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Artykuły w czasopismach na temat „Non-ketotic”

Autor: Grafiati

Data publikacji: 2 czerwca 2025

Data aktualizacji: 31 lipca 2025

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1

LEUNG, R. K. W. "NON-KETOTIC HYPERGLYCINAEMIA." Journal of Paediatrics and Child Health 29, no. 1 (1993): 71a—72. http://dx.doi.org/10.1111/j.1440-1754.1993.tb00448.x.

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2

Kalmanchey, R. "Non—ketotic hyperglycinaemia." European Journal of Paediatric Neurology 12 (May 2008): S8. http://dx.doi.org/10.1016/s1090-3798(08)70027-8.

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3

Mathew, Thomas, Nagabushan Hesarur, and Saji K John. "Non-ketotic hyperglycemia presenting as acute hemiparkinsonism." IP Indian Journal of Neurosciences 7, no. 3 (2021): 254–56. http://dx.doi.org/10.18231/j.ijn.2021.046.

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Non-ketotic hyperglycaemia is commonly associated with hyperkinetic movement disorders like chorea. Here we report a case of non-ketotic hyperglycaemia, in a 70 year old man with longstanding diabetes presenting as acute onset hemi-parkinsonism. Hypokinetic movement disorders are only rarely reported in non-ketotic hyperglycaemia.

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4

Brady, P. S., and L. J. Brady. "Hepatic carnitine palmitoyltransferase turnover and translation rates in fed, starved, streptozotocin-diabetic and diethylhexyl phthalate-treated rats." Biochemical Journal 246, no. 3 (1987): 641–49. http://dx.doi.org/10.1042/bj2460641.

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Hepatic carnitine palmitoyltransferase (CPT) turnover was studied in control and in non-ketotic hyperglycaemic streptozotocin-diabetic rats. The degradation constant (kd) and half-life (t1/2) did not appear to be altered by mild diabetes. The hepatic CPT (micrograms/g of liver) was not increased by the mild, non-ketotic, diabetes. However, the total hepatic CPT (micrograms/liver) was 37% greater in the diabetic animals, owing to the increased liver weight. This resulted from a 40% increase in the synthesis constant (ks). Hepatic CPT activity (total detergent-solubilized) and translation rates

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5

Munn, Alison. "Hyperosmolar non-ketotic hyperglycaemia." British Journal of Nursing 1, no. 4 (1992): 186–89. http://dx.doi.org/10.12968/bjon.1992.1.4.186.

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6

Nicolasjilwan, M., H. Ozer, M. Wintermark, and J. Matsumoto. "Neonatal non-ketotic hyperglycinemia." Journal of Neuroradiology 38, no. 4 (2011): 246–50. http://dx.doi.org/10.1016/j.neurad.2010.11.005.

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7

Borrone, C., C. Bachmann, M. Di Rocco, K. Tada, K. Hayasaka, and R. Gatti. "Atypical non-ketotic hyperglycinaemia." Journal of Inherited Metabolic Disease 9, no. 4 (1986): 402–3. http://dx.doi.org/10.1007/bf01800496.

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8

Gill, G. V., and K. G. M. M. Alberti. "Hyperosmolar non-ketotic coma." Practical Diabetes International 2, no. 3 (1985): 30–35. http://dx.doi.org/10.1002/pdi.1960020310.

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9

Shivane, V., T. Bandgar, A. Lila, and N. Shah. "Managing non-ketotic childhood hyperglycemia." Journal of Postgraduate Medicine 57, no. 4 (2011): 270. http://dx.doi.org/10.4103/0022-3859.90073.

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10

Gomes, Matheus Ferreira, Euripedes Gomes de Carvalho Neto, Fernando Kowacs, and Carlos R. M. Rieder. "Non-ketotic hyperosmolar hyperglycemic chorea." Revista da Associação Médica Brasileira 65, no. 2 (2019): 127–29. http://dx.doi.org/10.1590/1806-9282.65.2.127.

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11

Danve, Abhijeet, Supriya Kulkarni, and Girja Bhoite. "Non-ketotic hyperglycemia unmasks hemichorea." Journal of Community Hospital Internal Medicine Perspectives 5, no. 4 (2015): 27825. http://dx.doi.org/10.3402/jchimp.v5.27825.

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12

Lorber, Daniel. "Non-Ketotic Hypertonicity in Diabetes." Endocrinologist 3, no. 1 (1993): 29–38. http://dx.doi.org/10.1097/00019616-199301000-00006.

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13

Holmqvist, P., and S. Polberger. "Neonatal Non-Ketotic Hyperglycinemia (NKH)." Neuropediatrics 16, no. 04 (1985): 191–93. http://dx.doi.org/10.1055/s-2008-1059535.

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14

McMurray, J. J., P. H. Seidelin, and D. M. Fraser. "Hyperglycaemic non-ketotic focal epilepsy." Practical Diabetes International 4, no. 2 (1987): 78–79. http://dx.doi.org/10.1002/pdi.1960040210.

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15

Yıldırım, Serhan, Hakan Levent Gül, and Ülkü Türk Börü. "Non-Ketotik Hiperglisemiye Bağlı Gelişen Hemikore-Hemiballizm." Türk Nöroloji Dergisi 19, no. 4 (2013): 153–54. http://dx.doi.org/10.4274/tnd.93546.

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16

Mutlu, Mehmet, Yakup Aslan, and Berna Saygin. "Non-Ketotic Hyperglycinaemia: A Case Report." Tuberculin Skin Test in Children 11, no. 1 (2013): 29–31. http://dx.doi.org/10.5222/j.child.2011.029.

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17

Hennis, A., D. Corbin, and H. Fraser. "Focal seizures and non-ketotic hyperglycaemia." Journal of Neurology, Neurosurgery & Psychiatry 55, no. 3 (1992): 195–97. http://dx.doi.org/10.1136/jnnp.55.3.195.

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18

Boughammoura-Bouatay, A., S. Chebel, S. Younes-Mhenni, and M. Frih-Ayed. "Biballism due to non-ketotic hyperglycaemia." Diabetes & Metabolism 34, no. 6 (2008): 617–19. http://dx.doi.org/10.1016/j.diabet.2008.04.006.

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19

Lin, J. J., and M. K. Chang. "Hemiballism-hemichorea and non-ketotic hyperglycaemia." Journal of Neurology, Neurosurgery & Psychiatry 57, no. 6 (1994): 748–50. http://dx.doi.org/10.1136/jnnp.57.6.748.

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20

Cheema, H., D. Federman, and A. Kam. "Hemichorea–hemiballismus in non-ketotic hyperglycaemia." Journal of Clinical Neuroscience 18, no. 2 (2011): 293–94. http://dx.doi.org/10.1016/j.jocn.2010.04.036.

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21

Apostolidou, I., C. Papagaroufalis, H. Michelakakis, C. J. Stefanidis, and M. Xanthou. "Non-ketotic hyperglycinaemia: a therapeutic approach." Journal of Inherited Metabolic Disease 14, no. 5 (1991): 835–36. http://dx.doi.org/10.1007/bf01799960.

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22

Toone, J. R., D. A. Applegarth, and H. L. Levy. "Prenatal diagnosis of Non-ketotic hyperglycinaemia." Journal of Inherited Metabolic Disease 15, no. 5 (1992): 713–19. http://dx.doi.org/10.1007/bf01800011.

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23

Inoue, F., S. Matsuo, H. Yoshioka, et al. "Tryptophan therapy for non-ketotic hyperglycinaemia." Journal of Inherited Metabolic Disease 15, no. 3 (1992): 399–401. http://dx.doi.org/10.1007/bf02435987.

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24

Fletcher, J. M., A. M. E. Bye, V. Nayanar, and B. Wilcken. "Non-ketotic hyperglycinaemia presenting as pachygyria." Journal of Inherited Metabolic Disease 18, no. 6 (1995): 665–68. http://dx.doi.org/10.1007/bf02436754.

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25

Applegarth, D. A., H. L. Levy, V. E. Shih, et al. "Prenatal diagnosis of non-ketotic hyperglycinemia." Prenatal Diagnosis 6, no. 4 (1986): 257–63. http://dx.doi.org/10.1002/pd.1970060405.

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26

Ozer, Feriha, Aytul Mutlu, and Tufan Ozkayran. "Reflex epilepsy and non‐ketotic hyperglycemia." Epileptic Disorders 5, no. 3 (2003): 165–68. http://dx.doi.org/10.1684/j.1950-6945.2003.tb00008.x.

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Epileptic seizures are paroxysmal events, and it is likely that many, if not most, of them are precipitated by known or unknown factors acting on a central nervous system that is predisposed to the production of epileptic discharges by the presence of an organic lesion, a genetically determined neuronal hyperexcitability, or both. Known precipitating influences are quite varied. We report the case of a 58 years‐old patient, followed for non‐ketotic hyperglycemia, who presented with focal seizures exclusively induced by specific, active or passive, postures and movements of the right arm or han

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27

Kauppinen, K. "Annual Milk Yield and Reproductive Performance of Ketotic and Non-Ketotic Dairy Cows." Zentralblatt für Veterinärmedizin Reihe A 31, no. 1-10 (2010): 694–704. http://dx.doi.org/10.1111/j.1439-0442.1984.tb01328.x.

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28

Bergh, Claes-Håkan, Lennart Ransnäs, Åke Hjalmarson, Anders Waldenström, and Bo Jacobsson. "Effects of Acute Ketotic and Non-ketotic Diabetes on the Myocardial Muscarinic Receptors." Acta Pharmacologica et Toxicologica 55, no. 5 (2009): 373–79. http://dx.doi.org/10.1111/j.1600-0773.1984.tb01997.x.

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29

Choudhury, Tarak, Soumi Kundu, G. C. Das, and Malay Kumar Dasgupta. "Transient Non-Ketotic Hyperglycinemia in a Newborn." Journal of Nepal Paediatric Society 36, no. 3 (2017): 303–6. http://dx.doi.org/10.3126/jnps.v36i3.16047.

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In encephalopathic infants, cerebrospinal fluid hyperglycinemia and elevated cerebrospinal fluid to plasma glycine ratio are considered pathognomonic of Non-ketotic hyperglycinemia (NKH). It is due to a defect of the glycine cleavage system and has poor prognosis. We present a case of transient NKH presented to us with hypotonia, recurrent apnea and seizure. Increased ratio of cerebrospinal fluid to plasma glycine concentrations of 0.16 was seen as a strong diagnostic indicator of Non-ketotic hyperglycinemia.J Nepal Paediatr Soc 2016;36(3):303-306

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30

Setiawan, Regina Caecilia, William Septian Sonyo, and Luh Kadek Trisna Lestari. "CASE REPORT: HEMICHOREA-HEMIBALLISMUS IN NON-KETOTIC HYPERGLYCEMIA AND NON-HEMORRHAGIC STROKE PATIENT WITH BASAL GANGLIA HYPERDENSITY." Callosum Neurology 2, no. 2 (2019): 74–80. http://dx.doi.org/10.29342/cnj.v2i2.78.

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Background : Hemichorea-hemiballismus (HC-HB) is a hyperkinetic disorder characterized by uncontrolled movements, non patterned, occurring mostly in the proximal extremity on one side of the body. The etiology that most often causes HC-HB is acute cerebrovascular disorder. Non-ketotic hyperglycemia is another etiology that is very important because it is the second most common cause of HC-HB and can be manifested as an initial symptom or complication of diabetes mellitus. This case is rare and the prevalence is unknown. Case : A diabetic patient with non-ketotic hyperglycemia reported wi

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31

Bereda, Gudisa. "Differences between hyperglycemic hyperosmolar non-ketotic syndrome and diabetic ketoacidosis." BOHR International Journal of Current Research in Diabetes and Preventive Medicine 1, no. 1 (2023): 20–23. http://dx.doi.org/10.54646/bijrdpm.2023.03.

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Since high blood glucose levels might result from inadequate insulin levels, diabetic ketoacidosis is more commonin those with insulin-dependent diabetes mellitus. Diabetic ketoacidosis develops only when there is insufficientinsulin in the body to convert blood sugar into energy. The liver then uses the acids created by this process,known as ketones, to breakdown fat for energy. Osmotic diuresis, which results in significant amounts of urineproduction and volume depletion, as well as dehydration, occurs when an excessive amount of glucose entersthe renal tubules of an individual with diabetes

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32

Gusti Bagus Widiamatra Linggabudi, I., Rani Salsabilla, and Elvika Aulia Fitroningtyas. "Hyperosmolar Hyperglycemic State (HHS)." Jurnal Syntax Fusion 2, no. 02 (2022): 234–42. http://dx.doi.org/10.54543/fusion.v2i02.150.

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Hyperosmolar hyperglycemic syndrome (HHS) is a clinical condition arising from complications of diabetes mellitus. This clinical condition was previously called a non-ketotic hyperglycemic coma; non-ketotic hyperosmolar hyperglycemic syndrome, and non-ketotic hyperosmolar coma (KHONK). Current HHS diagnostic criteria include plasma glucose levels >600 mg/dL and an increase in effective plasma osmolality >320 mOsm/kg in the absence of ketoacidosis. Hyperosmolar hyperglycemic syndrome (HHS) usually occurs with lower insulinopenia levels compared to diabetic ketoacidosis (DKA), but its path

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33

Sharma, Praveen K., Abdul Majith Seeni Mohammed, Seetha Rashi, and Sakthi Ganesh Subramonian. "Non-ketotic hyperglycemia-induced hemichorea-hemiballism – A case presentation and literature review." Romanian Journal of Neurology 23, no. 3 (2024): 316–23. http://dx.doi.org/10.37897/rjn.2024.3.14.

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Non-ketotic hyperglycemia-induced hemichorea-hemiballism (NKHHH) is an infrequent hyperkinetic movement disorder, also known as diabetic striatopathy or Chorea hyperglycemia basal ganglia syndrome (C-H-BG), characterized by repetitive, uncontrollable movements in the unilateral or bilateral limbs. An insult to the contralateral basal ganglia causes NKHHH to develop. NKHHH is caused by ischemia, followed by non-ketotic hyperglycemia and poorly controlled diabetes. NKHHH is a rare condition with a unique cause that only affects one side of the corpus striatum (caudate nucleus and putamen). Clini

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34

Levine, Steven N., and Trudy H. Sanson. "Treatment of Hyperglycaemic Hyperosmolar Non-Ketotic Syndrome." Drugs 38, no. 3 (1989): 462–72. http://dx.doi.org/10.2165/00003495-198938030-00007.

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35

Biju, Sijin T., Siby Joseph, and Sunu Kurian. "Non Ketotic Hyperglycaemic Chorea – A Case Report." Asian Journal of Pharmaceutical and Health Sciences 12, no. 2 (2022): 2671–73. http://dx.doi.org/10.5530/ajphs.2022.12.12.

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36

Astroulakis, Z., P. Collinson, and A. Rhodes. "Hypernatraemia complicating hyperosmolar non-ketotic diabetic coma." Clinical Intensive Care 12, no. 2 (2001): 81–84. http://dx.doi.org/10.3109/tcic.12.2.81.84.

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37

Pinsker, Jordan E., Keivan Shalileh, Veronica J. Rooks, and Richard W. Pinsker. "Hemichorea-Hemiballism Secondary to Non-Ketotic Hyperglycemia." Journal of Clinical Medicine Research 7, no. 9 (2015): 729–30. http://dx.doi.org/10.14740/jocmr2259w.

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38

Chakrabarti, Subrata. "Hemifacial spasm due to non-ketotic hyperglycemia." International Journal of Advanced Medical and Health Research 1, no. 2 (2014): 90. http://dx.doi.org/10.4103/2349-4220.148016.

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39

Atay, Enver, Abdulkadir Bozaykut, and Gonul Sezer. "Four cases of neonatal non-ketotic hyperglycinaemia." Annals of Tropical Paediatrics 24, no. 4 (2004): 345–47. http://dx.doi.org/10.1179/027249304225019172.

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40

Wang, Weijing, Xiaomei Tang, Hao Feng, et al. "Clinical manifestation of non-ketotic hyperglycemia chorea." Medicine 99, no. 22 (2020): e19801. http://dx.doi.org/10.1097/md.0000000000019801.

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41

Chang, M. H., J. Y. Li, S. R. Lee, and C. Y. Men. "Non-ketotic hyperglycaemic chorea: a SPECT study." Journal of Neurology, Neurosurgery & Psychiatry 60, no. 4 (1996): 428–30. http://dx.doi.org/10.1136/jnnp.60.4.428.

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42

Hernando, C. "1.245 HEMICHOREA-HEMIBALLISM: NON KETOTIC HYPERGLYCEMIA SYMPTOM." Parkinsonism & Related Disorders 18 (January 2012): S58. http://dx.doi.org/10.1016/s1353-8020(11)70303-0.

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43

Tada, K., and K. Hayasaka. "Non-ketotic hyperglycinaemia: clinical and biochemical aspects." European Journal of Pediatrics 146, no. 3 (1987): 221–27. http://dx.doi.org/10.1007/bf00716464.

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44

Trump, D., S. O'Hanlon, M. Rinsler, and P. Sharp. "Hyperosmolar non-ketotic diabetic coma and rhabdomyolysis." Postgraduate Medical Journal 70, no. 819 (1994): 44–46. http://dx.doi.org/10.1136/pgmj.70.819.44.

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45

Grant, C., and C. Warlow. "Focal epilepsy in diabetic non-ketotic hyperglycaemia." BMJ 290, no. 6476 (1985): 1204–5. http://dx.doi.org/10.1136/bmj.290.6476.1204.

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46

Cole, D. E. C., and D. C. Meek. "Juvenile Non-ketotic hyperglycinaemia in three siblings." Journal of Inherited Metabolic Disease 8, S2 (1985): 123–24. http://dx.doi.org/10.1007/bf01811489.

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47

Chikthimmah, V., C. Hopkins, P. Wai, C. Soh, and M. Silverdale. "Severe reversible chorea complicating non-ketotic hyperglycaemia." Practical Diabetes International 26, no. 8 (2009): 331–32. http://dx.doi.org/10.1002/pdi.1412.

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48

Shin, Hae-Won, Kwang-Yeol Park, and Young Chul Youn. "Recurrent hemichorea-hemiballism with non-ketotic hyperglycemia." Neurological Sciences 35, no. 6 (2014): 933–34. http://dx.doi.org/10.1007/s10072-014-1673-0.

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49

K Sharma, Dr Praveen, Dr Keerthivatsan Mani, Dr Sai Sindhura G, and Dr Muthiah P. "Non-Ketotic Hyperglycemia-Induced Hemichorea-Hemiballism, A Case Presentation." Journal of University of Shanghai for Science and Technology 23, no. 09 (2021): 439–49. http://dx.doi.org/10.51201/jusst/21/09575.

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Hemiballism is a rare hyperkinetic movement disorder characterized by repetitive, uncontrolled movements unilateral /or bilateral extremities, develops as a result of insult to the contralateral basal ganglia. The leading source for this disorder is ischemia, followed by non-ketotic hyperglycemia with poorly controlled diabetes. Non-ketotic hyperglycemic induced hemichorea-hemiballism is an uncommon but unique etiology of unilateral neuro-parenchymal findings restricted to corpus striatum (caudate nucleus and putamen). Nonketotic hyperglycemia-induced hemichorea-hemiballism diagnosed by Cross-

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50

Elghobashy, Maiar, Rousseau Gama, and Raashda Ainuddin Sulaiman. "Investigation and Causes of Spontaneous (Non-Diabetic) Hypoglycaemia in Adults: Pitfalls to Avoid." Diagnostics 13, no. 20 (2023): 3275. http://dx.doi.org/10.3390/diagnostics13203275.

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Although adult spontaneous (non-diabetic) hypoglycaemia is rare, its recognition is important for the preventative or curative treatment of the underlying cause. Establishing Whipple’s triad—low blood glucose, neuroglycopaenia and resolution of neuroglycopaenia on increasing blood glucose levels to normal or above—is essential to verify hypoglycaemia. Awareness that hypoglycaemia may occur in severely ill patients is important for its prevention. Further investigation in such cases is unnecessary unless another cause of hypoglycaemia is suspected. Patients are often asymptomatic and normoglyca

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