U.S. flag

An official website of the United States government

Format

Send to:

Choose Destination

Anal stenosis

MedGen UID:
82644
Concept ID:
C0262374
Anatomical Abnormality
Synonym: Anal stricture
SNOMED CT: Stricture of anus (69914001); Anal stricture (69914001)
 
HPO: HP:0002025

Definition

Abnormal narrowing of the anal opening. [from HPO]

Term Hierarchy

Conditions with this feature

Metaphyseal chondrodysplasia, McKusick type
MedGen UID:
67398
Concept ID:
C0220748
Congenital Abnormality
The cartilage-hair hypoplasia – anauxetic dysplasia (CHH-AD) spectrum disorders are a continuum that includes the following phenotypes: Metaphyseal dysplasia without hypotrichosis (MDWH). Cartilage-hair hypoplasia (CHH). Anauxetic dysplasia (AD). CHH-AD spectrum disorders are characterized by severe disproportionate (short-limb) short stature that is usually recognized in the newborn, and occasionally prenatally because of the short extremities. Other findings include joint hypermobility, fine silky hair, immunodeficiency, anemia, increased risk for malignancy, gastrointestinal dysfunction, and impaired spermatogenesis. The most severe phenotype, AD, has the most pronounced skeletal phenotype, may be associated with atlantoaxial subluxation in the newborn, and may include cognitive deficiency. The clinical manifestations of the CHH-AD spectrum disorders are variable, even within the same family.
FG syndrome 1
MedGen UID:
113106
Concept ID:
C0220769
Disease or Syndrome
MED12-related disorders include the phenotypes of FG syndrome type 1 (FGS1), Lujan syndrome (LS), X-linked Ohdo syndrome (XLOS), Hardikar syndrome (HS), and nonspecific intellectual disability (NSID). FGS1 and LS share the clinical findings of cognitive impairment, hypotonia, and abnormalities of the corpus callosum. FGS1 is further characterized by absolute or relative macrocephaly, tall forehead, downslanted palpebral fissures, small and simple ears, constipation and/or anal anomalies, broad thumbs and halluces, and characteristic behavior. LS is further characterized by large head, tall thin body habitus, long thin face, prominent nasal bridge, high narrow palate, and short philtrum. Carrier females in families with FGS1 and LS are typically unaffected. XLOS is characterized by intellectual disability, blepharophimosis, and facial coarsening. HS has been described in females with cleft lip and/or cleft palate, biliary and liver anomalies, intestinal malrotation, pigmentary retinopathy, and coarctation of the aorta. Developmental and cognitive concerns have not been reported in females with HS. Pathogenic variants in MED12 have been reported in an increasing number of males and females with NSID, with affected individuals often having clinical features identified in other MED12-related disorders.
Cerebro-costo-mandibular syndrome
MedGen UID:
120537
Concept ID:
C0265342
Disease or Syndrome
Cerebrocostomandibular syndrome (CCMS) is characterized mainly by severe micrognathia, rib defects, and mental retardation. A spectrum of rib gap defects have been reported ranging from a few dorsal rib segments to complete absence of ossification. In about half of the 65 reported cases to date, there is cerebral involvement including mental retardation, microcephaly, and histologic anomalies. Both autosomal dominant and autosomal recessive forms of the disorder have been described (Zeevaert et al., 2009). See CDG2G (611209) for a cerebrocostomandibular-like syndrome.
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.
Pallister-Killian syndrome
MedGen UID:
120540
Concept ID:
C0265449
Disease or Syndrome
Pallister-Killian syndrome (PKS) is a dysmorphic condition involving most organ systems, but is also characterized by a tissue-limited mosaicism; most fibroblasts have 47 chromosomes with an extra small metacentric chromosome, whereas the karyotype of lymphocytes is normal. The extra metacentric chromosome is an isochromosome for part of the short arm of chromosome 12: i(12)(p10) (Peltomaki et al., 1987; Warburton et al., 1987).
Cat eye syndrome
MedGen UID:
120543
Concept ID:
C0265493
Disease or Syndrome
Cat eye syndrome (CES) is characterized clinically by the combination of coloboma of the iris and anal atresia with fistula, downslanting palpebral fissures, preauricular tags and/or pits, frequent occurrence of heart and renal malformations, and normal or near-normal mental development. A small supernumerary chromosome (smaller than chromosome 21) is present, frequently has 2 centromeres, is bisatellited, and represents an inv dup(22)(q11).
Microcephaly, normal intelligence and immunodeficiency
MedGen UID:
140771
Concept ID:
C0398791
Disease or Syndrome
Nijmegen breakage syndrome (NBS) is characterized by progressive microcephaly, early growth deficiency that improves with age, recurrent respiratory infections, an increased risk for malignancy (primarily lymphoma), and premature ovarian failure in females. Developmental milestones are attained at the usual time during the first year; however, borderline delays in development and hyperactivity may be observed in early childhood. Intellectual abilities tend to decline over time. Recurrent pneumonia and bronchitis may result in respiratory failure and early death. Other reported malignancies include solid tumors (e.g., medulloblastoma, glioma, rhabdomyosarcoma).
Kindler syndrome
MedGen UID:
96060
Concept ID:
C0406557
Disease or Syndrome
Kindler syndrome (KS), a rare subtype of inherited epidermolysis bullosa, is characterized by skin fragility and acral blister formation beginning at birth, diffuse cutaneous atrophy, photosensitivity (most prominent during childhood and usually decreasing after adolescence), poikiloderma, diffuse palmoplantar hyperkeratosis, and pseudosyndactyly. Mucosal manifestations are also common and include hemorrhagic mucositis and gingivitis, periodontal disease, premature loss of teeth, and labial leukokeratosis. Other mucosal findings can include ectropion, urethral stenosis, and severe phimosis. Severe long-term complications of KS include periodontitis, mucosal strictures, and aggressive squamous cell carcinomas. Manifestations can range from mild to severe.
Osteopathia striata with cranial sclerosis
MedGen UID:
96590
Concept ID:
C0432268
Disease or Syndrome
Most females with osteopathia striata with cranial sclerosis (OS-CS) present with macrocephaly and characteristic facial features (frontal bossing, hypertelorism, epicanthal folds, depressed nasal bridge, and prominent jaw). Approximately half have associated features including orofacial clefting and hearing loss, and a minority have some degree of developmental delay (usually mild). Radiographic findings of cranial sclerosis, sclerosis of long bones, and metaphyseal striations (in combination with macrocephaly) can be considered pathognomonic. Males can present with a mild or severe phenotype. Mildly affected males have clinical features similar to affected females, including macrocephaly, characteristic facial features, orofacial clefting, hearing loss, and mild-to-moderate learning delays. Mildly affected males are more likely than females to have congenital or musculoskeletal anomalies. Radiographic findings include cranial sclerosis and sclerosis of the long bones; Metaphyseal striations are more common in males who are mosaic for an AMER1 pathogenic variant. The severe phenotype manifests in males as a multiple-malformation syndrome, lethal in mid-to-late gestation, or in the neonatal period. Congenital malformations include skeletal defects (e.g., polysyndactyly, absent or hypoplastic fibulae), congenital heart disease, and brain, genitourinary, and gastrointestinal anomalies. Macrocephaly is not always present and longitudinal metaphyseal striations have not been observed in severely affected males, except for those who are mosaic for the AMER1 pathogenic variant.
Curry-Jones syndrome
MedGen UID:
167083
Concept ID:
C0795915
Disease or Syndrome
Curry-Jones syndrome is a multisystem disorder characterized by patchy skin lesions, polysyndactyly, diverse cerebral malformations, unicoronal craniosynostosis, iris colobomas, microphthalmia, and intestinal malrotation with myofibromas or hamartomas (summary by Twigg et al., 2016).
Kabuki syndrome
MedGen UID:
162897
Concept ID:
C0796004
Congenital Abnormality
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.
Elsahy-Waters syndrome
MedGen UID:
923028
Concept ID:
C0809936
Disease or Syndrome
The core phenotype of Elsahy-Waters syndrome consists of brachycephaly, facial asymmetry, marked hypertelorism, proptosis, blepharochalasis, midface hypoplasia, broad nose with concave nasal ridge, and prognathism; radicular dentin dysplasia with consequent obliterated pulp chambers, apical translucent cysts, recurrent infections, and early loss of teeth; vertebral fusions, particularly at C2-C3; and moderate mental retardation. Skin wrinkling over the glabellar region seems common, and in males, hypospadias has always been present. Inter- and intrafamilial variability has been reported regarding the presence of vertebral fusions, hearing loss, and dentigerous cysts. Midface hypoplasia, facial asymmetry, progressive dental anomalies, and impaired cognitive development become more evident in adulthood (summary by Castori et al., 2010).
Currarino triad
MedGen UID:
323460
Concept ID:
C1531773
Disease or Syndrome
Currarino syndrome (CS) is a rare congenital disease characterized by the triad of anorectal malformations (ARMs) (usually anal stenosis), presacral mass (commonly anterior sacral meningocele (ASM) or teratoma) and sacral anomalies (i.e. total or partial agenesis of the sacrum and coccyx or deformity of the sacral vertebrae).
Duane-radial ray syndrome
MedGen UID:
301647
Concept ID:
C1623209
Disease or Syndrome
SALL4-related disorders include Duane-radial ray syndrome (DRRS, Okihiro syndrome), acro-renal-ocular syndrome (AROS), and SALL4-related Holt-Oram syndrome (HOS) – three phenotypes previously thought to be distinct entities. DRRS is characterized by uni- or bilateral Duane anomaly and radial ray malformation that can include thenar hypoplasia and/or hypoplasia or aplasia of the thumbs, hypoplasia or aplasia of the radii, shortening and radial deviation of the forearms, triphalangeal thumbs, and duplication of the thumb (preaxial polydactyly). AROS is characterized by radial ray malformations, renal abnormalities (mild malrotation, ectopia, horseshoe kidney, renal hypoplasia, vesicoureteral reflux, bladder diverticula), ocular coloboma, and Duane anomaly. Rarely, pathogenic variants in SALL4 may cause clinically typical HOS (i.e., radial ray malformations and cardiac malformations without additional features).
Axenfeld-Rieger syndrome type 2
MedGen UID:
316937
Concept ID:
C1832229
Disease or Syndrome
Axenfeld-Rieger syndrome is a disorder of morphogenesis that results in abnormal development of the anterior segment of the eye, which results in blindness from glaucoma in approximately 50% of affected individuals. Systemic abnormalities, including cardiac and dental anomalies, are associated. For a general phenotypic description and a discussion of genetic heterogeneity and nomenclature of Axenfeld-Rieger syndrome, see RIEG1 (180500).
Bartsocas-Papas syndrome
MedGen UID:
337894
Concept ID:
C1849718
Disease or Syndrome
Bartsocas-Papas syndrome-1 (BPS1) is an autosomal recessive disorder characterized by multiple popliteal pterygia, ankyloblepharon, filiform bands between the jaws, cleft lip and palate, and syndactyly. Early lethality is common, although survival into childhood and beyond has been reported (summary by Mitchell et al., 2012). Genetic Heterogeneity of Bartsocas-Papas Syndrome Bartsocas-Papas syndrome-2 (BPS2) is caused by mutation in the CHUK gene (600664). A less severe form of popliteal pterygium syndrome (PPS; 119500) is caused by mutation in the IRF6 gene (607199).
Oculotrichoanal syndrome
MedGen UID:
383680
Concept ID:
C1855425
Disease or Syndrome
FREM1 autosomal recessive disorders include: Manitoba oculotrichoanal (MOTA) syndrome, bifid nose with or without anorectal and renal anomalies (BNAR syndrome), and isolated congenital anomalies of kidney and urinary tract (CAKUT). MOTA syndrome is characterized by an aberrant hairline (unilateral or bilateral wedge-shaped extension of the anterior hairline from the temple region to the ipsilateral eye) and anomalies of the eyes (widely spaced eyes, anophthalmia/microphthalmia and/or cryptophthalmos, colobomas of the upper eyelid, and corneopalpebral synechiae), nose (bifid or broad nasal tip), abdominal wall (omphalocele or umbilical hernia), and anus (stenosis and/or anterior displacement of the anal opening). The manifestations and degree of severity vary even among affected members of the same family. Growth and psychomotor development are normal. BNAR syndrome is characterized by a bifid or wide nasal tip, anorectal anomalies, and renal malformations (e.g., renal agenesis, renal dysplasia). Typically the eye manifestations of MOTA syndrome are absent. FREM1-CAKUT was identified in one individual with bilateral vesicoureteral reflux (VUR) and a second individual with VUR and renal hypodysplasia.
Ectrodactyly, ectodermal dysplasia, and cleft lip-palate syndrome 3
MedGen UID:
347666
Concept ID:
C1858562
Disease or Syndrome
The TP63-related disorders comprise six overlapping phenotypes: Ankyloblepharon-ectodermal defects-cleft lip/palate (AEC) syndrome (which includes Rapp-Hodgkin syndrome). Acro-dermo-ungual-lacrimal-tooth (ADULT) syndrome. Ectrodactyly, ectodermal dysplasia, cleft lip/palate syndrome 3 (EEC3). Limb-mammary syndrome. Split-hand/foot malformation type 4 (SHFM4). Isolated cleft lip/cleft palate (orofacial cleft 8). Individuals typically have varying combinations of ectodermal dysplasia (hypohidrosis, nail dysplasia, sparse hair, tooth abnormalities), cleft lip/palate, split-hand/foot malformation/syndactyly, lacrimal duct obstruction, hypopigmentation, hypoplastic breasts and/or nipples, and hypospadias. Findings associated with a single phenotype include ankyloblepharon filiforme adnatum (tissue strands that completely or partially fuse the upper and lower eyelids), skin erosions especially on the scalp associated with areas of scarring, and alopecia, trismus, and excessive freckling.
Ulnar-mammary syndrome
MedGen UID:
357886
Concept ID:
C1866994
Disease or Syndrome
Ulnar-mammary syndrome (UMS) is an autosomal dominant disorder characterized by posterior limb deficiencies or duplications, apocrine/mammary gland hypoplasia and/or dysfunction, abnormal dentition, delayed puberty in males, and genital anomalies (Bamshad et al., 1996).
Syndactyly-telecanthus-anogenital and renal malformations syndrome
MedGen UID:
394424
Concept ID:
C2678045
Disease or Syndrome
Syndrome with the association of toe syndactyly, facial dysmorphism including telecanthus and a broad nasal tip, urogenital malformations and anal atresia. Around ten cases have been reported so far. The syndrome is caused by mutations in the FAM58A gene (located on the X chromosome) encoding a protein of unknown function.
Multiple congenital anomalies-hypotonia-seizures syndrome 1
MedGen UID:
481405
Concept ID:
C3279775
Disease or Syndrome
Multiple congenital anomalies-hypotonia-seizures syndrome is an autosomal recessive disorder characterized by neonatal hypotonia, lack of psychomotor development, seizures, dysmorphic features, and variable congenital anomalies involving the cardiac, urinary, and gastrointestinal systems. Most affected individuals die before 3 years of age (summary by Maydan et al., 2011). The disorder is caused by a defect in glycosylphosphatidylinositol biosynthesis; see GPIBD1 (610293). Genetic Heterogeneity of Multiple Congenital Anomalies-Hypotonia-Seizures Syndrome MCAHS2 (300868) is caused by mutation in the PIGA gene (311770) on chromosome Xp22, MCAHS3 (615398) is caused by mutation in the PIGT gene (610272) on chromosome 20q13, and MCAHS4 (618548) is caused by mutation in the PIGQ gene (605754) on chromosome 16p13. Knaus et al. (2018) provided a review of the main clinical features of the different types of MCAHS, noting that patients with mutations in the PIGN, PIGA, and PIGT genes have distinct patterns of facial anomalies that can be detected by computer-assisted comparison. Some individuals with MCAHS may have variable increases in alkaline phosphatase (AP) as well as variable decreases in GPI-linked proteins that can be detected by flow cytometry. However, there was no clear correlation between AP levels or GPI-linked protein abnormalities and degree of neurologic involvement, mutation class, or gene involved. Knaus et al. (2018) concluded that a distinction between MCAHS and HPMRS1 (239300), which is also caused by mutation in genes involved in GPI biosynthesis, may be artificial and even inaccurate, and that all these disorders should be considered and classified together under the more encompassing term of 'GPI biosynthesis defects' (GPIBD).
Hyperphosphatasia with intellectual disability syndrome 2
MedGen UID:
766551
Concept ID:
C3553637
Disease or Syndrome
Hyperphosphatasia with impaired intellectual development syndrome-2 (HPMRS2) is an autosomal recessive disorder characterized by moderately to severely delayed psychomotor development, facial dysmorphism, brachytelephalangy, and increased serum alkaline phosphatase (hyperphosphatasia). Some patients may have additional features, such as cardiac septal defects or seizures (summary by Krawitz et al., 2012). The disorder is caused by a defect in glycosylphosphatidylinositol (GPI) biosynthesis. For a discussion of genetic heterogeneity of hyperphosphatasia with impaired intellectual development syndrome, see HPMRS1 (239300). For a discussion of genetic heterogeneity of GPI biosynthesis defects, see GPIBD1 (610293).
Axenfeld-Rieger syndrome type 1
MedGen UID:
811487
Concept ID:
C3714873
Disease or Syndrome
Axenfeld-Rieger syndrome is an autosomal dominant disorder of morphogenesis that results in abnormal development of the anterior segment of the eye, and results in blindness from glaucoma in approximately 50% of affected individuals (Fitch and Kaback, 1978). Systemic anomalies are associated, including dental hypoplasia, failure of involution of periumbilical skin, and maxillary hypoplasia (Alkemade, 1969). Genetic Heterogeneity of Axenfeld-Rieger Syndrome Linkage studies indicate that a second type of Axenfeld-Rieger syndrome maps to chromosome 13q14 (RIEG2; 601499). A third form of Axenfeld-Rieger syndrome (RIEG3; 602482) is caused by mutation in the FOXC1 gene (601090) on chromosome 6p25. See 109120 for a form of Axenfeld-Rieger syndrome associated with partially absent eye muscles, hydrocephalus, and skeletal abnormalities.
Meier-Gorlin syndrome 7
MedGen UID:
934705
Concept ID:
C4310738
Disease or Syndrome
Any Meier-Gorlin syndrome in which the cause of the disease is a mutation in the CDC45 gene.
Townes-Brocks syndrome 1
MedGen UID:
1635275
Concept ID:
C4551481
Disease or Syndrome
Townes-Brocks syndrome (TBS) is characterized by the triad of imperforate anus (84%), dysplastic ears (87%; overfolded superior helices and preauricular tags; frequently associated with sensorineural and/or conductive hearing impairment [65%]), and thumb malformations (89%; triphalangeal thumbs, duplication of the thumb [preaxial polydactyly], and rarely hypoplasia of the thumbs). Renal impairment (42%), including end-stage renal disease (ESRD), may occur with or without structural abnormalities (mild malrotation, ectopia, horseshoe kidney, renal hypoplasia, polycystic kidneys, vesicoutereral reflux). Congenital heart disease occurs in 25%. Foot malformations (52%; flat feet, overlapping toes) and genitourinary malformations (36%) are common. Intellectual disability occurs in approximately 10% of individuals. Rare features include iris coloboma, Duane anomaly, Arnold-Chiari malformation type 1, and growth retardation.

Recent clinical studies

Etiology

Lorenzo C, Travessa AM, Ferreira AC, Modamio-Høybjør S, Heath KE, Pereira C
Am J Med Genet A 2023 Jan;191(1):280-283. Epub 2022 Sep 26 doi: 10.1002/ajmg.a.62980. PMID: 36164748
Gallo G, Picciariello A, Di Tanna GL, Pelizzo P, Altomare DF, Trompetto M, Santoro GA, Roviello F, Felice C, Grossi U
Colorectal Dis 2022 Dec;24(12):1462-1471. Epub 2022 Jul 31 doi: 10.1111/codi.16248. PMID: 35792887
Gallo G, Stratta E, Realis Luc A, Clerico G, Trompetto M
Colorectal Dis 2020 Oct;22(10):1388-1395. Epub 2020 Jun 10 doi: 10.1111/codi.15118. PMID: 32401371
Halleran DR, Sanchez AV, Rentea RM, Ahmad H, Weaver L, Reck C, Gasior AC, Levitt MA, Wood RJ
J Pediatr Surg 2019 Jan;54(1):118-122. Epub 2018 Oct 5 doi: 10.1016/j.jpedsurg.2018.10.006. PMID: 30366721
Gülen M, Leventoğlu S, Ege B, Menteş BB
Dis Colon Rectum 2016 Mar;59(3):230-5. doi: 10.1097/DCR.0000000000000530. PMID: 26855398

Diagnosis

Bizimana W, Kaukone R, Jerguigue H, Latib R, Omor Y
Pan Afr Med J 2020;37:195. Epub 2020 Oct 29 doi: 10.11604/pamj.2020.37.195.23625. PMID: 33505564Free PMC Article
Chiarelli M, Guttadauro A, Maternini M, Lo Bianco G, Tagliabue F, Achilli P, Terragni S, Gabrielli F
Ann Ital Chir 2018;89:237-241. PMID: 30588920
Durchschein F, Schreiber F, Högenauer C
Endoscopy 2014;46 Suppl 1 UCTN:E529-30. Epub 2014 Nov 19 doi: 10.1055/s-0034-1377640. PMID: 25409054
Katdare MV, Ricciardi R
Surg Clin North Am 2010 Feb;90(1):137-45, Table of Contents. doi: 10.1016/j.suc.2009.10.002. PMID: 20109638
Brisinda G, Vanella S, Cadeddu F, Marniga G, Mazzeo P, Brandara F, Maria G
World J Gastroenterol 2009 Apr 28;15(16):1921-8. doi: 10.3748/wjg.15.1921. PMID: 19399922Free PMC Article

Therapy

Iida Y, Honda K, Iida R, Saitou H, Munemoto Y, Tanaka A, Tanaka H
J Visc Surg 2022 Aug;159(4):267-272. Epub 2021 Jul 21 doi: 10.1016/j.jviscsurg.2021.07.002. PMID: 34303637
Acar T, Acar N, Tosun F, Ayaroğlu Ç, Haciyanli M
Tech Coloproctol 2020 Mar;24(3):261-262. Epub 2020 Jan 14 doi: 10.1007/s10151-019-02139-y. PMID: 31939044
Chiarelli M, Guttadauro A, Maternini M, Lo Bianco G, Tagliabue F, Achilli P, Terragni S, Gabrielli F
Ann Ital Chir 2018;89:237-241. PMID: 30588920
Asfar S
World J Surg 2018 Sep;42(9):3015-3020. doi: 10.1007/s00268-018-4561-6. PMID: 29508023
Gülen M, Leventoğlu S, Ege B, Menteş BB
Dis Colon Rectum 2016 Mar;59(3):230-5. doi: 10.1097/DCR.0000000000000530. PMID: 26855398

Prognosis

Tajima Y, Hanai T, Katsuno H, Masumori K, Koide Y, Ashida K, Matsuoka H, Hiro J, Endo T, Kamiya T, Chong Y, Maeda K, Uyama I
World J Surg Oncol 2021 Jan 13;19(1):14. doi: 10.1186/s12957-021-02121-9. PMID: 33441169Free PMC Article
Asfar S
World J Surg 2018 Sep;42(9):3015-3020. doi: 10.1007/s00268-018-4561-6. PMID: 29508023
Lane VA, Wood RJ, Reck C, Skerritt C, Levitt MA
Tech Coloproctol 2016 Apr;20(4):249-54. Epub 2016 Feb 22 doi: 10.1007/s10151-016-1435-5. PMID: 26902368
Gülen M, Leventoğlu S, Ege B, Menteş BB
Dis Colon Rectum 2016 Mar;59(3):230-5. doi: 10.1097/DCR.0000000000000530. PMID: 26855398
Duieb Z, Appu S, Hung K, Nguyen H
ANZ J Surg 2010 May;80(5):337-40. doi: 10.1111/j.1445-2197.2009.05044.x. PMID: 20557507

Clinical prediction guides

Gallo G, Picciariello A, Di Tanna GL, Pelizzo P, Altomare DF, Trompetto M, Santoro GA, Roviello F, Felice C, Grossi U
Colorectal Dis 2022 Dec;24(12):1462-1471. Epub 2022 Jul 31 doi: 10.1111/codi.16248. PMID: 35792887
Iida Y, Honda K, Iida R, Saitou H, Munemoto Y, Tanaka A, Tanaka H
J Visc Surg 2022 Aug;159(4):267-272. Epub 2021 Jul 21 doi: 10.1016/j.jviscsurg.2021.07.002. PMID: 34303637
Gallo G, Stratta E, Realis Luc A, Clerico G, Trompetto M
Colorectal Dis 2020 Oct;22(10):1388-1395. Epub 2020 Jun 10 doi: 10.1111/codi.15118. PMID: 32401371
Asfar S
World J Surg 2018 Sep;42(9):3015-3020. doi: 10.1007/s00268-018-4561-6. PMID: 29508023
Gülen M, Leventoğlu S, Ege B, Menteş BB
Dis Colon Rectum 2016 Mar;59(3):230-5. doi: 10.1097/DCR.0000000000000530. PMID: 26855398

Recent systematic reviews

Lie H, Caesarini EF, Purnama AA, Irawan A, Sudirman T, Jeo WS, Budiono BP, Prabowo E, Rivai MI, Sitepu RK
Lasers Med Sci 2022 Dec;37(9):3621-3630. Epub 2022 Sep 12 doi: 10.1007/s10103-022-03643-8. PMID: 36094598
Gallo G, Picciariello A, Di Tanna GL, Pelizzo P, Altomare DF, Trompetto M, Santoro GA, Roviello F, Felice C, Grossi U
Colorectal Dis 2022 Dec;24(12):1462-1471. Epub 2022 Jul 31 doi: 10.1111/codi.16248. PMID: 35792887
Pathak M, Saxena AK
Pediatr Surg Int 2020 Nov;36(11):1299-1307. Epub 2020 Sep 26 doi: 10.1007/s00383-020-04748-3. PMID: 32980932
Du T, Quan S, Dong T, Meng Q
Int J Colorectal Dis 2019 Jun;34(6):1001-1012. Epub 2019 Mar 30 doi: 10.1007/s00384-019-03288-0. PMID: 30929052
Han Y, Xia Z, Guo S, Yu X, Li Z
PLoS One 2017;12(1):e0170421. Epub 2017 Jan 18 doi: 10.1371/journal.pone.0170421. PMID: 28099464Free PMC Article

Supplemental Content

Table of contents

    Clinical resources

    Consumer resources

    Recent activity

    Your browsing activity is empty.

    Activity recording is turned off.

    Turn recording back on

    See more...
    Support Center