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Glucose intolerance

MedGen UID:
75760
Concept ID:
C0271650
Disease or Syndrome
Synonyms: Glucose Intolerance; Glucose Intolerances; Glucose Tolerance, Impaired; Glucose Tolerances, Impaired; Impaired Glucose Tolerance; Impaired Glucose Tolerances; Intolerance, Glucose; Intolerances, Glucose; Tolerance, Impaired Glucose; Tolerances, Impaired Glucose
SNOMED CT: Impaired glucose tolerance (9414007); Prediabetic nonclinical diabetes (9414007); Latent diabetes (9414007); Chemical diabetes (9414007); Malabsorption of glucose (267426009); IGT - Impaired glucose tolerance (9414007)
 
HPO: HP:0001952
Monarch Initiative: MONDO:0001076

Definition

Glucose intolerance (GI) can be defined as dysglycemia that comprises both prediabetes and diabetes. It includes the conditions of impaired fasting glucose (IFG) and impaired glucose tolerance (IGT) and diabetes mellitus (DM). [from HPO]

Term Hierarchy

CClinical test,  RResearch test,  OOMIM,  GGeneReviews,  VClinVar  
  • CROGVGlucose intolerance

Conditions with this feature

Ataxia-telangiectasia syndrome
MedGen UID:
439
Concept ID:
C0004135
Disease or Syndrome
Classic ataxia-telangiectasia (A-T) is characterized by progressive cerebellar ataxia beginning between ages one and four years, oculomotor apraxia, choreoathetosis, telangiectasias of the conjunctivae, immunodeficiency, frequent infections, and an increased risk for malignancy, particularly leukemia and lymphoma. Individuals with A-T are unusually sensitive to ionizing radiation. Non-classic forms of A-T have included adult-onset A-T and A-T with early-onset dystonia.
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.
Williams syndrome
MedGen UID:
59799
Concept ID:
C0175702
Disease or Syndrome
Williams syndrome (WS) is characterized by cardiovascular disease (elastin arteriopathy, peripheral pulmonary stenosis, supravalvar aortic stenosis, hypertension), distinctive facies, connective tissue abnormalities, intellectual disability (usually mild), a specific cognitive profile, unique personality characteristics, growth abnormalities, and endocrine abnormalities (hypercalcemia, hypercalciuria, hypothyroidism, and early puberty). Feeding difficulties often lead to poor weight gain in infancy. Hypotonia and hyperextensible joints can result in delayed attainment of motor milestones.
Pituitary dependent hypercortisolism
MedGen UID:
66381
Concept ID:
C0221406
Disease or Syndrome
AIP familial isolated pituitary adenoma (AIP-FIPA) is defined as the presence of an AIP germline pathogenic variant in an individual with a pituitary adenoma (regardless of family history). The most commonly occurring pituitary adenomas in this disorder are growth hormone-secreting adenomas (somatotropinoma), followed by prolactin-secreting adenomas (prolactinoma), growth hormone and prolactin co-secreting adenomas (somatomammotropinoma), and nonfunctioning pituitary adenomas (NFPA). Rarely TSH-secreting adenomas (thyrotropinomas) are observed. Clinical findings result from excess hormone secretion, lack of hormone secretion, and/or mass effects (e.g., headaches, visual field loss). Within the same family, pituitary adenomas can be of the same or different type. Age of onset in AIP-FIPA is usually in the second or third decade.
Aniridia 1
MedGen UID:
576337
Concept ID:
C0344542
Congenital Abnormality
PAX6-related aniridia occurs either as an isolated ocular abnormality or as part of the Wilms tumor-aniridia-genital anomalies-retardation (WAGR) syndrome. Aniridia is a pan ocular disorder affecting the cornea, iris, intraocular pressure (resulting in glaucoma), lens (cataract and lens subluxation), fovea (foveal hypoplasia), and optic nerve (optic nerve coloboma and hypoplasia). Individuals with aniridia characteristically show nystagmus and impaired visual acuity (usually 20/100 - 20/200); however, milder forms of aniridia with subtle iris architecture changes, good vision, and normal foveal structure do occur. Other ocular involvement may include strabismus and occasionally microphthalmia. Although the severity of aniridia can vary between and within families, little variability is usually observed in the two eyes of an affected individual. WAGR syndrome. The risk for Wilms tumor is 42.5%-77%; of those who develop Wilms tumor, 90% do so by age four years and 98% by age seven years. Genital anomalies in males can include cryptorchidism and hypospadias (sometimes resulting in ambiguous genitalia), urethral strictures, ureteric abnormalities, and gonadoblastoma. While females typically have normal external genitalia, they may have uterine abnormalities and streak ovaries. Intellectual disability (defined as IQ <74) is observed in 70%; behavioral abnormalities include attention-deficit/hyperactivity disorder (ADHD), autism spectrum disorder, anxiety, depression, and obsessive-compulsive disorder. Other individuals with WAGR syndrome can have normal intellect without behavioral problems.
Renal cysts and diabetes syndrome
MedGen UID:
96569
Concept ID:
C0431693
Disease or Syndrome
The 17q12 recurrent deletion syndrome is characterized by variable combinations of the three following findings: structural or functional abnormalities of the kidney and urinary tract, maturity-onset diabetes of the young type 5 (MODY5), and neurodevelopmental or neuropsychiatric disorders (e.g., developmental delay, intellectual disability, autism spectrum disorder, schizophrenia, anxiety, and bipolar disorder). Using a method of data analysis that avoids ascertainment bias, the authors determined that multicystic kidneys and other structural and functional kidney anomalies occur in 85% to 90% of affected individuals, MODY5 in approximately 40%, and some degree of developmental delay or learning disability in approximately 50%. MODY5 is most often diagnosed before age 25 years (range: age 10-50 years).
Primrose syndrome
MedGen UID:
162911
Concept ID:
C0796121
Disease or Syndrome
Primrose syndrome is characterized by macrocephaly, hypotonia, developmental delay, intellectual disability with expressive speech delay, behavioral issues, a recognizable facial phenotype, radiographic features, and altered glucose metabolism. Additional features seen in adults: sparse body hair, distal muscle wasting, and contractures. Characteristic craniofacial features include brachycephaly, high anterior hairline, deeply set eyes, ptosis, downslanted palpebral fissures, high palate with torus palatinus, broad jaw, and large ears with small or absent lobes. Radiographic features include calcification of the external ear cartilage, multiple Wormian bones, platybasia, bathrocephaly, slender bones with exaggerated metaphyseal flaring, mild epiphyseal dysplasia, and spondylar dysplasia. Additional features include hearing impairment, ocular anomalies, cryptorchidism, and nonspecific findings on brain MRI.
SHORT syndrome
MedGen UID:
164212
Concept ID:
C0878684
Disease or Syndrome
SHORT syndrome is a mnemonic for short stature, hyperextensibility, ocular depression (deeply set eyes), Rieger anomaly, and teething delay. It is now recognized that the features most consistently observed in SHORT syndrome are mild intrauterine growth restriction (IUGR); mild to moderate short stature; partial lipodystrophy (evident in the face, and later in the chest and upper extremities, often sparing the buttocks and legs); and a characteristic facial gestalt. Insulin resistance may be evident in mid-childhood or adolescence, although diabetes mellitus typically does not develop until early adulthood. Other frequent features include Axenfeld-Rieger anomaly or related ocular anterior chamber dysgenesis, delayed dentition and other dental issues, and sensorineural hearing loss.
Mandibuloacral dysplasia with type B lipodystrophy
MedGen UID:
332940
Concept ID:
C1837756
Disease or Syndrome
Mandibuloacral dysplasia with type B lipodystrophy (MADB) is a rare autosomal recessive disorder characterized by postnatal growth retardation, craniofacial anomalies such as mandibular hypoplasia, skeletal anomalies such as progressive osteolysis of the terminal phalanges and clavicles, and skin changes such as mottled hyperpigmentation and atrophy. The lipodystrophy is characterized by generalized loss of subcutaneous fat involving the face, trunk, and extremities. Some patients have a progeroid appearance. Metabolic complications associated with insulin resistance have been reported (Schrander-Stumpel et al., 1992; summary by Simha et al., 2003). For a general phenotypic description of lipodystrophy associated with mandibuloacral dysplasia, see MADA (248370).
Skeletal dysplasia-intellectual disability syndrome
MedGen UID:
326949
Concept ID:
C1839729
Disease or Syndrome
This syndrome combines skeletal anomalies (short stature, ridging of the metopic suture, fusion of cervical vertebrae, thoracic hemivertebrae, scoliosis, sacral hypoplasia and short middle phalanges) and mild intellectual deficit. It has been described in four male cousins in three sibships. Glucose intolerance was present in three cases, and imperforated anus in one case. Carrier females had minor manifestations (fusion of cervical vertebrae and glucose intolerance). Transmission seems to be X-linked.
Male hypergonadotropic hypogonadism-intellectual disability-skeletal anomalies syndrome
MedGen UID:
334557
Concept ID:
C1843994
Disease or Syndrome
This syndrome is characterized by hypergonadotropic hypogonadism, intellectual deficit, congenital skeletal anomalies involving the cervical spine and superior ribs, and diabetes mellitus.
Hemochromatosis type 4
MedGen UID:
340044
Concept ID:
C1853733
Disease or Syndrome
Hemochromatosis type 4 (HFE4) is a dominantly inherited iron overload disorder with heterogeneous phenotypic manifestations that can be classified into 2 groups. One group is characterized by an early rise in ferritin (see 134790) levels with low to normal transferrin (190000) saturation and iron accumulation predominantly in macrophages. The other group is similar to classical hemochromatosis, with high transferrin saturation and prominent parenchymal iron loading (summary by De Domenico et al., 2005). For general background information and a discussion of genetic heterogeneity of hereditary hemochromatosis, see 235200.
Progressive external ophthalmoplegia with mitochondrial DNA deletions, autosomal dominant 4
MedGen UID:
350480
Concept ID:
C1864668
Disease or Syndrome
Progressive external ophthalmoplegia-4 is an autosomal dominant form of mitochondrial disease that variably affects skeletal muscle, the nervous system, the liver, and the gastrointestinal tract. Age at onset ranges from infancy to adulthood. The phenotype ranges from relatively mild, with adult-onset skeletal muscle weakness and weakness of the external eye muscles, to severe, with a multisystem disorder characterized by delayed psychomotor development, lactic acidosis, constipation, and liver involvement (summary by Young et al., 2011). For a general phenotypic description and a discussion of genetic heterogeneity of autosomal dominant progressive external ophthalmoplegia, see PEOA1 (157640).
Coronary artery disease, autosomal dominant 2
MedGen UID:
370259
Concept ID:
C1970440
Disease or Syndrome
Any coronary artery disease in which the cause of the disease is a mutation in the LRP6 gene.
Microcephaly-cerebellar hypoplasia-cardiac conduction defect syndrome
MedGen UID:
482322
Concept ID:
C3280692
Disease or Syndrome
The Zaki-Gleeson syndrome is an autosomal recessive neurodevelopmental disorder characterized by profound mental retardation, severe microcephaly, poor growth, cerebellar hypoplasia, and second-degree cardiac conduction defects (Zaki et al., 2011).
Hemochromatosis type 1
MedGen UID:
854011
Concept ID:
C3469186
Disease or Syndrome
HFE hemochromatosis is characterized by inappropriately high absorption of iron by the small intestinal mucosa. The phenotypic spectrum of HFE hemochromatosis includes: Persons with clinical HFE hemochromatosis, in whom manifestations of end-organ damage secondary to iron overload are present; Individuals with biochemical HFE hemochromatosis, in whom transferrin-iron saturation is increased and the only evidence of iron overload is increased serum ferritin concentration; and Non-expressing p.Cys282Tyr homozygotes, in whom neither clinical manifestations of HFE hemochromatosis nor iron overload are present. Clinical HFE hemochromatosis is characterized by excessive storage of iron in the liver, skin, pancreas, heart, joints, and anterior pituitary gland. In untreated individuals, early symptoms include: abdominal pain, weakness, lethargy, weight loss, arthralgias, diabetes mellitus; and increased risk of cirrhosis when the serum ferritin is higher than 1,000 ng/mL. Other findings may include progressive increase in skin pigmentation, congestive heart failure, and/or arrhythmias, arthritis, and hypogonadism. Clinical HFE hemochromatosis is more common in men than women.
Partial lipodystrophy, congenital cataracts, and neurodegeneration syndrome
MedGen UID:
813897
Concept ID:
C3807567
Disease or Syndrome
Lipodystrophies are rare disorders characterized by loss of body fat from various regions and predisposition to metabolic complications of insulin resistance and lipid abnormalities. FPLD7 is an autosomal dominant disorder with a highly variable phenotype. Additional features, including early-onset cataracts and later onset of spasticity of the lower limbs, have been noted in some patients (summary by Garg et al., 2015). For a general phenotypic description and a discussion of genetic heterogeneity of familial partial lipodystrophy (FPLD), see 151660.
Estrogen resistance syndrome
MedGen UID:
815580
Concept ID:
C3809250
Disease or Syndrome
Estrogen resistance (ESTRR) is characterized by absence of puberty with elevated estradiol and gonadotropic hormones, as well as markedly delayed bone maturation. Female patients show absent breast development, small uterus, and enlarged multicystic ovaries; male patients may show small testes (Bernard et al., 2017). Some patients exhibit continued growth into adulthood (Smith et al., 1994).
Short-rib thoracic dysplasia 10 with or without polydactyly
MedGen UID:
816505
Concept ID:
C3810175
Disease or Syndrome
Short-rib thoracic dysplasia (SRTD) with or without polydactyly refers to a group of autosomal recessive skeletal ciliopathies that are characterized by a constricted thoracic cage, short ribs, shortened tubular bones, and a 'trident' appearance of the acetabular roof. SRTD encompasses Ellis-van Creveld syndrome (EVC) and the disorders previously designated as Jeune syndrome or asphyxiating thoracic dystrophy (ATD), short rib-polydactyly syndrome (SRPS), and Mainzer-Saldino syndrome (MZSDS). Polydactyly is variably present, and there is phenotypic overlap in the various forms of SRTDs, which differ by visceral malformation and metaphyseal appearance. Nonskeletal involvement can include cleft lip/palate as well as anomalies of major organs such as the brain, eye, heart, kidneys, liver, pancreas, intestines, and genitalia. Some forms of SRTD are lethal in the neonatal period due to respiratory insufficiency secondary to a severely restricted thoracic cage, whereas others are compatible with life (summary by Huber and Cormier-Daire, 2012 and Schmidts et al., 2013). There is phenotypic overlap with the cranioectodermal dysplasias (Sensenbrenner syndrome; see CED1, 218330). For a discussion of genetic heterogeneity of short-rib thoracic dysplasia, see SRTD1 (208500).
Seckel syndrome 10
MedGen UID:
934614
Concept ID:
C4310647
Disease or Syndrome
Any Seckel syndrome in which the cause of the disease is a mutation in the NSMCE2 gene.
Mandibuloacral dysplasia progeroid syndrome
MedGen UID:
1741713
Concept ID:
C5436867
Disease or Syndrome
Mandibuloacral dysplasia progeroid syndrome (MDPS) is an autosomal recessive severe laminopathy-like disorder characterized by growth retardation, bone resorption, arterial calcification, renal glomerulosclerosis, and hypertension (Elouej et al., 2020).
Hypertriglyceridemia 1
MedGen UID:
1787149
Concept ID:
C5444012
Disease or Syndrome
Combined oxidative phosphorylation defect type 26
MedGen UID:
1799164
Concept ID:
C5567741
Disease or Syndrome
Peripheral neuropathy with variable spasticity, exercise intolerance, and developmental delay (PNSED) is an autosomal recessive multisystemic disorder with highly variable manifestations, even within the same family. Some patients present in infancy with hypotonia and global developmental delay with poor or absent motor skill acquisition and poor growth, whereas others present as young adults with exercise intolerance and muscle weakness. All patients have signs of a peripheral neuropathy, usually demyelinating, with distal muscle weakness and atrophy and distal sensory impairment; many become wheelchair-bound. Additional features include spasticity, extensor plantar responses, contractures, cerebellar signs, seizures, short stature, and rare involvement of other organ systems, including the heart, pancreas, and kidney. Biochemical analysis may show deficiencies in mitochondrial respiratory complex enzyme activities in patient tissue, although this is not always apparent. Lactate is frequently increased, suggesting mitochondrial dysfunction (Powell et al., 2015; Argente-Escrig et al., 2022). For a discussion of genetic heterogeneity of combined oxidative phosphorylation deficiency, see COXPD1 (609060).

Professional guidelines

PubMed

Mantovani G, Bastepe M, Monk D, de Sanctis L, Thiele S, Usardi A, Ahmed SF, Bufo R, Choplin T, De Filippo G, Devernois G, Eggermann T, Elli FM, Freson K, García Ramirez A, Germain-Lee EL, Groussin L, Hamdy N, Hanna P, Hiort O, Jüppner H, Kamenický P, Knight N, Kottler ML, Le Norcy E, Lecumberri B, Levine MA, Mäkitie O, Martin R, Martos-Moreno GÁ, Minagawa M, Murray P, Pereda A, Pignolo R, Rejnmark L, Rodado R, Rothenbuhler A, Saraff V, Shoemaker AH, Shore EM, Silve C, Turan S, Woods P, Zillikens MC, Perez de Nanclares G, Linglart A
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Legro RS
Semin Reprod Med 2012 Dec;30(6):496-506. Epub 2012 Oct 16 doi: 10.1055/s-0032-1328878. PMID: 23074008Free PMC Article

Recent clinical studies

Etiology

Derrou S, Bouziane T, Salhi H, El Ouahabi H
Ann Afr Med 2021 Jan-Mar;20(1):42-45. doi: 10.4103/aam.aam_13_20. PMID: 33727511Free PMC Article
Kalra B, Punyani H, Malhotra N, Kalra S
J Pak Med Assoc 2020 Apr;70(4):762-763. PMID: 32296232
Pastore I, Chiefari E, Vero R, Brunetti A
Endocrine 2018 Mar;59(3):481-494. Epub 2017 Aug 14 doi: 10.1007/s12020-017-1388-0. PMID: 28808874
Buysschaert M, Bergman M
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Abdul-Ghani MA, DeFronzo RA
Curr Diab Rep 2009 Jun;9(3):193-9. doi: 10.1007/s11892-009-0032-7. PMID: 19490820

Diagnosis

Chen B, Du YR, Zhu H, Sun ML, Wang C, Cheng Y, Pang H, Ding G, Gao J, Tan Y, Tong X, Lv P, Zhou F, Zhan Q, Xu ZM, Wang L, Luo D, Ye Y, Jin L, Zhang S, Zhu Y, Lin X, Wu Y, Jin L, Zhou Y, Yan C, Sheng J, Flatt PR, Xu GL, Huang H
Nature 2022 May;605(7911):761-766. Epub 2022 May 18 doi: 10.1038/s41586-022-04756-4. PMID: 35585240
Derrou S, Bouziane T, Salhi H, El Ouahabi H
Ann Afr Med 2021 Jan-Mar;20(1):42-45. doi: 10.4103/aam.aam_13_20. PMID: 33727511Free PMC Article
Thayer SM, Lo JO, Caughey AB
Obstet Gynecol Clin North Am 2020 Sep;47(3):383-396. Epub 2020 May 31 doi: 10.1016/j.ogc.2020.04.002. PMID: 32762924Free PMC Article
Kalra B, Punyani H, Malhotra N, Kalra S
J Pak Med Assoc 2020 Apr;70(4):762-763. PMID: 32296232
Buysschaert M, Bergman M
Med Clin North Am 2011 Mar;95(2):289-97, vii. doi: 10.1016/j.mcna.2010.11.002. PMID: 21281833

Therapy

Kawahara T, Suzuki G, Mizuno S, Inazu T, Kasagi F, Kawahara C, Okada Y, Tanaka Y
BMJ 2022 May 25;377:e066222. doi: 10.1136/bmj-2021-066222. PMID: 35613725Free PMC Article
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Hostalek U, Campbell I
Curr Med Res Opin 2021 Oct;37(10):1705-1717. Epub 2021 Jul 28 doi: 10.1080/03007995.2021.1955667. PMID: 34281467
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N Engl J Med 2001 May 3;344(18):1343-50. doi: 10.1056/NEJM200105033441801. PMID: 11333990

Prognosis

Sato M, Tamura Y, Nakagata T, Someya Y, Kaga H, Yamasaki N, Kiya M, Kadowaki S, Sugimoto D, Satoh H, Kawamori R, Watada H
J Clin Endocrinol Metab 2021 Apr 23;106(5):e2053-e2062. doi: 10.1210/clinem/dgab052. PMID: 33512496
Gong Q, Zhang P, Wang J, Ma J, An Y, Chen Y, Zhang B, Feng X, Li H, Chen X, Cheng YJ, Gregg EW, Hu Y, Bennett PH, Li G; Da Qing Diabetes Prevention Study Group
Lancet Diabetes Endocrinol 2019 Jun;7(6):452-461. Epub 2019 Apr 26 doi: 10.1016/S2213-8587(19)30093-2. PMID: 31036503Free PMC Article
Garro R, Warshaw B, Felner E
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N Engl J Med 2001 May 3;344(18):1343-50. doi: 10.1056/NEJM200105033441801. PMID: 11333990
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Clinical prediction guides

DeMayo F, Molinsky R, Tahir MJ, Roy S, Genkinger JM, Papapanou PN, Jacobs DR Jr, Demmer RT
J Clin Periodontol 2021 May;48(5):638-647. Epub 2021 Mar 12 doi: 10.1111/jcpe.13450. PMID: 33710636Free PMC Article
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Recent systematic reviews

Szabó A, Váncsa S, Hegyi P, Váradi A, Forintos A, Filipov T, Ács J, Ács N, Szarvas T, Nyirády P, Kopa Z
Reprod Biol Endocrinol 2023 Jan 18;21(1):5. doi: 10.1186/s12958-023-01054-0. PMID: 36653793Free PMC Article
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Azukaitis K, Palmer SC, Strippoli GF, Hodson EM
Cochrane Database Syst Rev 2022 Mar 1;3(3):CD001537. doi: 10.1002/14651858.CD001537.pub5. PMID: 35230699Free PMC Article
Tinguely D, Gross J, Kosinski C
Curr Diab Rep 2021 Aug 27;21(9):32. doi: 10.1007/s11892-021-01399-z. PMID: 34448957Free PMC Article
Brown J, Alwan NA, West J, Brown S, McKinlay CJ, Farrar D, Crowther CA
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