Necrotizing arteriolitis

Necrotizing arteriolitis, also called necrotizing arteritis is a life-threatening^[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 and most notably, hypertension.

Necrotizing arteriolitis
Pronunciation	nek'rō-tīz-ing ahr-tēr'ē-ō-lī'tis [1]
Specialty	Nephrology
Symptoms	Necrosis, numbness, peripheral neuropathy and severe inflammation of the arteries
Causes	Polyarteritis nodosa; Granulomatosis with polyangiitis; Lupus erythematosus; Hepatitis C; Autoimmune response
Prevention	There is no known way of preventing the disease.
Treatment	Administering corticosteroids and immunosuppresive drugs

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]

Symptoms

The symptoms include:

• Severe inflammation of the arteries
• Peripheral neuropathy^[5]
• Axonal degeneration ^[6]
• Fever ^[7][8]
• Necrosis
• Numbness ^[9]
• Ulcers that do not heal
• Hypertension ^[10]
• Lesions
• General pain

Emergency symptoms

• Anisocoria could be a sign of the disease.
• Speech problems
• Disphagia ^[9]
• 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]

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]

The intestinal version of the disease may be a reaction in collagen disease. ^[13]

Treatment

In most cases, corticosteroids are adminstered. 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] at the cost of exhacerbating the risk of infections and autoimmune diseases.^[14]

It has been found that appliying allylamine delayed the healing of the lesions.^[4]