The first step is defining the disease with as much certainty as possible. This involves confirming Sjögren’s and distinguishing it from overlap syndromes or mimicking conditions. Objective testing such as antibody studies (SSA/SSB, ANA, RF), salivary flow measurement, Schirmer’s testing, imaging, ultrasound, or minor salivary gland biopsy can provide the foundation for every subsequent decision. Note that some patients may have a diagnosis without ‘meeting classification criteria’. Sometimes a diagnosis cannot be fully established. Ultimately, the most important thing is to establish whether there is an immunological basis for symptoms.

Once the diagnosis is established, the next priority is determining where the disease lives. Sjögren’s can affect multiple organ systems, both glandular and extraglandular. Careful organ domain-based mapping, such as using clinically validated tools like the ESSDAI, can help identify involvement of the lungs, kidneys, nervous system, skin, blood, and other tissues. It should be acknowledged that ESSDAI does not capture all aspects of disease (such as liver involvement and autonomic dysfunction).

Beyond organ system inflammation, Sjögren’s profoundly impacts quality of life. This step focuses on how the disease is experienced on a day-to-day basis: fatigue, pain, dryness, dysautonomia, and cognitive changes. Structured patient-reported outcome measures (such as ESSPRI) and testing for cognitive dysfunction, fatigue, and disability help capture the full burden of illness.

Not all symptoms reflect active inflammation. Here, we quantify both disease activity and symptom burden to help distinguish immune-driven pathology from fixed tissue damage or secondary phenomena. Disease activity indices, blood tests, and imaging can be integrated with patient reports to create a full assessment. This helps us prognosticate a given patient’s Sjögren’s.

Once immune activity is clearly defined, therapy may be appropriate depending on the patient-specific factors. We align treatment to the underlying mechanism, whether through B-cell depletion, pyrimidine inhibition, or modulation of antigen presentation. Each plan is individualized to the patient’s suspected immune signature and pattern of organ involvement. A risk vs. benefits discussion is essential before starting such treatment.

In parallel, we address physiologic dysfunction that drives daily symptoms. This includes management of dryness, fatigue, pain, neuropathy, and mood changes through an integrated approach that depends on the symptom burden of the patient.

Autoimmune disease does not exist in isolation. This step focuses on optimizing the overall terrain on which immunity operates such as managing environmental exposures (eg. UV light), vitamin D levels, lipids, thyroid function, bone density, and metabolic health. These modifiable factors can influence Sjögren’s.

Our hope is to get as many patients to Step 8. After active disease and symptom domains are controlled, attention shifts to fine-tuning. The objective is to minimize residual inflammation and symptom load while reducing medication exposure when possible. Regular reassessment, dose tapering, and non-pharmacologic interventions help sustain equilibrium.

The final step focuses on long-term vigilance such as preventing flares, disease progression, and secondary complications. This includes monitoring immunoglobulins, screening for lymphoma or interstitial lung disease (if appropriate), maintaining vaccination, and evolving the management plan as new research emerges.