— The award-winning actor feels lucky to be alive after his health scare
by Michele R. Berman, MD January 3, 2023
In a clip from an episode of the Paramount+ docuseries "The Checkup: With Dr. David Agus" actor Ashton Kutcher talks about a previous health struggle. About 3 years ago, the "That '70s Show" star "woke up one day and was having vision issues [and] could hardly see," he said. "[It] knocked out my hearing, which threw off my equilibrium, my balance, and I couldn't walk."
Kutcher was subsequently diagnosed, he explained, with a "rare form of [autoimmune] vasculitis."
Concern for Kutcher's health started in August, when "Access Hollywood" aired a sneak peak of a then-upcoming episode of the National Geographic show "Running Wild With Bear Grylls: The Challenge" (now streaming on Disney+), where he and Grylls had to navigate the jungles of Costa Rica. Kutcher told Grylls that he had "this weird, super-rare form of vasculitis that knocked out my vision, it knocked out my hearing, it knocked out like all my equilibrium," and that "it took me like a year to build it all back up."
Kutcher then elaborated on Twitter: "Before there are a bunch of rumors/chatter/whatever out there. Yes, I had a rare vasculitis episode 3yrs ago. (Autoimmune flair up) I had some impairments hear, vision, balance issues right after. I fully recovered. All good. Moving on."
Kutcher told Grylls he believes he is "lucky to be alive," and that he is using the health scare as a learning experience: "The minute you start seeing your obstacles as things that are made for you, to give you what you need, then life starts to get fun, right? You start surfing on top of your problems instead of living underneath them."
Vasculitis
Vasculitis is an inflammation of the blood vessels (i.e., veins, arteries, and capillaries). The problem can affect blood vessels of any type, size, or location, including those in the brain and spinal cord. The primary site is the wall of the blood vessel.
Inflammation from vasculitis can cause the walls of blood vessels to weaken, stretch, thicken, swell, or develop scarring. This can narrow the vessel and slow or completely stop the normal flow of blood. Focal lesions within the vessel wall may also cause weakening with the subsequent development of aneurysms and/or rupture, with bleeding into surrounding tissues.
There are several types of vasculitis. The most commonly used classification system for vasculitis (2012 International Chapel Hill Consensus Conference Nomenclature of Vasculitides) is defined by the size of the vessel predominantly affected -- i.e., small, medium, large, or variable vessel disease. The classification is as follows:
- Systemic vasculitis: Large-vessel vasculitis, giant cell arteritis, Takayasu arteritis
- Medium-vessel vasculitis: Polyarteritis nodosa, Kawasaki disease
- Small-vessel vasculitis
- Anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis: Microscopic polyangiitis, granulomatosis with polyangiitis, eosinophilic granulomatosis with polyangiitis
- Immune complex vasculitis: Anti-glomerular basem*nt membrane disease, cryoglobulinemic vasculitis, immunoglobulin A vasculitis (Henoch-Schonlein purpura), hypocomplementemic urticarial vasculitis
- Variable vessel vasculitis: Behcet's disease, Cogan's syndrome
Vasculitis can affect a single organ or involve several organs and systems. Systemic vasculitis is considered primary when no etiological factor is identified.
Secondary vasculitis can be related to infections (such as hepatitis C or HIV), drugs (propylthiouracil, hydralazine), drug abuse (levamisole-induced vasculitis), systemic autoimmune diseases (systemic lupus erythematosus, rheumatoid arthritis, and Sjogren's syndrome), or to cancer.
The exact pathogenesis of vasculitis is unknown, but several immunologic mechanisms are believed to play a role:
- Immune complex deposition on vessel walls
- Autoantibodies (e.g., anti-endothelial antibodies and ANCA-antineutrophil cytoplasmic antibodies)
- Cell and molecular immune responses
- Granuloma formation
- Injury to endothelial cells
- Aberrant CD4+ T cell polarization
T cells can "polarize" into T1 and T2 effector cell types in response to distinct cytokines. Polarization restricts the ability of a T cell to produce either T1 or T2 patterns of cytokines. T1 cytokines participate in immune responses targeted at the destruction of cells infected with intracellular parasites such as bacteria and viruses.
T2 cytokines, on the other hand, are involved in immune responses effective against extracellular pathogens, such as antibody response or granulocyte activation. T1 cytokines include interleukin (IL)-2 and interferon γ. T2 cytokines include IL-4, IL-5, IL-6, and IL-10.
Symptoms
The symptoms of vasculitis vary depending on the type of vasculitis, the organs involved, and the severity of illness. Some people may have few symptoms, while others may have generalized or multiorgan symptoms.
Symptoms may develop suddenly over a few days or weeks, or gradually over months. Generalized symptoms may include any of the following:
- Tiredness
- Fever
- General aches and pains
- Loss of appetite
- Weight loss
Organ-specific symptoms include:
- Ear and nose: Sinus infections, inner ear infections, open sores in the nose, runny nose, dizziness, ringing in the ears, hearing loss, deafness
- Eye: Redness, itching, burning, changes in vision; blindness in one eye may be the first sign of giant cell arteritis
- GI tract: Open sores in the mouth or stomach area, diarrhea, vomiting blood, abdominal pain
- Genital: Ulcers
- Head: Headache, scalp tenderness, pain with chewing
- Heart: Palpitations
- Joints: Pain
- Lung: Shortness of breath, bleeding in the lung, hemoptysis
- Nerves: Numbness, tingling, weakness, loss of strength in hands and feet, shooting pain
- Skin: Rashes, purpura, petechiae, bruises, hives, itching
If inflammation blocks normal blood flow, it can cause damage to the part of the body involved. Serious, potentially life-threatening problems include aneurysms or aortic dissection, arrhythmias, coronary heart disease, deep vein thrombosis, myocardial infarction, myocarditis, high or low blood pressure, kidney disease, and strokes and transient ischemic attacks.
Treatment
The goal of treatment for vasculitis is to reduce inflammation and avoid possible long-term complications. The treatment approach for any vasculitis generally includes the three components of remission induction, remission maintenance, and monitoring.
Corticosteroids are the first line of treatment for many individuals with vasculitis, and may be used alone or with other immunosuppressive agents such as methotrexate, azathioprine, mycophenolate, cyclophosphamide, and rituximab.
Over the past decade, there have been major advances in the pathogenesis of vasculitis. The recent identification of target molecules is leading to novel therapeutic approaches that target key cytokine and cellular effectors of the inflammatory cascade.
An extensive list of clinical trials for patients with vasculitis can be found at ClinicalTrials.gov.
Michele R. Berman, MD, is a pediatrician-turned-medical journalist. She trained at Johns Hopkins, Washington University in St. Louis, and St. Louis Children's Hospital. Her mission is both journalistic and educational: to report on common diseases affecting uncommon people and summarize the evidence-based medicine behind the headlines.
