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Necrotizing arteriolitis
Type of vasculitis From Wikipedia, the free encyclopedia
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Necrotizing arteriolitis, also called necrotizing arteritis is an[2] inflammation of medium-sized blood vessels and arterial walls, also called vasculitis, that leads to tissue necrosis. It presents with symptoms such as fever, inflammation, muscle weakness, abdominal pain[citation needed] and most notably, hypertension.
![]() | It has been suggested that this article be merged into Systemic vasculitis. (Discuss) Proposed since August 2025. |
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History
Kussmaul and Maier gave the first detailed description of systemic necrotizing arteritis in 1866.[3]
In 1919 Karl Theodor Fahr[4] described acute arterial lesions which were always present in malignant nephrosclerosis. These injuries were the most severe and widespread in the kidneys and occurred less frequently and severely in other organs, particularly in the pancreas, adrenals and intestines. Fahr believed that necrotizing arteriolitis was the primary cause of the lesions, malignant necrosis and hypertension in these cases by narrowing the renal vascular bed.[3]
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Symptoms
The symptoms include:
- Severe inflammation of the arteries[citation needed]
- Peripheral neuropathy[5][failed verification]
- Axonal degeneration[6]
- Fever[7][8][failed verification]
- Necrosis [citation needed]
- Numbness[9][failed verification]
- Ulcers that do not heal [citation needed]
- Hypertension[10]
- Lesions [citation needed]
- General pain [citation needed]
Emergency symptoms
- Anisocoria could be a sign of the disease.[citation needed]
- Speech problems [citation needed]
- Disphagia[9][failed verification]
- Kidney failure[11]
The organ most damaged by the disease is the kidney. Hypertension is one of the principal symptoms of the disease, as the most damaged by the disease is the kidney. This has been mostly studied by Harry Goldblatt.[3][12]
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Causes
Necrotizing arteriolitis may be the primary condition in patients with polyarteritis nodosa or granulomatosis with polyangiitis. It could also be a result of another disorder, such as lupus erythematosus or hepatitis C. What causes the inflammation is not known, but is likely related to the autoimmune response.[9][failed verification]
The intestinal version of the disease may be a reaction in collagen disease.[13]
Treatment
In most cases, corticosteroids are administered. For severe cases, Cytoxan used to be administered, but is being fased out in favor of Rituxan, a less toxic alternative. Some immunosupressive drugs such as azathioprine, methotrexate and mycophenolate have been used to treat the disease,[9][failed verification] at the cost of exhacerbating the risk of infections and autoimmune diseases.[14] [non-primary source needed]
It has been found that appliying allylamine delayed the healing of the lesions.[4][non-primary source needed]
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References
Further reading
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