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{{CMG}} {{AE}} {{CLG}} {{MAD}}
{{CMG}} {{AE}} {{CLG}} {{MAD}}


==== Overview ====
== Overview ==
Causes of hypoglycemia depend on age; neonatal causes are transient neonatal hypoglycemia, [[Prematurity]], [[intrauterine growth retardation]], [[perinatal asphyxia]]., [[Sepsis|sepsis,]] congenital [[hypopituitarism]], beta sympathomimetic drugs[[Congenital hyperinsulinism|, congenital hyperinsulinism]], [[Infant of diabetic mother (patient information)|infant of a diabetic mother]][[Beckwith-Wiedemann syndrome|, Beckwith-Wiedemann syndrome and]] [[Inborn error of metabolism|inborn errors of carbohydrate metabolism]]. Cause of adult hypoglycemia are: [[insulin]] or insulin secretagogue drugs, [[alcohol]], hepatic, renal, or cardiac failure, sepsis, non-islet cell pancreatic tumors, [[insulinoma]], reactive hypoglycemia, post [[Gastric bypass surgery|gastric bypass]] hypoglycemia, autoimmune hypoglycemia.  
Causes of hypoglycemia depend on age; neonatal causes are transient neonatal hypoglycemia, [[Prematurity]], [[intrauterine growth retardation]], [[perinatal asphyxia]], [[Sepsis|sepsis,]] congenital [[hypopituitarism]], beta sympathomimetic drugs[[Congenital hyperinsulinism|, congenital hyperinsulinism]], [[Infant of diabetic mother (patient information)|infant of a diabetic mother]][[Beckwith-Wiedemann syndrome|, Beckwith-Wiedemann syndrome]] and [[Inborn error of metabolism|inborn errors of carbohydrate metabolism]]. Causes of adult hypoglycemia are: [[insulin]] or insulin secretagogue drugs, [[alcohol]], [[hepatic failure]], [[Renal insufficiency|renal failure]], [[cardiac failure]], [[sepsis]], non-islet cell [[Pancreatic cancer|pancreatic tumors]], [[insulinoma]], reactive hypoglycemia, post [[Gastric bypass surgery|gastric bypass]] hypoglycemia, and [[Autoimmune|autoimmune]]<nowiki/>e hypoglycemia.  
== Causes of hypoglycemia ==
== Causes of hypoglycemia ==
=== Hypoglycemia in Newborn Infants ===
=== Hypoglycemia in Newborn Infants ===
*Transient neonatal hypoglycemia: blood glucose level in healthy newborns falls due to loss of the mothers' glucose supply that passes the placenta.<ref name="pmid25819173">{{cite journal| author=Stanley CA, Rozance PJ, Thornton PS, De Leon DD, Harris D, Haymond MW et al.| title=Re-evaluating "transitional neonatal hypoglycemia": mechanism and implications for management. | journal=J Pediatr | year= 2015 | volume= 166 | issue= 6 | pages= 1520-5.e1 | pmid=25819173 | doi=10.1016/j.jpeds.2015.02.045 | pmc=4659381 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25819173  }}</ref>Plasma glucose level is corrected by glycogenolysis and gluconeogenesis.<ref name="pmid10202173">{{cite journal| author=Stanley CA, Baker L| title=The causes of neonatal hypoglycemia. | journal=N Engl J Med | year= 1999 | volume= 340 | issue= 15 | pages= 1200-1 | pmid=10202173 | doi=10.1056/NEJM199904153401510 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10202173  }}</ref>
*Transient neonatal hypoglycemia:
**[[Blood glucose]] level in healthy newborns falls due to loss of the mothers' [[glucose]] supply that passes the [[placenta]].<ref name="pmid25819173">{{cite journal| author=Stanley CA, Rozance PJ, Thornton PS, De Leon DD, Harris D, Haymond MW et al.| title=Re-evaluating "transitional neonatal hypoglycemia": mechanism and implications for management. | journal=J Pediatr | year= 2015 | volume= 166 | issue= 6 | pages= 1520-5.e1 | pmid=25819173 | doi=10.1016/j.jpeds.2015.02.045 | pmc=4659381 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25819173  }}</ref> [[Plasma glucose]] level is corrected by [[glycogenolysis]] and [[gluconeogenesis]].<ref name="pmid10202173">{{cite journal| author=Stanley CA, Baker L| title=The causes of neonatal hypoglycemia. | journal=N Engl J Med | year= 1999 | volume= 340 | issue= 15 | pages= 1200-1 | pmid=10202173 | doi=10.1056/NEJM199904153401510 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10202173  }}</ref>


* [[Prematurity]], [[intrauterine growth retardation]] and [[perinatal asphyxia]]
* [[Prematurity]]
* [[Intrauterine growth retardation]]
* [[perinatal asphyxia]]
* Maternal hyperglycemia due to [[diabetes]] or iatrogenic glucose administration
* Maternal hyperglycemia due to [[diabetes]] or iatrogenic glucose administration
* [[Sepsis]]
* [[Sepsis]]
* Congenital [[Hypopituitarism|hypopituitarism:]] cortisol and growth hormone regulate glucose level.
* Congenital [[Hypopituitarism|hypopituitarism:]]
* Maternal treatment with beta-sympathomimetics, which interrupts [[glycogenolysis]] by blocking [[Epinephrine|epinephrine']]<nowiki/>s effect.<ref name="pmid27577580">{{cite journal| author=Bateman BT, Patorno E, Desai RJ, Seely EW, Mogun H, Maeda A et al.| title=Late Pregnancy β Blocker Exposure and Risks of Neonatal Hypoglycemia and Bradycardia. | journal=Pediatrics | year= 2016 | volume= 138 | issue= 3 | pages=  | pmid=27577580 | doi=10.1542/peds.2016-0731 | pmc=5005024 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27577580  }}</ref>
** [[Cortisol]] and [[growth hormone]] regulate [[glucose]] level
* Hypothermic infants who have diminished the availability of glucose and increased rates of glucose utilization.
* Maternal use of [[Beta agonist|beta-sympathomimetics]]
* Severe [[hepatic]] dysfunction leads to impairment of both [[glycogenolysis]] and [[gluconeogenesis]].
** Interrupts [[glycogenolysis]] by blocking [[Epinephrine|epinephrine']]<nowiki/>s effect.<ref name="pmid27577580">{{cite journal| author=Bateman BT, Patorno E, Desai RJ, Seely EW, Mogun H, Maeda A et al.| title=Late Pregnancy β Blocker Exposure and Risks of Neonatal Hypoglycemia and Bradycardia. | journal=Pediatrics | year= 2016 | volume= 138 | issue= 3 | pages=  | pmid=27577580 | doi=10.1542/peds.2016-0731 | pmc=5005024 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27577580  }}</ref>
*[[Congenital hyperinsulinism]]:
* [[Hypothermia|Hypothermic]] infants who have increased rates of glucose utilization and decreased glucose availability.
**[[Infant of diabetic mother (patient information)|Infant of a diabetic mothe]]<nowiki/>r is the most common cause of hypoglycemia due to [[hyperinsulinism]]. Prolonged intrapartum [[hyperglycemia]] in [[fetus]] leads to hypertrophied and hyperfunctioning [[beta cells]] causing [[hyperinsulinism]]. It is transient and resolves two days after birth.  
* Severe [[hepatic]] dysfunction
** Leads to impairment of both [[glycogenolysis]] and [[gluconeogenesis]].
*[[Congenital hyperinsulinism]]:<ref name="pmid23739646">{{cite journal| author=Buraczewska B, Kopacz K, Myśliwiec M| title=Hyperinsulinism as a common cause of hypoglycemia in children - pathogenesis, diagnosis and treatment. | journal=Pediatr Endocrinol Diabetes Metab | year= 2013 | volume= 19 | issue= 1 | pages= 24-8 | pmid=23739646 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23739646  }}</ref>
**[[Infant of diabetic mother (patient information)|Infant of a diabetic mothe]]<nowiki/>r is most commonly affected by hypoglycemia due to [[hyperinsulinism]]. Prolonged intrapartum [[hyperglycemia]] in [[fetus]] leads to [[Hypertrophy (medical)|hypertrophied]] and hyperfunctioning [[beta cells]] causing [[hyperinsulinism]]. It is transient and resolves two days after birth.  
**[[Beckwith-Wiedemann syndrome]]
**[[Beckwith-Wiedemann syndrome]]
**[[Persistent hyperinsulinemic hypoglycemia of infancy]]: it is a mutation in genes encoding enzymes that control intracellular metabolic pathways of the [[pancreatic]] beta cell.  
**[[Persistent hyperinsulinemic hypoglycemia of infancy]]: it is a mutation in genes encoding [[enzymes]] that control [[intracellular]] [[metabolic]] pathways of the [[pancreatic]] beta cell.  
**Excess exogenous [[insulin]] given to newborns with [[hyperglycemia]] may result in hypoglycemia.<ref name="pmid19588439">{{cite journal| author=Sinclair JC, Bottino M, Cowett RM| title=Interventions for prevention of neonatal hyperglycemia in very low birth weight infants. | journal=Cochrane Database Syst Rev | year= 2009 | volume=  | issue= 3 | pages= CD007615 | pmid=19588439 | doi=10.1002/14651858.CD007615.pub2 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19588439  }}</ref>
**Excess [[exogenous]] [[insulin]] given to newborns with [[hyperglycemia]] may result in hypoglycemia.<ref name="pmid19588439">{{cite journal| author=Sinclair JC, Bottino M, Cowett RM| title=Interventions for prevention of neonatal hyperglycemia in very low birth weight infants. | journal=Cochrane Database Syst Rev | year= 2009 | volume=  | issue= 3 | pages= CD007615 | pmid=19588439 | doi=10.1002/14651858.CD007615.pub2 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19588439  }}</ref>
**Neonatal conditions associated with excessive [[insulin]] secretion include alloimmune hemolytic disease of the newborn, [[heart failure]] and [[sepsis]].<ref name="pmid10331464">{{cite journal| author=Sue CM, Hirano M, DiMauro S, De Vivo DC| title=Neonatal presentations of mitochondrial metabolic disorders. | journal=Semin Perinatol | year= 1999 | volume= 23 | issue= 2 | pages= 113-24 | pmid=10331464 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10331464  }}</ref>
**Neonatal conditions associated with excessive [[insulin]] secretion include [[alloimmune]] [[Hemolytic disease of the newborn|hemolytic disease]] of the newborn, [[heart failure]] and [[sepsis]].<ref name="pmid10331464">{{cite journal| author=Sue CM, Hirano M, DiMauro S, De Vivo DC| title=Neonatal presentations of mitochondrial metabolic disorders. | journal=Semin Perinatol | year= 1999 | volume= 23 | issue= 2 | pages= 113-24 | pmid=10331464 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10331464  }}</ref>
**[[Polycythemia]] may lead to greater glucose utilization by the increased mass of red blood cells.  
**[[Polycythemia]] may lead to greater glucose utilization by the increased mass of red blood cells.  
*[[Inborn error of metabolism|Inborn errors of metabolism]]:
**[[Nesidioblastosis]]
*[[Inborn error of metabolism|Inborn errors of metabolism]]:<ref name="pmid9832597">{{cite journal| author=Burton BK| title=Inborn errors of metabolism in infancy: a guide to diagnosis. | journal=Pediatrics | year= 1998 | volume= 102 | issue= 6 | pages= E69 | pmid=9832597 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9832597  }}</ref>
**Disorders of [[gluconeogenesis]]: [[Fructose bisphosphatase deficiency|fructose-1,6-bisphosphatase]] deficiency, [[pyruvate carboxylase deficiency]].
**Disorders of [[gluconeogenesis]]: [[Fructose bisphosphatase deficiency|fructose-1,6-bisphosphatase]] deficiency, [[pyruvate carboxylase deficiency]].
**Disorders of [[carbohydrate metabolism]]: [[hereditary fructose intolerance]], [[Galactosemia|galactosemia.]]
**Disorders of [[carbohydrate metabolism]]: [[hereditary fructose intolerance]], [[Galactosemia|galactosemia.]]
**Disorders of [[Fatty acid metabolism|fatty acid metabolism:]] medium or [[Long-chain 3-hydroxyacyl-coenzyme A dehydrogenase deficiency|long-chain acyl-CoA dehydrogenase deficiency]]).<ref name="pmid7726385">{{cite journal| author=Worthen HG, al Ashwal A, Ozand PT, Garawi S, Rahbeeni Z, al Odaib A et al.| title=Comparative frequency and severity of hypoglycemia in selected organic acidemias, branched chain amino acidemia, and disorders of fructose metabolism. | journal=Brain Dev | year= 1994 | volume= 16 Suppl | issue=  | pages= 81-5 | pmid=7726385 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7726385  }}</ref>
**Disorders of [[Fatty acid metabolism|fatty acid metabolism:]] medium or [[Long-chain 3-hydroxyacyl-coenzyme A dehydrogenase deficiency|long-chain acyl-CoA dehydrogenase deficiency]]).<ref name="pmid7726385">{{cite journal| author=Worthen HG, al Ashwal A, Ozand PT, Garawi S, Rahbeeni Z, al Odaib A et al.| title=Comparative frequency and severity of hypoglycemia in selected organic acidemias, branched chain amino acidemia, and disorders of fructose metabolism. | journal=Brain Dev | year= 1994 | volume= 16 Suppl | issue=  | pages= 81-5 | pmid=7726385 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7726385  }}</ref>
====Hypoglycemia in Older Adults====
===Hypoglycemia in Adults===
* Drugs: they are the most common cause of hypoglycemia.<ref name="pmid19088155">{{cite journal| author=Cryer PE, Axelrod L, Grossman AB, Heller SR, Montori VM, Seaquist ER et al.| title=Evaluation and management of adult hypoglycemic disorders: an Endocrine Society Clinical Practice Guideline. | journal=J Clin Endocrinol Metab | year= 2009 | volume= 94 | issue= 3 | pages= 709-28 | pmid=19088155 | doi=10.1210/jc.2008-1410 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19088155  }}</ref>
* Drugs are the most common cause of hypoglycemia in adults.<ref name="pmid19088155">{{cite journal| author=Cryer PE, Axelrod L, Grossman AB, Heller SR, Montori VM, Seaquist ER et al.| title=Evaluation and management of adult hypoglycemic disorders: an Endocrine Society Clinical Practice Guideline. | journal=J Clin Endocrinol Metab | year= 2009 | volume= 94 | issue= 3 | pages= 709-28 | pmid=19088155 | doi=10.1210/jc.2008-1410 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19088155  }}</ref> The most important causes of hypoglycemia in adults include:
**[[Insulin]] or insulin secretagogue such as [[sulfonylurea]] and glyburide are the most common drugs induce hypoglycemia due to longer duration of action.<ref name="pmid16324923">{{cite journal| author=Szoke E, Gosmanov NR, Sinkin JC, Nihalani A, Fender AB, Cryer PE et al.| title=Effects of glimepiride and glyburide on glucose counterregulation and recovery from hypoglycemia. | journal=Metabolism | year= 2006 | volume= 55 | issue= 1 | pages= 78-83 | pmid=16324923 | doi=10.1016/j.metabol.2005.07.009 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16324923  }}</ref>They suppress hepatic [[glucose]] production and stimulate glucose utilization causing hypoglycemia.
**[[Insulin]] or insulin secretagogues such as [[sulfonylurea]] and glyburide are the most common drugs that may cause hypoglycemia due to longer duration of action<ref name="pmid16324923">{{cite journal| author=Szoke E, Gosmanov NR, Sinkin JC, Nihalani A, Fender AB, Cryer PE et al.| title=Effects of glimepiride and glyburide on glucose counterregulation and recovery from hypoglycemia. | journal=Metabolism | year= 2006 | volume= 55 | issue= 1 | pages= 78-83 | pmid=16324923 | doi=10.1016/j.metabol.2005.07.009 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16324923  }}</ref>. They suppress hepatic [[glucose]] production and stimulate glucose utilization which may result in hypoglycemia.
**Other drugs in nondiabetic patients: quinolones, pentamidine, quinine, beta blockers, angiotensin-converting enzyme inhibitors, and [[Insulin-like growth factor-I|IGF-1]] especially in older patients with underlying renal or hepatic dysfunctions.<ref name="pmid25179404">{{cite journal| author=Parekh TM, Raji M, Lin YL, Tan A, Kuo YF, Goodwin JS| title=Hypoglycemia after antimicrobial drug prescription for older patients using sulfonylureas. | journal=JAMA Intern Med | year= 2014 | volume= 174 | issue= 10 | pages= 1605-12 | pmid=25179404 | doi=10.1001/jamainternmed.2014.3293 | pmc=4878670 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25179404  }}  [https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25686188 Review in: Ann Intern Med. 2015 Feb 17;162(4):JC13]</ref>
**[[Quinolones]]
**[[Alcohol]]: due to hepatic glycogen depletion in fasting patients. Alcohol can induce hypoglycemia alone or associated with other hypoglycemic drugs.
**[[Pentamidine]]
* Critical illnesses: [[hepatic]], [[renal]], or [[Congestive heart failure|cardiac failure]], sepsis. It occurs due to impaired liver [[gluconeogenesis]]. [[Sepsis]] induced [[cytokines]] secretion cause suppression of [[gluconeogenesis]].<ref name="pmid10807013">{{cite journal| author=Maitra SR, Wojnar MM, Lang CH| title=Alterations in tissue glucose uptake during the hyperglycemic and hypoglycemic phases of sepsis. | journal=Shock | year= 2000 | volume= 13 | issue= 5 | pages= 379-85 | pmid=10807013 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10807013  }}</ref>
**[[Quinine]]
* Hormone deficiency: cortisol in acquired [[adrenal insufficiency|adrenal insufficiency or]] acquired [[hypopituitarism]]
**[[Beta blockers]]
* Nonislet cell tumor: Hypoglycemia usually occurs as a result of tumor production of [[Insulin-like growth factor 2|IGF-2]]
**[[Angiotensin-converting enzyme inhibitors]]
**[[Insulin-like growth factor-I|IGF-1]]  
***Especially in older patients with underlying [[renal]] or [[hepatic]] dysfunction<ref name="pmid25179404">{{cite journal| author=Parekh TM, Raji M, Lin YL, Tan A, Kuo YF, Goodwin JS| title=Hypoglycemia after antimicrobial drug prescription for older patients using sulfonylureas. | journal=JAMA Intern Med | year= 2014 | volume= 174 | issue= 10 | pages= 1605-12 | pmid=25179404 | doi=10.1001/jamainternmed.2014.3293 | pmc=4878670 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25179404  }}  [https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25686188 Review in: Ann Intern Med. 2015 Feb 17;162(4):JC13]</ref>
**[[Alcohol]]
***Due to [[hepatic]] [[glycogen]] depletion in fasting patients
***[[Alcohol]] can induce hypoglycemia alone or associated with other hypoglycemic drugs
* Critical illnesses:
** [[Hepatic failure]]
** [[Renal failure]]
** [[Congestive heart failure|Cardiac failure]]  
** [[Sepsis]]
*** It occurs due to impaired liver [[gluconeogenesis]]
*** [[Sepsis]] induced [[cytokines]] secretion cause suppression of [[gluconeogenesis]]<ref name="pmid10807013">{{cite journal| author=Maitra SR, Wojnar MM, Lang CH| title=Alterations in tissue glucose uptake during the hyperglycemic and hypoglycemic phases of sepsis. | journal=Shock | year= 2000 | volume= 13 | issue= 5 | pages= 379-85 | pmid=10807013 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10807013  }}</ref>
* [[Hormone]] deficiency: [[cortisol]] in acquired [[adrenal insufficiency|adrenal insufficiency or]] acquired [[hypopituitarism]]<ref name="pmid26563979">{{cite journal| author=Odenwald B, Nennstiel-Ratzel U, Dörr HG, Schmidt H, Wildner M, Bonfig W| title=Children with classic congenital adrenal hyperplasia experience salt loss and hypoglycemia: evaluation of adrenal crises during the first 6 years of life. | journal=Eur J Endocrinol | year= 2016 | volume= 174 | issue= 2 | pages= 177-86 | pmid=26563979 | doi=10.1530/EJE-15-0775 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26563979  }}</ref>
* [[Islet cell|Non islet cell]] [[tumor]]: hypoglycemia usually occurs as a result of [[tumor]] production of [[Insulin-like growth factor 2|IGF-2]]
* [[Insulinoma]]
* [[Insulinoma]]
* Reactive hypoglycemia or postprandial:  it is a hypoglycemia that occurs as a reaction to food ingestion within 4 hours after meals due to [[Hyperinsulinism|functional hyperinsulinism]].
* [[Reactive hypoglycemia]] or postprandial
*[[Gastric bypass|Post gastric bypass]] hypoglycemia: rapid [[Jejunum|jejunal]] emptying with exaggerated [[insulin]] response.
** A hypoglycemia that occurs as a reaction to food ingestion within 4 hours after meals due to [[Hyperinsulinism|functional hyperinsulinism]]<ref name="pmid24246338">{{cite journal| author=Galati SJ, Rayfield EJ| title=Approach to the patient with postprandial hypoglycemia. | journal=Endocr Pract | year= 2014 | volume= 20 | issue= 4 | pages= 331-40 | pmid=24246338 | doi=10.4158/EP13132.RA | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24246338  }}</ref>
* [[Insulin]] autoimmune hypoglycemia: it occurs in patients who have [[antibodies]] directed to endogenous [[insulin]] or to the [[insulin]] receptor.<ref name="pmid19440117">{{cite journal| author=Lupsa BC, Chong AY, Cochran EK, Soos MA, Semple RK, Gorden P| title=Autoimmune forms of hypoglycemia. | journal=Medicine (Baltimore) | year= 2009 | volume= 88 | issue= 3 | pages= 141-53 | pmid=19440117 | doi=10.1097/MD.0b013e3181a5b42e | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19440117  }}</ref>
*[[Gastric bypass|Post gastric bypass]] hypoglycemia
**Rapid [[Jejunum|jejunal]] emptying with exaggerated [[insulin]] response
* [[Insulin]] [[autoimmune]] hypoglycemia
** Occurs in patients who have [[antibodies]] directed to endogenous [[insulin]] or to the [[insulin]] [[receptor]]<ref name="pmid19440117">{{cite journal| author=Lupsa BC, Chong AY, Cochran EK, Soos MA, Semple RK, Gorden P| title=Autoimmune forms of hypoglycemia. | journal=Medicine (Baltimore) | year= 2009 | volume= 88 | issue= 3 | pages= 141-53 | pmid=19440117 | doi=10.1097/MD.0b013e3181a5b42e | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19440117  }}</ref>
* Accidental, surreptitious, or malicious hypoglycemia
* Accidental, surreptitious, or malicious hypoglycemia
==References==
==References==
{{Reflist|2}}
{{Reflist|2}}

Latest revision as of 19:03, 15 November 2017

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Carlos A Lopez, M.D. [2] Mohammed Abdelwahed M.D[3]

Overview

Causes of hypoglycemia depend on age; neonatal causes are transient neonatal hypoglycemia, Prematurity, intrauterine growth retardation, perinatal asphyxia, sepsis, congenital hypopituitarism, beta sympathomimetic drugs, congenital hyperinsulinism, infant of a diabetic mother, Beckwith-Wiedemann syndrome and inborn errors of carbohydrate metabolism. Causes of adult hypoglycemia are: insulin or insulin secretagogue drugs, alcohol, hepatic failure, renal failure, cardiac failure, sepsis, non-islet cell pancreatic tumors, insulinoma, reactive hypoglycemia, post gastric bypass hypoglycemia, and autoimmunee hypoglycemia.

Causes of hypoglycemia

Hypoglycemia in Newborn Infants

Hypoglycemia in Adults

References

  1. ↑ Stanley CA, Rozance PJ, Thornton PS, De Leon DD, Harris D, Haymond MW; et al. (2015). "Re-evaluating "transitional neonatal hypoglycemia": mechanism and implications for management". J Pediatr. 166 (6): 1520–5.e1. doi:10.1016/j.jpeds.2015.02.045. PMC 4659381. PMID 25819173.
  2. ↑ Stanley CA, Baker L (1999). "The causes of neonatal hypoglycemia". N Engl J Med. 340 (15): 1200–1. doi:10.1056/NEJM199904153401510. PMID 10202173.
  3. ↑ Bateman BT, Patorno E, Desai RJ, Seely EW, Mogun H, Maeda A; et al. (2016). "Late Pregnancy β Blocker Exposure and Risks of Neonatal Hypoglycemia and Bradycardia". Pediatrics. 138 (3). doi:10.1542/peds.2016-0731. PMC 5005024. PMID 27577580.
  4. ↑ Buraczewska B, Kopacz K, Myśliwiec M (2013). "Hyperinsulinism as a common cause of hypoglycemia in children - pathogenesis, diagnosis and treatment". Pediatr Endocrinol Diabetes Metab. 19 (1): 24–8. PMID 23739646.
  5. ↑ Sinclair JC, Bottino M, Cowett RM (2009). "Interventions for prevention of neonatal hyperglycemia in very low birth weight infants". Cochrane Database Syst Rev (3): CD007615. doi:10.1002/14651858.CD007615.pub2. PMID 19588439.
  6. ↑ Sue CM, Hirano M, DiMauro S, De Vivo DC (1999). "Neonatal presentations of mitochondrial metabolic disorders". Semin Perinatol. 23 (2): 113–24. PMID 10331464.
  7. ↑ Burton BK (1998). "Inborn errors of metabolism in infancy: a guide to diagnosis". Pediatrics. 102 (6): E69. PMID 9832597.
  8. ↑ Worthen HG, al Ashwal A, Ozand PT, Garawi S, Rahbeeni Z, al Odaib A; et al. (1994). "Comparative frequency and severity of hypoglycemia in selected organic acidemias, branched chain amino acidemia, and disorders of fructose metabolism". Brain Dev. 16 Suppl: 81–5. PMID 7726385.
  9. ↑ Cryer PE, Axelrod L, Grossman AB, Heller SR, Montori VM, Seaquist ER; et al. (2009). "Evaluation and management of adult hypoglycemic disorders: an Endocrine Society Clinical Practice Guideline". J Clin Endocrinol Metab. 94 (3): 709–28. doi:10.1210/jc.2008-1410. PMID 19088155.
  10. ↑ Szoke E, Gosmanov NR, Sinkin JC, Nihalani A, Fender AB, Cryer PE; et al. (2006). "Effects of glimepiride and glyburide on glucose counterregulation and recovery from hypoglycemia". Metabolism. 55 (1): 78–83. doi:10.1016/j.metabol.2005.07.009. PMID 16324923.
  11. ↑ Parekh TM, Raji M, Lin YL, Tan A, Kuo YF, Goodwin JS (2014). "Hypoglycemia after antimicrobial drug prescription for older patients using sulfonylureas". JAMA Intern Med. 174 (10): 1605–12. doi:10.1001/jamainternmed.2014.3293. PMC 4878670. PMID 25179404. Review in: Ann Intern Med. 2015 Feb 17;162(4):JC13
  12. ↑ Maitra SR, Wojnar MM, Lang CH (2000). "Alterations in tissue glucose uptake during the hyperglycemic and hypoglycemic phases of sepsis". Shock. 13 (5): 379–85. PMID 10807013.
  13. ↑ Odenwald B, Nennstiel-Ratzel U, Dörr HG, Schmidt H, Wildner M, Bonfig W (2016). "Children with classic congenital adrenal hyperplasia experience salt loss and hypoglycemia: evaluation of adrenal crises during the first 6 years of life". Eur J Endocrinol. 174 (2): 177–86. doi:10.1530/EJE-15-0775. PMID 26563979.
  14. ↑ Galati SJ, Rayfield EJ (2014). "Approach to the patient with postprandial hypoglycemia". Endocr Pract. 20 (4): 331–40. doi:10.4158/EP13132.RA. PMID 24246338.
  15. ↑ Lupsa BC, Chong AY, Cochran EK, Soos MA, Semple RK, Gorden P (2009). "Autoimmune forms of hypoglycemia". Medicine (Baltimore). 88 (3): 141–53. doi:10.1097/MD.0b013e3181a5b42e. PMID 19440117.
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