Once thought to be rare, Sjogren’s disease is now known to be the second most common autoimmune rheumatic disease behind rheumatoid arthritis (RA)—and up to half of patients with Sjogren’s present with another autoimmune disease such as RA or lupus.^1,2 What’s more, the heterogeneous and often nonspecific manifestations are easily mistaken for other conditions. Such challenges help explain why it can take an average of three years for patients to receive a diagnosis.² This lag time can pave the way for Sjogren’s progression, greatly impacting a patient’s quality of life (QoL) and increasing vulnerability to organ involvement.

“Diagnosis in Sjogren’s disease is quite tricky,” confirms Teja Kapoor, MD, director of the Columbia Sjogren’s Center at Columbia University Irving Medical Center in New York City. She points to several factors:

• Frequent misunderstanding of what Sjogren’s disease is and how it can manifest.
• Lack of attention on Sjogren’s disease, because other autoimmune conditions are more publicized by popular media, and treatments are less commonly seen in advertisements. “It is kind of an invisible disease,” says Dr. Kapoor.
• Physician referrals for autoimmune disease evaluations often focus on RA or lupus, making Sjogren’s more of an afterthought, she points out. 

It’s important for clinicians to consider Sjogren’s if a patient presents with complaints of dryness and/or systemic symptoms like joint pain and fatigue. “The earlier you can diagnose a patient, the better it is for their QoL, and in some cases, will prevent damage that manifests with the disease,” says Dr. Kapoor. In fact, clinicians from multiple disciplines can play a role in recognizing symptoms and using validated testing to direct patients to the correct specialists for treatment. The following expert recommendations can help facilitate the process.

Tuning into symptoms

“We need a lot more education about Sjogren’s disease,” says Dr. Kapoor. The presentation of the disease is not always obvious, and symptoms are nonspecific. For example:

• The most common symptoms include dryness (eyes, mouth, skin, airway and vagina), fatigue and musculoskeletal pain.
• Systemic manifestations may lead to joint swelling, shortness of breath and cough (interstitial lung disease; ILD), rash (skin vasculitis), paresthesias and/or weakness (peripheral neuropathy), dizziness, nausea, dyspepsia, lower urinary tract symptoms, abnormal sweating (autonomic dysfunction) and many others.

In the past, Sjogren’s was categorized as “primary” and “secondary,” with secondary indicating the presence of another autoimmune condition. Today, however, specialists say these labels are outdated. “While Sjogren’s often overlaps with another autoimmune disease, such as lupus or RA, Sjogren’s is viewed as its own diagnosis,” says Adam L. Dore, DO, division chief of rheumatology at Allegheny Health Network in Pennsylvania. This is important to recognize in order for patients to receive the therapies that manage and reduce often-debilitating symptoms.

Overall, there is a misconception that Sjogren’s is a “dryness disease.” While dryness is a hallmark symptom, some patients experience minimal issues in this area, says Dr. Kapoor. “Clinicians may see a group of patients where dryness is the main symptom. However, up to 40% of patients have systemic manifestations.”

Pinpointing patients

Another misconception is about the type of patient that Sjogren’s affects. Although the disease is diagnosed in women vs. men at a 9:1 ratio,¹ clinicians should still consider this diagnosis in their male patients. “Men can have a more profoundly aggressive disease due to delayed diagnosis as a result of perceptions of Sjogren's as a disease primarily affecting women,” says Dr. Dore.

Additionally, whereas the average patient age upon diagnosis is between 45 and 55,¹ Sjogren’s develops in people of all ages. “Younger patients face the reality of living with their diagnosis for many years longer compared to those diagnosed at midlife, and face a greater risk of complications down the road,” says Dr. Dore. “This makes early recognition all the more critical.”

Recognizing the benefits of early intervention

Dr. Dore and Dr. Kapoor emphasize that timely treatment achieves several crucial goals, including the following:

Improved quality of life.
“Sjogren’s disease impacts patients’ lives all day, every day,” says Dr. Dore. Research shows that Sjogren’s is associated with decreased physical, psychological and social QoL compared with those who do not have the disease. In addition, patients report more symptoms of anxiety and depression.

But perhaps the most impactful symptom affecting patients’ QoL is fatigue, says Dr. Kapoor, estimating that she sees this in 70%-80% of patients. “This is very, very severe fatigue. It is not just regular tiredness but an overwhelming flu-like fatigue that stops them from functioning normally.”

Reduced risk of complications. 
Treatment is key for stalling disease progression. This is true when it comes to the effects of severe dryness itself as well as the systemic damage that may occur. Consider the following examples:

• Keratoconjunctivitis may cause blurry vision or eye discomfort initially; however, without treatment patients can develop corneal erosions, says Dr. Kapoor.
• Xerostomia can drive tooth decay, gum disease, oral thrush and changes in taste. Dry mouth also impairs one’s ability to physically eat comfortably: “I have patients who have lost significant amounts of weight because the joy of food is not there anymore,” says Dr. Kapoor.
• Vaginal dryness causes painful intercourse and increases the risk of vulvovaginitis and urinary tract infections.
• Systemic involvement can cause damage to the kidneys, GI tract, nerves, brain, blood vessels, skin and lungs.

Heightened awareness of comorbidities.
On average, patients are diagnosed with comorbidities—predominantly fibromyalgia, depression and pain—about 2.5 years after a diagnosis of Sjogren’s.⁵ Research shows that among male patients with Sjogren’s, an increased risk for heart attacks, atherosclerosis, cardiomyopathy and congestive heart failure are the most common comorbidities.⁵ Men with Sjogren’s are also more likely to have ILD, as well as develop certain cancers like lymphoma, requiring a need for more frequent monitoring.⁶

Increased well-being and confidence in providers.
Clinicians who listen to their patients and pursue an accurate diagnosis provide immense psychological benefits. Research shows that more than 80% of patients with autoimmune rheumatic diseases who reported being misdiagnosed with a psychosomatic or psychiatric issue said their self-worth was damaged as a result of their experience of trying to get properly diagnosed.⁷ Not only did this have detrimental effects on their mental health, they also reported lower levels of satisfaction with their medical care, including under-reporting symptoms and avoiding healthcare providers due to fears of not being believed or being misunderstood again.

Coordinated multidisciplinary care.
Considering that Sjogren’s can affect multiple organ systems, rheumatologists can ensure timely referral to specialists for monitoring and additional treatment based on a patient’s symptoms and complications. Key team members include an eye care professional to monitor for eye complications and a dental provider to maintain oral health and offer more frequent cleanings as needed. In addition, patients may require referral to other specialists, such as a pulmonologist, cardiologist, nephrologist or neurologist, for management of organ or tissue damage.  

—by Jessica Migala

It’s been decades since Swedish ophthalmologist Henrik Sjögren first noticed that some patients suffered from a trio of symptoms—dry eyes, dry mouth and joint pain in multiple joints. In the years since, clinicians have treated patients with Sjogren’s disease with therapies to manage the symptoms. Drops could lubricate and reduce eye inflammation. Medications could boost saliva production. Painkillers could address sore joints. What’s been lacking: FDA-approved medications designed to treat the underlying cause and systemic nature of the disease. Experts say that may soon change.

Several disease-modifying agents in Phase III clinical trials show promise for halting the immune system’s attack on exocrine glands and other bodily tissues. If these trials are successful, certain medications may reach the market in as little as two years. “It’s an incredibly exciting time for rheumatologists who take care of people with Sjogren’s disease,” says Teresa Tarrant, MD, associate professor of medicine and director of the Clinical Immunology Lab at Duke University in Durham, NC. “We’re going to be able to talk to patients about so much more than drinking fluids and using tear drops. We’ll have a lot more to offer.”

The challenge of clinical biomarkers

In Sjogren’s disease, lymphocytes attack the exocrine glands, especially the lacrimal and salivary glands. As these glands become damaged, they produce less tears and saliva—leading to the cardinal symptoms of dry eyes and mouth. However, not everyone with Sjogren’s exhibits the same symptoms or disease progression. In some individuals, the immune system also attacks other organs, resulting in neurological, cutaneous, skeletal or musculoskeletal symptoms. Still others might develop kidney or lung damage, and there is an overall increased risk of lymphoma.¹

Additionally, clinical manifestations can differ from patient to patient. For example, results of serum autoantibody testing often show anti-Sjogren’s syndrome type A (SSA) and/or anti-Sjogren’s syndrome type B (SSB) autoantibodies.^2,3 These autoantibodies may stop Ro60 and Ro52 antigens from completing their task of cell maintenance as a protein binding Y RNA or protein E3 ubiquitin ligase, respectively. “When people have a positive anti-Ro60 antibody and/or an anti-Ro52 antibody, this can help us diagnose Sjogren’s disease,” explains Sara McCoy, MD, PhD, assistant professor of rheumatology at the University of Wisconsin and director of the UW Health Sjogren’s Disease Clinic in Madison. However, not every patient has these clinical markers. Just as importantly, some people with anti-Ro52 antibodies may not have Sjogren’s disease at all, but rather another condition such as lupus, myositis or ovarian cancer, notes Dr. McCoy.

These challenges have made Sjogren’s disease difficult to diagnose and to study, explains Dr. McCoy. For example, some disease-modifying medications may only be effective in people who are positive for anti-SSA autoantibodies.

Immunotherapies on the horizon

Disease-modifying agents currently under development target autoimmunity in various ways, helping to reduce symptoms and potentially slowing or halting damage to organs and tissue. Some promising therapies include:

BAFF inhibitors
The B-cell activating factor (BAFF) receptor is involved in the activation and survival of autoreactive B cells that attack healthy tissue. Antibodies that target the BAFF receptor stop it from activating the B cells. Once these agents muffle the BAFF signals, autoreactive B cells undergo programmed cell death, and levels of these harmful cells drop to reduce levels of autoantibodies.

In a randomized, dose-ranging Phase IIb study involving 190 people with Sjogren’s, treatment with a BAFF inhibitor at the highest dose showed improvement in tear and saliva flow and fatigue that was sustained through the 52-week follow-up, with a favorable safety profile through up to two years of follow-up.⁴ The therapy has since progressed to a Phase III trial.

Other medications in this class target the BAFF receptor along with a proliferation-inducing ligand (APRIL), a protein that is part of the tumor necrosis factor family that is thought to be involved in Sjogren’s disease.

FcRn blockers
When attaching to healthy tissue, immunoglobulin G (IgG) recruits immune cells to attack. The neonatal Fc receptor (FcRn) protects IgG from degrading and recycles it for circulation. FcRn blockers interrupt this process, preventing IgG from being recycled, thus reducing levels of IgG and anti-Ro60 autoantibodies. 

In a placebo-controlled, double-blind Phase II clinical trial with 163 people with Sjogren’s, treatment with an FcRn-blocking agent resulted in clinically meaningful improvements and symptom relief versus placebo. Levels of IgG and anti-Ro60 dropped, and the drug was well-tolerated.⁵ The therapy has since progressed to a Phase III trial. If the drug eventually receives FDA approval for Sjogren's disease, it will likely be used in patients with anti-SSA and anti-SSB antibodies, says Dr. Tarrant. 

CD40 ligand antagonists
These drugs block the crosstalk between the cluster differentiation 40 (CD40) protein on B cells and the CD40 ligand on T cells. “When T and B cells talk to each other, that’s an important part of immune activation,” explains Dr. Tarrant. “CD40 ligand antagonists inhibit overactive T cells from stimulating B cells and vice versa.” By interrupting this pathway, CD40 ligand antagonists are thought to reduce the production of autoantibodies.⁶

In the past, attempts to block this pathway have resulted in undesirable side effects, including increased blood clotting. However, drug formulations have since been re-engineered to prevent this dangerous side effect, says Dr. Tarrant. Following successful Phase II trial results, one agent in this class is now enrolling patients in a Phase III clinical trial.⁶

More agents in the pipeline

In addition to the disease-modifying therapies above, other potential Sjogren’s medications are being studied, including:

• Bruton’s tyrosine kinase (BTK) inhibitors, which may help to block pathogenic B-cell signaling and activation.
• Inhibitors of the Janus kinases-signal transducer and activator of transcription (JAK-STAT) pathway, which is thought to be involved in the inflammatory response.
• Anti-CD20 medications that bind to and deplete CD20-expressing B cells.

Many other potential pathways also exist, which is promising news for clinicians who care for individuals with Sjogren’s disease. “Each of these pathways is different,” says Dr. Tarrant. “That’s exciting to me as a rheumatologist because there could be a Sjogren’s patient who might respond better to one class of immune-modulating medicine than another.”

The power of personalization

All of this underscores the importance of making a correct diagnosis, which often requires serum autoantibody testing and, in those whose bloodwork is negative for SSA, a labial salivary gland biopsy. (For more on testing, see above.) Once disease-modifying treatments gain FDA approval, clinicians may need to verify whether someone is positive for anti-SSA in order for a treatment to be authorized.

Additionally, some medications may be approved for people with mild disease, while others might work better in patients with moderate to severe disease. Because of that, clinicians may need to start becoming more familiar with the European Alliance of Associations for Rheumatology (EULAR) Sjogren’s Syndrome Disease Activity Index (ESSDAI), a research tool that evaluates 12 domains to assess disease severity, says Dr. Tarrant. For these reasons, the advent of disease-modifying medications is leading toward a paradigm shift in diagnosis and treatment of Sjogren’s disease, says Dr. McCoy. “I’m so happy to be able to be proactive rather than reactive when treating people with this disease.”  

—by Alisa Bowman

“Sjogren’s is a multifaceted disease that goes beyond affecting the saliva and lacrimal glands to concerns that we can’t measure, but that matter to patients,” observes rheumatologist Ghaith Noaiseh, MD, director of the University of Kansas Sjogren’s Clinic and an associate professor at the university. “The buzzword is symptom management.”

Self-care is so vital to symptom management that guidelines published in the last decade by the American College of Rheumatology,¹ the Sjogren’s Foundation² and other rheumatology organizations³ included it as a cornerstone of treatment. But before directing them toward nonmedical strategies, clinicians should assess exactly how Sjogren’s is affecting patients. 

Get subjective feedback—face-to-face

A 2021 Sjogren’s Foundation survey⁴ illustrates just how varied and life-altering symptoms can be. Participants reported frequency of one or more of 48 symptoms in the prior 12 months. Answers ranged from 30% (rash or migraine) to 95% (dry eyes) of the time, with eight symptoms having the greatest impact (see box below). So it is not surprising that 81% said that the disease was a significant emotional burden and that 66% struggled to cope every day, citing the disease’s effect on work, relationships, activities of daily living and their ability to care for home and family.

In addition to using a quality of life (QoL) survey such as the European League Against Rheumatism (EULAR) Sjogren’s Syndrome Patient Reported Index (ESSPRI)⁵, Dr. Noaiseh recommends asking patients directly what’s bothering them the most. “Face-to-face conversation about a patient’s own experience is essential,” he says. This can also sidestep a common disconnect between clinical assessments of Sjogren’s activity and how patients feel.

For example, measurement of lacrimal gland activity did not align with patients’ subjective reports about dry eyes in a 2024 study⁶ from the Medical University of Graz, Austria.

“Discussions about symptoms and self-care strategies such as exercise and stress reduction are very important,” confirms rheumatologist and Sjogren’s disease specialist Donald E. Thomas, Jr., MD, FACP, FACR, RhMSUS, Arthritis and Pain Associates of Prince Georges County, Greenbelt, MD; professor of medicine at the Uniformed Services University, Bethesda, MD; and immediate past chair of the national board of the Sjogren’s Foundation.

Admittedly, clinicians may not be equipped to manage the wide diversity of Sjogren’s symptoms. But what they can do is share key strategies for those within their domain and offer specialist referrals. “I recommend physicians develop lists of specialists familiar with Sjogren’s, including neurologists, dermatologists, pulmonologists, gastroenterologists as well as ophthalmologists and dentists they can refer patients to,” says Dr. Thomas.

In addition, both he and Dr. Noaiseh recommend sharing educational materials provided by the Sjogren’s Foundation (sjogrens.org). “Hand-outs save precious time during a visit,” says Dr. Noaiseh.

Emphasize physical activity

“The most important symptom-relief strategy for Sjogren’s is exercise,” Dr. Noaiseh says. “Physicians must explain why it’s important and how to do it. I often use the expression ‘start low and go slow.’ ” In a 2025 Brazilian meta-analysis⁷ of studies involving 269 women with Sjogren’s, exercise interventions led to notable improvements in pain, fatigue, QoL and aerobic capacity.

“Fatigue can be the most significant and impactful symptom,” says Dr. Noaiseh. (However, he cautions that it’s important to rule out treatable, non-Sjogren’s causes of fatigue such as hypothyroidism, low vitamin D and B12, obstructive sleep apnea and side effects of medications such as beta blockers and opioids.)

“It’s a pervasive, relentless lack of vitality.” Often, he says, the fatigue is accompanied by one or more top Sjogren’s symptoms such as musculoskeletal pain, insomnia and depression/anxiety. “Each symptom fuels the others in ways we don’t fully understand. It’s a common cluster that can be addressed together.”

To combat the fatigue, Dr. Noaiseh says he generally recommends exercise. “If a patient hasn’t been active because they’re tired and in pain, suggest they start with five minutes of slow walking around the house or riding an exercise bike at low intensity. “I tell my patients to find their comfort zone. Then, after three to four weeks, add three to five more minutes.”

He then encourages patients to add more time in another three or four weeks. “I tell them, ‘Within nine months you’ll be exercising for 30 to 40 minutes at a time.’ It’s do-able if patients understand their chronic disease and their physical limits. There will be good days and bad days.” As they progress, he instructs them to add one to two strength-training sessions a week, which has been study-proven to improve fatigue, pain, functional capacity, mood and vitality.⁸

“Some patients will say ‘How can you ask me to exercise when I hurt so bad and I’m so tired?’ ” says Dr. Thomas. “Starting slowly is the key. For someone who cannot exercise, clinicians need to make a referral to physical therapy. The physical therapist can design a safe and effective program that considers common co-morbidities like arthritis and neuropathy that could interfere with exercising.”

Share symptom-relief strategies

Be sure to remind patients that they may have to try several strategies and/or combine strategies to find relief, Dr. Thomas says. He suggests the following:

For dry eyes and dry skin:

• Discuss OTC and prescription tears, gels, ointments and emulsions, as well as wraparound sunglasses and even daytime and nighttime goggles to reduce evaporation. For dry skin, remind patients to take short, warm baths or showers. Dr. Thomas recommends “an oil-based soap for underarms, private areas and feet and a body cream containing ceramides to wash the rest of your skin.” After bathing, moisturize with petroleum jelly or even canola or safflower oil to help preserve natural oils.
• Although hydration is important, Dr. Thomas says it’s smart to spread fluid intake across the day to avoid disrupting sleep with extra bathroom trips.
• When reading or looking at TV or device screens, take a break every 20 minutes and look at something 20 feet away for 20 seconds—and blink several times, closing eyes firmly. “This step squeezes moisturizing oils out of meibomian glands along the eyelids,” explains Dr. Thomas.

For effective pain relief:

• Patients may be uncertain whether heat or ice will address their musculoskeletal pain. Dr. Thomas says, “Five minutes of a cold compress is usually best for relieving inflammation and 20 minutes of a heating pad can help muscle spasms, but patients can experiment to see what works best.”
• Clinicians can counsel patients about the best doses of acetaminophen to get results without raising risk for liver injury. “I oftentimes see that patients don’t take enough or don’t take it as often as they should,” he says.
• Topical capsaicin, NSAID creams and gels and lidocaine patches (applied per label directions) are effective but may have to be used consistently for up to three weeks for optimal relief from joint and muscle pain—or, in the case of lidocaine, for neuropathy—notes Dr. Thomas. 

For better sleep:

• Addressing symptoms that don’t seem related to sleep could improve slumber and boost daytime energy, Dr. Thomas says. “For example, patients can keep an artificial saliva product on their bedside table and use xylitol-based pastilles at night to maintain oral moisture and reduce nighttime wakeups due to mouth discomfort.”
• Dr. Thomas notes that GERD caused by low saliva flow can also disrupt sleep. “Advise patients to avoid foods like chocolate, alcohol and high-fat items that can relax the lower esophageal sphincter. And advise your patients not to eat within three hours of bedtime.”

Support acceptance of the new normal

“When you have a chronic disease, you lose something of yourself,” says Dr. Noaiseh. “You have to reset your expectations.” How you can help: from the start, let your patients know that accepting they have a chronic condition like Sjogren’s is not easy. “Fighting against it can deplete energy and potentially contribute to stress, anxiety, depression and even brain fog,” he notes. To address these issues, advise patients to try limiting major activities to one per day and using sticky notes and smartphone alarms as reminders to take a break. Clinicians can also recommend stress-reduction techniques like mindfulness and breathing exercises.   

—by Sari Harrar

Special thanks to our medical reviewer:

Chadwick R. Johr, MD
Director of the Penn Sjogren's Center, Associate Professor of Clinical Medicine, Division of Rheumatology, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA 

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