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External genital hypoplasia

MedGen UID:
344478
Concept ID:
C1855333
Finding
Synonyms: Hypogenitalism; Small genitalia
 
HPO: HP:0003241

Definition

Underdevelopment of part or all of the external reproductive organs. [from HPO]

Conditions with this feature

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.
CHARGE association
MedGen UID:
75567
Concept ID:
C0265354
Disease or Syndrome
CHD7 disorder encompasses the entire phenotypic spectrum of heterozygous CHD7 pathogenic variants that includes CHARGE syndrome as well as subsets of features that comprise the CHARGE syndrome phenotype. The mnemonic CHARGE syndrome, introduced in the premolecular era, stands for coloboma, heart defect, choanal atresia, retarded growth and development, genital hypoplasia, ear anomalies (including deafness). Following the identification of the genetic cause of CHD7 disorder, the phenotypic spectrum expanded to include cranial nerve anomalies, vestibular defects, cleft lip and/or palate, hypothyroidism, tracheoesophageal anomalies, brain anomalies, seizures, and renal anomalies. Life expectancy highly depends on the severity of manifestations; mortality can be high in the first few years when severe birth defects (particularly complex heart defects) are present and often complicated by airway and feeding issues. In childhood, adolescence, and adulthood, decreased life expectancy is likely related to a combination of residual heart defects, infections, aspiration or choking, respiratory issues including obstructive and central apnea, and possibly seizures. Despite these complications, the life expectancy for many individuals can be normal.
Harrod syndrome
MedGen UID:
162895
Concept ID:
C0795970
Disease or Syndrome
The association of intellectual deficit, facial dysmorphism (a highly arched palate, pointed chin, and small mouth, hypotelorism, a long nose and large protruding ears), arachnodactyly, hypogenitalism (undescended testes and hypospadias) and failure to thrive. So far, it has been described in three males (including two brothers). An autosomal recessive mode of transmission has been suggested.
Mesoaxial hexadactyly and cardiac malformation
MedGen UID:
167099
Concept ID:
C0796057
Disease or Syndrome
A syndrome of mental retardation, short stature, delayed puberty, polydactyly, synmetracarpalia, ocular torticollis, orofacial dysmorphism, and multiple cardiac malformations.
Warburg micro syndrome 1
MedGen UID:
333142
Concept ID:
C1838625
Disease or Syndrome
RAB18 deficiency is the molecular deficit underlying both Warburg micro syndrome (characterized by eye, nervous system, and endocrine abnormalities) and Martsolf syndrome (characterized by similar – but milder – findings). To date Warburg micro syndrome comprises >96% of reported individuals with genetically defined RAB18 deficiency. The hallmark ophthalmologic findings are bilateral congenital cataracts, usually accompanied by microphthalmia, microcornea (diameter <10), and small atonic pupils. Poor vision despite early cataract surgery likely results from progressive optic atrophy and cortical visual impairment. Individuals with Warburg micro syndrome have severe to profound intellectual disability (ID); those with Martsolf syndrome have mild to moderate ID. Some individuals with RAB18 deficiency also have epilepsy. In Warburg micro syndrome, a progressive ascending spastic paraplegia typically begins with spastic diplegia and contractures during the first year, followed by upper-limb involvement leading to spastic quadriplegia after about age five years, often eventually causing breathing difficulties. In Martsolf syndrome infantile hypotonia is followed primarily by slowly progressive lower-limb spasticity. Hypogonadism – when present – manifests in both syndromes, in males as micropenis and/or cryptorchidism and in females as hypoplastic labia minora, clitoral hypoplasia, and small introitus.
Retinitis pigmentosa inversa with deafness
MedGen UID:
341447
Concept ID:
C1849405
Disease or Syndrome
Bardet-Biedl syndrome 6
MedGen UID:
347610
Concept ID:
C1858054
Disease or Syndrome
BBS6 is an autosomal recessive disorder with cardinal features of postaxial polydactyly, retinitis pigmentosa, kidney defects, obesity, and mental retardation (Slavotinek et al., 2000). Zaghloul and Katsanis (2009) estimated that mutations in the MKKS gene account for 5.8% of the total BBS mutational load. For a general phenotypic description and a discussion of genetic heterogeneity of Bardet-Biedl syndrome, see BBS1 (209900).
Bardet-Biedl syndrome 3
MedGen UID:
347179
Concept ID:
C1859564
Disease or Syndrome
BBS3 is a rare autosomal recessive disorder characterized by retinal dystrophy, polydactyly, renal structural abnormalities, and history of obesity. Although mental retardation has been considered part of the BBS phenotype, several patients with BBS3 and normal intelligence have been reported. Additionally, the obesity in several BBS3 patients has been reversible with caloric restriction and exercise (Young et al., 1998; Ghadami et al., 2000). For a general phenotypic description and a discussion of genetic heterogeneity of Bardet-Biedl syndrome, see BBS1 (209900).
Microcephaly, growth retardation, cataract, hearing loss, and unusual appearance
MedGen UID:
416652
Concept ID:
C2751870
Disease or Syndrome
Bardet-Biedl syndrome 2
MedGen UID:
422453
Concept ID:
C2936863
Disease or Syndrome
BBS2 is an autosomal recessive ciliopathy characterized by retinal degeneration, polydactyly, renal disease, hypogonadism, obesity, dysmorphic features, and variable degrees of cognitive impairment (Innes et al., 2010). Mutation in the BBS2 gene is the third most frequent cause of BBS, accounting for approximately 8% of cases (Zaghloul and Katsanis, 2009). For a general phenotypic description and a discussion of genetic heterogeneity of Bardet-Biedl syndrome, see BBS1 (209900).
Bardet-Biedl syndrome 4
MedGen UID:
423627
Concept ID:
C2936864
Disease or Syndrome
BBS4 is a rare multisystemic disorder characterized primarily by retinal dystrophy, obesity, polydactyly, and renal dysfunction that accounts for less than 3% of BBS (Katsanis et al., 2002). Anosmia has been described in patients with BBS4 (Iannaccone et al., 2005), as well as polydactyly confined to the hands (Carmi et al., 1995). For a general phenotypic description and a discussion of genetic heterogeneity of Bardet-Biedl syndrome, see BBS1 (209900).
Palmoplantar keratoderma-XX sex reversal-predisposition to squamous cell carcinoma syndrome
MedGen UID:
461281
Concept ID:
C3149931
Disease or Syndrome
Palmoplantar keratoderma-XX sex reversal-predisposition to squamous cell carcinoma syndrome is characterised by sex reversal in males with a 46, XX (SRY-negative) karyotype, palmoplantar hyperkeratosis and a predisposition to squamous cell carcinoma. To date, five cases (four of whom were brothers) have been described. The aetiology is unknown.
Fanconi anemia complementation group O
MedGen UID:
462003
Concept ID:
C3150653
Disease or Syndrome
Fanconi anemia (FA) is characterized by physical abnormalities, bone marrow failure, and increased risk for malignancy. Physical abnormalities, present in approximately 75% of affected individuals, include one or more of the following: short stature, abnormal skin pigmentation, skeletal malformations of the upper and/or lower limbs, microcephaly, and ophthalmic and genitourinary tract anomalies. Progressive bone marrow failure with pancytopenia typically presents in the first decade, often initially with thrombocytopenia or leukopenia. The incidence of acute myeloid leukemia is 13% by age 50 years. Solid tumors – particularly of the head and neck, skin, and genitourinary tract – are more common in individuals with FA.
Microcephaly, epilepsy, and diabetes syndrome
MedGen UID:
481870
Concept ID:
C3280240
Disease or Syndrome
Microcephaly, epilepsy, and diabetes syndrome-1 (MEDS1) is an autosomal recessive neurodevelopmental disorder characterized by microcephaly, simplified gyral pattern, severe epilepsy, and infantile diabetes (summary by Poulton et al., 2011). Genetic Heterogeneity of Microcephaly, Epilepsy, and Diabetes Syndrome MEDS2 (619278) is caused by mutation in the YIPF5 gene (611483) on chromosome 5q31.
Meckel syndrome, type 1
MedGen UID:
811346
Concept ID:
C3714506
Disease or Syndrome
Meckel syndrome, also known as Meckel-Gruber syndrome, is a severe pleiotropic autosomal recessive developmental disorder caused by dysfunction of primary cilia during early embryogenesis. There is extensive clinical variability and controversy as to the minimum diagnostic criteria. Early reports, including that of Opitz and Howe (1969) and Wright et al. (1994), stated that the classic triad of Meckel syndrome comprises (1) cystic renal disease; (2) a central nervous system malformation, most commonly occipital encephalocele; and (3) polydactyly, most often postaxial. However, based on a study of 67 patients, Salonen (1984) concluded that the minimum diagnostic criteria are (1) cystic renal disease; (2) CNS malformation, and (3) hepatic abnormalities, including portal fibrosis or ductal proliferation. In a review of Meckel syndrome, Logan et al. (2011) stated that the classic triad first described by Meckel (1822) included occipital encephalocele, cystic kidneys, and fibrotic changes to the liver. Genetic Heterogeneity of Meckel Syndrome See also MKS2 (603194), caused by mutation in the TMEM216 gene (613277) on chromosome 11q12; MKS3 (607361), caused by mutation in the TMEM67 gene (609884) on chromosome 8q; MKS4 (611134), caused by mutation in the CEP290 gene (610142) on chromosome 12q; MKS5 (611561), caused by mutation in the RPGRIP1L gene (610937) on chromosome 16q12; MKS6 (612284), caused by mutation in the CC2D2A gene (612013) on chromosome 4p15; MKS7 (267010), caused by mutation in the NPHP3 (608002) gene on chromosome 3q22; MKS8 (613885), caused by mutation in the TCTN2 gene (613846) on chromosome 12q24; MKS9 (614209), caused by mutation in the B9D1 gene (614144) on chromosome 17p11; MKS10 (614175), caused by mutation in the B9D2 gene (611951) on chromosome 19q13; MKS11 (615397), caused by mutation in the TMEM231 gene (614949) on chromosome 16q23; MKS12 (616258), caused by mutation in the KIF14 gene (611279) on chromosome 1q32; MKS13 (617562), caused by mutation in the TMEM107 gene (616183) on chromosome 17p13; and MKS14 (619879), caused by mutation in the TXNDC15 gene (617778) on chromosome 5q31.
Autosomal recessive congenital ichthyosis 2
MedGen UID:
854762
Concept ID:
C3888093
Disease or Syndrome
Autosomal recessive congenital ichthyosis (ARCI) encompasses several forms of nonsyndromic ichthyosis. Although most neonates with ARCI are collodion babies, the clinical presentation and severity of ARCI may vary significantly, ranging from harlequin ichthyosis, the most severe and often fatal form, to lamellar ichthyosis (LI) and (nonbullous) congenital ichthyosiform erythroderma (CIE). These phenotypes are now recognized to fall on a continuum; however, the phenotypic descriptions are clinically useful for clarification of prognosis and management. Infants with harlequin ichthyosis are usually born prematurely and are encased in thick, hard, armor-like plates of cornified skin that severely restrict movement. Life-threatening complications in the immediate postnatal period include respiratory distress, feeding problems, and systemic infection. Collodion babies are born with a taut, shiny, translucent or opaque membrane that encases the entire body and lasts for days to weeks. LI and CIE are seemingly distinct phenotypes: classic, severe LI with dark brown, plate-like scale with no erythroderma and CIE with finer whiter scale and underlying generalized redness of the skin. Affected individuals with severe involvement can have ectropion, eclabium, scarring alopecia involving the scalp and eyebrows, and palmar and plantar keratoderma. Besides these major forms of nonsyndromic ichthyosis, a few rare subtypes have been recognized, such as bathing suit ichthyosis, self-improving collodion ichthyosis, or ichthyosis-prematurity syndrome.
Bardet-Biedl syndrome 16
MedGen UID:
855172
Concept ID:
C3889474
Disease or Syndrome
BBS16 is an autosomal recessive ciliopathy characterized by retinal degeneration, obesity, renal disease, and cognitive impairment. Although polydactyly is considered a primary feature of BBS overall, it has not been reported in any BBS16 patient (Billingsley et al., 2012). For a general phenotypic description and a discussion of genetic heterogeneity of Bardet-Biedl syndrome, see BBS1 (209900).
Bardet-Biedl syndrome 19
MedGen UID:
855173
Concept ID:
C3889475
Disease or Syndrome
Bardet-Biedl syndrome-19 (BBS19) is an autosomal recessive ciliopathy characterized by obesity, impaired intellectual development, polydactyly, renal failure, retinitis pigmentosa, and hypogonadism (Aldahmesh et al., 2014). For a general phenotypic description and a discussion of genetic heterogeneity of Bardet-Biedl syndrome, see BBS1 (209900).
Bardet-Biedl syndrome 5
MedGen UID:
856141
Concept ID:
C3892039
Disease or Syndrome
BBS5 is a ciliopathy associated with severe and early-onset retinal dystrophy, postaxial polydactyly, obesity, renal dysfunction, hypogonadism, and learning difficulties (summary by Scheidecker et al., 2015). Patients described by Young et al. (1999) and Moore et al. (2005) with mutations in the BBS5 gene did not have polydactyly. The contribution of BBS5 mutations to all cases of BBS has been estimated at 2% (Li et al., 2004) and 0.40% (Zaghloul and Katsanis, 2009). For a general phenotypic description and a discussion of genetic heterogeneity of Bardet-Biedl syndrome, see BBS1 (209900).
RAB23-related Carpenter syndrome
MedGen UID:
1644017
Concept ID:
C4551510
Disease or Syndrome
Carpenter syndrome is a rare autosomal recessive disorder with the cardinal features of acrocephaly with variable synostosis of the sagittal, lambdoid, and coronal sutures; peculiar facies; brachydactyly of the hands with syndactyly; preaxial polydactyly and syndactyly of the feet; congenital heart defects; growth retardation; mental retardation; hypogenitalism; and obesity. In addition, cerebral malformations, oral and dental abnormalities, coxa valga, genu valgum, hydronephrosis, precocious puberty, and hearing loss may be observed (summary by Altunhan et al., 2011). Genetic Heterogeneity of Carpenter Syndrome Carpenter syndrome-2 (CRPT2; 614976), in which the features of Carpenter syndrome are sometimes associated with defective lateralization, is caused by mutation in the MEGF8 gene (604267).
Short stature and microcephaly with genital anomalies
MedGen UID:
1684791
Concept ID:
C5231467
Disease or Syndrome
Short stature and microcephaly with genital anomalies (SSMGA) is characterized by severe growth failure, with extreme short stature, microcephaly, and delayed and dissociated bone age. Global psychomotor developmental delay may be present, although the brain appears structurally normal. Pubertal delay and genital anomalies have been observed (Hung et al., 2017).

Recent clinical studies

Etiology

Mallmann MR, Gembruch U
Arch Gynecol Obstet 2022 Dec;306(6):1847-1862. Epub 2022 Feb 27 doi: 10.1007/s00404-022-06441-3. PMID: 35220478Free PMC Article
López-Soto Á, Meseguer-González JL, Garví-Morcillo J, Beltrán-Sánchez A, Jódar-Pérez Á, Martínez-Rivero I, García-Izquierdo O, Urbano-Reyes M, López-Pérez R, Martínez-Cendán JP
Eur J Obstet Gynecol Reprod Biol 2021 Aug;263:50-55. Epub 2021 Jun 15 doi: 10.1016/j.ejogrb.2021.06.016. PMID: 34167033
Dumeige L, Chatelais L, Bouvattier C, De Kerdanet M, Hyon C, Esteva B, Samara-Boustani D, Zenaty D, Nicolino M, Baron S, Metz-Blond C, Naud-Saudreau C, Dupuis C, Léger J, Siffroi JP, Donadille B, Christin-Maitre S, Carel JC, Coutant R, Martinerie L
Eur J Endocrinol 2018 Sep;179(3):181-190. Epub 2018 Jul 4 doi: 10.1530/EJE-18-0309. PMID: 29973376
Wang S, Shi M, Zhu D, Mathews R, Zheng Z
Urology 2018 Mar;113:179-186. Epub 2017 Nov 16 doi: 10.1016/j.urology.2017.11.002. PMID: 29155192
Hester AG, Kogan SJ
J Pediatr Urol 2017 Oct;13(5):492.e1-492.e5. Epub 2017 Mar 1 doi: 10.1016/j.jpurol.2017.01.019. PMID: 28319024

Diagnosis

Pinson K, Melber DJ, Nguyen NH, Montaney L, Basu R, Mims J, Pretorius D, Lamale-Smith L
J Ultrasound Med 2023 Feb;42(2):293-307. Epub 2022 Aug 16 doi: 10.1002/jum.16080. PMID: 35975397
Işık E, Onay H, Atik T, Solmaz AE, Özen S, Çoğulu Ö, Darcan Ş, Özkınay F
J Clin Res Pediatr Endocrinol 2020 Mar 19;12(1):113-116. Epub 2019 May 15 doi: 10.4274/jcrpe.galenos.2019.2019.0023. PMID: 31088041Free PMC Article
Yan M, Dilihuma J, Luo Y, Reyilanmu B, Shen Y, Mireguli M
J Clin Res Pediatr Endocrinol 2019 May 28;11(2):211-217. Epub 2018 Nov 16 doi: 10.4274/jcrpe.galenos.2018.2018.0197. PMID: 30444213Free PMC Article
Dumeige L, Chatelais L, Bouvattier C, De Kerdanet M, Hyon C, Esteva B, Samara-Boustani D, Zenaty D, Nicolino M, Baron S, Metz-Blond C, Naud-Saudreau C, Dupuis C, Léger J, Siffroi JP, Donadille B, Christin-Maitre S, Carel JC, Coutant R, Martinerie L
Eur J Endocrinol 2018 Sep;179(3):181-190. Epub 2018 Jul 4 doi: 10.1530/EJE-18-0309. PMID: 29973376
Baldinger L, Mudegowdar A, Shukla AR
Clin Perinatol 2014 Sep;41(3):709-24. Epub 2014 Jul 23 doi: 10.1016/j.clp.2014.05.016. PMID: 25155737

Therapy

Wei L, Xie X, Liu J, Zhao Y, Chen W, Zhao C, Wang S, Liao X, Shou Q, Qiu Y, Qiao Y, Saah AJ
Vaccine 2019 Jun 12;37(27):3617-3624. Epub 2018 Aug 16 doi: 10.1016/j.vaccine.2018.08.009. PMID: 30122646
Bernabé KJ, Nokoff NJ, Galan D, Felsen D, Aston CE, Austin P, Baskin L, Chan YM, Cheng EY, Diamond DA, Ellens R, Fried A, Greenfield S, Kolon T, Kropp B, Lakshmanan Y, Meyer S, Meyer T, Delozier AM, Mullins LL, Palmer B, Paradis A, Reddy P, Reyes KJS, Schulte M, Swartz JM, Yerkes E, Wolfe-Christensen C, Wisniewski AB, Poppas DP
J Pediatr Urol 2018 Apr;14(2):157.e1-157.e8. Epub 2018 Feb 2 doi: 10.1016/j.jpurol.2017.11.019. PMID: 29398588Free PMC Article
Adekanye AO, Adefemi SA, Onawola KA, James JA, Adeleke IT, Francis M, Sheshi EU, Atakere ME, Jibril AD
Afr Health Sci 2017 Dec;17(4):1120-1125. doi: 10.4314/ahs.v17i4.20. PMID: 29937883Free PMC Article
Wonkam A, Extermann P, Birraux J, Fokstuen S
Congenit Anom (Kyoto) 2011 Jun;51(2):96-9. doi: 10.1111/j.1741-4520.2010.00291.x. PMID: 20727000
Ozoemena OF, Mbah AU
Niger J Clin Pract 2007 Jun;10(2):120-5. PMID: 17902503

Prognosis

Yan M, Dilihuma J, Luo Y, Reyilanmu B, Shen Y, Mireguli M
J Clin Res Pediatr Endocrinol 2019 May 28;11(2):211-217. Epub 2018 Nov 16 doi: 10.4274/jcrpe.galenos.2018.2018.0197. PMID: 30444213Free PMC Article
Wei L, Xie X, Liu J, Zhao Y, Chen W, Zhao C, Wang S, Liao X, Shou Q, Qiu Y, Qiao Y, Saah AJ
Vaccine 2019 Jun 12;37(27):3617-3624. Epub 2018 Aug 16 doi: 10.1016/j.vaccine.2018.08.009. PMID: 30122646
Dumeige L, Chatelais L, Bouvattier C, De Kerdanet M, Hyon C, Esteva B, Samara-Boustani D, Zenaty D, Nicolino M, Baron S, Metz-Blond C, Naud-Saudreau C, Dupuis C, Léger J, Siffroi JP, Donadille B, Christin-Maitre S, Carel JC, Coutant R, Martinerie L
Eur J Endocrinol 2018 Sep;179(3):181-190. Epub 2018 Jul 4 doi: 10.1530/EJE-18-0309. PMID: 29973376
Hester AG, Kogan SJ
J Pediatr Urol 2017 Oct;13(5):492.e1-492.e5. Epub 2017 Mar 1 doi: 10.1016/j.jpurol.2017.01.019. PMID: 28319024
Baldinger L, Mudegowdar A, Shukla AR
Clin Perinatol 2014 Sep;41(3):709-24. Epub 2014 Jul 23 doi: 10.1016/j.clp.2014.05.016. PMID: 25155737

Clinical prediction guides

Yan M, Dilihuma J, Luo Y, Reyilanmu B, Shen Y, Mireguli M
J Clin Res Pediatr Endocrinol 2019 May 28;11(2):211-217. Epub 2018 Nov 16 doi: 10.4274/jcrpe.galenos.2018.2018.0197. PMID: 30444213Free PMC Article
Dumeige L, Chatelais L, Bouvattier C, De Kerdanet M, Hyon C, Esteva B, Samara-Boustani D, Zenaty D, Nicolino M, Baron S, Metz-Blond C, Naud-Saudreau C, Dupuis C, Léger J, Siffroi JP, Donadille B, Christin-Maitre S, Carel JC, Coutant R, Martinerie L
Eur J Endocrinol 2018 Sep;179(3):181-190. Epub 2018 Jul 4 doi: 10.1530/EJE-18-0309. PMID: 29973376
Matsushita S, Suzuki K, Murashima A, Kajioka D, Acebedo AR, Miyagawa S, Haraguchi R, Ogino Y, Yamada G
Nat Rev Urol 2018 Jun;15(6):358-368. doi: 10.1038/s41585-018-0008-y. PMID: 29670181
Bernabé KJ, Nokoff NJ, Galan D, Felsen D, Aston CE, Austin P, Baskin L, Chan YM, Cheng EY, Diamond DA, Ellens R, Fried A, Greenfield S, Kolon T, Kropp B, Lakshmanan Y, Meyer S, Meyer T, Delozier AM, Mullins LL, Palmer B, Paradis A, Reddy P, Reyes KJS, Schulte M, Swartz JM, Yerkes E, Wolfe-Christensen C, Wisniewski AB, Poppas DP
J Pediatr Urol 2018 Apr;14(2):157.e1-157.e8. Epub 2018 Feb 2 doi: 10.1016/j.jpurol.2017.11.019. PMID: 29398588Free PMC Article
Nemec SF, Nemec U, Weber M, Rotmensch S, Brugger PC, Kasprian G, Krestan CR, Rimoin DL, Graham JM Jr, Prayer D
Ultrasound Obstet Gynecol 2011 Dec;38(6):695-700. Epub 2011 Feb 28 doi: 10.1002/uog.8973. PMID: 21584884

Recent systematic reviews

Grimbizis GF, Di Spiezio Sardo A, Saravelos SH, Gordts S, Exacoustos C, Van Schoubroeck D, Bermejo C, Amso NN, Nargund G, Timmerman D, Athanasiadis A, Brucker S, De Angelis C, Gergolet M, Li TC, Tanos V, Tarlatzis B, Farquharson R, Gianaroli L, Campo R
Hum Reprod 2016 Jan;31(1):2-7. Epub 2015 Nov 4 doi: 10.1093/humrep/dev264. PMID: 26537921
Dietrich JE, Millar DM, Quint EH
J Pediatr Adolesc Gynecol 2014 Dec;27(6):386-95. Epub 2014 Jul 17 doi: 10.1016/j.jpag.2014.07.001. PMID: 25438707
Utomo E, Groen J, Blok BF
Cochrane Database Syst Rev 2014 May 24;(5):CD004927. doi: 10.1002/14651858.CD004927.pub4. PMID: 24859260

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