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What Every Rheumatoid Arthritis Patient Needs to Know About Shingles

It’s a cruel twist, but rheumatoid arthritis (RA) patients have an increased risk for another painful condition—the skin rash known as shingles (or herpes zoster).

This peculiar disease is caused by a common childhood infection that lies silent in the body for years before it is reanimated and causes havoc in adulthood. The misery is usually over in a few weeks for most sufferers, but shingles may produce long-term complications that can mean months of pain. Here’s what every rheumatoid arthritis patient should know about shingles.

What is shingles?

Shingles is caused by a germ known as varicella-zoster virus, which is also responsible for chicken pox, the contagious childhood disease that produces an itchy skin rash. After the symptoms of chicken pox subside, the varicella-zoster virus takes up residence in nerves, where it remains dormant, or inactive, for years. Then, for reasons that aren’t clear, the virus reawakens in some people and triggers an attack of shingles.

A bout with shingles usually begins as pain, itching, or tingling on one side of the body. Soon red, bumpy patches form on the skin, often forming a swath that wraps from the spine to the abdomen or chest. However, the rash may form on the face and other body parts. The red patches turn to blisters, which break and leave behind crusty formations that eventually fall off. Shingles can also cause fever, headache, upset stomach, and other symptoms.

A case of shingles usually clears up in a few weeks, but pain can linger for months in some unlucky individuals who develop a complication known as postherpetic neuralgia (PHN), which is caused by nerve damage.

If a rash forms on your face, your eyes or ears may become inflamed, too. And while no one knows why, the risk for suffering a heart attack or stroke rises immediately after you develop shingles, though the increased threat is greatest for the first month or so, then gradually fades away.

Medication as a trigger

Anyone can develop shingles, though for unknown reasons women appear to have a higher risk than men. Moreover, the varicella-zoster virus becomes more likely to reactivate and cause symptoms as you age, with about half of all shingles cases in the United States occurring in people over 60.

Although it’s not known what causes the varicella-zoster virus to reawaken, it appears that the immune system’s capacity to keep the virus in check declines over time. This means that medical conditions that cause dysfunction in the immune system—like rheumatoid arthritis—can make shingles a bigger threat.

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Furthermore, many rheumatoid arthritis drugs work by suppressing the immune system, which may explain why people who have this form of inflammatory arthritis are two to three times more likely than others to develop shingles.

There are questions about which drugs are most likely to increase a rheumatoid arthritis patient’s risk for shingles. It’s known that the potent anti-inflammatory medications called corticosteroids (such as prednisone) can increase your odds as much as twofold. Meanwhile, there’s little evidence that the widely prescribed disease-modifying drug (DMARD) methotrexate can trigger an attack.

Less clear is the connection between shingles and a newer class of medicines known as biologic response modifiers (BRMs), or biologics. These medications have dramatically improved the treatment of rheumatoid arthritis and other forms of inflammatory arthritis, but they are also known to increase the risk for infections. However, whether these medicines reactivate the shingles virus is controversial.

A few studies have suggested that biologic drugs may stir up shingles. Notably, in 2009 a group of German researchers reported in JAMA that people with RA treated with a category of biologics known as monoclonal antibodies—which include adalimumab (Humira) and infliximab (Remicade)—may increase their risk for shingles by 82 percent.

However, a subsequent study published in JAMA four years laterinvolving about six times more patients exonerated adalimumab and infliximab, indicating that they don’t cause shingles. And a more recent study published in Arthritis Care & Research in 2015 evaluated eight different biologic drugs and found no evidence that they increase the risk for shingles.

One possible explanation for the contrasting results may be that some patients in the earlier studies were also taking high doses of corticosteroids, which would account for their higher rates of shingles.

Finally, one newer nonbiologic rheumatoid arthritis medicine has been linked to shingles. Studies suggest that taking the drug tofacitinib (Xeljanz) may double your odds of acquiring the disease.

Choosing the right drug to manage your rheumatoid arthritis always requires a careful balancing of benefit and risk, so the threat of shingles should be part of the conversation when you discuss drug therapy with your physician.

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Treatment and prevention

If you think you might be developing shingles, call your doctor right away. He or she can prescribe an antiviral medication, which may shorten the duration of your symptoms and make them less severe.

But these drugs work best when taken soon after the onset of symptoms, ideally within three days. Your doctor may also suggest you take a pain reliever and an antihistamine (to relieve itching). Skin creams or lotions may help, too.

There wasn’t much you could do to lower your risk for shingles until 2006, when the Food and Drug Administration approved the vaccine Zostavax for people 50 and older. A vaccine works by exposing the body to a tiny amount of a germ, which teaches the immune system to recognize and control it. Zostavax contains a live dose of the varicella-zoster virus.

Although the virus has been chemically weakened, Zostavax isn’t recommended for people whose immune systems are compromised by disease or suppressed by medication, since it may trigger an attack of shingles.

That complicates the decision of whether or not to get the shingles vaccine for rheumatoid arthritis patients. About 1 in 4 Americans over age 60 receive the vaccine, compared to only about 1 percent of rheumatoid arthritis patients, possibly because physicians are reluctant to recommend it to people being treated with drugs that quiet the immune system.

However, the Advisory Committee on Immunization Practices considers the shingles vaccine to be safe for people taking a short course or low doses of corticosteroids, or low doses of methotrexate. And the American College of Rheumatology (ACR) states that rheumatoid arthritis patients can safely receive the shingles vaccine as long as they wait at least two weeks before starting treatment with a biologic or tofacitinib. The ACR does not recommend the shingles vaccine for patients already taking a biologic drug, but some research has questioned whether that precaution is necessary.

Getting the shingles vaccine does not guarantee you won’t get the disease; it cuts the risk by about half. However, the vaccine also reduces the chances of suffering severe complications such as postherpetic neuralgia by about two-thirds, making it a shot in the arm worth considering.

Vaccines for RA patients

Rheumatoid arthritis patients have double the risk for serious infections, yet a large study showed that just 1 in 4 get the recommended vaccinations that can guard against several of these threats. The ACR advises rheumatoid arthritis patients to receive the following vaccinations:

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• Influenza vaccine: every year before flu season

• Pneumococcal vaccine: any time, then repeated five years later

• Shingles (herpes zoster) vaccine: after turning 50 and before starting therapy with a biologic drug or tofacitinib

Learn more about the flu and pneumonia vaccines.

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