Management Approach to Hypoglycemia
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Hepatic Glycogen Storage Diseases: Pathogenesis, Clinical Symptoms and Therapeutic Management
State of the art paper Hepatology Hepatic glycogen storage diseases: pathogenesis, clinical symptoms and therapeutic management Edyta Szymańska1, Dominika A. Jóźwiak-Dzięcielewska2, Joanna Gronek2, Marta Niewczas3, Wojciech Czarny4, Dariusz Rokicki1, Piotr Gronek2 1Department of Gastroenterology, Hepatology, Feeding Disorders and Pediatrics, Corresponding author: The Children’s Memorial Health Institute, Warsaw, Poland Edyta Szymańska MD, PhD 2Laboratory of Genetics, Department of Gymnastics and Dance, University School Department of Physical Education, Poznan, Poland of Gastroenterology, 3Department of Sport, Faculty of Physical Education, University of Rzeszow, Rzeszow, Hepatology, Feeding Poland Disorders and 4Department of Human Sciences, Faculty of Physical Education, University of Rzeszow, Pediatrics Rzeszow, Poland The Children’s Memorial Health Institute Submitted: 13 October 2017; Accepted: 8 December 2017; Al. Dzieci Polskich 20 Online publication: 18 February 2019 Warsaw, Poland Phone: +48 22 815 74 94 Arch Med Sci 2021; 17 (2): 304–313 E-mail: edyta.szymanska@ DOI: https://doi.org/10.5114/aoms.2019.83063 ipczd.pl Copyright © 2019 Termedia & Banach Abstract Glycogen storage diseases (GSDs) are genetically determined metabolic diseases that cause disorders of glycogen metabolism in the body. Due to the enzymatic defect at some stage of glycogenolysis/glycogenesis, excess glycogen or its pathologic forms are stored in the body tissues. The first symptoms of the disease usually appear during the first months of life and are thus the domain of pediatricians. Due to the fairly wide access of the authors to unpublished materials and research, as well as direct contact with the GSD patients, the article addresses the problem of actual diag- nostic procedures for patients with the suspected diseases. -
What Is Ketotic Hypoglycemia?
KETOTICHYPOGLYCEMIA.ORGv Ketotic Hypoglycemia International Who we are, what we do and why Ketotic Hypoglycemia INTERNATIONAL What is ketotic hypoglycemia? “Ketotic hypoglycemia may be unexplained, or idiopathic (IKH). This is a challenge and should urge for more research” For the patients In a normal person, fuel for the brain and the general cell metabolism primarily comes from the burning of sugar deposits (glycogen). When the glycogen stores are depleted, the body will switch to burn fat deposits. The fat burn lead to two fuels for the brain, both glucose (sugar) and ketone bodies. However, ketones in the blood will lead to nausea and eventually vomiting. This will lead to a vicious circle, where you cannot eat or drink sugar-rich items, which again leads to further fat burn and production of ketone bodies. In a KH-patient, the glycogen stores are somehow insufficient. This leads to For the doctors decreased fasting tolerance with earlier Ketotic hypoglycemia can be seen in children Emergency treatment constitutes of oral onset of fat burn and hence ketone bodies. In because of growth hormone deficiency, cortisol or i.v. glucose, eventually i.m. glucagon, to most patients, the hypoglycemia is relatively deficiency, metabolic diseases with intact fatty raise the plasma glucose, which will prevent mild, and the ketone bodies helps to provide acid consumption, including glycogen storage further lipolysis. However, the ketones can fuel to the brain, which prevents loss of diseases (glycogenosis; GSD) type 0, III, VI, and take hours to be eliminated. In more severely consciousness and convulsions. However, in IX, or disturbances in transport or metabolism affected patients, the ketone production relatively few patients, the condition is more of ketone bodies. -
Reactive Hypoglycemia from Metformin Immediate-Release Monotherapy Resolved by a Switch to Metformin Extended-Release: Conceptualizing Their Concentration-Time Curves
Open Access Case Report DOI: 10.7759/cureus.16112 Reactive Hypoglycemia From Metformin Immediate-Release Monotherapy Resolved by a Switch to Metformin Extended-Release: Conceptualizing Their Concentration-Time Curves Ayesha Akram 1, 2 1. Internal Medicine, Combined Military Hospital, Rawalpindi, PAK 2. Internal Medicine, Rawalpindi Medical University, Rawalpindi, PAK Corresponding author: Ayesha Akram, [email protected] Abstract Metformin rarely, if ever, causes hypoglycemia when it is used as labeled. A 55-year-old woman presented to the medicine ward with an altered level of consciousness. She had been reviewed in an outpatient department three days earlier and prescribed 500 mg two times per day of metformin immediate-release (Met IR) for newly diagnosed type 2 diabetes mellitus (T2DM), to which she had been adherent; however, she had been experiencing intermittent episodes of hypoglycemia after taking the medication prescribed to treat her T2DM. On physical examination, she was diaphoretic and disoriented but responsive to sensory stimuli. In the ward, she received 25 ml of intravenous dextrose as the initial blood glucose reading was low at 54 mg/dl, and 4 ounces of apple juice additionally two hours later as her blood glucose level fell below 70 mg/dl again. She was no longer hypoglycemic a few hours later, and there was a significant neurological improvement. The remainder of the laboratory results, including serum renal and liver function tests, were normal. Met IR was discontinued, and metformin extended-release (Met XR) 500 mg/day was initiated at discharge. The patient's hypoglycemic episodes resolved within days after the initiation of Met XR. -
Recurrent Severe Hypoglycemia Due to Isolated Growth Hormone
C O R R E S P O N D E N C E Recurrent Severe Hypoglycemia hyperinsulinism, ketotic hypoglycemia and hormonal deficiencies such as cortisol, GH and thyroxine [1]. GH due to Isolated Growth Hormone deficiency may occasionally manifest as recurrent Deficiency hypoglycemia as seen in our patient. The mechanisms of hypoglycemia in GH deficiency are increased insulin sensitivity and hypoglycemia unawareness [2]. Additionally, GH deficiency impairs carbohydrate meta- A 6-year-old boy presented to us with repeated episodes bolism resulting in deceased basal insulin level, impaired of seizures since early infancy. He was born small for insulin secretion and carbohydrate intolerance with gestational age to non-consanguineous parents at term. reactive hypoglycemia [1,2]. Although hypoglycemia is During neonatal period, he suffered multiple episodes of described in GH deficiency, severe symptomatic hypoglycemia requiring intravenous dextrose but no hypoglycemia is extremely rare and usually occurs in etiological investigations were done. Three of the four association with another causative factor such as hypoglycemic events beyond neonatal age were glycogen storage disorder [3,4]. Children with even associated with seizures. There were no precipitating complete GH deficiency do not usually manifest factors for hypoglycemia such as prolonged fasting, an hypoglycemia [5]. Our patient unusually developed intercurrent illness or intake of medications. There was recurrent episodes of severe symptomatic hypoglycemia no family history of similar illness, metabolic disorders or due to an isolated GH deficiency. an unexplained death. DEVI DAYAL AND JAIVINDER Y ADAV* On examination, he was short (106 cm, -2.02 z-score) Department of Pediatrics, and underweight (13.8 kg, -3.15 z-score) and had normal PGIMER, Chandigarh, India. -
Table of Contents
DISCLAIMER The information contained within this document is restricted to and intended for professional use by licensed health care providers. The statements made should not be construed as a claim, nor does it represent any particular product procedure or advice as constituting a specific cure, whether palliative or ameliorative. Procedures and products mentioned are designed to support the client’s health and may be considered as support for other procedures deemed necessary by the practitioner. Although specific manufacturers make the supplements, herbs and homeopathies referenced in this document, the opinions expressed are those of the author and are not those of any of the manufacturers. This document is not designed to replace medical advice or medical treatments, but to be used adjunctively in the care and support of health and vitality. 9 © Copyright 2005 Return to Table of Contents . CHAPTER II: SUGAR HANDLING BLOOD SUGAR STABILIZATION RELATED CONDITIONS • Hypoglycemia PROTOCOL AT A GLANCE • Reactive Hypoglycemia • Low blood sugar Primary Supplemental Support • Syndrome X Bio-Glycozyme Forte • Triglycerides high Biomega-3 • Carbohydrate sensitivity Secondary Supplemental Support • Pre-diabetic Whey Protein Isolate • B vitamin deficiency Amino Acid Quick Sorb • Sugar sensitivity Beta-TCP • Food cravings ADHS Cytozyme-PAN • Carbohydrate cravings Cytozyme-LV Cytozyme-AD PHYSIOLOGIC CONSIDERATIONS Tri-Chol Blood sugar problems begin in childhood with excess use of sugary snacks and drinks. This is extremely common today. The U.S. Department of Agriculture estimates that the average American consumes from 150 to 180 pounds of sugar each year––an unbelievable amount compared to two or three hundred years ago when normal sugar consumption was one to five pounds per year. -
Acid-Base Disorders in Critical Care
Update in Anaesthesia Acid-base disorders in critical care Alex Grice Correspondence Email: [email protected] INTRODUCTION assess severity (and likely outcome) and allow the Metabolic acidosis is a common component of critical clinician to determine whether current treatments are cid-base disorders illness. Evaluation of this component can aid diagnosis, working. A CASE EXAMPLES was dehydrated and hypotensive. Admission bloods revealed Na+ 134, K+ 2.5, Cl- 122, urea 15.4, creatinine Case 1 280, and blood gas analysis revealed: Summary A known diabetic patient presented with severe diabetic ketoacidosis. He was drowsy, exhibited pH 7.21 Disorders in acid-base balance are commonly classical Kussmaul respiration and proceeded to PaCO 2.9 kPa have a respiratory arrest whilst being admitted to 2 found in critically ill patients. Clinicians responsible for the ICU. After immediate intubation the trainee PaO 19.5 kPa 2 these patients need a clear ventilated the patient with the ventilator’s default HCO - 6.4mmol.L-1 understanding of acid-base settings (rate 12, tidal volume 500ml, PEEP 5, FiO 0.5) 3 2 pathophysiology in order to and attempted to secure arterial and central venous • Describe the acid-base disorder present. What provide effective treatment access. Shortly after intubation the patient became is the likely cause? for these disorders. This asystolic and could not be resuscitated. • Is her compensation adequate? article concentrates on • Why did this patient have a respiratory arrest? aspects of metabolic acidosis often seen in intensive care, Case 4 • Why did he deteriorate after intubation? including poisoning with the A man was brought in to the emergency room heavily alcohols (ethanol, methanol Case 2 intoxicated. -
Neurologic Manifestations of Hypoglycemia
13 Neurologic Manifestations of Hypoglycemia William P. Neil and Thomas M. Hemmen University of California, San Diego United States of America (USA) 1. Introduction Unlike most other body tissues, the brain requires a continuous supply of glucose. It has very limited endogenous glycogen stores, and does not produce glucose intrinsically.1 Although it accounts for 2% of body weight, the brain utilizes 25% of the body’s glucose due to its high metabolic rate.2, 3 Evidence for the brains sole reliance on glucose came from obtaining a respiratory quotient of one after measuring differences between arterial and venous content of oxygen and carbon dioxide in blood traveling through the brain.4 In the past, neurons were thought to directly metabolize glucose, however, more recent studies suggest astrocytes may play an important role in glucose metabolism.5 Astrocytic foot processes surround brain capillaries, which deliver glucose to the brain. With this, they form the first cellular barrier for entering glucose.5 Astrocytes contain the non-insulin dependent GLUT1 transporter, as well as the insulin dependent GLUT4 transporter, suggesting a possible role for astrocytes in regulating and storing brain glucose in an insulin dependent and independent manner (see figure 1).6-8 In addition to glucose, the brain contains a very limited store of glycogen, (between 0.5 and 1.5 g, or about 0.1% of total brain weight). Unlike peripheral tissue, where glycogen is readily mobilized during hypoglycemia, the brain can only function normally for a limited duration. Glycogen content seems to fall in areas of highest brain metabolic rate, suggesting at least some, albeit limited role as fuel during hypoglycemia.7 Although the brain relies primarily on glucose during normal conditions, it can use ketone bodies during starvation. -
1 Jasvinder Chawla, MD, MBA Chief Neurology, Hines Veterans Affairs
Jasvinder Chawla, MD, MBA Chief Neurology, Hines Veterans Affairs Hospital, Professor of Neurology, Loyola University Medical Medical Center Jasvinder Chawla, MD, MBA is a member of the following medical societies: American Academy of Neurology, American Association of Neuromuscular and Electrodiagnostic Medicine, American Clinical Neurophysiology Society, American Medical Association. Specialty Editor Board Francisco Talavera, PharmD, PhD Adjuct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Editor-in-Chief, Medscape Drug Reference Howard S Kirshner, MD Professor of Neurology, Psychiatry and Hearing and Speech Sciences, Vice Chairman, Department of Neurology, Vanderbilt University School of Medicine, Director, Vanderbilt Stroke Center, Program Director, Stroke Service, Vanderbilt Stallworth Rehabilitation Hospital, Consulting Staff, Department of Neurology, Nashville Veterans Affairs Medical Center. Chief Editor Helmi L Letsep, MD Professor and Vice Chair, Department of Neurology, Oregon Health and Science University School of Medicine, Associate Director, OHSU Stoke Center Additional Contributors Pitchaiah Mandava, MD, PhD Assistant Professor, Department of Neurology, Baylor College of Medicine, Consulting Staff, Department of Neurology, Michael E DeBakey Veterans Affairs Medical Center. Richard M Zweifler, MD Chief of Neurosciences, Sentara Healthcare, Professor and Chair of Neurology, Eastern Virginia Medical School. 1 Thomas A Kent, MD Professor and Director of Stroke Research and Education, Department -
First Do No Harm…Hypoglycemia Or Hyperglycemia? Dr
First do no harm…Hypoglycemia or hyperglycemia? Dr. Van den Berghe has received a research grant from Novo Nordisk to the University of Leuven. Copyright © 2006 by the Society of Critical Care Medicine and Lippincott Williams & Wilkins DOI: 10.1097/01.CCM.0000242913.88721.6E 2843 Crit Care Med 2006 Vol. 34, No. 11 Hyperglycemia is common in intensive care unit (ICU) patients, and severity of hyperglycemia has been repeatedly associated with adverse outcome of a variety of illnesses including critical illness (1). Traditionally, insulin was not administered until blood glucose exceeded 180–200 mg/dL based on the rationale that such mild increases were not deleterious and tighter control might be complicated by life- threatening hypoglycemia. In 2001, our large, randomized, controlled study revealed that intensive insulin therapy to maintain normal blood glucose levels (<110 mg/dL) saves lives and prevents debilitating and expensive complications in a predominantly surgical ICU population (2). The level of blood glucose control rather than the insulin dose explained the benefits (3). This study was followed by a publication by Krinsley (4), who reported that when intensive insulin therapy is implemented in real life intensive care, the benefits on morbidity and mortality can be largely reproduced. Our subsequent randomized, controlled study of intensive insulin therapy in a very ill medical ICU population, with a high co-morbidity and a high risk of death, confirmed the morbidity benefits and, when blood glucose control is continued for at least a third day, also the reduced mortality (5). Furthermore, analysis of healthcare resource utilization clearly revealed substantial cost savings (6, 7). -
(Idiopathic) Ketotic Hypoglycemia in Children
(Idiopathic) Ketotic hypoglycemia in children *Leena Priyambada, **Srinivas Raghavan *E-mail: [email protected] **Department of Pediatrics, Jawaharlal Institute of Medical Education and Research, Puducherry, India Abstract Idiopathic Ketotic Hypoglycemia is the most common non-iatrogenic cause of hypoglycemia in children beyond infancy. It improves with age and is rare after puberty. Early morning hypoglycemia, responding promptly to glucose, is a typical presentation. Etiology of hypoglycemia is unclear; deficiency of gluconeogenic substrate (hypoalaninemia) has been widely proposed. Idiopathic Ketotic Hypoglycemia is a diagnosis of exclusion. Rule out specific etiologies first. Ketonuria precedes hypoglycemia by several hours, testing for ketonuria helps in early detection. For prevention, avoiding fasting states and bedtime snacks are helpful. Keywords: Ketotic hypoglycemia, children, hypoalaninemia Introduction classic presentation is the appearance of ‘G, a 4 yr old developmentally normal girl, recurrent episodes of hypoglycemia and ketosis presented with recurrent seizures (3 episodes) provoked by fasting for 12 to 24 hours. Early for the past three months. The seizures were morning hypoglycemia before breakfast generalised tonic clonic in nature, preceded by especially when associated with strenuous vomiting early in the morning and responding physical activity the previous evening or during immediately to glucose. There was no suggestive intercurrent illnesses is a classic presentation. past, neonatal or family history. Clinical These episodes respond promptly to glucose examination, baseline biochemical, neurological administration and neurological sequelae are investigations in the interictal period when the rare. child was referred to us was normal. Fasting IKH usually presents between 18 months and test resulted in blood sugar of 26 mg/dl with five years of age. -
Effect of Ketone Bodies on Glucose Production and Utilization in the Miniature Pig
Effect of ketone bodies on glucose production and utilization in the miniature pig. M J Müller, … , U Paschen, H J Seitz J Clin Invest. 1984;74(1):249-261. https://doi.org/10.1172/JCI111408. Research Article The effect of ketone bodies on glucose production (Ra) and utilization (Rd) was investigated in the 24-h starved, conscious unrestrained miniature pig. Infusing Na-DL-beta-OH-butyrate (Na-DL-beta-OHB) and thus shifting the blood pH from 7.40 to 7.56 resulted in a decrease of Ra by 52% and of Rd by 45%, as determined by the isotope dilution technique. Simultaneously, the concentrations of arterial insulin and glucagon were slightly enhanced, whereas the plasma levels of glucose, lactate, pyruvate, alanine, alpha-amino-N, and free fatty acids (FFA) were all reduced. Infusion of Na- bicarbonate, which yielded a similar shift in blood pH, did not mimick these effects. Infusion of equimolar amounts of the ketoacid, yielding a blood pH of 7.35, induced similar metabolic alterations with respect to plasma glucose, Ra, Rd, and insulin; however, plasma alanine and alpha-amino-N increased. Infusing different amounts of Na-DL-beta-OHB resulting in plasma steady state levels of ketones from 0.25 to 1.5 mM had similar effects on arterial insulin and glucose kinetics. No dose dependency was observed. Prevention of the Na-DL-beta-OHB-induced hypoalaninemia by simultaneous infusion of alanine (1 mumol/kg X min) did not prevent hypoglycemia. Infusion of Na-DL-beta-OHB plus insulin (0.4 mU/kg X min) showed no additive effect on the inhibition of Ra. -
Blood Sugar the Hidden Factor in Health
Blood Sugar The Hidden Factor in Health Disorders in blood sugar balance disrupt all aspects of human physiology. To understand this, we must keep in mind that our bodies primarily produce their energy from converting glucose (blood sugar) into ATP. If this system is not working properly, health cannot be achieved. Blood sugar disorders are extraordinarily common in the U.S. today. Much (but not all) of the prob- lem can be placed on the Standard American Diet that is high in saturated fats and sugars while being low in essential fatty acids and fiber. In the past decade, there has been an explosion in the number of cases of diabetes, which only figures to grow in the decades ahead. Insulin Insulin is a protein hormone secreted by the pancreas. Its primary job is to stimulate the uptake of glucose from our blood into our cells. Cell membranes have a lipid layer thru which glucose cannot pass on its own. It has to be carried across with the assistance of insulin. Once inside the cells, glu- cose can be used for energy. All foods are ultimately converted into glucose. An increase of glucose in the bloodstream stimulates the release of more insulin. Insulin promotes the production of glycogen, which is the form that glucose is stored in, for later use. Insulin also promotes the formation of lipids, triglyceride and protein. Alterations in insulin are responsible for causing metabolic disorders such as hypoglycemia and diabetes. Hypoglycemia If the pancreas overreacts to a sudden surge in glucose, it will release excess insulin which will subsequently cause a drop in blood sugar.