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Journal articles on the topic 'Diabetes Insipidus'

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

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1

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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2

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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3

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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4

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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5

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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6

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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7

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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8

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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9

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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10

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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11

Samarasinghe, Shanika, and Tamara Vokes. "Diabetes insipidus." Expert Review of Anticancer Therapy 6, sup1 (September 2006): S63—S74. http://dx.doi.org/10.1586/14737140.6.9s.s63.

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12

Baylis, P. H., and T. Cheetham. "Diabetes insipidus." Archives of Disease in Childhood 79, no. 1 (July 1, 1998): 84–89. http://dx.doi.org/10.1136/adc.79.1.84.

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13

Bianco, Coleen M. "Diabetes Insipidus." American Journal of Nursing 96, no. 8 (August 1996): 30–31. http://dx.doi.org/10.1097/00000446-199608000-00027.

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14

Holcomb, Susan Simmons. "Diabetes Insipidus." Dimensions of Critical Care Nursing 21, no. 3 (May 2002): 94–97. http://dx.doi.org/10.1097/00003465-200205000-00004.

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15

Perkins, Amanda. "Diabetes insipidus." Nursing Made Incredibly Easy! 18, no. 3 (2020): 28–37. http://dx.doi.org/10.1097/01.nme.0000658172.72738.c2.

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16

Ball, Stephen. "Diabetes insipidus." Medicine 33, no. 11 (November 2005): 18–19. http://dx.doi.org/10.1383/medc.2005.33.11.18.

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17

Baylis, Peter H. "Diabetes Insipidus." Medicine 29, no. 11 (November 2001): 13–16. http://dx.doi.org/10.1383/medc.29.11.13.28426.

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18

BLEVINS, LEWIS S., and GARY S. WAND. "Diabetes insipidus." Critical Care Medicine 20, no. 1 (January 1992): 69–79. http://dx.doi.org/10.1097/00003246-199201000-00019.

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19

Bell, Tally N. "Diabetes Insipidus." Critical Care Nursing Clinics of North America 6, no. 4 (December 1994): 675–85. http://dx.doi.org/10.1016/s0899-5885(18)30441-6.

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20

Ball, Stephen. "Diabetes insipidus." Medicine 37, no. 8 (August 2009): 414–15. http://dx.doi.org/10.1016/j.mpmed.2009.05.014.

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21

Ball, Stephen. "Diabetes insipidus." Medicine 41, no. 9 (September 2013): 519–21. http://dx.doi.org/10.1016/j.mpmed.2013.06.001.

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22

Kochhar, Rupinder Singh, and Stephen Ball. "Diabetes insipidus." Medicine 45, no. 8 (August 2017): 488–91. http://dx.doi.org/10.1016/j.mpmed.2017.05.002.

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23

Robertson, Gary L. "Diabetes Insipidus." Endocrinology and Metabolism Clinics of North America 24, no. 3 (September 1995): 549–72. http://dx.doi.org/10.1016/s0889-8529(18)30031-8.

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24

Ober, K. Patrick. "Diabetes Insipidus." Critical Care Clinics 7, no. 1 (January 1991): 109–25. http://dx.doi.org/10.1016/s0749-0704(18)30326-9.

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25

Hendy, Geoffrey N., and Daniel G. Bichet. "Diabetes insipidus." Baillière's Clinical Endocrinology and Metabolism 9, no. 3 (July 1995): 509–24. http://dx.doi.org/10.1016/s0950-351x(95)80570-2.

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26

Refardt, Julie, Bettina Winzeler, and Mirjam Christ-Crain. "Diabetes Insipidus." Endocrinology and Metabolism Clinics of North America 49, no. 3 (September 2020): 517–31. http://dx.doi.org/10.1016/j.ecl.2020.05.012.

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27

Leroy, Clara, Wassila Karrouz, Claire Douillard, Christine Do Cao, Christine Cortet, Jean-Louis Wémeau, and Marie-Christine Vantyghem. "Diabetes insipidus." Annales d'Endocrinologie 74, no. 5-6 (December 2013): 496–507. http://dx.doi.org/10.1016/j.ando.2013.10.002.

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28

Biswas, Rabi. "Paediatric Diabetes Insipidus: A Review." Dhaka Shishu (Children) Hospital Journal 37, no. 1 (April 12, 2022): 64–70. http://dx.doi.org/10.3329/dshj.v37i1.59119.

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Diabetes insipidus is a disease characterized by partial or total inability to concentrate urine due to a vasopressin secretion deficiency (central diabetes insipidus), a resistance to its action (nephrogenic diabetes insipidus) or an excessive consumption of water (primary polydipsia). The main signs and symptoms of the disease are polydipsia, polyuria, and nocturia; central diabetes insipidus has an insidious onset, whereas nephrogenic diabetes insipidus has a gradual onset. Because of the advances in clinical, laboratory, imaging techniques and molecular biology, the etiologic diagnosis of diabetes insipidus has improved, from 50% of patients with idiopathic diabetes insipidus to 10%-20% of patients; therefore, it has been achieved more timely treatments, resulting in reduction of the risk of sequelae. Accordingly, it is pivotal to rule out secondary causes of diabetes insipidus, such as drug consumption or metabolic disorders in patients with nephrogenic diabetes insipidus, brain tumors, encephalic trauma, infiltrative diseases, autoimmune disorders or central nervous system infections in case of patients suffering from central diabetes insipidus. Regarding treatment, it is recommended the use of desmopressin, an analogue of vasopressin, for the treatment of central diabetes insipidus, whereas water consumption, decrease of salt consumption and treatment with diuretic and non-steroidal anti inflammatory drugs are recommended for treatment of patients with nephrogenic diabetes insipidus. DS (Child) H J 2021; 37(1): 64-70
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29

Rifa'i, Achmad. "DIABETES INSIPIDUS DENGAN HIPOKALEMIA REFRAKTER." Jurnal Ilmiah Kesehatan Media Husada 11, no. 2 (November 10, 2022): 105–9. http://dx.doi.org/10.33475/jikmh.v11i2.319.

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Abstract Diabetes insipidus is a poluuria polydipsia syndrome with hyperexcretion of hypotonic urine. It is still rare in the world. Generally, diagnosed by dehydration and vasopressin test. It was reported that woman experienced with recurrent hypokalemia, the cause is unknown. After examination of collected urine and urine and plasma osmolarity, it was found that diabetes insipidus waspresent. A test was performed using intranasal desmopressin and it was proven that patient had nephrogenic diabetes insipidus. Woman, 44-years old with refractory hypokalemia and polyuria, suspected of having diabetes insipidus. The patient underwent a desmopressin test using 20mcg of intranasal desmopressin and there was no change in urine osmolarity. The patient was diagnosed with nephrogenic diabetes insipidus and received supportive treatment using NDAIDs. Keywords : diabetes insipidus; refractory hypokalemia. Abstrak Penyakit Diabetes Insipidus merupakan sindroma polyuria polidipsi dengan hiperekskresi urin yang hipotonis. Kejadiannya masih sangat jarang di dunia. Penentuan diagnosis umumnya dengan tes dehidrasi dan tes vasopressin. Dilaporkan seorang wanita dengan hipokalemia berulang, belum diketahui sebabnya. Setelah pemeriksaan urin tampung dan osmolaritas urin serta plasma diketahui adanya diabetes insipidus. Dilakukan tes menggunakan desmopressin intranasal dan terbukti bahwa pasien menderita diabetes insipidus nefrogenik. Wanita 44 tahun dengan hipokalemia refrakter dan polyuria, dicurigai diabetes insipidus. Pasien menjalani tes desmopressin menggunakan 20 mcg desmopressin intranasal dan tidak didapatkan perubahan dari osmolarita urin. Pasien didiagnosa diabetes insipidus nefrogenik dan mendapatkan pengobatan suportif menggunakan NSAID. Kata kunci: diabetes insipidus; hypokalemia refrakter.
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30

Benchimol, C. "Nephrogenic Diabetes Insipidus." Pediatrics in Review 17, no. 4 (April 1, 1996): 145–46. http://dx.doi.org/10.1542/pir.17-4-145.

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31

Sands, Jeff M., and Daniel G. Bichet. "Nephrogenic Diabetes Insipidus." Annals of Internal Medicine 144, no. 3 (February 7, 2006): 186. http://dx.doi.org/10.7326/0003-4819-144-3-200602070-00007.

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32

ALBERTAZZI, ELENA, DEBORAH ZANCHETTA, PASCALINE BARBIER, SARA FARANDA, ANNALISA FRATTINI, PAOLO VEZZONI, MIRELLA PROCACCIO, et al. "Nephrogenic Diabetes Insipidus." Journal of the American Society of Nephrology 11, no. 6 (June 2000): 1033–43. http://dx.doi.org/10.1681/asn.v1161033.

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Abstract. The aim of this study was to identify loss-of-function mutations of the V2 vasopressin receptor gene (AVPR2) in Italian patients affected by X-linked nephrogenic diabetes insipidus (NDI). Mutations were found in 15 of the 18 unrelated families investigated: nine of these mutations were previously unknown, including two affecting residues located in regions known to be important for determining the pharmacologic properties of the receptor, which were therefore functionally investigated. The first (A84D) involves a residue located near an aspartic acid (D85) that is highly conserved in all G protein-coupled receptors and that is believed to play a role in the process of their isomerization into functionally active and inactive states. The present study indicates that this mutation not only affects receptor folding in such a way as to lead to its retention inside the intracellular compartments but, as expected, also has profound effects on its binding and coupling properties. The second was a mutation of a tryptophan located at the beginning of the first extracellular loop (W99R) that greatly impaired the binding properties of the receptor and had a minor effect on its intracellular routing. Molecular analysis of the first extracellular loop bearing this mutation suggests that this residue plays a fundamental role in stabilizing the peptide/receptor interactions responsible for the high-affinity binding of agonists to the V2 receptor.
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33

Benchimol, Corrine. "Nephrogenic Diabetes Insipidus." Pediatrics In Review 17, no. 4 (April 1, 1996): 145–46. http://dx.doi.org/10.1542/pir.17.4.145.

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Nephrogenic diabetes insipidus (NDI) is a disorder, either congenital or acquired, in which antidiuretic hormone (ADH) secretion is normal, but the ability to concentrate urine is reduced because of insensitivity of the collecting tubule to ADH. The antidiuretic action of arginine vasopressin requires binding of the hormone to the renal type V2 receptor on the basolateral membrane of the collecting duct principal cell. Binding results in activation of adenylate cyclase, generation of cAMP, and increased reabsorption of water across the apical membrane of the renal collecting duct cell. The defect in NDI may be located at any of the steps from binding of vasopressin to the final effect of the hormone on the luminal membrane.
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34

Bononi, Patricia L., and Alan G. Robinson. "Central Diabetes Insipidus." Endocrinologist 1, no. 3 (June 1991): 180–86. http://dx.doi.org/10.1097/00019616-199106000-00007.

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35

MCCONNELL, EDWINA A. "… About diabetes insipidus." Nursing 33, no. 6 (June 2003): 84. http://dx.doi.org/10.1097/00152193-200306000-00065.

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36

Chong, P. L., J. Pisharam, A. Abdullah, and V. H. Chong. "Gestational diabetes insipidus." QJM: An International Journal of Medicine 112, no. 2 (October 29, 2018): 123–24. http://dx.doi.org/10.1093/qjmed/hcy252.

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37

Kavanagh, Catherine, and Natalie S. Uy. "Nephrogenic Diabetes Insipidus." Pediatric Clinics of North America 66, no. 1 (February 2019): 227–34. http://dx.doi.org/10.1016/j.pcl.2018.09.006.

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38

Bichet, Daniel G. "Nephrogenic Diabetes Insipidus." Advances in Chronic Kidney Disease 13, no. 2 (April 2006): 96–104. http://dx.doi.org/10.1053/j.ackd.2006.01.006.

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39

Sindhwani, A., D. Singhal, and N. Jerath. "Nephrogenic Diabetes Insipidus." Apollo Medicine 4, no. 2 (June 2007): 149–51. http://dx.doi.org/10.1016/s0976-0016(11)60125-7.

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40

Jane, John A., Mary Lee Vance, and Edward R. Laws. "Neurogenic diabetes insipidus." Pituitary 9, no. 4 (October 31, 2006): 327–29. http://dx.doi.org/10.1007/s11102-006-0414-7.

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41

Surapolchai, Pacharapan, Shau-Yin Ha, Godfrey Chi-Fung Chan, Johannes B. Lukito, Thomas S. K. Wan, Chi-Chiu So, and Alan Kwok-Shing Chiang. "Central Diabetes Insipidus." Journal of Pediatric Hematology/Oncology 35, no. 2 (March 2013): e84-e87. http://dx.doi.org/10.1097/mph.0b013e3182580d88.

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42

Morello, Jean-Pierre, and Daniel G. Bichet. "Nephrogenic Diabetes Insipidus." Annual Review of Physiology 63, no. 1 (March 2001): 607–30. http://dx.doi.org/10.1146/annurev.physiol.63.1.607.

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43

Bockenhauer, D., and Daniel G. Bichet. "Nephrogenic diabetes insipidus." Current Opinion in Pediatrics 29, no. 2 (April 2017): 199–205. http://dx.doi.org/10.1097/mop.0000000000000473.

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44

MERCER, MELINDA E. "ABOUT DIABETES INSIPIDUS." Nursing 20, no. 5 (May 1990): 20–21. http://dx.doi.org/10.1097/00152193-199005000-00010.

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45

Deen, Peter M. T., Nannette Marr, Erik-Jan Kamsteeg, and Bas W. M. van Balkom. "Nephrogenic diabetes insipidus." Current Opinion in Nephrology and Hypertension 9, no. 6 (November 2000): 591–95. http://dx.doi.org/10.1097/00041552-200011000-00001.

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46

Seckl, J., and D. Dunger. "Postoperative diabetes insipidus." BMJ 298, no. 6665 (January 7, 1989): 2–3. http://dx.doi.org/10.1136/bmj.298.6665.2.

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47

Monson, J. P., M. I. Mccarthy, and G. C. Toms. "Postoperative diabetes insipidus." BMJ 298, no. 6671 (February 18, 1989): 459. http://dx.doi.org/10.1136/bmj.298.6671.459-b.

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48

Childs, Barton. "Nephrogenic Diabetes Insipidus." Archives of Pediatrics & Adolescent Medicine 149, no. 2 (February 1, 1995): 181. http://dx.doi.org/10.1001/archpedi.1995.02170140063010.

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49

Bellastella, Antonio, Antonio Bizzarro, Caterina Colella, Giuseppe Bellastella, Antonio A. Sinisi, and Annamaria De Bellis. "Subclinical diabetes insipidus." Best Practice & Research Clinical Endocrinology & Metabolism 26, no. 4 (August 2012): 471–83. http://dx.doi.org/10.1016/j.beem.2011.11.008.

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50

Greger, Nancy G. "Central Diabetes Insipidus." American Journal of Diseases of Children 140, no. 6 (June 1, 1986): 551. http://dx.doi.org/10.1001/archpedi.1986.02140200061028.

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