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Duodenal ulcer

MedGen UID:
Concept ID:
Disease or Syndrome
Synonym: Duodenal ulcer (disease)
SNOMED CT: Duodenal ulcer (51868009); DU - Duodenal ulcer (51868009); Ulcer of duodenum (51868009); DUD - Duodenal ulcer disease (51868009); Duodenal ulcer disease (51868009)
HPO: HP:0002588
Monarch Initiative: MONDO:0005412


An erosion of the mucous membrane in a portion of the duodenum. [from HPO]

Term Hierarchy

Conditions with this feature

Duodenal ulcer, hyperpepsinogenemic 1
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Disease or Syndrome
Duodenal ulcer due to antral G-cell hyperfunction
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Disease or Syndrome
Tremor-nystagmus-duodenal ulcer syndrome
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Disease or Syndrome
A rare hyperkinetic movement disorder with characteristics of mild to severe, progressive essential tremor, nystagmus (principally horizontal), duodenal ulceration and a narcolepsy-like sleep disturbance. Refractive errors and cerebellar signs such as gait ataxia and adiadochokinesia may be associated. There have been no further descriptions in the literature since 1976.
Plasminogen deficiency, type I
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Disease or Syndrome
Congenital plasminogen deficiency is a rare autosomal recessive disorder characterized clinically by chronic mucosal pseudomembranous lesions consisting of subepithelial fibrin deposition and inflammation. The most common clinical manifestation is ligneous ('wood-like') conjunctivitis, a redness and subsequent formation of pseudomembranes mostly on the palpebral surfaces of the eye that progress to white, yellow-white, or red thick masses with a wood-like consistency that replace the normal mucosa. The lesions may be triggered by local injury and/or infection and often recur after local excision. Pseudomembranous lesions of other mucous membranes often occur in the mouth, nasopharynx, trachea, and female genital tract. Some affected children also have congenital occlusive hydrocephalus. A slightly increased female:male ratio has been observed (1.4:1 to 2:1) (Schuster and Seregard, 2003; Tefs et al., 2006). Type I plasminogen deficiency is characterized by decreased serum plasminogen activity, decreased plasminogen antigen levels, and clinical symptoms, whereas type II plasminogen deficiency, also known as 'dysplasminogenemia,' is characterized by decreased plasminogen activity with normal or slightly reduced antigen levels. Patients with type II deficiency are usually asymptomatic. Ligneous conjunctivitis and pseudomembranous formation has only been associated with type I plasminogen deficiency. Presumably, normal amounts of plasminogen antigen with decreased activity, as seen in type II, is sufficient for normal wound healing (Schuster and Seregard, 2003).
Coffin-Siris syndrome 1
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Disease or Syndrome
Coffin-Siris syndrome (CSS) is classically characterized by aplasia or hypoplasia of the distal phalanx or nail of the fifth and additional digits, developmental or cognitive delay of varying degree, distinctive facial features, hypotonia, hirsutism/hypertrichosis, and sparse scalp hair. Congenital anomalies can include malformations of the cardiac, gastrointestinal, genitourinary, and/or central nervous systems. Other findings commonly include feeding difficulties, slow growth, ophthalmologic abnormalities, and hearing impairment.
Spondylo-ocular syndrome
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Disease or Syndrome
Spondylo-ocular syndrome is a very rare association of spinal and ocular manifestations that is characterized by dense cataracts, and retinal detachment along with generalized osteoporosis and platyspondyly. Mild craniofacial dysphormism has been reported including short neck, large head and prominent eyebrows.
Hyper-IgE recurrent infection syndrome 1, autosomal dominant
MedGen UID:
Concept ID:
Disease or Syndrome
STAT3 hyper IgE syndrome (STAT3-HIES) is a primary immune deficiency syndrome characterized by elevated serum IgE, eczema, and recurrent skin and respiratory tract infections, together with several nonimmune features. This disorder typically manifests in the newborn period with a rash (often diagnosed as eosinophilic pustulosis) that subsequently evolves into an eczematoid dermatitis. Recurrent staphylococcal skin boils and bacterial pneumonias usually manifest in the first years of life. Pneumatoceles and bronchiectasis often result from aberrant healing of pneumonias. Mucocutaneous candidiasis is common. Nonimmune features may include retained primary teeth, scoliosis, bone fractures following minimal trauma, joint hyperextensibility, and characteristic facial appearance, which typically emerges in adolescence. Vascular abnormalities have been described and include middle-sized artery tortuosity and aneurysms, with infrequent clinical sequelae of myocardial infarction and subarachnoid hemorrhage. Gastrointestinal (GI) manifestations include gastroesophageal reflux disease, esophageal dysmotility, and spontaneous intestinal perforations (some of which are associated with diverticuli). Fungal infections of the GI tract (typically histoplasmosis, Cryptococcus, and Coccidioides) also occur infrequently. Survival is typically into adulthood, with most individuals now living into or past the sixth decade. Most deaths are associated with gram-negative (Pseudomonas) or filamentous fungal pneumonias resulting in hemoptysis. Lymphomas occur at an increased frequency.
Menke-Hennekam syndrome 2
MedGen UID:
Concept ID:
Disease or Syndrome
Menke-Hennekam syndrome-2 (MKHK2) is a congenital disorder characterized by variable impairment of intellectual development and facial dysmorphisms. Feeding difficulties, autistic behavior, recurrent upper airway infections, and hearing impairment are also frequently seen. Although mutations in the same gene cause Rubinstein-Taybi syndrome-2 (RSTS2; 613684), patients with MKHK1 do not resemble the striking phenotype of RSTS2. For a discussion of genetic heterogeneity of Menke-Hennekam syndrome, see MKHK1 (618332).
Immunodeficiency 82 with systemic inflammation
MedGen UID:
Concept ID:
Disease or Syndrome
Immunodeficiency-82 with systemic inflammation (IMD82) is a complex autosomal dominant immunologic disorder characterized by recurrent infections with various organisms, as well as noninfectious inflammation manifest as lymphocytic organ infiltration with gastritis, colitis, and lung, liver, CNS, or skin disease. One of the more common features is inflammation of the stomach and bowel. Most patients develop symptoms in infancy or early childhood; the severity is variable. There may be accompanying fever, elevated white blood cell count, decreased B cells, hypogammaglobulinemia, increased C-reactive protein (CRP; 123260), and a generalized hyperinflammatory state. Immunologic workup shows variable B- and T-cell abnormalities such as skewed subgroups. Patients have a propensity for the development of lymphoma, usually in adulthood. At the molecular level, the disorder results from a gain-of-function mutation that leads to constitutive and enhanced activation of the intracellular inflammatory signaling pathway. Treatment with SYK inhibitors rescued human cell abnormalities and resulted in clinical improvement in mice (Wang et al., 2021).
Cytosolic phospholipase-A2 alpha deficiency associated bleeding disorder
MedGen UID:
Concept ID:
Disease or Syndrome
Recurrent gastrointestinal ulceration with dysfunctional platelets (GURDP) is an autosomal recessive disorder characterized by onset of severe gastrointestinal mucosal ulceration in early childhood. Affected individuals may have secondary iron deficiency anemia or malnourishment. Studies of platelet aggregation show a functional defect associated with decreased thromboxane-A2 production and decreased eicosanoid biosynthesis. The gastrointestinal disease is believed to result from decreased or absent production of prostaglandins that protect the gut mucosa (summary by Adler et al., 2008 and Faioni et al., 2014).

Professional guidelines


Expert Panel on Gastrointestinal Imaging, Vij A, Zaheer A, Kamel IR, Porter KK, Arif-Tiwari H, Bashir MR, Fung A, Goldstein A, Herr KD, Kamaya A, Kobi M, Landler MP, Russo GK, Thakrar KH, Turturro MA, Wahab SA, Wardrop RM 3rd, Wright CL, Yang X, Carucci LR
J Am Coll Radiol 2021 Nov;18(11S):S330-S339. doi: 10.1016/j.jacr.2021.08.006. PMID: 34794592
de Brito BB, da Silva FAF, Soares AS, Pereira VA, Santos MLC, Sampaio MM, Neves PHM, de Melo FF
World J Gastroenterol 2019 Oct 7;25(37):5578-5589. doi: 10.3748/wjg.v25.i37.5578. PMID: 31602159Free PMC Article
Satoh K, Yoshino J, Akamatsu T, Itoh T, Kato M, Kamada T, Takagi A, Chiba T, Nomura S, Mizokami Y, Murakami K, Sakamoto C, Hiraishi H, Ichinose M, Uemura N, Goto H, Joh T, Miwa H, Sugano K, Shimosegawa T
J Gastroenterol 2016 Mar;51(3):177-94. Epub 2016 Feb 15 doi: 10.1007/s00535-016-1166-4. PMID: 26879862

Recent clinical studies


Malik M, Magsi AM, Parveen S, Khan MI, Iqbal M
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Endoscopy 1985 May;17(3):94-8. doi: 10.1055/s-2007-1018469. PMID: 4006874

Clinical prediction guides

Malik M, Magsi AM, Parveen S, Khan MI, Iqbal M
J Pak Med Assoc 2023 Jul;73(7):1506-1510. doi: 10.47391/JPMA.4768. PMID: 37469068
Mignon M, Vallot T
Aliment Pharmacol Ther 1993;7 Suppl 1:37-40, discussion 61-6. doi: 10.1111/j.1365-2036.1993.tb00587.x. PMID: 8490078
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Recent systematic reviews

Clinch D, Damaskos D, Di Marzo F, Di Saverio S
J Trauma Acute Care Surg 2021 Oct 1;91(4):748-758. doi: 10.1097/TA.0000000000003357. PMID: 34254960
Huang HB, Jiang W, Wang CY, Qin HY, Du B
Crit Care 2018 Jan 28;22(1):20. doi: 10.1186/s13054-017-1937-1. PMID: 29374489Free PMC Article
Prescrire Int 2016 Jan;25(167):18-23. PMID: 26942258
Tomtitchong P, Siribumrungwong B, Vilaichone RK, Kasetsuwan P, Matsukura N, Chaiyakunapruk N
Helicobacter 2012 Apr;17(2):148-52. doi: 10.1111/j.1523-5378.2011.00928.x. PMID: 22404446
Leontiadis GI, Moayyedi P, Ford AC
BMJ Clin Evid 2009 Oct 1;2009 PMID: 21718575Free PMC Article

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