Status: current, Not sufficiently defined by necessary conditions definition status (core metadata concept). Date: 31-Jan 2002. Module: SNOMED CT core
Descriptions:
| Id | Description | Lang | Type | Status | Case? | Module |
| 5034965011 | A rare non-histaminic angioedema characterised by potentially life-threatening episodes of oedema of subcutaneous and/or mucosal tissues without urticaria, caused by excessive consumption of C1 esterase inhibitor (C1-INH) in the context of lymphoproliferative or autoimmune diseases. Patients typically present in the fourth decade of life or later and without a family history of angioedema. Clinical manifestation includes nonpitting oedema of the skin predominantly involving the face, but also the limbs or genitals, as well as abdominal pain due to involvement of the gastrointestinal mucosa and severe oedema of the upper airway and oral mucosa. Laboratory examination shows low C1-INH activity and low C3, C4, and C1q levels. Autoantibodies to C1-INH are frequently detectable. | en | Definition | Active | Entire term case sensitive (core metadata concept) | SNOMED CT core |
| 5034966012 | A rare non-histaminic angioedema characterized by potentially life-threatening episodes of edema of subcutaneous and/or mucosal tissues without urticaria, caused by excessive consumption of C1 esterase inhibitor (C1-INH) in the context of lymphoproliferative or autoimmune diseases. Patients typically present in the fourth decade of life or later and without a family history of angioedema. Clinical manifestation includes nonpitting edema of the skin predominantly involving the face, but also the limbs or genitals, as well as abdominal pain due to involvement of the gastrointestinal mucosa and severe edema of the upper airway and oral mucosa. Laboratory examination shows low C1-INH activity and low C3, C4, and C1q levels. Autoantibodies to C1-INH are frequently detectable. | en | Definition | Active | Entire term case sensitive (core metadata concept) | SNOMED CT core |
| 362175013 | Acquired C1 esterase inhibitor deficiency | en | Synonym (core metadata concept) | Active | Only initial character case insensitive (core metadata concept) | SNOMED CT core |
| 631293015 | Acquired C1 esterase inhibitor deficiency (disorder) | en | Fully specified name | Active | Only initial character case insensitive (core metadata concept) | SNOMED CT core |
| 3915188019 | Acquired angioedema | en | Synonym (core metadata concept) | Active | Entire term case insensitive (core metadata concept) | SNOMED CT core |
| 3915189010 | Acquired angio-oedema | en | Synonym (core metadata concept) | Active | Entire term case insensitive (core metadata concept) | SNOMED CT core |
| 5034960018 | Acquired angioedema with C1Inh (C1 esterase inhibitor) deficiency | en | Synonym (core metadata concept) | Active | Only initial character case insensitive (core metadata concept) | SNOMED CT core |
| 5034961019 | Acquired angioneurotic edema with C1Inh (C1 esterase inhibitor) deficiency | en | Synonym (core metadata concept) | Active | Only initial character case insensitive (core metadata concept) | SNOMED CT core |
| 5034963016 | Acquired angioneurotic oedema with C1Inh (C1 esterase inhibitor) deficiency | en | Synonym (core metadata concept) | Active | Only initial character case insensitive (core metadata concept) | SNOMED CT core |
| 5034964010 | Acquired angioneurotic edema with C1 inhibitor deficiency | en | Synonym (core metadata concept) | Active | Only initial character case insensitive (core metadata concept) | SNOMED CT core |
| 5034967015 | Acquired angioneurotic oedema with C1 inhibitor deficiency | en | Synonym (core metadata concept) | Active | Only initial character case insensitive (core metadata concept) | SNOMED CT core |
| 2960041000005118 | erhvervet C1-esterase-inhibitor-mangel | da | Synonym (core metadata concept) | Active | Only initial character case insensitive (core metadata concept) | Danish module (core metadata concept) |
| Outbound Relationships | Type | Target | Active | Characteristic | Refinability | Group | Values |
| A rare non-histaminic angioedema characterised by potentially life-threatening episodes of oedema of subcutaneous and/or mucosal tissues without urticaria, caused by excessive consumption of C1 esterase inhibitor (C1-INH) in the context of lymphoproliferative or autoimmune diseases. Patients typically present in the fourth decade of life or later and without a family history of angioedema. Clinical manifestation includes nonpitting oedema of the skin predominantly involving the face, but also the limbs or genitals, as well as abdominal pain due to involvement of the gastrointestinal mucosa and severe oedema of the upper airway and oral mucosa. Laboratory examination shows low C1-INH activity and low C3, C4, and C1q levels. Autoantibodies to C1-INH are frequently detectable. | Is a | Inherited form of angioedema caused by decreased levels or function of C1 inhibitor or other mechanisms including mutations of the genes encoding coagulation factor XII, angiopoietin-1, plasminogen and as yet undefined factors. | false | Inferred relationship | Some | ||
| A rare non-histaminic angioedema characterised by potentially life-threatening episodes of oedema of subcutaneous and/or mucosal tissues without urticaria, caused by excessive consumption of C1 esterase inhibitor (C1-INH) in the context of lymphoproliferative or autoimmune diseases. Patients typically present in the fourth decade of life or later and without a family history of angioedema. Clinical manifestation includes nonpitting oedema of the skin predominantly involving the face, but also the limbs or genitals, as well as abdominal pain due to involvement of the gastrointestinal mucosa and severe oedema of the upper airway and oral mucosa. Laboratory examination shows low C1-INH activity and low C3, C4, and C1q levels. Autoantibodies to C1-INH are frequently detectable. | Finding site | Structure of immune system (body structure) | false | Inferred relationship | Some | ||
| A rare non-histaminic angioedema characterised by potentially life-threatening episodes of oedema of subcutaneous and/or mucosal tissues without urticaria, caused by excessive consumption of C1 esterase inhibitor (C1-INH) in the context of lymphoproliferative or autoimmune diseases. Patients typically present in the fourth decade of life or later and without a family history of angioedema. Clinical manifestation includes nonpitting oedema of the skin predominantly involving the face, but also the limbs or genitals, as well as abdominal pain due to involvement of the gastrointestinal mucosa and severe oedema of the upper airway and oral mucosa. Laboratory examination shows low C1-INH activity and low C3, C4, and C1q levels. Autoantibodies to C1-INH are frequently detectable. | Finding site | Skin structure | false | Inferred relationship | Some | ||
| A rare non-histaminic angioedema characterised by potentially life-threatening episodes of oedema of subcutaneous and/or mucosal tissues without urticaria, caused by excessive consumption of C1 esterase inhibitor (C1-INH) in the context of lymphoproliferative or autoimmune diseases. Patients typically present in the fourth decade of life or later and without a family history of angioedema. Clinical manifestation includes nonpitting oedema of the skin predominantly involving the face, but also the limbs or genitals, as well as abdominal pain due to involvement of the gastrointestinal mucosa and severe oedema of the upper airway and oral mucosa. Laboratory examination shows low C1-INH activity and low C3, C4, and C1q levels. Autoantibodies to C1-INH are frequently detectable. | Associated morphology | A raised, erythematous papule or cutaneous plaque, usually representing short-lived dermal edema. | false | Inferred relationship | Some | 1 | |
| A rare non-histaminic angioedema characterised by potentially life-threatening episodes of oedema of subcutaneous and/or mucosal tissues without urticaria, caused by excessive consumption of C1 esterase inhibitor (C1-INH) in the context of lymphoproliferative or autoimmune diseases. Patients typically present in the fourth decade of life or later and without a family history of angioedema. Clinical manifestation includes nonpitting oedema of the skin predominantly involving the face, but also the limbs or genitals, as well as abdominal pain due to involvement of the gastrointestinal mucosa and severe oedema of the upper airway and oral mucosa. Laboratory examination shows low C1-INH activity and low C3, C4, and C1q levels. Autoantibodies to C1-INH are frequently detectable. | Associated morphology | Inflammation | false | Inferred relationship | Some | ||
| A rare non-histaminic angioedema characterised by potentially life-threatening episodes of oedema of subcutaneous and/or mucosal tissues without urticaria, caused by excessive consumption of C1 esterase inhibitor (C1-INH) in the context of lymphoproliferative or autoimmune diseases. Patients typically present in the fourth decade of life or later and without a family history of angioedema. Clinical manifestation includes nonpitting oedema of the skin predominantly involving the face, but also the limbs or genitals, as well as abdominal pain due to involvement of the gastrointestinal mucosa and severe oedema of the upper airway and oral mucosa. Laboratory examination shows low C1-INH activity and low C3, C4, and C1q levels. Autoantibodies to C1-INH are frequently detectable. | Has definitional manifestation | Immune system finding | false | Inferred relationship | Some | ||
| A rare non-histaminic angioedema characterised by potentially life-threatening episodes of oedema of subcutaneous and/or mucosal tissues without urticaria, caused by excessive consumption of C1 esterase inhibitor (C1-INH) in the context of lymphoproliferative or autoimmune diseases. Patients typically present in the fourth decade of life or later and without a family history of angioedema. Clinical manifestation includes nonpitting oedema of the skin predominantly involving the face, but also the limbs or genitals, as well as abdominal pain due to involvement of the gastrointestinal mucosa and severe oedema of the upper airway and oral mucosa. Laboratory examination shows low C1-INH activity and low C3, C4, and C1q levels. Autoantibodies to C1-INH are frequently detectable. | Is a | allergisk Quinckes ødem forårsaget af C1-esterase-inhibitor-forstyrrelse | false | Inferred relationship | Some | ||
| A rare non-histaminic angioedema characterised by potentially life-threatening episodes of oedema of subcutaneous and/or mucosal tissues without urticaria, caused by excessive consumption of C1 esterase inhibitor (C1-INH) in the context of lymphoproliferative or autoimmune diseases. Patients typically present in the fourth decade of life or later and without a family history of angioedema. Clinical manifestation includes nonpitting oedema of the skin predominantly involving the face, but also the limbs or genitals, as well as abdominal pain due to involvement of the gastrointestinal mucosa and severe oedema of the upper airway and oral mucosa. Laboratory examination shows low C1-INH activity and low C3, C4, and C1q levels. Autoantibodies to C1-INH are frequently detectable. | Is a | Angioedema due to disorder of kinin metabolism | true | Inferred relationship | Some | ||
| A rare non-histaminic angioedema characterised by potentially life-threatening episodes of oedema of subcutaneous and/or mucosal tissues without urticaria, caused by excessive consumption of C1 esterase inhibitor (C1-INH) in the context of lymphoproliferative or autoimmune diseases. Patients typically present in the fourth decade of life or later and without a family history of angioedema. Clinical manifestation includes nonpitting oedema of the skin predominantly involving the face, but also the limbs or genitals, as well as abdominal pain due to involvement of the gastrointestinal mucosa and severe oedema of the upper airway and oral mucosa. Laboratory examination shows low C1-INH activity and low C3, C4, and C1q levels. Autoantibodies to C1-INH are frequently detectable. | Occurrence | Adulthood | false | Inferred relationship | Some | 2 | |
| A rare non-histaminic angioedema characterised by potentially life-threatening episodes of oedema of subcutaneous and/or mucosal tissues without urticaria, caused by excessive consumption of C1 esterase inhibitor (C1-INH) in the context of lymphoproliferative or autoimmune diseases. Patients typically present in the fourth decade of life or later and without a family history of angioedema. Clinical manifestation includes nonpitting oedema of the skin predominantly involving the face, but also the limbs or genitals, as well as abdominal pain due to involvement of the gastrointestinal mucosa and severe oedema of the upper airway and oral mucosa. Laboratory examination shows low C1-INH activity and low C3, C4, and C1q levels. Autoantibodies to C1-INH are frequently detectable. | Associated morphology | Angioedema | true | Inferred relationship | Some | 1 | |
| A rare non-histaminic angioedema characterised by potentially life-threatening episodes of oedema of subcutaneous and/or mucosal tissues without urticaria, caused by excessive consumption of C1 esterase inhibitor (C1-INH) in the context of lymphoproliferative or autoimmune diseases. Patients typically present in the fourth decade of life or later and without a family history of angioedema. Clinical manifestation includes nonpitting oedema of the skin predominantly involving the face, but also the limbs or genitals, as well as abdominal pain due to involvement of the gastrointestinal mucosa and severe oedema of the upper airway and oral mucosa. Laboratory examination shows low C1-INH activity and low C3, C4, and C1q levels. Autoantibodies to C1-INH are frequently detectable. | Occurrence | Any period of life commencing after birth, but before death. | true | Inferred relationship | Some | 1 | |
| A rare non-histaminic angioedema characterised by potentially life-threatening episodes of oedema of subcutaneous and/or mucosal tissues without urticaria, caused by excessive consumption of C1 esterase inhibitor (C1-INH) in the context of lymphoproliferative or autoimmune diseases. Patients typically present in the fourth decade of life or later and without a family history of angioedema. Clinical manifestation includes nonpitting oedema of the skin predominantly involving the face, but also the limbs or genitals, as well as abdominal pain due to involvement of the gastrointestinal mucosa and severe oedema of the upper airway and oral mucosa. Laboratory examination shows low C1-INH activity and low C3, C4, and C1q levels. Autoantibodies to C1-INH are frequently detectable. | Causative agent | Kallidin I | true | Inferred relationship | Some | 1 |
| Inbound Relationships | Type | Active | Source | Characteristic | Refinability | Group |
| Acquired angioedema due to activation of the classical complement pathway related to an underlying lymphoreticular disorder particularly lymphoma or monoclonal gammopathy of unknown significance (MGUS) | Is a | True | A rare non-histaminic angioedema characterised by potentially life-threatening episodes of oedema of subcutaneous and/or mucosal tissues without urticaria, caused by excessive consumption of C1 esterase inhibitor (C1-INH) in the context of lymphoproliferative or autoimmune diseases. Patients typically present in the fourth decade of life or later and without a family history of angioedema. Clinical manifestation includes nonpitting oedema of the skin predominantly involving the face, but also the limbs or genitals, as well as abdominal pain due to involvement of the gastrointestinal mucosa and severe oedema of the upper airway and oral mucosa. Laboratory examination shows low C1-INH activity and low C3, C4, and C1q levels. Autoantibodies to C1-INH are frequently detectable. | Inferred relationship | Some | |
| Acquired angio-oedema due to the presence of neutralising antibodies against C1 inhibitor. | Is a | True | A rare non-histaminic angioedema characterised by potentially life-threatening episodes of oedema of subcutaneous and/or mucosal tissues without urticaria, caused by excessive consumption of C1 esterase inhibitor (C1-INH) in the context of lymphoproliferative or autoimmune diseases. Patients typically present in the fourth decade of life or later and without a family history of angioedema. Clinical manifestation includes nonpitting oedema of the skin predominantly involving the face, but also the limbs or genitals, as well as abdominal pain due to involvement of the gastrointestinal mucosa and severe oedema of the upper airway and oral mucosa. Laboratory examination shows low C1-INH activity and low C3, C4, and C1q levels. Autoantibodies to C1-INH are frequently detectable. | Inferred relationship | Some |
This concept is not in any reference sets
FHIR