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Skin ulcer

MedGen UID:
Concept ID:
Disease or Syndrome
Synonyms: Skin Ulcer; Skin Ulcers; Ulcer, Skin; Ulcers, Skin
SNOMED CT: Skin ulcer (46742003); Cutaneous ulcer (46742003)
HPO: HP:0200042


A discontinuity of the skin exhibiting complete loss of the epidermis and often portions of the dermis and even subcutaneous fat. [from HPO]

Conditions with this feature

Chilblain lupus 1
MedGen UID:
Concept ID:
Disease or Syndrome
Chilblain lupus is a cutaneous form of systemic lupus erythematosus (SLE; 152700) characterized by the appearance of painful bluish-red papular or nodular lesions of the skin in acral locations (including the dorsal aspects of fingers and toes, heels, nose, cheeks, ears, and, in some cases, knees) precipitated by cold and wet exposure (summary by Lee-Kirsch et al., 2006). Genetic Heterogeneity of Chilblain Lupus See also CHBL2 (614415), caused by mutation in the SAMHD1 gene (606754) on chromosome 20q11. Mutations in the TREX1 and SAMHD1 genes also cause Aicardi-Goutieres syndrome (AGS1, 225750 and AGS5, 612952, respectively).
Prolidase deficiency
MedGen UID:
Concept ID:
Disease or Syndrome
Prolidase deficiency is characterized by skin lesions (typically severe, chronic, recalcitrant, and painful skin ulcers of the lower extremities and telangiectasias of the face and hands), recurrent infections (particularly of the skin and respiratory tract), dysmorphic facial features, variable intellectual disability, and organomegaly (typically splenomegaly but occasionally associated with hepatomegaly) with elevated liver enzymes. Skeletal anomalies, chronic pulmonary disease, anemia, thrombocytopenia, hypergammaglobulinemia, and hypocomplementemia are observed in a minority of affected individuals. An association between prolidase deficiency and autoimmune conditions – particularly systemic lupus erythematosus (SLE) – has been described.
Leukocyte adhesion deficiency 1
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Concept ID:
Disease or Syndrome
Leukocyte adhesion deficiency (LAD) is an autosomal recessive disorder of neutrophil function resulting from a deficiency of the beta-2 integrin subunit of the leukocyte cell adhesion molecule. The leukocyte cell adhesion molecule is present on the surface of peripheral blood mononuclear leukocytes and granulocytes and mediates cell-cell and cell-extracellular matrix adhesion. LAD is characterized by recurrent bacterial infections; impaired pus formation and wound healing; abnormalities of a wide variety of adhesion-dependent functions of granulocytes, monocytes, and lymphocytes; and a lack of beta-2/alpha-L, beta-2/alpha-M, and beta-2/alpha-X expression. Genetic Heterogeneity of Leukocyte Adhesion Deficiency Also see LAD2 (266265), caused by mutation in the SLC35C1 gene (605881), and LAD3 (612840), caused by mutation in the FERMT3 gene (607901).
Laryngo-onycho-cutaneous syndrome
MedGen UID:
Concept ID:
Disease or Syndrome
Junctional epidermolysis bullosa 2C (JEB2C), also known as laryngoonychocutaneous syndrome (LOCS), is an autosomal recessive disorder characterized by skin erosions, nail dystrophy, dental anomalies, and excessive vascular granulation tissue of the conjunctiva and larynx. Onset is characterized by a hoarse cry soon after birth. Beginning in infancy, chronic skin ulcers and conjunctival lesions appear. Patients may die in childhood secondary to acute or chronic respiratory obstruction. Long-term survivors have visual loss and often require tracheostomy (McLean et al., 2003). For a discussion of genetic heterogeneity of the subtypes of JEB, see JEB1A (226650). Reviews Has et al. (2020) reviewed the clinical and genetic aspects, genotype-phenotype correlations, disease-modifying factors, and natural history of epidermolysis bullosa.
MHC class I deficiency
MedGen UID:
Concept ID:
Disease or Syndrome
Bare lymphocyte syndrome type I (BLS I) is an inherited disorder of the immune system (primary immunodeficiency). Immunodeficiencies are conditions in which the immune system is not able to protect the body effectively from foreign invaders such as bacteria or viruses. Starting in childhood, most people with BLS I develop recurrent bacterial infections in the lungs and airways (respiratory tract). These recurrent infections can lead to a condition called bronchiectasis, which damages the passages leading from the windpipe to the lungs (bronchi) and can cause breathing problems.\n\nMany people with BLS I also have open sores (ulcers) on their skin, usually on the face, arms, and legs. These ulcers typically develop in adolescence or young adulthood. Some people with BLS I have no symptoms of the condition.\n\nPeople with BLS I have a shortage of specialized immune proteins called major histocompatibility complex (MHC) class I proteins on cells, including infection-fighting white blood cells (lymphocytes), which is where the condition got its name.
Neuropathy, hereditary sensory and autonomic, type 1C
MedGen UID:
Concept ID:
Disease or Syndrome
Hereditary sensory and autonomic neuropathy type IC (HSAN1C) is an autosomal dominant neurologic disorder characterized by sensory neuropathy with variable autonomic and motor involvement. Most patients have adult onset of slowly progressive distal sensory impairment manifest as numbness, tingling, or pain, as well as distal muscle atrophy. Complications include ulceration and osteomyelitis. Some patients may have a more severe phenotype with onset in childhood. Electrophysiologic studies show a predominantly axonal neuropathy with some demyelinating features. Some patients may have evidence of central nervous system involvement, including macular telangiectasia type 2 and/or pyramidal signs. Affected individuals have increased levels of plasma 1-deoxysphingolipids (1-deoxySLs), which are thought to be neurotoxic. (summary by Rotthier et al., 2010, Gantner et al., 2019, and Triplett et al., 2019). Oral supplementation with serine decreases 1-deoxySL and may offer some clinical benefits (Fridman et al., 2019). For a discussion of genetic heterogeneity of HSAN, see HSAN1A (162400).
Granulomatosis with polyangiitis
MedGen UID:
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Disease or Syndrome
Granulomatosis with polyangiitis, formerly termed Wegener granulomatosis, is a systemic disease with a complex genetic background. It is characterized by necrotizing granulomatous inflammation of the upper and lower respiratory tract, glomerulonephritis, vasculitis, and the presence of antineutrophil cytoplasmatic autoantibodies (ANCAs) in patient sera. These ANCAs are antibodies to a defined target antigen, proteinase-3 (PR3, PRTN3; 177020), which is present within primary azurophil granules of neutrophils (PMNs) and lysozymes of monocytes. On cytokine priming of PMNs, PR3 translocates to the cell surface, where PR3-ANCAs can interact with their antigens and activate PMNs. PMNs from patients with active GPA express PR3 on their surface, produce respiratory burst, and release proteolytic enzymes after activation with PR3-ANCAs. The consequence is a self-sustaining inflammatory process (Jagiello et al., 2004).
Vasculitis due to ADA2 deficiency
MedGen UID:
Concept ID:
Disease or Syndrome
Adenosine deaminase 2 deficiency (DADA2) is a complex systemic autoinflammatory disorder in which vasculopathy/vasculitis, dysregulated immune function, and/or hematologic abnormalities may predominate. Inflammatory features include intermittent fevers, rash (often livedo racemosa/reticularis), and musculoskeletal involvement (myalgia/arthralgia, arthritis, myositis). Vasculitis, which usually begins before age ten years, may manifest as early-onset ischemic (lacunar) and/or hemorrhagic strokes, or as cutaneous or systemic polyarteritis nodosa. Hypertension and hepatosplenomegaly are often found. More severe involvement may lead to progressive central neurologic deficits (dysarthria, ataxia, cranial nerve palsies, cognitive impairment) or to ischemic injury to the kidney, intestine, and/or digits. Dysregulation of immune function can lead to immunodeficiency or autoimmunity of varying severity; lymphadenopathy may be present and some affected individuals have had lymphoproliferative disease. Hematologic disorders may begin early in life or in late adulthood, and can include lymphopenia, neutropenia, pure red cell aplasia, thrombocytopenia, or pancytopenia. Of note, both interfamilial and intrafamilial phenotypic variability (e.g., in age of onset, frequency and severity of manifestations) can be observed; also, individuals with biallelic ADA2 pathogenic variants may remain asymptomatic until adulthood or may never develop clinical manifestations of DADA2.
Disabling pansclerotic morphea of childhood
MedGen UID:
Concept ID:
Disease or Syndrome
Disabling pansclerotic morphea of childhood is the most severe subtype of deep morphea within the spectrum of juvenile localized scleroderma. Patients affected by this systemic inflammatory disorder experience poor wound healing with rapidly progressive deep fibrosis involving the mucous membranes, dermis, subcutaneous fat, fascia, muscles, and bone, leading to contractures, musculoskeletal atrophy, and articular ankylosis. Systemic manifestations include cytopenias and hypogammaglobulinemia, but scleroderma-associated autoantibodies are usually not present. The disorder is associated with high morbidity and mortality due to squamous cell carcinoma, restrictive pulmonary disease, sepsis, and gangrene (Baghdassarian et al., 2023).
Blau syndrome
MedGen UID:
Concept ID:
Disease or Syndrome
Blau syndrome is characterized by the triad of granulomatous arthritis, uveitis, and dermatitis. First described in 1985, it was considered to be distinct from sarcoidosis due to the early age of onset and autosomal dominant inheritance pattern. Published reports of sporadic cases of children with 'early-onset sarcoidosis' (EOS) with granulomatous involvement of different organs, primarily affecting joints, eyes, and skin, were suspected to represent the same disorder because the patients' characteristics were nearly identical. Subsequently, identical NOD2 mutations were identified in patients with Blau syndrome as well as in patients diagnosed with EOS, confirming earlier suspicions that they represented the same disease (summary by Borzutzky et al., 2010). Unlike older children diagnosed with sarcoidosis, these patients have no apparent pulmonary involvement; however, the disease is progressive and may result in severe complications such as blindness and/or joint destruction (Shetty and Gedalia, 1998).

Professional guidelines


Garcіa-Fernandez FP, Soldevilla-Agreda JJ, Rodriguez-Palma M, Parra-Anguita L, Pancorbo-Hidalgo PL
J Tissue Viability 2022 Nov;31(4):575-578. Epub 2022 Sep 24 doi: 10.1016/j.jtv.2022.09.005. PMID: 36175255
Machado RS, Viana S, Sbruzzi G
Lasers Med Sci 2017 May;32(4):937-944. Epub 2017 Jan 23 doi: 10.1007/s10103-017-2150-9. PMID: 28116536
Woo KY
Int Wound J 2014 Aug;11(4):431-7. Epub 2014 Mar 16 doi: 10.1111/iwj.12237. PMID: 24629019Free PMC Article

Recent clinical studies


Shavit E, Alavi A
Adv Skin Wound Care 2022 Jun 1;35(6):306-313. doi: 10.1097/01.ASW.0000826864.20824.b5. PMID: 35703852
Hashemi DA, Rosenbach M
JAMA Dermatol 2019 Feb 1;155(2):238. doi: 10.1001/jamadermatol.2018.3597. PMID: 30566195
Powers JG, Higham C, Broussard K, Phillips TJ
J Am Acad Dermatol 2016 Apr;74(4):607-25; quiz 625-6. doi: 10.1016/j.jaad.2015.08.070. PMID: 26979353
Willenborg S, Eming SA
J Dtsch Dermatol Ges 2014 Mar;12(3):214-21, 214-23. doi: 10.1111/ddg.12290. PMID: 24580874
Jung P, Trautinger F
J Dtsch Dermatol Ges 2013 Aug;11(8):731-6. Epub 2013 Jun 5 doi: 10.1111/ddg.12137. PMID: 23738531


Frech TM, Frech M, Saknite I, O'Connell KA, Ghosh S, Baba J, Tkaczyk ER
Best Pract Res Clin Rheumatol 2022 Dec;36(4):101813. Epub 2023 Jan 5 doi: 10.1016/j.berh.2022.101813. PMID: 36609122
Shavit E, Alavi A
Adv Skin Wound Care 2022 Jun 1;35(6):306-313. doi: 10.1097/01.ASW.0000826864.20824.b5. PMID: 35703852
Hashemi DA, Rosenbach M
JAMA Dermatol 2019 Feb 1;155(2):238. doi: 10.1001/jamadermatol.2018.3597. PMID: 30566195
Papi M, Papi C
Int J Low Extrem Wounds 2016 Mar;15(1):6-16. Epub 2015 Dec 11 doi: 10.1177/1534734615621220. PMID: 26657344
Hoffman MD
Dermatol Ther 2013 May-Jun;26(3):222-35. doi: 10.1111/dth.12048. PMID: 23742283


Shavit E, Alavi A
Adv Skin Wound Care 2022 Jun 1;35(6):306-313. doi: 10.1097/01.ASW.0000826864.20824.b5. PMID: 35703852
Hughes M, Pauling JD
Semin Arthritis Rheum 2019 Apr;48(5):888-894. Epub 2018 Aug 11 doi: 10.1016/j.semarthrit.2018.08.001. PMID: 30205981
Galluccio F, Allanore Y, Czirjak L, Furst DE, Khanna D, Matucci-Cerinic M
Rheumatology (Oxford) 2017 Sep 1;56(suppl_5):v67-v71. doi: 10.1093/rheumatology/kex200. PMID: 28992171Free PMC Article
Patel BK, Wolfe KS, Pohlman AS, Hall JB, Kress JP
JAMA 2016 Jun 14;315(22):2435-41. doi: 10.1001/jama.2016.6338. PMID: 27179847Free PMC Article
Fernandez R, Griffiths R
Cochrane Database Syst Rev 2012 Feb 15;(2):CD003861. doi: 10.1002/14651858.CD003861.pub3. PMID: 22336796


Mousa AK, Elshenawy AA, Maklad SM, Bebars SMM, Burezq HA, Sayed SE
Int Wound J 2022 May;19(4):895-909. Epub 2021 Sep 18 doi: 10.1111/iwj.13690. PMID: 34535972Free PMC Article
Br J Surg 2019 Mar;106(4):341. doi: 10.1002/bjs.11040. PMID: 30811048
Zhong J, Lan Y, Fu S, Zhang J, Lu S, He Y, Zhang JM
Int J Low Extrem Wounds 2019 Mar;18(1):97-103. Epub 2019 Jan 29 doi: 10.1177/1534734618816589. PMID: 30696317
Riyaz N, Sehgal VN
Skinmed 2017;15(1):45-51. Epub 2017 Feb 1 PMID: 28270310
Rongioletti F, Caputo V
G Ital Dermatol Venereol 2013 Aug;148(4):419-25. PMID: 23900163

Clinical prediction guides

Frech TM, Frech M, Saknite I, O'Connell KA, Ghosh S, Baba J, Tkaczyk ER
Best Pract Res Clin Rheumatol 2022 Dec;36(4):101813. Epub 2023 Jan 5 doi: 10.1016/j.berh.2022.101813. PMID: 36609122
Jerjen R, Nikpour M, Krieg T, Denton CP, Saracino AM
J Am Acad Dermatol 2022 Nov;87(5):957-978. Epub 2022 Feb 4 doi: 10.1016/j.jaad.2021.10.066. PMID: 35131401
Jung P, Trautinger F
J Dtsch Dermatol Ges 2013 Aug;11(8):731-6. Epub 2013 Jun 5 doi: 10.1111/ddg.12137. PMID: 23738531
Li W, Dasgeb B, Phillips T, Li Y, Chen M, Garner W, Woodley DT
Dermatol Clin 2005 Apr;23(2):181-92. doi: 10.1016/j.det.2004.09.004. PMID: 15837149
Lancet 1990 May 5;335(8697):1078-80. PMID: 1970380

Recent systematic reviews

Yon H, Shin H, Shin JI, Shin JU, Shin YH, Lee J, Rhee SY, Koyanagi A, Jacob L, Smith L, Lee SW, Rahmati M, Ahmad S, Cho W, Yon DK
Rev Med Virol 2023 Jul;33(4):e2446. Epub 2023 Apr 13 doi: 10.1002/rmv.2446. PMID: 37056203
Machado Velho JC, França TA, Malagutti-Ferreira MJ, Albuquerque ER, Lívero FADR, Soares MR, Soares AEE, Ribeiro-Paes JT
Arch Dermatol Res 2023 May;315(4):943-955. Epub 2022 Nov 23 doi: 10.1007/s00403-022-02455-8. PMID: 36418601
Saeg F, Orazi R, Bowers GM, Janis JE
Plast Reconstr Surg 2021 Jul 1;148(1):226-238. doi: 10.1097/PRS.0000000000008061. PMID: 34181622
Oldroyd AGS, Allard AB, Callen JP, Chinoy H, Chung L, Fiorentino D, George MD, Gordon P, Kolstad K, Kurtzman DJB, Machado PM, McHugh NJ, Postolova A, Selva-O'Callaghan A, Schmidt J, Tansley S, Vleugels RA, Werth VP, Aggarwal R
Rheumatology (Oxford) 2021 Jun 18;60(6):2615-2628. doi: 10.1093/rheumatology/keab166. PMID: 33599244Free PMC Article
Hesseler MJ, Shyam N
J Am Acad Dermatol 2019 Sep;81(3):834-846. Epub 2019 Apr 19 doi: 10.1016/j.jaad.2019.04.037. PMID: 31009668

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