenic Diabetes Insipidus (NDI). Wistar rats received lithium (40 mmol/kg food) or not for 4 weeks (Li or control), some rats also receiving sildenafil (200 mg/kg food) in weeks 2-4, with or without lithium (Li+Sil orSil). Animals in Li group developed polyuria, decreased urinary osmolality and decreased expression of AQP2 in both the cytoplasmic fraction and the cell membrane and Sil reversed these changes. We also demonstrated that intracellular cGMP concentration was increased in papillary tubules treated with Sil. We found that PKA may be involved in the pathway of cGMP induced AQP2 phosphorylation. In addition, Sil treatment increases Creb phosphorylation. Creb phosphorylation, acts as AQP2 gene transcription factor. We also observed that Li decreases eNOS expression and treatment with Sil normalizes this alteration. We conclude that Sil treatment improves polyuria by increasing production and insertion of AQP2. Sil treatment may be beneficial to patients suffering from induced DIN Li
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Villarreal-Engelhardt, Gabriele. "Extensive glomerular immaturity associated with renal tubular acidosis, nephrogenic diabetes insipidus and nephrocalcinosis /." [S.l : s.n.], 1987. http://www.ub.unibe.ch/content/bibliotheken_sammlungen/sondersammlungen/dissen_bestellformular/index_ger.html.

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Sanches, Talita Rojas Cunha. "Estudo da ação do inibidor de fosfodiesterase (sildenafil) no diabetes insipidus induzido pelo lítio." Universidade de São Paulo, 2008. http://www.teses.usp.br/teses/disponiveis/5/5148/tde-20012009-112638/.

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Os pacientes que usam lítio (Li) para tratamento do transtorno bipolar freqüentemente apresentam poliúria e deficiência de concentração urinária, sintomas do Diabetes Insipidus nefrogênico (DIN). Animais tratados com Li apresentam baixos níveis de produção de adenosina monofosfato cíclico (AMPc) em resposta ao hormônio antidiurético (HAD). O Sildenafil (Sil), um inibidor da fosfodiesterase 5 (PDE5), eleva os níveis intracelulares de guanosina monofosfato cíclico (GMPc), levando a inserção de aquaporina 2 (AQP2) na membrana plasmática das células do ducto coletor. Portanto, inibidores de PDE podem promover a inserção de AQP2 na membrana plasmática mesmo sem a ativação do receptor de HAD, indicando a participação de uma via alternativa mediada pelo GMPc. Nós investigamos o efeito do Sil na expressão renal das proteínas de membrana AQP2, UT-A1, NKCC2, NHE3, P-ENaC em ratos com DIN induzido pelo Li. Ratos Wistar foram divididos nos seguintes grupos: grupo controle, recebendo dieta alimentar normal durante quatro semanas; grupo Li, recebendo dieta alimentar normal com 40 mmol Li por quilo de dieta durante quatro semanas; grupo Li + Sil, recebendo dieta alimentar normal com 40 mmol Li por quilo de dieta durante quatro semanas e 200 mg por quilo de dieta de Sil a partir da segunda semana; grupo Sil, recebendo dieta alimentar normal durante a primeira semana e a partir da segunda semana recebendo dieta normal com 200 mg de Sil por quilo de dieta. Os animais do grupo Li desenvolveram poliúria, diminuição da osmolalidade urinária e diminuição da expressão da AQP2. No grupo Li+Sil, o Sil foi capaz de reverter parcialmente a poliúria, diminuir o clearance de água livre, aumentar a osmolalidade urinária e aumentar a expressão da AQP2. A expressão de UTA1 foi completamente normalizada com o tratamento com Sil. A expressão das proteínas NKCC2 e NHE3 apresentaram-se aumentadas no grupo tratado com Li, e o Sil não foi capaz de reverter tal alteração. Além disso, o tratamento com Sil reverteu completamente o aumento da resistência vascular renal. Assim, concluímos que o tratamento com Sil em ratos com DIN melhora a poliúria, aumenta a smolalidade urinária e diminui o clearance de água livre pelo aumento da expressão de AQP2 e UT-A1. O tratamento com Sil pode ser benéfico para pacientes que sofrem com DIN induzida pelo Li.
Patients taking lithium to treat bipolar disorder often present polyuria and urinary concentrating defect. In addition, lithium-treated animals present lower cyclic adenosine monophosphate production in response to vasopressin. Sildenafil (Sil), a phosphodiesterase 5 (PDE5) inhibitor, elevates intracellular cyclic guanosine monophosphate (cGMP) levels, leading to plasma membrane accumulation of aquaporin 2 (AQP2). Therefore, PDE inhibitors might induce AQP2 membrane insertion even without vasopressin receptor activation by activating a parallel cGMP-mediated signal transduction pathway. We investigated the effect of sildenafil on renal expression of AQP2, UT-A1, sodium/hydrogen exchanger (NHE3), type 1 bumetanide-sensitive Na-K-2Cl cotransporter (NKCC2), and the epithelial sodium channel alpha subunit (P-ENaC). Wistar rats received lithium (40 mmol/kg food) or not for 4 weeks (Li or control), some rats also receiving sildenafil (200 mg/kg food) in weeks 2-4, with or without lithium (Li+Sil or Sil). In Li+Sil rats, urine output was markedly lower, as was water free clearance, whereas urine osmolality was higher. Semiquantitative immunoblotting revealed the following: AQP2 expression was partially normalized; UT-A1 expression was completely normalized; expression of NKCC2 and NHE3 was significantly higher in Li rats (although not significantly different between Li+Sil rats and Li rats); and P-ENaC protein expression was unaltered in all groups. Sildenafil treatment completely reversed the lithium-induced increase in renal vascular resistance. In conclusion, sildenafil treatment of lithium-induced nephrogenic diabetes insipidus (NDI) improves polyuria, increases urinary osmolality, and decreases free water clearance via upregulation of renal AQP2 and UT-A1. Sildenafil treatment could be beneficial in patients with lithium-induced NDI.
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Poulsen, Søren Brandt, Tina Bøgelund Kristensen, Heddwen L. Brooks, Donald E. Kohan, Timo Rieg, and Robert A. Fenton. "Role of adenylyl cyclase 6 in the development of lithium-induced nephrogenic diabetes insipidus." AMER SOC CLINICAL INVESTIGATION INC, 2017. http://hdl.handle.net/10150/623931.

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Psychiatric patients treated with lithium (Li+) may develop nephrogenic diabetes insipidus (NDI). Although the etiology of Li+-induced NDI (Li-NDI) is poorly understood, it occurs partially due to reduced aquaporin-2 (AQP2) expression in the kidney collecting ducts. A mechanism postulated for this is that Li+ inhibits adenylyl cyclase (AC) activity, leading to decreased cAMP, reduced AQP2 abundance, and less membrane targeting. We hypothesized that Li-NDI would not develop in mice lacking AC6. Whole-body AC6 knockout (AC6(-/-)) mice and potentially novel connecting tubule/principal cell-specific AC6 knockout (AC6(loxloxCre)) mice had approximately 50% lower urine osmolality and doubled water intake under baseline conditions compared with controls. Dietary Li+ administration increased water intake and reduced urine osmolality in control, AC6(-/)-, and AC6(loxloxCre) mice. Consistent with AC6(-/-) mice, medullary AQP2 and pS256-AQP2 abundances were lower in AC6(loxloxCre) mice compared with controls under standard conditions, and levels were further reduced after Li+ administration. AC6loxloxCre and control mice had a similar increase in the numbers of proliferating cell nuclear antigen-positive cells in response to Li+. However, AC6(loxloxCre) mice had a higher number of H+-ATPase B1 subunit-positive cells under standard conditions and after Li+ administration. Collectively, AC6 has a minor role in Li-NDI development but may be important for determining the intercalated cell-to-principal cell ratio.
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Schliebe, Nicole. "Die molekulare Pathophysiologie der hypothalamisch-renalen Osmoregulation bei Mäusen mit X-chromosomalem nephrogenen Diabetes insipidus." Leipzig Leipziger Univ.-Verl, 2009. http://d-nb.info/998766585/04.

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Geddes, Brad J. "Adenovirus as gene therapy vectors in the CNS : evaluation in a model of hypothalamic diabetes insipidus." Thesis, University of Bristol, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.265302.

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Books on the topic "Diabetes Insipidus"

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National Kidney and Urologic Diseases Information Clearinghouse (U.S.) and National Institute of Diabetes and Digestive and Kidney Diseases (U.S.), eds. Diabetes insipidus. [Bethesda, Md.]: National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, 2001.

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V. V. A. M. van Knoers. Nephrogenic Diabetes Insipidus. [s.l.]: [s.n.], 1990.

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International Symposium on Diabetes Insipidus in Man (1984 Paris, France). Diabetes insipidus in man. Edited by Czernichow P and Robinson A. G. Basel ; New York: Karger, 1985.

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Alter, Craig A., ed. Diabetes Insipidus in Children. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-83248-3.

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International Symposium on Diabetes Insipidus in Man (1984 Paris, France). Diabetes insipidus in man: International Symposium on Diabetes Insipidus in Man, Paris, January 18-19, 1984. Edited by Czernichow P. ed and Robinson Alan G. ed. Basel: Karger, 1985.

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Graham, Olive. Diabetes insipidus: What kind of diabetes is that? : study guide. [Bethesda, Md.?]: U.S. Dept. of Health and Human Services, Public Health Service, National Institutes of Health, Clinical Center Communications, 1988.

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Patsy, McCabe, and National Institutes of Health (U.S.). Office of Clinical Center Communications, eds. Diabetes insipidus: What kind of diabetes is that? : study guide. [Bethesda, Md.?]: U.S. Department of Health and Human Services, Public Health Service, National Institutes of Health, Clinical Center Communications, 1988.

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Hamburg, Universität, ed. Heterologe Expression des normalen und eines mutanten Vasopressin-Neurophysin-Vorläufers in einer Hypophysentumorzellinie der Maus als Modellsystem für den familiären hypothalamischen Diabetes insipidus. [s.l.]: [s.n.], 1997.

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Diabetes Insipidus. Exon Publications, 2024. http://dx.doi.org/10.36255/diabetes-insipidus.

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Diabetes Insipidus is a rare condition characterized by an imbalance of water in the body, leading to excessive thirst and urination. This article is organized to provide an understanding of Diabetes Insipidus for patients, their loved ones, and the public. It begins with an introduction to the condition, explaining its types and the differences between them. The article discusses the risk factors and epidemiology of Diabetes Insipidus, followed by an exploration of its causes and symptoms. The pathophysiology section explains how the condition affects the body, while the complications section highlights potential risks if not managed properly. Diagnosis methods are described, along with the various treatment options available, including medications and lifestyle changes. The prognosis of living with Diabetes Insipidus is also covered, providing a complete overview of managing the condition. All information is presented in simple terms to ensure it is understandable for all readers.
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Kamoi, Kyuzi, ed. Diabetes Insipidus. InTech, 2011. http://dx.doi.org/10.5772/860.

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Book chapters on the topic "Diabetes Insipidus"

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Grant, Frederick D. "Diabetes Insipidus." In Pediatric Endocrinology, 215–30. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-73782-9_10.

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Colao, Annamaria, Claudia Pivonello, and Enrico Riccio. "Diabetes Insipidus." In Encyclopedia of Pathology, 1–3. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-319-28845-1_5104-1.

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Kannan, C. R. "Diabetes Insipidus." In The Pituitary Gland, 545–64. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4613-1849-1_20.

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Srivatsa, Abhinash, and Frederick D. Grant. "Diabetes Insipidus." In Pediatric Endocrinology, 151–66. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-60761-395-4_9.

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Al-Tubaikh, Jarrah Ali. "Diabetes Insipidus." In Internal Medicine, 370–72. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-03709-2_73.

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Bockenhauer, Detlef, and Daniel G. Bichet. "Diabetes Insipidus." In Pediatric Kidney Disease, 993–1010. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-52972-0_37.

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Traill, Catherine, and Stephen H. Halpern. "Diabetes Insipidus." In Consults in Obstetric Anesthesiology, 161–62. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-59680-8_44.

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Annamalai, Aniyizhai. "Diabetes Insipidus." In Medical Management of Psychotropic Side Effects, 109–13. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-51026-2_15.

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Burkitt Creedon, Jamie M. "Diabetes Insipidus." In Textbook of Small Animal Emergency Medicine, 757–61. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2018. http://dx.doi.org/10.1002/9781119028994.ch117.

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Colao, Annamaria, Claudia Pivonello, and Enrico Riccio. "Diabetes Insipidus." In Endocrine Pathology, 174–76. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-62345-6_5104.

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Conference papers on the topic "Diabetes Insipidus"

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Vicente, V., J. Corrales, J. Miralles, and I. Alberca. "DDAVP IN DIABETES INSIPIDUS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644126.

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In order to investigate whether the response of von Willebrand factor (vWF), Factor VIII (FVIII) and tissue plasminogen activator (t-PA) to DDAVP infusion is governed by the integrity of the hypothaLamo neurohypophyseal axis, we studied the behaviours >of these proteins (FVIII, one stage; vWF antigen by electroimmunoassay and t-PA was measured in the plasma auglobulin fraction with added C-1 inactivator on fibrin plates) after DDAVP infusion (0.3 ug/Kg) in five patients with cranial diabetes insipidus, comparing them with the responses obtained in six healthy subjects.In spite of receiving a daily therapeutic dose of 10-20 ug of DDAVP the patients with diabetes insipidus showed normal basal levels of FVIII, vWF and t-PA. The increase in these parameters following DDAVP infusion were not significantly different in the two groups. These findings suggest that the integrity of the hypothalamo-hypophyseal axis is not neccessary for a response by vWF, FVIII and t-PA to occur after DDAVP infusion.
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Chai, A. L., R. Rakocevic, F. M. El-Baba, and K. Killu. "Transient Diabetes Insipidus After Vasopressin Discontinuation." In American Thoracic Society 2023 International Conference, May 19-24, 2023 - Washington, DC. American Thoracic Society, 2023. http://dx.doi.org/10.1164/ajrccm-conference.2023.207.1_meetingabstracts.a5282.

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Nga, Telema, Duy An T Minior, Basema Dibas, and Weili Chang. "Congenital Nephrogenic Diabetes Insipidus Presenting in Premature Neonate." In Selection of Abstracts From NCE 2015. American Academy of Pediatrics, 2017. http://dx.doi.org/10.1542/peds.140.1_meetingabstract.69.

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Noy, Kerry, Mohamad Hilal, and Jayabharathi Sakamudi. "P291 Nephrogenic diabetes insipidus in a female infant." In Faculty of Paediatrics of the Royal College of Physicians of Ireland, 9th Europaediatrics Congress, 13–15 June, Dublin, Ireland 2019. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2019. http://dx.doi.org/10.1136/archdischild-2019-epa.641.

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Rodrigues, Dalianna Luise Andrade Souto, Giovana Gabriela Koptian, Luiz Felipe Adsuara de Sousa, Gabriela Araújo Munhoz, and Dawton Yukito Torigoe. "GRANULOMATOSIS WITH POLYANGIITIS MANIFESTING WITH CRANIAL DIABETES INSIPIDUS." In XXXIX Congresso Brasileiro de Reumatologia. Sociedade Brasileiro de Reumatologia, 2022. http://dx.doi.org/10.47660/cbr.2022.2146.

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Noy, KS, M. Hilal, J. Sakamudi, and J. Van Der Voort. "G234(P) Nephrogenic diabetes insipidus in a female infant." In Royal College of Paediatrics and Child Health, Abstracts of the RCPCH Conference and exhibition, 13–15 May 2019, ICC, Birmingham, Paediatrics: pathways to a brighter future. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2019. http://dx.doi.org/10.1136/archdischild-2019-rcpch.228.

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Parasher, Arjun, David Lerner, Jordan Glicksman, James Palmer, and Nithin Adappa. "In-hospital Costs Associated with Diabetes Insipidus Following Pituitary Surgery." In 29th Annual Meeting North American Skull Base Society. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1679526.

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Stroescu, Ramona, Mihai Gafencu, Adela Chiriţ&acaron;, Raluca Isac, and Gabriela Doroş. "P95 A rare cause for failure to thrive: nephrogenic diabetes insipidus." In 8th Europaediatrics Congress jointly held with, The 13th National Congress of Romanian Pediatrics Society, 7–10 June 2017, Palace of Parliament, Romania, Paediatrics building bridges across Europe. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2017. http://dx.doi.org/10.1136/archdischild-2017-313273.183.

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Bassey-Akamune, Felicia, and Naaz F. Nasar. "Congenital Nephrogenic Diabetes Insipidus: Delayed Onset of Symptoms in Breastfed Infant." In Selection of Abstracts From NCE 2016. American Academy of Pediatrics, 2018. http://dx.doi.org/10.1542/peds.141.1_meetingabstract.695.

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Sass, S. J., E. Wiens, J. Ziegler, and A. Sharma. "Granulomatosis with Polyangiitis as an Acute Cause of Central Diabetes Insipidus." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a3102.

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Reports on the topic "Diabetes Insipidus"

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Figueredo, Luisa, Liliana Martinez, and Joao Paulo Almeida. Current role of Endoscopic Endonasal Approach for Craniopharyngiomas. A 10-year Systematic review and Meta-Analysis Comparison with the Open Transcranial Approach. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, January 2023. http://dx.doi.org/10.37766/inplasy2023.1.0045.

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Abstract:
Review question / Objective: To identify and review studies published in the last ten years, presenting the efficacy and outcomes of EEA and TCA for patients with cranio-pharyngiomas. Eligibility criteria: Studies meeting the following criteria were included: (a) retrospective and prospective studies and (b) observational studies (i.e., cross-sectional, case-control, case-series). The outcomes included visual outcomes (improvement, no changes, worsening), endocrinological outcomes (permanent diabetes insipidus and hypopituitarism), operatory site infection, meningitis, cerebrospinal fluid leak, stroke, hemorrhage, and mortality. Studies were excluded if they were determined to be: (a) case-report studies, (b) studies testing genetic disorders, (c) poster presentation abstracts without full-text availability, (d) systematic reviews, and (e) metanalyses.
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Gong, Xuan, Zhou Chen, Kui Yang, Chuntao Li, Songshan Feng, Mingyu Zhang, Zhixiong Liu, Hongshu Zhou, and Zhenyan Li. Endoscopic Transsphenoidal Surgery for Infra-Diaphragmatic Craniopharyngiomas: Impact of Diaphragm Sellae Competence on Hypothalamic Injury. International Journal of Surgery, May 2024. http://dx.doi.org/10.60122/j.ijs.2024.20.03.

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Objective: Investigate the impact of diaphragm sellae competence on surgical outcomes and risk factors for postoperative hypothalamic injury (HI) in patients undergoing endoscopic transsphenoidal surgery (ETS) for infra-diaphragmatic craniopharyngiomas (ICs). Methods: A retrospective analysis of 54 consecutive patients (2016-2023) with ICs treated by ETS was conducted. All tumors originated from the sellar region inferior to the diaphragm sellae and were classified into two subtypes in terms of diaphragm sellae competence: IC with competent diaphragm sellae (IC-CDS) and IC with incompetent diaphragm sellae (IC-IDS). Clinical features, intraoperative findings, and follow-up data were compared between subtypes. Postoperative HI was assessed using a magnetic resonance imaging-based scoring system. Results: Fifty-four patients (29 males, 25 females) were included in this study, with 12 (22.2%) under 18 years old. Overall, 35 cases were IC-CDS, while 19 were IC-IDS. Compared with IC-CDS, patients with IC-IDS tended to have hormone hypofunction before surgery (p = 0.03). Tumor volume in IC-IDS group (9.0 ± 8.6 cm3) was also higher than that in IC-CDS group (3.3 ±3.4 cm, p = 0.011). Thirty-seven patients underwent standard endoscopic transsphenoidal approach (SEA) and 17 underwent an extended endoscopic transsphenoidal approach (EEA). Gross total resection (GTR) was achieved in 50 cases (92.6%). Postoperative CSF leak was observed in four patients (7.4%). Permanent diabetes insipidus (DI) occurred in 13 patients (27.7%), six in IC-CDS and seven in IC-IDS. Postoperative HI occurred in 38.9% of patients. Univariate analysis revealed that large tumor size (p = 0.014), prior hypopituitarism (p = 0.048) and IC-IDS (p < 0.001) were significantly associated with postoperative HI. Multivariate analysis revealed that IC- IDS was the sole predictor of postoperative HI. Conclusion: To our knowledge, this is the largest case series in the literature to describe IC resected by endoscopic surgery in a single institution. Classification based on diaphragm sellae competence highlights distinct clinical features and surgical outcomes between IC-CDS and IC-IDS subtypes. Notably, IC-IDS is an independent risk factor for postoperative HI. Preoperative identification of subtype can guide surgical strategy and potentially minimize complications.
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