Ankylosing Spondylitis in Black Adults: Missed, Not Rare

Ankylosing spondylitis (AS) is a form of inflammatory arthritis that attacks the spine and the sacroiliac joints where the spine meets the pelvis. It causes chronic back pain and stiffness, and over years it can fuse vertebrae into a rigid column. The belief that it skips Black patients traces to one fact: the gene most tied to AS, HLA-B27, is less common in people of African descent. That fact got turned into a myth, and the myth costs Black patients years of delay. When Black Americans with AS do get diagnosed, their disease is on average further along than that of White patients seen in the same clinics.

AS sits under a larger umbrella called axial spondyloarthritis (axSpA). The immune system targets the joints of the spine and the sacroiliac joints, driving inflammation at the sites where ligaments and tendons anchor to bone. The body tries to heal that inflammation by laying down new bone. Over time that new bone can bridge across joints and fuse the spine, the change that gives the disease its name (ankylosis means fusion). Roughly 80% of people feel their first symptoms before age 30, and fewer than 5% are diagnosed after 45, so this is a young person's disease that often gets dismissed as a pulled muscle or a bad mattress.

It is more common in men than women, though women are diagnosed later and more often missed. Beyond the spine, AS travels with other inflammation: acute anterior uveitis (a painful, red, light-sensitive eye) affects 25% to 35% of patients, and psoriasis appears in roughly 1 in 10. Fatigue is near-universal and is part of the disease, not a character flaw.

Mechanical back pain (a strain, a disc) gets better with rest and worse with activity. Inflammatory back pain does the reverse, and that reversal is the single most useful clue. Rheumatologists look for at least four of these five features:

• Onset before age 40, gradual rather than from a single injury.
• Pain that improves with exercise and movement.
• No relief from rest; sitting still makes it worse.
• Night pain that eases once you get up and move.
• Morning stiffness that lasts longer than 30 minutes.

Two other patterns point toward AS: alternating buttock pain that shifts from one side to the other (inflammation of the sacroiliac joints), and deep fatigue that the pain alone does not explain. A red, painful eye in someone with chronic back pain is a flag that should send you to a rheumatologist, not just an eye doctor.

HLA-B27 is a genetic marker strongly linked to AS, and it is less common in Black Americans. In the US population, roughly 7.5% of non-Hispanic White people carry it versus about 1.1% of non-Hispanic Black people. Because the gene is rarer, clinicians and textbooks treated AS itself as rare in Black patients, and many learned to use a negative HLA-B27 result to wave the diagnosis away.

That logic breaks down at the patient level. Among Black Americans who do have AS, a smaller share are HLA-B27 positive than among White patients. A foundational 1977 study found B27 in 48% of Black AS patients versus 94% of White AS patients. A more recent cohort put it near 62.5% for Black patients versus 85.3% for White patients. A Black patient with real AS is more likely than a White patient to test B27-negative, so leaning on that test to rule the disease out misses exactly the patients it should catch. Researchers analyzing US clinical data concluded the racial gap looks like detection bias: only Black patients with classic features and a positive B27 tended to get diagnosed, while subtler presentations slipped through.

The under-diagnosis shows up in how advanced the disease is when Black patients finally get worked up. A cross-sectional study of 925 AS patients across three ethnic groups found Black patients had the highest disease activity, the worst physical function, and the most spinal damage of the three. The median BASDAI disease-activity score (0 to 10) was 5.9 for Black patients versus 3.5 for White patients. The median BASFI functional-impairment score was 62.5 for Black patients versus 27.8 for White patients. Radiographic damage measured by the mSASSS spine score was several times higher in Black patients. The authors' bottom line: Black patients have more severe AS than White or Latino patients.

Diagnostic delay is the engine behind that severity. Across the AS population, years often pass between the first inflammatory back pain and a diagnosis, and the delay runs longer for people facing social barriers to care. A 2025 analysis of patients with radiographic axial spondyloarthritis found that documented social need was tied to a 21% longer time from back pain to diagnosis, and flagged race and ethnicity among the factors trending toward longer delay. Every year of delay is a year inflammation keeps remodeling the spine.

There is no single test. A rheumatologist builds the diagnosis from the clinical picture plus imaging and labs:

• History and exam: the inflammatory back pain pattern, age of onset, family history, uveitis, psoriasis, or bowel disease, and reduced spinal mobility.
• Imaging of the sacroiliac joints: X-rays can show damage once it is established, but MRI catches active inflammation years earlier, before it shows on plain film. For a younger patient with inflammatory back pain and normal X-rays, MRI is the test that finds the disease.
• HLA-B27: useful when positive, but a negative result does not exclude AS, and that caveat matters most for Black patients.
• Inflammatory markers: C-reactive protein (CRP) and ESR can be elevated, though many patients with active disease have normal labs.

Inflammatory back pain for three months or more in someone under 45 warrants a rheumatology referral on its own. You do not need a positive gene test to earn the workup.

AS has no cure, but treatment controls inflammation and preserves mobility, and starting before the spine fuses is the whole game. The 2019 American College of Rheumatology guideline lays out the steps:

• NSAIDs first. Naproxen, ibuprofen, and similar drugs are first-line, and 70% to 80% of patients respond. Taken consistently, they control pain and stiffness.
• Biologics when NSAIDs fall short. TNF inhibitors (such as adalimumab, etanercept) are strongly recommended next. IL-17 inhibitors (secukinumab, ixekizumab, bimekizumab) are another option that targets a different inflammatory pathway.
• Physical therapy and movement. A structured exercise and posture program is core treatment, not an add-on. Staying mobile is how you keep the spine flexible while medication calms the inflammation.

For the wider inflammatory-arthritis picture, our explainer on rheumatoid arthritis in Black patients covers a different but overlapping autoimmune joint disease, and our guide to sciatica and low back pain in Black adults walks through the mechanical causes that AS is so often mistaken for.

The right specialist is a rheumatologist, and the goal is to be seen before the disease damages the spine. If your back pain fits the inflammatory pattern, ask your primary care doctor for a referral and bring the five inflammatory-back-pain features written down so the conversation starts in the right place. You can find a Black rheumatologist or a clinician who serves Black patients through our directory. A clinician who takes a Black patient's back pain seriously, and who does not dismiss the diagnosis over a negative gene test, is the difference between catching AS early and catching it after the spine has already fused.