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Polyphagia

MedGen UID:
9369
Concept ID:
C0020505
Finding
Synonyms: Hyperphagia; Overeating; Polyphagias
SNOMED CT: Overeats (58424009); Hyperphagia (267023007); Gluttony (267023007); Excessive oral food intake (58424009); Polyphagia (267023007); Excessive eating (267023007); Overeating (58424009)
 
HPO: HP:0002591

Definition

A neurological anomaly with gross overeating associated with an abnormally strong desire or need to eat. [from HPO]

Conditions with this feature

Diabetes mellitus type 1
MedGen UID:
41522
Concept ID:
C0011854
Disease or Syndrome
Type 1 diabetes mellitus (T1D), also designated insulin-dependent diabetes mellitus (IDDM), is a disorder of glucose homeostasis characterized by susceptibility to ketoacidosis in the absence of insulin therapy. It is a genetically heterogeneous autoimmune disease affecting about 0.3% of Caucasian populations (Todd, 1990). Genetic studies of T1D have focused on the identification of loci associated with increased susceptibility to this multifactorial phenotype. The classic phenotype of diabetes mellitus is polydipsia, polyphagia, and polyuria which result from hyperglycemia-induced osmotic diuresis and secondary thirst. These derangements result in long-term complications that affect the eyes, kidneys, nerves, and blood vessels.
Prader-Willi syndrome
MedGen UID:
46057
Concept ID:
C0032897
Disease or Syndrome
Prader-Willi syndrome (PWS) is characterized by severe hypotonia and feeding difficulties in early infancy, followed in later infancy or early childhood by excessive eating and gradual development of morbid obesity (unless eating is externally controlled). Motor milestones and language development are delayed. All individuals have some degree of cognitive impairment. A distinctive behavioral phenotype (with temper tantrums, stubbornness, manipulative behavior, and obsessive-compulsive characteristics) is common. Hypogonadism is present in both males and females and manifests as genital hypoplasia, incomplete pubertal development, and, in most, infertility. Short stature is common (if not treated with growth hormone); characteristic facial features, strabismus, and scoliosis are often present.
Kleine-Levin syndrome
MedGen UID:
61511
Concept ID:
C0206085
Disease or Syndrome
The Kleine-Levin hibernation syndrome, a rare disorder that occurs predominantly in males, is characterized by episodic attacks of aberrant behavior, hypersomnia, and increased feeding (megaphagia) and sex drives (Kleine, 1925; Levin, 1929).
Pick disease
MedGen UID:
116020
Concept ID:
C0236642
Disease or Syndrome
Pick disease refers to the neuropathologic finding of 'Pick bodies,' which are argyrophilic, intraneuronal inclusions, and 'Pick cells,' which are enlarged neurons. The clinical correlates of Pick disease of brain include those of frontotemporal dementia, which encompass the behavioral variant of FTD, semantic dementia, and progressive nonfluent aphasia (summary by Piguet et al., 2011). Kertesz (2003) suggested the term 'Pick complex' to represent the overlapping syndromes of FTD, primary progressive aphasia (PPA), corticobasal degeneration (CBD), progressive supranuclear palsy (601104), and FTD with motor neuron disease. He noted that frontotemporal dementia may also be referred to as 'clinical Pick disease,' and that the term 'Pick disease' should be restricted to the pathologic finding of Pick bodies.
Weaver syndrome
MedGen UID:
120511
Concept ID:
C0265210
Disease or Syndrome
EZH2-related overgrowth includes EZH2-related Weaver syndrome at one end of the spectrum and tall stature at the other. Although most individuals diagnosed with a heterozygous EZH2 pathogenic variant have been identified because of a clinical suspicion of Weaver syndrome, a minority have been identified through molecular genetic testing of family members of probands or individuals with overgrowth who did not have a clinical diagnosis of Weaver syndrome. Thus, the extent of the phenotypic spectrum associated with a heterozygous EZH2 pathogenic variant is not yet known. Weaver syndrome is characterized by tall stature, variable intellect (ranging from normal intellect to severe intellectual disability), characteristic facial appearance, and a range of associated clinical features including advanced bone age, poor coordination, soft doughy skin, camptodactyly of the fingers and/or toes, umbilical hernia, abnormal tone, and hoarse low cry in infancy. Brain MRI has identified abnormalities in a few individuals with EZH2-related overgrowth. Neuroblastoma occurs at a slightly increased frequency in individuals with a heterozygous EZH2 pathogenic variant but data are insufficient to determine absolute risk. There is currently no evidence that additional malignancies (including hematologic malignancies) occur with increased frequency.
Frontotemporal dementia
MedGen UID:
83266
Concept ID:
C0338451
Disease or Syndrome
Frontotemporal dementia (FTD) refers to a clinical manifestation of the pathologic finding of frontotemporal lobar degeneration (FTLD). FTD, the most common subtype of FTLD, is a behavioral variant characterized by changes in social and personal conduct with loss of volition, executive dysfunction, loss of abstract thought, and decreased speech output. A second clinical subtype of FTLD is 'semantic dementia,' characterized by specific loss of comprehension of language and impaired facial and object recognition. A third clinical subtype of FTLD is 'primary progressive aphasia' (PPA), characterized by a reduction in speech production, speech errors, and word retrieval difficulties resulting in mutism and an inability to communicate. All subtypes have relative preservation of memory, at least in the early stages. FTLD is often associated with parkinsonism or motor neuron disease (MND) resembling amyotrophic lateral sclerosis (ALS; 105400) (reviews by Tolnay and Probst, 2002 and Mackenzie and Rademakers, 2007). Mackenzie et al. (2009, 2010) provided a classification of FTLD subtypes according to the neuropathologic findings (see PATHOGENESIS below). Clinical Variability of Tauopathies Tauopathies comprise a clinically variable group of neurodegenerative diseases characterized neuropathologically by accumulation of abnormal MAPT-positive inclusions in nerve and/or glial cells. In addition to frontotemporal dementia, semantic dementia, and PPA, different clinical syndromes with overlapping features have been described, leading to confusion in the terminology (Tolnay and Probst, 2002). Other terms used historically include parkinsonism and dementia with pallidopontonigral degeneration (PPND) (Wszolek et al., 1992); disinhibition-dementia-parkinsonism-amyotrophy complex (DDPAC) (Lynch et al., 1994); frontotemporal dementia with parkinsonism (FLDEM) (Yamaoka et al., 1996); and multiple system tauopathy with presenile dementia (MSTD) (Spillantini et al., 1997). These disorders are characterized by variable degrees of frontal lobe dementia, parkinsonism, motor neuron disease, and amyotrophy. Other neurodegenerative associated with mutations in the MAPT gene include Pick disease (172700) and progressive supranuclear palsy (PSP; 601104), Inherited neurodegenerative tauopathies linked to chromosome 17 and caused by mutation in the MAPT gene have also been collectively termed 'FTDP17' (Lee et al., 2001). Kertesz (2003) suggested the term 'Pick complex' to represent the overlapping syndromes of FTD, primary progressive aphasia (PPA), corticobasal degeneration (CBD), PSP, and FTD with motor neuron disease. He noted that frontotemporal dementia may also be referred to as 'clinical Pick disease' and that the term 'Pick disease' should be restricted to the pathologic finding of Pick bodies. Genetic Heterogeneity of Frontotemporal Lobar Degeneration Mutations in several different genes can cause frontotemporal dementia and frontotemporal lobar degeneration, with or without motor neuron disease. See FTLD with TDP43 inclusions (607485), caused by mutation in the GRN gene (138945) on chromosome 17q21; FTLALS7 (600795), caused by mutation in the CHMP2B gene (609512) on chromosome 3p11; inclusion body myopathy with Paget disease and FTD (IBMPFD; 167320), caused by mutation in the VCP gene (601023) on chromosome 9p13; ALS6 (608030), caused by mutation in the FUS gene (137070) on 16p11; ALS10 (612069), caused by mutation in the TARDBP gene (605078) on 1p36; and FTDALS1 (105550), caused by mutation in the C9ORF72 gene (614260) on 9p21. In 1 family with FTD, a mutation was identified in the presenilin-1 gene (PSEN1; 104311) on chromosome 14, which is usually associated with a familial form of early-onset Alzheimer disease (AD3; 607822).
Congenital generalized lipodystrophy type 1
MedGen UID:
318592
Concept ID:
C1720862
Disease or Syndrome
Berardinelli-Seip congenital lipodystrophy (BSCL) is usually diagnosed at birth or soon thereafter. Because of the absence of functional adipocytes, lipid is stored in other tissues, including muscle and liver. Affected individuals develop insulin resistance and approximately 25%-35% develop diabetes mellitus between ages 15 and 20 years. Hepatomegaly secondary to hepatic steatosis and skeletal muscle hypertrophy occur in all affected individuals. Hypertrophic cardiomyopathy is reported in 20%-25% of affected individuals and is a significant cause of morbidity from cardiac failure and early mortality.
Congenital generalized lipodystrophy type 2
MedGen UID:
318593
Concept ID:
C1720863
Congenital Abnormality
Berardinelli-Seip congenital lipodystrophy (BSCL) is usually diagnosed at birth or soon thereafter. Because of the absence of functional adipocytes, lipid is stored in other tissues, including muscle and liver. Affected individuals develop insulin resistance and approximately 25%-35% develop diabetes mellitus between ages 15 and 20 years. Hepatomegaly secondary to hepatic steatosis and skeletal muscle hypertrophy occur in all affected individuals. Hypertrophic cardiomyopathy is reported in 20%-25% of affected individuals and is a significant cause of morbidity from cardiac failure and early mortality.
Chromosome 1p36 deletion syndrome
MedGen UID:
334629
Concept ID:
C1842870
Disease or Syndrome
The constitutional deletion of chromosome 1p36 results in a syndrome with multiple congenital anomalies and mental retardation (Shapira et al., 1997). Monosomy 1p36 is the most common terminal deletion syndrome in humans, occurring in 1 in 5,000 births (Shaffer and Lupski, 2000; Heilstedt et al., 2003). See also neurodevelopmental disorder with or without anomalies of the brain, eye, or heart (NEDBEH; 616975), which shows overlapping features and is caused by heterozygous mutation in the RERE gene (605226) on proximal chromosome 1p36. See also Radio-Tartaglia syndrome (RATARS; 619312), caused by mutation in the SPEN gene (613484) on chromosome 1p36, which shows overlapping features.
GRN-related frontotemporal lobar degeneration with Tdp43 inclusions
MedGen UID:
375285
Concept ID:
C1843792
Disease or Syndrome
The spectrum of GRN frontotemporal dementia (GRN-FTD) includes the behavioral variant (bvFTD), primary progressive aphasia (PPA; further subcategorized as progressive nonfluent aphasia [PNFA] and semantic dementia [SD]), and movement disorders with extrapyramidal features such as parkinsonism and corticobasal syndrome (CBS). A broad range of clinical features both within and between families is observed. The age of onset ranges from 35 to 87 years. Behavioral disturbances are the most common early feature, followed by progressive aphasia. Impairment in executive function manifests as loss of judgment and insight. In early stages, PPA often manifests as deficits in naming, word finding, or word comprehension. In late stages, affected individuals often become mute and lose their ability to communicate. Early findings of parkinsonism include rigidity, bradykinesia or akinesia (slowing or absence of movements), limb dystonia, apraxia (loss of ability to carry out learned purposeful movements), and disequilibrium. Late motor findings may include myoclonus, dysarthria, and dysphagia. Most affected individuals eventually lose the ability to walk. Disease duration is three to 12 years.
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.
Graves disease, susceptibility to, 1
MedGen UID:
341307
Concept ID:
C1848795
Finding
Graves disease (GRD) is an autoimmune disorder in which antibodies to the thyrotropin receptor (TSHR; 603372) result in constitutive activation of the receptor and increased levels of thyroid hormone. Wilkin (1990) reviewed endocrine disorders of hormone excess and hormone deficiency resulting from receptor autoimmunity. Genetic Heterogeneity of Graves Disease Susceptibility to Graves disease-1 (GRD1) has been mapped to chromosome 14q31. Other susceptibility loci for Graves disease include GRD2 (603388) on chromosome 20q13, GRDX1 (300351) on Xp11, and GRDX2 (see 300351) on Xq21.33-q22. Graves disease has also been mapped to several loci that confer susceptibility to autoimmune thyroid diseases, including Hashimoto thyroiditis (HT; 140300): AITD1 (608173) on 6p11; AITD2 (608174) on 5q31-q33; AITD3 (608175) on 8q24; AITD4 (608176) on 10q, and AITD5 (601941) on 18q21.
Obesity due to pro-opiomelanocortin deficiency
MedGen UID:
341863
Concept ID:
C1857854
Disease or Syndrome
Early-onset obesity with adrenal insuficiency and red hair (OBAIRH) is an autosomal recessive endocrine disorder characterized by early-onset obesity due to severe hyperphagia, pigmentary abnormalities, mainly pale skin and red hair, and secondary hypocortisolism. In the neonatal period, affected individuals are prone to hypoglycemia, hyperbilirubinemia, and cholestasis that may result in death if not treated. The disorder results from mutation in the POMC gene, which encodes a preproprotein that is processed into a range of bioactive peptides, including alpha-melanocyte-stimulating hormone (MSH) and ACTH (summary by Kuhnen et al., 2016 and Clement et al., 2008).
Bardet-Biedl syndrome 9
MedGen UID:
347182
Concept ID:
C1859567
Disease or Syndrome
BBS9 is an autosomal recessive disorder characterized by obesity, polydactyly, renal anomalies, retinopathy, and mental retardation (Abu-Safieh et al., 2012). For a general phenotypic description and a discussion of genetic heterogeneity of Bardet-Biedl syndrome, see BBS1 (209900).
Intellectual disability, autosomal dominant 1
MedGen UID:
409857
Concept ID:
C1969562
Mental or Behavioral Dysfunction
MBD5 haploinsufficiency is a neurodevelopmental disorder characterized by developmental delay, intellectual disability, severe speech impairment, seizures, sleep disturbances, and abnormal behaviors. Most children lack speech entirely or have single words, short phrases, or short sentences. Seizures are present in more than 80% of children; onset is usually around age two years. Sleep disturbances, present in about 90%, can result in excessive daytime drowsiness. Abnormal behaviors can include autistic-like behaviors (80%) and self-injury and aggression (>60%).
Wilms tumor, aniridia, genitourinary anomalies, intellectual disability, and obesity syndrome
MedGen UID:
382718
Concept ID:
C2675904
Disease or Syndrome
For a detailed discussion of the WAGR syndrome, see 194072. In a subgroup of individuals with the WAGR syndrome, obesity develops. The phenotype in this subset is associated with haploinsufficiency for the BDNF gene.
Joubert syndrome 10
MedGen UID:
440688
Concept ID:
C2749019
Disease or Syndrome
Classic Joubert syndrome (JS) is characterized by three primary findings: A distinctive cerebellar and brain stem malformation called the molar tooth sign (MTS). Hypotonia. Developmental delays. Often these findings are accompanied by episodic tachypnea or apnea and/or atypical eye movements. In general, the breathing abnormalities improve with age, truncal ataxia develops over time, and acquisition of gross motor milestones is delayed. Cognitive abilities are variable, ranging from severe intellectual disability to normal. Additional findings can include retinal dystrophy, renal disease, ocular colobomas, occipital encephalocele, hepatic fibrosis, polydactyly, oral hamartomas, and endocrine abnormalities. Both intra- and interfamilial variation are seen.
Obesity, hyperphagia, and developmental delay
MedGen UID:
462653
Concept ID:
C3151303
Disease or Syndrome
OBHD is a neurodevelopmental disorder characterized by global developmental delay and hyperphagia resulting in obesity. Some patients may develop seizures (summary by Hamdan et al., 2017).
Familial renal glucosuria
MedGen UID:
757652
Concept ID:
C3245525
Disease or Syndrome
Patients with familial renal glucosuria have decreased renal tubular resorption of glucose form the urine in the absence of hyperglycemia and any other signs of tubular dysfunction. Glucosuria in these patients can range from less than 1 to over 150 g/1.73 m(2) per day (Santer and Calado, 2010).
Obesity due to congenital leptin deficiency
MedGen UID:
767138
Concept ID:
C3554224
Disease or Syndrome
Leptin deficiency or dysfunction (LEPD) is characterized by severe early-onset obesity, hyperphagia, hypogonadotropic hypogonadism, and neuroendocrine/metabolic dysfunction (Ozata et al., 1999).
Obesity due to leptin receptor gene deficiency
MedGen UID:
767139
Concept ID:
C3554225
Disease or Syndrome
Leptin receptor deficiency is characterized by severe early-onset obesity, major hyperphagia, hypogonadotropic hypogonadism, and neuroendocrine/metabolic dysfunction (summary by Dehghani et al., 2018).
Chromosome 22q13 duplication syndrome
MedGen UID:
816174
Concept ID:
C3809844
Disease or Syndrome
X-linked acrogigantism due to Xq26 microduplication
MedGen UID:
856021
Concept ID:
C3891556
Disease or Syndrome
X-linked acrogigantism is the occurrence of pituitary gigantism in an individual heterozygous or hemizygous for a germline or somatic duplication of GPR101. X-linked acrogigantism is characterized by acceleration of linear growth in early childhood – in most cases during the first two years of life – due to growth hormone (GH) excess. Most individuals with X-linked acrogigantism present with associated hyperprolactinemia due to a mixed GH- and prolactin-secreting pituitary adenoma with or without associated hyperplasia; less commonly they develop diffuse hyperplasia of the GH- and prolactin-secreting pituitary cells without a pituitary adenoma. Most affected individuals are females. Growth acceleration is the main presenting feature; other frequently observed clinical features include enlargement of hands and feet, coarsening of the facial features, and increased appetite. Neurologic signs or symptoms are rarely present. Untreated X-linked acrogigantism can lead to markedly increased stature, with obvious severe physical and psychological sequelae.
ADNP-related multiple congenital anomalies - intellectual disability - autism spectrum disorder
MedGen UID:
862975
Concept ID:
C4014538
Disease or Syndrome
ADNP-related disorder is characterized by hypotonia, severe speech and motor delay, mild-to-severe intellectual disability, and characteristic facial features (prominent forehead, high anterior hairline, wide and depressed nasal bridge, and short nose with full, upturned nasal tip) based on a cohort of 78 individuals. Features of autism spectrum disorder are common (stereotypic behavior, impaired social interaction). Other common findings include additional behavioral problems, sleep disturbance, brain abnormalities, seizures, feeding issues, gastrointestinal problems, visual dysfunction (hypermetropia, strabismus, cortical visual impairment), musculoskeletal anomalies, endocrine issues including short stature and hormonal deficiencies, cardiac and urinary tract anomalies, and hearing loss.
Luscan-Lumish syndrome
MedGen UID:
898669
Concept ID:
C4085873
Disease or Syndrome
Luscan-Lumish syndrome (LLS) is characterized by macrocephaly, intellectual disability, speech delay, low sociability, and behavioral problems. More variable features include postnatal overgrowth, obesity, advanced carpal ossification, developmental delay, and seizures (Luscan et al., 2014; Lumish et al., 2015)
Intellectual disability, autosomal dominant 39
MedGen UID:
909304
Concept ID:
C4225296
Disease or Syndrome
An autosomal dominant condition caused by mutation(s) in the MYT1L gene, encoding myelin transcription factor 1-like protein. It is characterized by intellectual disability and mild dysmorphic facial features.
BODY MASS INDEX QUANTITATIVE TRAIT LOCUS 19
MedGen UID:
1638030
Concept ID:
C4693522
Finding
Patients with biallelic mutations in the ADCY3 gene show hyperphagia within the first 2 years of life and develop severe obesity. Other features include hyposmia or anosmia, and some patients exhibit mild to moderate intellectual disability (Saeed et al., 2018).
BODY MASS INDEX QUANTITATIVE TRAIT LOCUS 20
MedGen UID:
1674972
Concept ID:
C4759928
Finding
Obesity due to mutation in the MC4R gene is the most common cause of monogenic obesity. Patients have early-onset severe obesity and hyperphagia (Farooqi et al., 2003).
CEBALID syndrome
MedGen UID:
1710973
Concept ID:
C5394044
Disease or Syndrome
Individuals with MN1 C-terminal truncation (MCTT) syndrome have mild-to-moderate intellectual disability, severe expressive language delay, dysmorphic facial features (midface hypoplasia, downslanting palpebral fissures, hypertelorism, exophthalmia, short upturned nose, and small low-set ears), and distinctive findings on brain imaging (including perisylvian polymicrogyria and atypical rhombencephalosynapsis). Mild-to-moderate prelingual hearing loss (usually bilateral, conductive, and/or sensorineural) is common. Generalized seizures (observed in the minority of individuals) are responsive to anti-seizure medication. There is an increased risk for craniosynostosis and, thus, increased intracranial pressure. To date, 25 individuals with MCTT syndrome have been identified.
Bardet-Biedl syndrome 22
MedGen UID:
1794146
Concept ID:
C5561936
Disease or Syndrome
Bardet-Biedl syndrome-22 (BBS22) is an autosomal recessive ciliopathy described in a single patient and characterized by retinitis pigmentosa, obesity, polydactyly, hypogonadism, and intellectual disability (Lindstrand et al., 2016). For a general phenotypic description and a discussion of genetic heterogeneity of Bardet-Biedl syndrome, see BBS1 (209900).
Schaaf-Yang syndrome
MedGen UID:
1807366
Concept ID:
C5575066
Disease or Syndrome
Schaaf-Yang syndrome (SYS) is a rare neurodevelopmental disorder that shares multiple clinical features with the genetically related Prader-Willi syndrome. It usually manifests at birth with muscular hypotonia in all and distal joint contractures in a majority of affected individuals. Gastrointestinal/feeding problems are particularly pronounced in infancy and childhood, but can transition to hyperphagia and obesity in adulthood. Respiratory distress is present in many individuals at birth, with approximately half requiring intubation and mechanical ventilation, and approximately 20% requiring tracheostomy. Skeletal manifestations such as joint contractures, scoliosis, and decreased bone mineral density are frequently observed. All affected individuals show developmental delay, resulting in intellectual disability of variable degree, from low-normal intelligence to severe intellectual disability. Other findings may include short stature, seizures, eye anomalies, and hypogonadism.
Hypermetabolism due to uncoupled mitochondrial oxidative phosphorylation 2
MedGen UID:
1824010
Concept ID:
C5774237
Disease or Syndrome
Hypermetabolism due to uncoupled mitochondrial oxidative phosphorylation-2 (HUMOP2) is characterized by failure to thrive apparent in infancy despite adequate caloric intake. Affected individuals show normal thyroid function, hyperphagia, tachypnea, increased basal temperature, and increased sweating. Biochemical studies demonstrate increased mitochondrial oxygen consumption with inefficient production of ATP in the final steps of oxidative phosphorylation due to an uncoupling defect (Ganetzky et al., 2022). Genetic Heterogeneity of Hypermetabolism due to Uncoupled Mitochondrial Oxidative Phosphorylation See also HUMOP1 (238800).
Obesity and hypopigmentation
MedGen UID:
1824062
Concept ID:
C5774289
Disease or Syndrome
Obesity and hypopigmentation (OBHP) is characterized by early-onset severe obesity and hypopigmentation of the skin. Some affected individuals have red hair, and some experience increased appetite and exhibit reduced energy expenditure (Kempf et al., 2022).
Intellectual developmental disorder, autosomal dominant 71, with behavioral abnormalities
MedGen UID:
1841073
Concept ID:
C5830437
Mental or Behavioral Dysfunction
Autosomal dominant intellectual developmental disorder-71 with behavioral abnormalities (MRD71) is a neurodevelopmental disorder characterized by global developmental delay with hypotonia, speech delay, and variably impaired cognitive development. Almost all affected individuals show marked behavioral manifestations, including autism spectrum disorder (ASD), ADHD, hypersensitivity, and aggression. Many have dysmorphic features, although there is not a common gestalt (Harris et al., 2021).
Intellectual developmental disorder, autosomal dominant 72
MedGen UID:
1841248
Concept ID:
C5830612
Mental or Behavioral Dysfunction
Autosomal dominant intellectual developmental disorder-72 (MRD72) is characterized by developmental delay, predominant speech delay, autistic or attention-deficit/hyperactivity disorder features, overfriendliness, generalized hypotonia, overweight/obesity, and dysmorphic features (Cuinat et al., 2022).

Professional guidelines

PubMed

Bettencourt-Silva R, Aguiar B, Sá-Araújo V, Barreira R, Guedes V, Marques Ribeiro MJ, Carvalho D, Östlundh L, Paulo MS
BMJ Open 2019 Jun 14;9(6):e028604. doi: 10.1136/bmjopen-2018-028604. PMID: 31203247Free PMC Article
Westerberg DP
Am Fam Physician 2013 Mar 1;87(5):337-46. PMID: 23547550
Jonasson O, Hoversten GH
Surg Annu 1978;10:1-21. PMID: 416507

Recent clinical studies

Etiology

Gao Y, Zhou J, Xie YC, Qiu LJ, Duan L, A ZX, Wu HF, Lv MX
BMC Pediatr 2023 Aug 24;23(1):420. doi: 10.1186/s12887-023-04209-5. PMID: 37620840Free PMC Article
Chen F, Ge L, Jiang X, Lai Y, Huang P, Hua J, Lin Y, Lin Y, Jiang X
PLoS One 2022;17(9):e0273703. Epub 2022 Sep 15 doi: 10.1371/journal.pone.0273703. PMID: 36107823Free PMC Article
Byashalira KC, Chamba NG, Alkabab Y, Mbelele PM, Ntinginya NE, Ramaiya KL, Alimohamed MZ, Heysell SK, Mmbaga BT, Bygbjerg IC, Christensen DL, Mpagama SG, Lillebaek T; ADEPT Consortium
BMC Infect Dis 2022 Mar 16;22(1):260. doi: 10.1186/s12879-022-07249-x. PMID: 35296241Free PMC Article
Kissani N, Cherkaoui Rhazouani O, Berrhoute L, Chraa M, Louhab N
Rev Neurol (Paris) 2021 Jan-Feb;177(1-2):80-84. Epub 2020 Jul 30 doi: 10.1016/j.neurol.2020.05.006. PMID: 32741562
Soskolne WA, Klinger A
Ann Periodontol 2001 Dec;6(1):91-8. doi: 10.1902/annals.2001.6.1.91. PMID: 11887477

Diagnosis

Gao Y, Zhou J, Xie YC, Qiu LJ, Duan L, A ZX, Wu HF, Lv MX
BMC Pediatr 2023 Aug 24;23(1):420. doi: 10.1186/s12887-023-04209-5. PMID: 37620840Free PMC Article
Bettencourt-Silva R, Aguiar B, Sá-Araújo V, Barreira R, Guedes V, Marques Ribeiro MJ, Carvalho D, Östlundh L, Paulo MS
BMJ Open 2019 Jun 14;9(6):e028604. doi: 10.1136/bmjopen-2018-028604. PMID: 31203247Free PMC Article
Teti C, Castelletti L, Allegretti L, Talco M, Zona G, Minuto F, Boschetti M, Ferone D
Pituitary 2015 Oct;18(5):592-7. doi: 10.1007/s11102-014-0612-7. PMID: 25311104
Westerberg DP
Am Fam Physician 2013 Mar 1;87(5):337-46. PMID: 23547550
Hochberg I, Hochberg Z
Obes Rev 2010 Oct;11(10):709-21. doi: 10.1111/j.1467-789X.2010.00727.x. PMID: 20233310

Therapy

Chen F, Ge L, Jiang X, Lai Y, Huang P, Hua J, Lin Y, Lin Y, Jiang X
PLoS One 2022;17(9):e0273703. Epub 2022 Sep 15 doi: 10.1371/journal.pone.0273703. PMID: 36107823Free PMC Article
Bettencourt-Silva R, Aguiar B, Sá-Araújo V, Barreira R, Guedes V, Marques Ribeiro MJ, Carvalho D, Östlundh L, Paulo MS
BMJ Open 2019 Jun 14;9(6):e028604. doi: 10.1136/bmjopen-2018-028604. PMID: 31203247Free PMC Article
Westerberg DP
Am Fam Physician 2013 Mar 1;87(5):337-46. PMID: 23547550
Hochberg I, Hochberg Z
Obes Rev 2010 Oct;11(10):709-21. doi: 10.1111/j.1467-789X.2010.00727.x. PMID: 20233310
Schaad U, Vassella F, Zuppinger K, Oetliker O
Helv Paediatr Acta 1979 Feb;34(1):63-76. PMID: 429194

Prognosis

Xu T, He P, namWangdu S, Xu C, Hou B, Ma P, Wang Z, Zhang L, Du G, Ring T, Ji T, Qiang G
J Ethnopharmacol 2024 Jan 30;319(Pt 2):117254. Epub 2023 Sep 29 doi: 10.1016/j.jep.2023.117254. PMID: 37778519
Byashalira KC, Chamba NG, Alkabab Y, Mbelele PM, Ntinginya NE, Ramaiya KL, Alimohamed MZ, Heysell SK, Mmbaga BT, Bygbjerg IC, Christensen DL, Mpagama SG, Lillebaek T; ADEPT Consortium
BMC Infect Dis 2022 Mar 16;22(1):260. doi: 10.1186/s12879-022-07249-x. PMID: 35296241Free PMC Article
Peng W, Yuan J, Chiavaroli V, Dong G, Huang K, Wu W, Ullah R, Jin B, Lin H, Derraik JGB, Fu J
Front Endocrinol (Lausanne) 2021;12:653519. Epub 2021 Apr 27 doi: 10.3389/fendo.2021.653519. PMID: 33986725Free PMC Article
Shera AS, Miyan Z, Basit A, Maqsood A, Ahmadani MY, Fawwad A, Riaz M
Pediatr Diabetes 2008 Aug;9(4 Pt 2):401-6. doi: 10.1111/j.1399-5448.2007.00309.x. PMID: 18221426
Pogson C
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Clinical prediction guides

Xu T, He P, namWangdu S, Xu C, Hou B, Ma P, Wang Z, Zhang L, Du G, Ring T, Ji T, Qiang G
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