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Items: 12

1.

Takayasu arteritis

A large vessel granulomatous vasculitis affecting the aorta or its main branches and pulmonary arteries with angiographic findings of stenosis, occlusion, or aneurysm. Clinical findings include absent or asymmetric pulses (discrepancy in four limb blood pressure), bruits, hypertension, or elevation in acute phase reactants. [from NCI_NICHD]

MedGen UID:
21458
Concept ID:
C0039263
Disease or Syndrome
2.

Purpura

Purpura (from Latin: purpura, meaning \ [from HPO]

MedGen UID:
19584
Concept ID:
C0034150
Disease or Syndrome; Finding
3.

Polyarteritis nodosa

Childhood-onset polyarteritis nodosa is an autosomal recessive systemic vascular inflammatory disorder characterized mainly by involvement of the skin, nervous system, kidney, and gastrointestinal tract. There is considerable variability in the severity and age at onset, although most patients have onset of symptoms in the first decade. Features include recurrent ischemic stroke affecting the small vessels of the brain and resulting in neurologic dysfunction, recurrent fever, elevated acute-phase proteins, myalgias, and livedo racemosa or reticularis with an inflammatory vasculitis on biopsy. Some patients develop hypertension, aneurysms, or ischemic necrosis of the digits (summary by Zhou et al., 2014 and Navon Elkan et al., 2014). Some patients present with clinical immunodeficiency (van Eyck et al., 2014). [from OMIM]

MedGen UID:
14681
Concept ID:
C0031036
Disease or Syndrome
4.

Arteritis

INFLAMMATION of any ARTERIES. [from MeSH]

MedGen UID:
13916
Concept ID:
C0003860
Pathologic Function
5.

Granulomatosis with polyangiitis

MedGen UID:
879743
Concept ID:
CN206346
Finding
6.

Granulomatosis with polyangiitis

Granulomatosis with polyangiitis (GPA), previously known as Wegener's granulomatosis, is a rare disease. It is a type of vasculitis, or inflammation of the blood vessels. The inflammation limits the flow of blood to important organs, causing damage. It can affect any organ, but it mainly affects the sinuses, nose, trachea (windpipe), lungs, and kidneys. . The cause of GPA is unknown. It can affect people at any age. Men and women are equally affected. It is more common in whites. Symptoms may include joint pain, weakness, tiredness, and cold symptoms such as a runny nose that doesn't get better. Doctors use blood tests, chest X-rays, and biopsies to diagnose GPA and rule out other causes of the symptoms. Early treatment is important. Most people improve with medicines to slow or stop the inflammation. . NIH: National Institute of Allergy and Infectious Diseases.  [from MedlinePlus]

MedGen UID:
811223
Concept ID:
C3495801
Disease or Syndrome
7.

Immunoglobulin A vasculitis

Schönlein-Henoch purpura (SHP) is a systemic IgA vasculitis that affects small vessels. It is characterized by skin purpura, arthritis, and abdominal and/or renal involvement. [from ORDO]

MedGen UID:
799309
Concept ID:
CN205724
Finding
8.

Polyarteritis

MedGen UID:
539001
Concept ID:
C0264992
Disease or Syndrome
9.

Granulomatosis

Formation of multiple granulomas, i.e., localized nodular foci inflammation. [from HPO]

MedGen UID:
488910
Concept ID:
C0521173
Disease or Syndrome
10.

Henoch-Schönlein purpura

A systemic, usually self-limited immune complex vasculitis, characterized by immunoglobulin A deposition in the small vessels and kidneys. It is manifested with small hemorrhages in the skin, gastrointestinal symptoms, arthritis, and nephropathy. [from NCI]

MedGen UID:
48265
Concept ID:
C0034152
Disease or Syndrome
11.

Wegener granulomatosis

Wegener granulomatosis (WG) 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), that 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 WG 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). [from OMIM]

MedGen UID:
12144
Concept ID:
C0043092
12.

Pulse deficit

MedGen UID:
536717
Concept ID:
C0237313
Finding
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