Related Research Articles
Hypoglycemia, also called low blood sugar, is a fall in blood sugar to levels below normal, typically below 70 mg/dL (3.9 mmol/L). Whipple's triad is used to properly identify hypoglycemic episodes. It is defined as blood glucose below 70 mg/dL (3.9 mmol/L), symptoms associated with hypoglycemia, and resolution of symptoms when blood sugar returns to normal. Hypoglycemia may result in headache, tiredness, clumsiness, trouble talking, confusion, fast heart rate, sweating, shakiness, nervousness, hunger, loss of consciousness, seizures, or death. Symptoms typically come on quickly.
Hyperinsulinemic hypoglycemia describes the condition and effects of low blood glucose caused by excessive insulin. Hypoglycemia due to excess insulin is the most common type of serious hypoglycemia. It can be due to endogenous or injected insulin.
Hyperinsulinism refers to an above normal level of insulin in the blood of a person or animal. Normal insulin secretion and blood levels are closely related to the level of glucose in the blood, so that a given level of insulin can be normal for one blood glucose level but low or high for another. Hyperinsulinism can be associated with several types of medical problems, which can be roughly divided into two broad and largely non-overlapping categories: those tending toward reduced sensitivity to insulin and high blood glucose levels (hyperglycemia), and those tending toward excessive insulin secretion and low glucose levels (hypoglycemia).
Whipple's triad is a collection of three signs that suggests that a patient's symptoms result from hypoglycaemia that may indicate insulinoma. The essential conditions are symptoms of hypoglycaemia, low blood plasma glucose concentration, and relief of symptoms when plasma glucose concentration is increased. It was first described by the pancreatic surgeon Allen Whipple, who aimed to establish criteria for exploratory pancreatic surgery to look for insulinoma.
Congenital hyperinsulinism is a medical term referring to a variety of congenital disorders in which hypoglycemia is caused by excessive insulin secretion. Congenital forms of hyperinsulinemic hypoglycemia can be transient or persistent, mild or severe. These conditions are present at birth and most become apparent in early infancy. Mild cases can be treated by frequent feedings, more severe cases can be controlled by medications that reduce insulin secretion or effects.
Ketotic hypoglycemia is a medical term used in two ways: (1) broadly, to refer to any circumstance in which low blood glucose is accompanied by ketosis, and (2) also nutritional ketosis. It remains one of the more common causes of hypoglycemia in the age range.
Reactive hypoglycemia, postprandial hypoglycemia, or sugar crash is a term describing recurrent episodes of symptomatic hypoglycemia occurring within four hours after a high carbohydrate meal in people with and without diabetes. The term is not necessarily a diagnosis since it requires an evaluation to determine the cause of the hypoglycemia.
Glycogen storage disease type 0 is a disease characterized by a deficiency in the glycogen synthase enzyme (GSY). Although glycogen synthase deficiency does not result in storage of extra glycogen in the liver, it is often classified as a glycogen storage disease because it is another defect of glycogen storage and can cause similar problems. There are two isoforms (types) of glycogen synthase enzyme; GSY1 in muscle and GSY2 in liver, each with a corresponding form of the disease. Mutations in the liver isoform (GSY2), causes fasting hypoglycemia, high blood ketones, increased free fatty acids and low levels of alanine and lactate. Conversely, feeding in these patients results in hyperglycemia and hyperlactatemia.
Seale Harris was an American physician and researcher born in Cedartown, Georgia. He was nicknamed "the Benjamin Franklin of Medicine" by contemporaries for his leadership and writing on a wide range of medical and political topics. Dr. Harris' most celebrated accomplishments were his 1924 hypothesis of hyperinsulinism as a cause of spontaneous hypoglycemia.
Kir6.2 is a major subunit of the ATP-sensitive K+ channel, a lipid-gated inward-rectifier potassium ion channel. The gene encoding the channel is called KCNJ11 and mutations in this gene are associated with congenital hyperinsulinism.
ATP-binding cassette transporter sub-family C member 8 is a protein that in humans is encoded by the ABCC8 gene. ABCC8 orthologs have been identified in all mammals for which complete genome data are available.
Neonatal hypoglycemia occurs when the neonate's blood glucose level is less than the newborn's body requirements for factors such as cellular energy and metabolism. There is inconsistency internationally for diagnostic thresholds. In the US, hypoglycemia is when the blood glucose level is below 30 mg/dL within the first 24 hours of life and below 45 mg/dL thereafter. In the UK, however, lower and more variable thresholds are used. The neonate's gestational age, birth weight, metabolic needs, and wellness state of the newborn has a substantial impact on the neonates blood glucose level. There are known risk factors that can be both maternal and neonatal. This is a treatable condition. Its treatment depends on the cause of the hypoglycemia. Though it is treatable, it can be fatal if gone undetected. Hypoglycemia is the most common metabolic problem in newborns.
Glucose-elevating agents are medications used to treat hypoglycemia by raising blood glucose. In diabetics, hypoglycemia can occur as a result of too much insulin or antidiabetic medication, insufficient food intake, or sudden increase in physical activity or exercise. The most common glucose-elevating agents used to treat diabetic hypoglycemia are glucose and glucagon injections when severe hypoglycemia occurs. Diazoxide, which is used to counter hypoglycemia in disease states such as insulinoma or congenital hyperinsulinism, increases blood glucose and decreases insulin secretion and glucagon accelerates breakdown of glycogen in the liver (glycogenolysis) to release glucose into the bloodstream.
References
- 1 2 3 4 Edwards, Taygen; Liu, Gordon; Battin, Malcolm; Harris, Deborah L.; Hegarty, Joanne E.; Weston, Philip J.; Harding, Jane E. (2022-03-18). "Oral dextrose gel for the treatment of hypoglycaemia in newborn infants". The Cochrane Database of Systematic Reviews. 2022 (3): CD011027. doi:10.1002/14651858.CD011027.pub3. ISSN 1469-493X. PMC 8932405 . PMID 35302645.
- ↑ "WHO ref. number WHO/CHD/97.1 / WHO/MSM/97.1" (PDF). Hypoglycaemia of the Newborn. Geneva: World Health Organization. 1997. pp. 4, 19. Retrieved 6 April 2010.
- ↑ H. Huopio1, S.-L. Shyng, T. Otonkoski3, and C. G. Nichols4 (2002-08-01). "KATP channels and insulin secretion disorders". American Journal of Physiology. Endocrinology and Metabolism. Ajpendo.physiology.org. 283 (2): E207–E216. doi:10.1152/ajpendo.00047.2002. PMID 12110524 . Retrieved 2012-03-10.
{{cite journal}}: CS1 maint: multiple names: authors list (link) - ↑ "Familial Leucine-Sensitive Hypoglycemia of Infancy Due to a Dominant Mutation of the β-Cell Sulfonylurea Receptor". Jcem.endojournals.org. 2004-09-01. Retrieved 2012-03-10.
- ↑ Umesh Masharani, MB, BS, MRCP(UK) (2007). "The Hypoglycemic states – Hypoglycemia". The Hypoglycemic states. Armenian Medical Network.
{{cite web}}: CS1 maint: multiple names: authors list (link)