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Neonatal hypoglycemia

MedGen UID:
57646
Concept ID:
C0158986
Disease or Syndrome; Finding
Synonyms: Hypoglycemia (neonatal); Hypoglycemia, neonatal
SNOMED CT: Neonatal hypoglycemia (52767006)
 
HPO: HP:0001998

Definition

Blood glucose concentration below the lower limit of established reference ranges in a newborn. [from NCI]

Term Hierarchy

CClinical test,  RResearch test,  OOMIM,  GGeneReviews,  VClinVar  
  • Neonatal hypoglycemia

Conditions with this feature

Beckwith-Wiedemann syndrome
MedGen UID:
2562
Concept ID:
C0004903
Disease or Syndrome
Beckwith-Wiedemann syndrome (BWS) is a growth disorder variably characterized by neonatal hypoglycemia, macrosomia, macroglossia, hemihyperplasia, omphalocele, embryonal tumors (e.g., Wilms tumor, hepatoblastoma, neuroblastoma, and rhabdomyosarcoma), visceromegaly, adrenocortical cytomegaly, renal abnormalities (e.g., medullary dysplasia, nephrocalcinosis, medullary sponge kidney, and nephromegaly), and ear creases/pits. BWS is considered a clinical spectrum, in which affected individuals may have many of these features or may have only one or two clinical features. Early death may occur from complications of prematurity, hypoglycemia, cardiomyopathy, macroglossia, or tumors. However, the previously reported mortality of 20% is likely an overestimate given better recognition of the disorder along with enhanced treatment options. Macroglossia and macrosomia are generally present at birth but may have postnatal onset. Growth rate slows around age seven to eight years. Hemihyperplasia may affect segmental regions of the body or selected organs and tissues.
Sotos syndrome
MedGen UID:
61232
Concept ID:
C0175695
Disease or Syndrome
Sotos syndrome is characterized by a distinctive facial appearance (broad and prominent forehead with a dolichocephalic head shape, sparse frontotemporal hair, downslanting palpebral fissures, malar flushing, long and narrow face, long chin); learning disability (early developmental delay, mild-to-severe intellectual impairment); and overgrowth (height and/or head circumference =2 SD above the mean). These three clinical features are considered the cardinal features of Sotos syndrome. Major features of Sotos syndrome include behavioral problems (most notably autistic spectrum disorder), advanced bone age, cardiac anomalies, cranial MRI/CT abnormalities, joint hyperlaxity with or without pes planus, maternal preeclampsia, neonatal complications, renal anomalies, scoliosis, and seizures.
Carnitine acylcarnitine translocase deficiency
MedGen UID:
91000
Concept ID:
C0342791
Disease or Syndrome
Carnitine-acylcarnitine translocase (CACT) is a critical component of the carnitine shuttle, which facilitates the transfer of long-chain fatty acylcarnitines across the inner mitochondrial membrane. CACT deficiency causes a defect in mitochondrial long-chain fatty acid ß-oxidation, with variable clinical severity. Severe neonatal-onset disease is most common, with symptoms evident within two days after birth; attenuated cases may present in the first months of life. Hyperammonemia and cardiac arrhythmia are prominent in early-onset disease, with high rates of cardiac arrest. Other clinical features are typical for disorders of long-chain fatty acid oxidation: poor feeding, lethargy, hypoketotic hypoglycemia, hypotonia, transaminitis, liver dysfunction with hepatomegaly, and rhabdomyolysis. Univentricular or biventricular hypertrophic cardiomyopathy, ranging from mild to severe, may respond to appropriate dietary and medical therapies. Hyperammonemia is difficult to treat and is an important determinant of long-term neurocognitive outcome. Affected individuals with early-onset disease typically experience brain injury at presentation, and have recurrent hyperammonemia leading to developmental delay / intellectual disability. Affected individuals with later-onset disease have milder symptoms and are less likely to experience recurrent hyperammonemia, allowing a better developmental outcome. Prompt treatment of the presenting episode to prevent hypoglycemic, hypoxic, or hyperammonemic brain injury may allow normal growth and development.
Pituitary hormone deficiency, combined, 2
MedGen UID:
209236
Concept ID:
C0878683
Disease or Syndrome
PROP1-related combined pituitary hormone deficiency (CPHD) is associated with deficiencies of: growth hormone (GH); thyroid-stimulating hormone (TSH); the two gonadotropins, luteinizing hormone (LH) and follicle-stimulating hormone (FSH); prolactin (PrL); and occasionally adrenocorticotropic hormone (ACTH). At birth, in contrast to individuals with congenital CPHD of other etiologies, neonates with PROP1-related CPHD lack perinatal signs of hypopituitarism. Mean birth weights and lengths are usually within the normal range and neonatal hypoglycemia and prolonged neonatal jaundice are not prevalent findings. Most affected individuals are ascertained because of short stature during childhood. Although TSH deficiency can present shortly after birth, TSH deficiency usually occurs with or after the onset of GH deficiency. Hypothyroidism is usually mild. FSH and LH deficiencies are typically identified at the age of onset of puberty. Affected individuals can have absent or delayed and incomplete secondary sexual development with infertility. Untreated males usually have a small penis and small testes. Some females experience menarche but subsequently require hormone replacement therapy. ACTH deficiency is less common and, when present, usually occurs in adolescence or adulthood. Neuroimaging of hypothalamic-pituitary region usually demonstrates a hypoplastic or normal anterior pituitary lobe and a normal posterior pituitary lobe.
Midface hypoplasia, obesity, developmental delay, and neonatal hypotonia
MedGen UID:
325238
Concept ID:
C1837730
Disease or Syndrome
Hypotonia-cystinuria syndrome
MedGen UID:
341133
Concept ID:
C1848030
Disease or Syndrome
A rare, genetic disorder of amino acid absorption and transport, characterized by generalized hypotonia at birth, neonatal/infantile failure to thrive (followed by hyperphagia and rapid weight gain in late childhood), cystinuria type 1, nephrolithiasis, growth retardation due to growth hormone deficiency, and minor facial dysmorphism. Dysmorphic features mainly include dolichocephaly and ptosis. Nephrolithiasis occurs at variable ages.
Lethal congenital glycogen storage disease of heart
MedGen UID:
337919
Concept ID:
C1849813
Disease or Syndrome
A rare glycogen storage disease with fetal or neonatal onset of severe cardiomyopathy with non-lysosomal glycogen accumulation and fatal outcome in infancy. Patients present with massive cardiomegaly, severe cardiac and respiratory complications and failure to thrive. Non-specific facial dysmorphism, bilateral cataracts, macroglossia, hydrocephalus, enlarged kidneys and skeletal muscle involvement have been reported in some cases.
Glycogen storage disorder due to hepatic glycogen synthase deficiency
MedGen UID:
343430
Concept ID:
C1855861
Disease or Syndrome
Glycogen storage disease type 0 (also known as GSD 0) is a condition caused by the body's inability to form a complex sugar called glycogen, which is a major source of stored energy in the body. GSD 0 has two types: in muscle GSD 0, glycogen formation in the muscles is impaired, and in liver GSD 0, glycogen formation in the liver is impaired.\n\nIndividuals with liver GSD 0 usually show signs and symptoms of the disorder in infancy. People with this disorder develop low blood sugar (glucose), known as hypoglycemia, after going long periods of time without food (fasting). Signs of hypoglycemia become apparent when affected infants begin sleeping through the night and stop late-night feedings; these infants exhibit extreme tiredness (lethargy), pale skin (pallor), and nausea. During episodes of fasting, ketone levels in the blood may increase (ketosis). Ketones are molecules produced during the breakdown of fats, which occurs when stored sugars (such as glycogen) are unavailable. These short-term signs and symptoms of liver GSD 0 often improve when food is eaten and glucose levels in the body return to normal. The features of liver GSD 0 vary; they can be mild and go unnoticed for years, or they can include developmental delay and growth failure.\n\nThe signs and symptoms of muscle GSD 0 typically begin in early childhood. Affected individuals often experience muscle pain and weakness or episodes of fainting (syncope) following moderate physical activity, such as walking up stairs. The loss of consciousness that occurs with fainting typically lasts up to several hours. Some individuals with muscle GSD 0 have a disruption of the heart's normal rhythm (arrhythmia) known as long QT syndrome. In all affected individuals, muscle GSD 0 impairs the heart's ability to effectively pump blood and increases the risk of cardiac arrest and sudden death, particularly after physical activity. Sudden death from cardiac arrest can occur in childhood or adolescence in people with muscle GSD 0.
Pituitary hormone deficiency, combined, 6
MedGen UID:
462790
Concept ID:
C3151440
Disease or Syndrome
Any combined pituitary hormone deficiencies, genetic form in which the cause of the disease is a mutation in the OTX2 gene.
Kabuki syndrome 2
MedGen UID:
477126
Concept ID:
C3275495
Disease or Syndrome
Kabuki syndrome (KS) is characterized by typical facial features (long palpebral fissures with eversion of the lateral third of the lower eyelid; arched and broad eyebrows; short columella with depressed nasal tip; large, prominent, or cupped ears), minor skeletal anomalies, persistence of fetal fingertip pads, mild-to-moderate intellectual disability, and postnatal growth deficiency. Other findings may include: congenital heart defects, genitourinary anomalies, cleft lip and/or palate, gastrointestinal anomalies including anal atresia, ptosis and strabismus, and widely spaced teeth and hypodontia. Functional differences can include: increased susceptibility to infections and autoimmune disorders, seizures, endocrinologic abnormalities (including isolated premature thelarche in females), feeding problems, and hearing loss.
Hypoinsulinemic hypoglycemia and body hemihypertrophy
MedGen UID:
480014
Concept ID:
C3278384
Disease or Syndrome
Hypoinsulinemic hypoglycemia and body hemihypertrophy is a rare, genetic, endocrine disease characterized by neonatal macrosomia, asymmetrical overgrowth (typically manifesting as left-sided hemihypertrophy) and recurrent, severe hypoinsulinemic (or hypoketotic hypo-fatty-acidemic) hypoglycemia in infancy, which results in episodes of reduced consciousness and seizures.
3-methylglutaconic aciduria type 8
MedGen UID:
934617
Concept ID:
C4310650
Disease or Syndrome
MGCA8 is an autosomal recessive metabolic disorder resulting in death in infancy. Features include hypotonia, abnormal movements, respiratory insufficiency with apneic episodes, and lack of developmental progress, often with seizures. Brain imaging is variable, but may show progressive cerebral atrophy. Laboratory studies show increased serum lactate and 3-methylglutaconic aciduria, suggesting a mitochondrial defect (summary by Mandel et al., 2016). For a phenotypic description and a discussion of genetic heterogeneity of 3-methylglutaconic aciduria, see MGCA type I (250950).
Intellectual disability, autosomal dominant 45
MedGen UID:
1616472
Concept ID:
C4539848
Mental or Behavioral Dysfunction
Orthostatic hypotension 1
MedGen UID:
1648402
Concept ID:
C4746777
Disease or Syndrome
Dopamine beta-hydroxylase (DBH) deficiency is characterized by lack of sympathetic noradrenergic function but normal parasympathetic and sympathetic cholinergic function. Affected individuals exhibit profound deficits in autonomic regulation of cardiovascular function that predispose to orthostatic hypotension. Although DBH deficiency appears to be present from birth, the diagnosis is not generally recognized until late childhood. The combination of ptosis of the eyelids in infants and children, together with hypotension, is suggestive of the disease. In the perinatal period, DBH deficiency has been complicated by vomiting, dehydration, hypotension, hypothermia, and hypoglycemia requiring repeated hospitalization; children have reduced exercise capacity. By early adulthood, individuals have profound orthostatic hypotension, greatly reduced exercise tolerance, ptosis of the eyelids, and nasal stuffiness. Presyncopal symptoms include dizziness, blurred vision, dyspnea, nuchal discomfort, and chest pain; symptoms may worsen in hot environments or after heavy meals or alcohol ingestion. Life expectancy is unknown, but some affected individuals have lived beyond age 60 years.
Basilicata-Akhtar syndrome
MedGen UID:
1684820
Concept ID:
C5231394
Disease or Syndrome
Basilicata-Akhtar syndrome (MRXSBA) is characterized by global developmental delay apparent from infancy, feeding difficulties, hypotonia, and poor or absent speech. Most patients are able to walk, although they may have an unsteady gait or spasticity. Additional findings include dysmorphic facial features and mild distal skeletal anomalies. Males and females are similarly affected (summary by Basilicata et al., 2018).
Silver-russell syndrome 2
MedGen UID:
1714148
Concept ID:
C5394446
Disease or Syndrome
Silver-Russell Syndrome (SRS) is typically characterized by asymmetric gestational growth restriction resulting in affected individuals being born small for gestational age, with relative macrocephaly at birth (head circumference =1.5 SD above birth weight and/or length), prominent forehead usually with frontal bossing, and frequently body asymmetry. This is followed by postnatal growth failure, and in some cases progressive limb length discrepancy and feeding difficulties. Additional clinical features include triangular facies, fifth-finger clinodactyly, and micrognathia with narrow chin. Except for the limb length asymmetry, the growth failure is proportionate and head growth normal. The average adult height in untreated individuals is ~3.1±1.4 SD below the mean. The Netchine-Harbison Clinical Scoring System (NH-CSS) is a sensitive diagnostic scoring system. Clinical diagnosis can be established in an individual who meets at least four of the NH-CSS clinical criteria – prominent forehead/frontal bossing and relative macrocephaly at birth plus two additional findings – and in whom other disorders have been ruled out.
Deeah syndrome
MedGen UID:
1756624
Concept ID:
C5436579
Disease or Syndrome
DEEAH syndrome is an autosomal recessive multisystemic disorder with onset in early infancy. Affected individuals usually present in the perinatal period with respiratory insufficiency, apneic episodes, and generalized hypotonia. The patients have failure to thrive and severely impaired global development with poor acquisition of motor, cognitive, and language skills. Other common features include endocrine, pancreatic exocrine, and autonomic dysfunction, as well as hematologic disturbances, mainly low hemoglobin. Patients also have dysmorphic and myopathic facial features. Additional more variable features include seizures, undescended testes, and distal skeletal anomalies. Death in early childhood may occur (summary by Schneeberger et al., 2020).
Mitochondrial complex 4 deficiency, nuclear type 3
MedGen UID:
1764816
Concept ID:
C5436682
Disease or Syndrome
Mitochondrial complex IV deficiency nuclear type 3 (MC4DN3) is an autosomal recessive multisystem metabolic disorder with a highly variable phenotype. Some patients present with encephalomyopathic features in early infancy, whereas others may present later in infancy or the first years of life after normal early development. Affected individuals show hypotonia, failure to thrive, and developmental delay or regression with poor eye contact and loss of motor skills with ataxia. Additional features observed in some patients include proximal renal tubulopathy, macrocytic anemia, sensorineural hearing loss, nystagmus, and hypertrophic cardiomyopathy, consistent with systemic involvement. Brain imaging in most patients shows lesions consistent with Leigh syndrome (see 256000). Laboratory studies show increased serum lactate and decreased levels and activity of mitochondrial respiratory complex IV. Most patients die in infancy (summary by Valnot et al., 2000 and Antonicka et al., 2003). For a discussion of genetic heterogeneity of mitochondrial complex IV (cytochrome c oxidase) deficiency, see 220110.
Mitochondrial complex 4 deficiency, nuclear type 12
MedGen UID:
1745691
Concept ID:
C5436695
Disease or Syndrome
Mitochondrial complex IV deficiency nuclear type 12 (MC4DN12) is an autosomal recessive metabolic disorder characterized by the onset of neurologic dysfunction in early infancy. Affected individuals demonstrate hypotonia with poor head control, profoundly delayed global development with inability to fix and follow, poor overall growth, abnormal spasms or myoclonus, and seizures. Most patients die in the first years of life; those that survive have spastic quadriplegia, feeding difficulties necessitating tube feeding, and profoundly impaired intellectual development with poor or absent communication. More variable features include cortical blindness, nystagmus, scoliosis, and hearing impairment. Brain imaging shows abnormalities consistent with Leigh syndrome (see 256000), as well as cystic cavitation. Laboratory studies show lactic acidosis, increased serum creatine kinase, and decreased levels and activity of mitochondrial respiratory complex IV (summary by Lim et al., 2014). For a discussion of genetic heterogeneity of mitochondrial complex IV (cytochrome c oxidase) deficiency, see 220110.
Neurologic, endocrine, and pancreatic disease, multisystem, infantile-onset 2
MedGen UID:
1778117
Concept ID:
C5543623
Disease or Syndrome
Infantile-onset multisystem neurologic, endocrine, and pancreatic disease-2 (IMNEPD2) is an autosomal recessive multisystemic disorder characterized by cholestatic hepatitis, poor feeding associated with poor overall growth, and hypoglycemia apparent from infancy. Most, but not all, patients have variable global developmental delay. Additional common features include sensorineural deafness, retinal abnormalities with visual defects, and hypotonia. Some patients have endocrine abnormalities, including hyperinsulinemic hypoglycemia, pancreatic dysfunction, hypothyroidism, and primary amenorrhea. Additional features may include hypertriglyceridemia, anemia, proteinuria, increased lactate, and recurrent infections. Brain imaging often shows dysmyelination, thin corpus callosum, cerebral atrophy, and white matter abnormalities. Although the clinical manifestations and severity of the disorder are highly variable, death in early childhood may occur (summary by Williams et al., 2019 and Zeiad et al., 2021). For a discussion of genetic heterogeneity of IMNEPD, see IMNEPD1 (616263).
3-methylglutaconic aciduria, type VIIB
MedGen UID:
1810214
Concept ID:
C5676893
Disease or Syndrome
CLPB (caseinolytic peptidase B) deficiency is characterized by neurologic involvement and neutropenia, which can range from severe to mild. In severe CLPB deficiency, death usually occurs at a few months of age due to significant neonatal neurologic involvement (hyperekplexia or absence of voluntary movements, hypotonia or hypertonia, swallowing problems, respiratory insufficiency, and epilepsy) and severe neutropenia associated with life-threatening infections. Individuals with moderate CLPB deficiency present with neurologic abnormalities in infancy including hypotonia and feeding problems, and develop spasticity, a progressive movement disorder (ataxia, dystonia, and/or dyskinesia), epilepsy, and intellectual disability. Neutropenia is variable, but not life threatening. In those with mild CLPB deficiency there is no neurologic involvement, intellect is normal, neutropenia is mild and intermittent, and life expectancy is normal.

Professional guidelines

PubMed

Roeper M, Hoermann H, Kummer S, Meissner T
Front Endocrinol (Lausanne) 2023;14:1179102. Epub 2023 Jun 8 doi: 10.3389/fendo.2023.1179102. PMID: 37361517Free PMC Article
Chatzakis C, Cavoretto P, Sotiriadis A
Curr Pharm Des 2021;27(36):3833-3840. doi: 10.2174/1381612827666210125155428. PMID: 33550962
Immanuel J, Simmons D
Curr Diab Rep 2017 Oct 2;17(11):115. doi: 10.1007/s11892-017-0943-7. PMID: 28971305

Recent clinical studies

Etiology

Hubbard EM, Hay WW Jr
Clin Perinatol 2021 Aug;48(3):665-679. doi: 10.1016/j.clp.2021.05.013. PMID: 34353586
De Angelis LC, Brigati G, Polleri G, Malova M, Parodi A, Minghetti D, Rossi A, Massirio P, Traggiai C, Maghnie M, Ramenghi LA
Front Endocrinol (Lausanne) 2021;12:634305. Epub 2021 Mar 16 doi: 10.3389/fendo.2021.634305. PMID: 33796072Free PMC Article
Chatzakis C, Cavoretto P, Sotiriadis A
Curr Pharm Des 2021;27(36):3833-3840. doi: 10.2174/1381612827666210125155428. PMID: 33550962
Paredes C, Hsu RC, Tong A, Johnson JR
Neoreviews 2021 Feb;22(2):e78-e87. doi: 10.1542/neo.22-2-e78. PMID: 33526637
Thompson-Branch A, Havranek T
Pediatr Rev 2017 Apr;38(4):147-157. doi: 10.1542/pir.2016-0063. PMID: 28364046

Diagnosis

Roeper M, Hoermann H, Kummer S, Meissner T
Front Endocrinol (Lausanne) 2023;14:1179102. Epub 2023 Jun 8 doi: 10.3389/fendo.2023.1179102. PMID: 37361517Free PMC Article
Casertano A, Rossi A, Fecarotta S, Rosanio FM, Moracas C, Di Candia F, Parenti G, Franzese A, Mozzillo E
Front Endocrinol (Lausanne) 2021;12:684011. Epub 2021 Aug 2 doi: 10.3389/fendo.2021.684011. PMID: 34408725Free PMC Article
Hubbard EM, Hay WW Jr
Clin Perinatol 2021 Aug;48(3):665-679. doi: 10.1016/j.clp.2021.05.013. PMID: 34353586
Kallem VR, Pandita A, Pillai A
J Matern Fetal Neonatal Med 2020 Feb;33(3):482-492. Epub 2018 Sep 9 doi: 10.1080/14767058.2018.1494710. PMID: 29947269
HAPO Study Cooperative Research Group, Metzger BE, Lowe LP, Dyer AR, Trimble ER, Chaovarindr U, Coustan DR, Hadden DR, McCance DR, Hod M, McIntyre HD, Oats JJ, Persson B, Rogers MS, Sacks DA
N Engl J Med 2008 May 8;358(19):1991-2002. doi: 10.1056/NEJMoa0707943. PMID: 18463375

Therapy

Dunne F, Newman C, Alvarez-Iglesias A, Ferguson J, Smyth A, Browne M, O'Shea P, Devane D, Gillespie P, Bogdanet D, Kgosidialwa O, Egan A, Finn Y, Gaffney G, Khattak A, O'Keeffe D, Liew A, O'Donnell M
JAMA 2023 Oct 24;330(16):1547-1556. doi: 10.1001/jama.2023.19869. PMID: 37786390Free PMC Article
Chatzakis C, Cavoretto P, Sotiriadis A
Curr Pharm Des 2021;27(36):3833-3840. doi: 10.2174/1381612827666210125155428. PMID: 33550962
Dude A, Niznik CM, Szmuilowicz ED, Peaceman AM, Yee LM
Am J Perinatol 2018 Sep;35(11):1119-1126. Epub 2018 Mar 13 doi: 10.1055/s-0038-1629903. PMID: 29534258Free PMC Article
Gyamfi-Bannerman C, Thom EA, Blackwell SC, Tita AT, Reddy UM, Saade GR, Rouse DJ, McKenna DS, Clark EA, Thorp JM Jr, Chien EK, Peaceman AM, Gibbs RS, Swamy GK, Norton ME, Casey BM, Caritis SN, Tolosa JE, Sorokin Y, VanDorsten JP, Jain L; NICHD Maternal–Fetal Medicine Units Network
N Engl J Med 2016 Apr 7;374(14):1311-20. Epub 2016 Feb 4 doi: 10.1056/NEJMoa1516783. PMID: 26842679Free PMC Article
Rowan JA, Hague WM, Gao W, Battin MR, Moore MP; MiG Trial Investigators
N Engl J Med 2008 May 8;358(19):2003-15. doi: 10.1056/NEJMoa0707193. PMID: 18463376

Prognosis

Zenker M, Mohnike K, Palm K
Front Endocrinol (Lausanne) 2023;14:1013874. Epub 2023 Mar 30 doi: 10.3389/fendo.2023.1013874. PMID: 37065762Free PMC Article
Harding JE, Hegarty JE, Crowther CA, Edlin RP, Gamble GD, Alsweiler JM; hPOD Study Group
PLoS Med 2021 Jan;18(1):e1003411. Epub 2021 Jan 28 doi: 10.1371/journal.pmed.1003411. PMID: 33507929Free PMC Article
Mottola MF, Davenport MH, Ruchat SM, Davies GA, Poitras V, Gray C, Jaramillo Garcia A, Barrowman N, Adamo KB, Duggan M, Barakat R, Chilibeck P, Fleming K, Forte M, Korolnek J, Nagpal T, Slater L, Stirling D, Zehr L
J Obstet Gynaecol Can 2018 Nov;40(11):1528-1537. Epub 2018 Oct 5 doi: 10.1016/j.jogc.2018.07.001. PMID: 30297272
Hartling L, Dryden DM, Guthrie A, Muise M, Vandermeer B, Aktary WM, Pasichnyk D, Seida JC, Donovan L
Evid Rep Technol Assess (Full Rep) 2012 Oct;(210):1-327. PMID: 24423035Free PMC Article
Brooks C
Neonatal Netw 1997 Mar;16(2):15-21. PMID: 9087008

Clinical prediction guides

Dunne F, Newman C, Alvarez-Iglesias A, Ferguson J, Smyth A, Browne M, O'Shea P, Devane D, Gillespie P, Bogdanet D, Kgosidialwa O, Egan A, Finn Y, Gaffney G, Khattak A, O'Keeffe D, Liew A, O'Donnell M
JAMA 2023 Oct 24;330(16):1547-1556. doi: 10.1001/jama.2023.19869. PMID: 37786390Free PMC Article
De Angelis LC, Brigati G, Polleri G, Malova M, Parodi A, Minghetti D, Rossi A, Massirio P, Traggiai C, Maghnie M, Ramenghi LA
Front Endocrinol (Lausanne) 2021;12:634305. Epub 2021 Mar 16 doi: 10.3389/fendo.2021.634305. PMID: 33796072Free PMC Article
Hartling L, Dryden DM, Guthrie A, Muise M, Vandermeer B, Aktary WM, Pasichnyk D, Seida JC, Donovan L
Evid Rep Technol Assess (Full Rep) 2012 Oct;(210):1-327. PMID: 24423035Free PMC Article
Rowan JA, Hague WM, Gao W, Battin MR, Moore MP; MiG Trial Investigators
N Engl J Med 2008 May 8;358(19):2003-15. doi: 10.1056/NEJMoa0707193. PMID: 18463376
HAPO Study Cooperative Research Group, Metzger BE, Lowe LP, Dyer AR, Trimble ER, Chaovarindr U, Coustan DR, Hadden DR, McCance DR, Hod M, McIntyre HD, Oats JJ, Persson B, Rogers MS, Sacks DA
N Engl J Med 2008 May 8;358(19):1991-2002. doi: 10.1056/NEJMoa0707943. PMID: 18463375

Recent systematic reviews

O'Brien M, Gilchrist C, Sadler L, Hegarty JE, Alsweiler JM
JAMA Pediatr 2023 Nov 1;177(11):1187-1196. doi: 10.1001/jamapediatrics.2023.3957. PMID: 37782488Free PMC Article
Sheng B, Ni J, Lv B, Jiang G, Lin X, Li H
Acta Diabetol 2023 May;60(5):595-608. Epub 2023 Jan 3 doi: 10.1007/s00592-022-02016-5. PMID: 36593391Free PMC Article
Wei J, Yan J, Yang H
Nutrients 2022 Jul 9;14(14) doi: 10.3390/nu14142831. PMID: 35889788Free PMC Article
Guo L, Ma J, Tang J, Hu D, Zhang W, Zhao X
J Diabetes Res 2019;2019:9804708. Epub 2019 Nov 4 doi: 10.1155/2019/9804708. PMID: 31781670Free PMC Article
Immanuel J, Simmons D
Curr Diab Rep 2017 Oct 2;17(11):115. doi: 10.1007/s11892-017-0943-7. PMID: 28971305

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