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


==== Overview ====
== Overview ==
Is when blood sugar decreases to below normal levels. This may result in a variety of symptoms including clumsiness, trouble talking, confusion, loss of consciousness, seizures, or death. Some causes of hypoglycemia are [[chloramphenicol]], [[addison's disease]], [[acute fatty liver of pregnancy]] and [[sepsis]].  
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 ====
===== Life Threatening Causes =====
* [[Adrenal cancer]]
* [[Acute meningitis]]
* [[Diabetes type 1]]
* [[ketotic hypoglycemia]]
* [[Septic shock]]
 
===== Common Causes =====
* [[Adrenal cortex insufficiency]]
* [[Burns]]
* [[Ethanol]]
* [[Glibenclamide]]
* [[Reye syndrome]]
 
== Causes ==
=== Hypoglycemia in Newborn Infants ===
=== Hypoglycemia in Newborn Infants ===
Hypoglycemia is a common problem in critically ill or extremely [[low birthweight infants]]. If not due to maternal hyperglycemia, in most cases it is multifactorial, transient and easily supported. In a minority of cases hypoglycemia turns out to be due to significant [[hyperinsulinism]], [[hypopituitarism]] or an [[inborn error of metabolism]] and presents more of a management challenge.
*Transient neonatal hypoglycemia:
*Transient neonatal hypoglycemia: With loss of the continuous transplacental supply of glucose, plasma glucose concentration in the healthy term newborn falls during the first two hours after delivery[1,2,6,7].  plasma glucose concentration is maintained by glycogenolysis during the first 8 to 12 hours then by gluconeogenesis.[8,9]
**[[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: cortisol and growth hormone regulate glucose level.
* Congenital [[Hypopituitarism|hypopituitarism:]]
* Maternal treatment with beta-sympathomimetic agents (eg, terbutaline and beta-blockers), which interrupts glycogenolysis by blocking epinephrine's effect [12]
** [[Cortisol]] and [[growth hormone]] regulate [[glucose]] level
* Hypothermic infants who have diminished availability of glucose and increased rates of glucose utilization
* Maternal use of [[Beta agonist|beta-sympathomimetics]]
* Severe hepatic dysfunction due 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 a diabetic mother is the most common cause of hypoglycemia due to hyperinsulinism. Prolonged intrapartum hyperglycemia in fetus leads to hypertrophied and hyperfunctioning beta cells causing hyperinsulinsim. It is transient and resolves two to four 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]]: mutations in genes encoding enzymes that control intracellular metabolic pathways of the pancreatic beta cell. The genes most often affected control the sulfonylurea receptor that control the functional ATP-dependent potassium channel in the beta cell membrane.
**[[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 16
**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 excess insulin secretion include alloimmune hemolytic disease of the newborn, heart failure and sepsis. These conditons increase anaerobic glycolysis due to decreased tissue perfusion.[17]
**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 result from 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 carbohydrate metabolism]]:
**[[Nesidioblastosis]]
**Disorders of gluconeogenesis: fructose-1,6-bisphosphatase deficiency, pyruvate carboxylase deficiency.
*[[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 carbohydrate metabolism: hereditary fructose intolerance, galactosemia.
**Disorders of [[gluconeogenesis]]: [[Fructose bisphosphatase deficiency|fructose-1,6-bisphosphatase]] deficiency, [[pyruvate carboxylase deficiency]].
**Disorders of fatty acid metabolism: medium or long-chain acyl-CoA dehydrogenase deficiency). 11
**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>
====Hypoglycemia in Young Children====
===Hypoglycemia in Adults===
Single episodes of hypoglycemia due to [[gastroenteritis]] or fasting, but recurrent episodes nearly always indicate either an [[inborn error of metabolism]], congenital hypopituitarism, or congenital hyperinsulinism
* 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:
*Prolonged fasting
**[[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.
**[[Diarrhea]]l illness in young children, especially [[rotavirus]] [[gastroenteritis]]
**[[Quinolones]]
*Idiopathic [[ketotic hypoglycemia]]
**[[Pentamidine]]
*Isolated [[growth hormone deficiency]], [[hypopituitarism]]
**[[Quinine]]
*[[Hyperinsulinemic hypoglycemia|Insulin excess]]
**[[Beta blockers]]
**Hyperinsulinism due to several [[congenital hyperinsulinism|congenital disorders of insulin secretion]]
**[[Angiotensin-converting enzyme inhibitors]]
**Insulin injected for type 1 diabetes
**[[Insulin-like growth factor-I|IGF-1]]  
*[[Gastric dumping syndrome]] (after gastrointestinal surgery)
***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>
*Other congenital metabolic diseases; some of the common include
**[[Alcohol]]
**[[Maple syrup urine disease]] and other [[organic aciduria]]s
***Due to [[hepatic]] [[glycogen]] depletion in fasting patients
**[[Glycogen storage disease|Type 1 glycogen storage disease]]
***[[Alcohol]] can induce hypoglycemia alone or associated with other hypoglycemic drugs
**Disorders of fatty acid oxidation
* Critical illnesses:
**[[Medium chain acylCoA dehydrogenase deficiency]] ([[MCAD]])
** [[Hepatic failure]]
*Accidental ingestions
** [[Renal failure]]
**[[Sulfonylurea]]s, [[propranolol]] and others
** [[Congestive heart failure|Cardiac failure]]  
**[[Ethanol]] (mouthwash, "leftover morning-after-the-party drinks")
** [[Sepsis]]
 
*** It occurs due to impaired liver [[gluconeogenesis]]
====Hypoglycemia in Older Children and Young Adults====
*** [[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>
By far the most common cause of severe hypoglycemia in this age range is insulin injected for [[type I diabetes|type 1 diabetes]]. Circumstances should provide clues fairly quickly for the new diseases causing severe hypoglycemia. All of the congenital metabolic defects, congenital forms of [[hyperinsulinism]], and congenital hypopituitarism are likely to have already been diagnosed or are unlikely to start causing new hypoglycemia at this age. [[Body mass]] is large enough to make starvation hypoglycemia and idiopathic [[ketotic hypoglycemia]] quite uncommon. Recurrent mild hypoglycemia may fit a [[reactive hypoglycemia]] pattern, but this is also the peak age for [[idiopathic postprandial syndrome]], and recurrent "spells" in this age group can be traced to [[orthostatic hypotension]] or [[hyperventilation]] as often as demonstrable hypoglycemia.
* [[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>
*Insulin-induced hypoglycemia
* [[Islet cell|Non islet cell]] [[tumor]]: hypoglycemia usually occurs as a result of [[tumor]] production of [[Insulin-like growth factor 2|IGF-2]]
**Insulin injected for type 1 diabetes
* [[Insulinoma]]
**Factitious insulin injection ([[Munchausen syndrome]])
* [[Reactive hypoglycemia]] or postprandial
**[[Insulin-secreting pancreatic tumor]]
** 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>
**[[Reactive hypoglycemia]] and [[idiopathic postprandial syndrome]]
*[[Gastric bypass|Post gastric bypass]] hypoglycemia
*[[Addison's disease]]
**Rapid [[Jejunum|jejunal]] emptying with exaggerated [[insulin]] response
*[[Sepsis]]
* [[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>
====Hypoglycemia in Older Adults====
The incidence of hypoglycemia due to complex drug interactions, especially involving oral hypoglycemic agents and insulin for diabetes rises with age. Though much rarer, the incidence of insulin-producing tumors also rises with advancing age. Most tumors causing hypoglycemia by mechanisms other than insulin excess occur in adults
* Drugs: they are the most common cause of hypoglycemia.[1]
 
* Insulin or insulin secretagogue: sulfonylureas, glyburide and less common glipizide or glimepiride due to  longer duration of action. [30]. They suppress hepatic glucose production and stimulate glucose utilization causing hypoglycemia.
* Other drugs in non-diabetic patients: quinolones, pentamidine, quinine, beta blockers, angiotensin-converting enzyme inhibitors, and IGF-1 especially in in older patients with underlying renal or hepatic dysfunctions. [32]
* Alcohol: due to hepatic glycogen depletion in fasting patients. Alcohol can induce hypoglycemia alone or associated with other hypoglycemic drugs.
 
* Critical illnesses: hepatic, renal, or cardiac failure, sepsis. [34] It occurs due to impaired liver gluconeogenesis. Sepsis induced cytokines secretion cause supression of gluconeogenesis. 36
* Hormone deficiency: cortisol in acquired [[adrenal insufficiency|adrenal insufficiency or]] acquired [[hypopituitarism]]
* Nonislet cell tumor: Hypoglycemia usually occurs as a result of tumor production of IGF-2. 1
* Insulinoma
* Reactive hypoglycemia: there are different kinds of reactive hypoglycemia:[http://www.alfediam.org/media/pdf/RevueBrunD&M5-2000.pdf <nowiki>[1]</nowiki>]  '''Alimentary Hypoglycemia''' (consequence of [[dumping syndrome]]; it occurs in about 15% of people who have had stomach surgery)  '''[[Helicobacter pylori]]-induced gastritis.'''  '''Congenital enzyme deficiencies''' (hereditary fructose intolerance, galactosemia, and leucine sensitivity of childhood).  '''Idiopathic reactive hypoglycemia'''  '''Late Hypoglycemia''' (Occult Diabetes; characterized by a delay in early insulin release from pancreatic B cells, resulting in initial exaggeration of hyperglycemia during a glucose tolerance test).
*Post gastric bypass hypoglycemia: rapid jejunal emptying with exaggerated insulin response.
* Insulin autoimmune hypoglycemia: it occurs in patients who have antibodies directed to endogenous insulin or to the insulin receptor. 41
* Accidental, surreptitious, or malicious hypoglycemia
* Accidental, surreptitious, or malicious hypoglycemia
==References==
==References==
{{Reflist|2}}
{{Reflist|2}}
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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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