Lupus, a chronic autoimmune disease, and shingles, a viral infection, are distinct conditions, yet their relationship often raises questions. While lupus does not directly cause shingles, it significantly increases an individual’s susceptibility to developing this painful rash. This increased risk stems from the complex interplay between lupus itself and the medications used to manage it, both of which can affect the immune system’s ability to keep latent viruses in check.
Understanding Lupus and Shingles
Systemic lupus erythematosus, commonly known as lupus, is a chronic autoimmune disease where the body’s immune system mistakenly attacks its own healthy tissues and organs. This misdirected immune response can lead to widespread inflammation affecting various parts of the body, including the skin, joints, kidneys, blood cells, brain, heart, and lungs.
Shingles, also known as herpes zoster, is a viral infection characterized by a painful rash. It is caused by the reactivation of the varicella-zoster virus (VZV), which is the same virus responsible for chickenpox. After a person recovers from chickenpox, the VZV remains dormant within nerve tissues near the spinal cord and brain. Shingles occurs when this dormant virus reactivates and travels along nerve pathways to the skin, causing a stripe of fluid-filled blisters on one side of the body or face.
The Connection: Lupus and Shingles Risk
Individuals with lupus face a higher risk of developing shingles primarily due to their compromised immune system. The immune dysregulation characteristic of lupus means the body’s defenses, which normally keep the varicella-zoster virus in a dormant state, are less effective. This creates an environment where the latent virus is more likely to reactivate and cause shingles.
Cellular immunity, especially T-cell responses, is crucial for controlling the dormant varicella-zoster virus. In lupus, the immune system’s ability to maintain this control is often diminished, contributing to the increased likelihood of VZV reactivation and shingles outbreaks.
Factors Increasing Shingles Risk in Lupus
Beyond the intrinsic immune system changes in lupus, several specific factors further elevate the risk of shingles. Lupus disease activity, especially during flares or with more serious manifestations like lupus nephritis, can weaken the immune system, increasing VZV reactivation risk.
Immunosuppressive medications, commonly prescribed to manage lupus symptoms and control disease activity, are another significant factor. These medications, which include corticosteroids (like prednisone), conventional synthetic disease-modifying antirheumatic drugs (e.g., azathioprine, mycophenolate mofetil, cyclophosphamide), and biologics, work by suppressing the immune system. While these treatments are important for controlling lupus, they can reduce the immune system’s ability to keep the varicella-zoster virus dormant, thereby increasing shingles risk.
Advanced age is a known risk factor for shingles, and this risk is compounded in individuals with lupus, meaning a younger lupus patient might face a similar risk as an older healthy individual.
Prevention and Management
Vaccination is a primary strategy for preventing shingles in individuals with lupus. The recombinant zoster vaccine, Shingrix, is recommended by the Centers for Disease Control and Prevention (CDC) for adults aged 19 and older who are immunocompromised due to conditions like lupus. This non-live vaccine is considered safe for lupus patients, including those on immunosuppressive medications, unlike older live-attenuated vaccines. It involves two doses administered a few months apart for effective protection.
Early recognition of shingles symptoms and prompt antiviral treatment are important for managing the infection and preventing complications. Early signs include burning, tingling, or pain, followed by a rash with fluid-filled blisters. If shingles is suspected, consulting a healthcare provider quickly is advised, as antiviral medications can reduce the severity and duration of the rash. Starting antiviral treatment within 72 hours of rash onset can lower the risk of postherpetic neuralgia, a persistent nerve pain that can linger long after the rash has healed.