Relevant bibliographies by topics / Metabolic decompensation

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters

Academic literature on the topic 'Metabolic decompensation'

Author: Grafiati
Published: 4 June 2021
Last updated: 15 February 2022

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Journal articles on the topic "Metabolic decompensation"

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Morris, A. A. M., and J. V. Leonard. "Early recognition of metabolic decompensation." Archives of Disease in Childhood 76, no. 6 (1997): 555–56. http://dx.doi.org/10.1136/adc.76.6.555.

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Cravino, Maria Marta, Felice Urso, Giuliana Arzilli, and Antonio Sechi. "Acute glyco-metabolic decompensation during septic shock." Emergency Care Journal 6, no. 3 (2010): 29. http://dx.doi.org/10.4081/ecj.2010.3.29.

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Starostina, E. G. "Acute metabolic decompensation in diabetes mellitus (lecture)." Problems of Endocrinology 44, no. 6 (1998): 32–39. http://dx.doi.org/10.14341/probl11667.

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The treatment of acute metabolic decompensation in diabetes mellitus (DM), especially its extreme manifestations - diabetic com - still presents significant difficulties for many endocrinologists, resuscitators and other doctors, although in practice they often have to deal with this. In the scope of this lecture, we are not able to dwell in detail on the pathogenesis, biochemical and clinical features of acute diabetic decompensation of metabolism, therefore, it will mainly examine the most important principles of its treatment and the most frequently encountered diagnostic and tactical error
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Roth, B., A. Younossi-Hartenstein, H. Skopnik, J. V. Leonard, and W. Lehnert. "Haemodialysis for metabolic decompensation in propionic acidaemia." Journal of Inherited Metabolic Disease 10, no. 2 (1987): 147–51. http://dx.doi.org/10.1007/bf01800040.

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Helmer, Drew A., Chin-Lin Tseng, Mangala Rajan, et al. "Can Ambulatory Care Prevent Hospitalization for Metabolic Decompensation?" Medical Care 46, no. 2 (2008): 148–57. http://dx.doi.org/10.1097/mlr.0b013e31815b9d66.

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Elpeleg, Orly N., Adina Joseph, David Branski, et al. "Recurrent metabolic decompensation in profound carnitine palmitoyltransferase II deficiency." Journal of Pediatrics 122, no. 6 (1993): 917–19. http://dx.doi.org/10.1016/s0022-3476(09)90019-1.

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Wathen, C. G., and I. R. Starkey. "Survival from Extreme Lactic and Keto-Acidosis in Diabetes Mellitus." Scottish Medical Journal 31, no. 4 (1986): 243–44. http://dx.doi.org/10.1177/003693308603100408.

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Feinstein, Jeffrey A., and Kevin OʼBrien. "Acute Metabolic Decompensation in an Adult Patient with Isovaleric Acidemia." Southern Medical Journal 96, no. 5 (2003): 500–503. http://dx.doi.org/10.1097/01.smj.0000051141.03668.1d.

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Burlina, Silvia, Maria Grazia Dalfrà, and Annunziata Lapolla. "Clinical and biochemical approach to predicting post-pregnancy metabolic decompensation." Diabetes Research and Clinical Practice 145 (November 2018): 178–83. http://dx.doi.org/10.1016/j.diabres.2018.02.035.

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Zwickler, Tamaris, Gisela Haege, Alina Riderer, et al. "Metabolic decompensation in methylmalonic aciduria: which biochemical parameters are discriminative?" Journal of Inherited Metabolic Disease 35, no. 5 (2012): 797–806. http://dx.doi.org/10.1007/s10545-011-9426-1.

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Dissertations / Theses on the topic "Metabolic decompensation"

1

Sabbah, E. (Emad). "Role of antibodies to glutamic acid decarboxylase in type 1 diabetes:relation to other autoantibodies, HLA risk markers and clinical characteristics." Doctoral thesis, University of Oulu, 2000. http://urn.fi/urn:isbn:951425628X.

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Abstract The purpose of this research was to assess the role of antibodies to glutamic acid decarboxylase (GAD) in children with newly diagnosed type 1 diabetes in relation to other disease-associated autoantibodies and HLA-defined genetic disease susceptibility, to evaluate the role of GAD antibodies (GADA) in relation to clinical characteristics at the diagnosis of type 1 diabetes and to compare the frequency and levels of GADA between adult and childhood onset type 1 diabetes.The study population comprised altogether 999 children and adolescents with type 1 diabetes, 100 affected adult subj
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Books on the topic "Metabolic decompensation"

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Morris, Andrew A. M. Disorders of Ketogenesis and Ketolysis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0009.

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Disorders of ketone body metabolism are characterized by episodes of metabolic decompensation. The initial episode usually occurs in the newborn period or early childhood during an infection with vomiting. The disorders of ketogenesis cause hypoglycemia and encephalopathy. Decompensation leads to severe ketoacidosis in defects of ketone body utilization (including MCT1 transporter deficiency). Treatment aims to prevent the catabolism that leads to decompensation. Prolonged fasting is avoided and glucose is provided, orally or intravenously, during illnesses. The risk of decompensation falls wi
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Lachmann, Robin H., and Elaine Murphy. Emergencies. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0076.

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Patients with an inherited metabolic disease can present acutely either with a metabolic decompensation, or due to an emerging complication. In either case, it is important to recognize the underlying metabolic condition as disease specific management is likely to be necessary. In this chapter we discuss some of the more prequent acute presentations which can be seen in adults with IMDs.
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Fraser, Jamie L., Frédéric Sedel, and Charles P. Vendetti. Disorders of Cobalamin and Folate Metabolism. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0027.

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Cobalamin C deficiency (cblC) and related disorders of intracellular cobalamin metabolism may present at any time from the prenatal period through adolescence/adulthood and are due to deficiency of the cobalamin cofactors adenosylcobalamin and methylcobalamin. Chronic complications of cblC depend on the age at presentation and may include poor growth, renal dysfunction, neuropsychiatric manifestations, intellectual disability, strokes, progressive leukoencephalopathy and spinal cord degeneration, psychiatric manifestations and executive function deficits, and optic nerve and retinal anomalies.
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Gropman, Andrea L., Belen Pappa, and Nicholas Ah Mew. The Urea Cycle Disorders. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0063.

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The urea cycle is the primary nitrogen disposal pathway in humans. The urea cycle requires the coordinated function of six enzymes and two mitochondrial transporters to catalyze the conversion of a molecule of ammonia, the α-nitrogen of aspartate and bicarbonate into urea. Whereas ammonia is toxic, urea is relatively inert, soluble in water, and readily excreted by the kidney in the urine. The accumulation of ammonia and other toxic intermediates of the cycle lead to predominantly neurological sequelae. All of the genes have been identified. The disorders may present at any age from the neonat
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Prunty, Helen, Jamie L. Fraser, Charles P. Venditti, and Robin H. Lachmann. Branched Chain Amino Acids. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0016.

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This chapter describes the four most common disorders affecting the degradation of branched chain amino acids: maple syrup urine disease, methylmalonic acidemia, propionic acidemia and isovaleric acidemia. These conditions most commonly present with encephalopathy in the newborn period, although cases with later onset have also been described. Although adult patients are less prone to acute metabolic decompensations, they do develop a number of long-term complications, both neurological and visceral. Management shares features with other disorders of protein metabolism and centers on a low-pro
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Book chapters on the topic "Metabolic decompensation"

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Paolisso, Giuseppe, and Michelangela Barbieri. "Metabolic decompensation in older people." In Diabetes in Old Age. John Wiley & Sons, Ltd, 2017. http://dx.doi.org/10.1002/9781118954621.ch17.

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Shanmugam, Naresh, and Roshni Vara. "Acute Metabolic Decompensation: Crisis Management." In Pediatric Liver Intensive Care. Springer Singapore, 2018. http://dx.doi.org/10.1007/978-981-13-1304-2_9.

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Parini, R., F. Furlan, A. Brambilla, et al. "Severe Neonatal Metabolic Decompensation in Methylmalonic Acidemia Caused by CblD Defect." In JIMD Reports. Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/8904_2013_232.

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Habets, D. D. J., N. C. Schaper, H. Rogozinski, et al. "Biochemical Monitoring and Management During Pregnancy in Patients with Isovaleric Acidaemia is Helpful to Prevent Metabolic Decompensation." In JIMD Reports. Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/8904_2011_66.

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Rodney, S., and A. Boneh. "Amino Acid Profiles in Patients with Urea Cycle Disorders at Admission to Hospital due to Metabolic Decompensation." In JIMD Reports. Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/8904_2012_186.

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Kannan, C. R. "Metabolic Decompensations in the Diabetic." In Essential Endocrinology. Springer US, 1986. http://dx.doi.org/10.1007/978-1-4899-1692-1_49.

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Barcat, Lucile, Patricia Monnier, Franz Schaefer, and Philippe Jouvet. "Dialytic Therapy of Inborn Errors of Metabolism in Case of Acute Decompensation." In Pediatric Dialysis. Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-66861-7_47.

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Sen, S., C. Steiner, A. Alisa, D. Kapoor, R. Williams, and R. Jalan. "Molecular Adsorbents Recirculating System (MARS) for acute decompensation of chronic liver disease: an early clinical experience." In Encephalopathy and Nitrogen Metabolism in Liver Failure. Springer Netherlands, 2003. http://dx.doi.org/10.1007/978-94-010-0159-5_39.

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Ravikumar, Nakul, Geoffrey R. Sheinfeld, and William T. McGee. "Hemodynamic Perspectives in Anemia." In Hemodynamics [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.99725.

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Oxygen delivery in normal physiologic states is determined by cardiac output, hemoglobin, oxygen saturation, and to a lesser extent, dissolved oxygen in the blood. Compensatory mechanisms such as an increase in stroke volume, heart rate, and re-distribution of blood flow helps in scenarios with increased oxygen demand. In cases of acute hemodynamic decompensation, this pre-existing physiologic relation between oxygen delivery and oxygen consumption is altered, resulting in tissue hypoxia and resultant anaerobic metabolism. A persistent state of sub-critical O2 delivery correlates with increased mortality. Oxygen consumption itself is usually independent of delivery unless a critical threshold is unmet. We can use various parameters such as serum lactate, oxygen extraction, and central venous oxygen saturation to determine this pathology. A basic understanding of this physiology will help better tailor therapy to improve outcomes in critically ill patients.
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Fdil, Naima, Es-Said Sabir, Karima Lafhal, et al. "Insights Into the COVID-19 Infection Related to Inherited Metabolic Diseases." In Handbook of Research on Pathophysiology and Strategies for the Management of COVID-19. IGI Global, 2022. http://dx.doi.org/10.4018/978-1-7998-8225-1.ch012.

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People with respiratory problems and people prone to decompensations are particularly vulnerable to COVID-19. These characteristics are often present in patients with inherited metabolic diseases (IMDs). It is therefore conceivable that patients with IMDs are at a greater risk of infection and may present a more serious form of COVID-19 disease. Currently available data about the impact of COVID-19 on patients suffering from IMDs are very scarce and no study has been able to confirm this hypothesis. In this chapter, the authors have tried to show that the severity of COVID-19 infection in patients with IMDs is specific to the group that the disease belongs. Indeed, lysosomal storage diseases caused by impaired degradation and accumulation of metabolites in lysosomes leads to dysfunction of lysosomal and possible impairment of the COVID-19 egress process. The fact that COVID-19 disease may be considered itself as an IMD was also discussed to highlight the interference which can exist between COVID-19 disease and IMDs in a patient.
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