Not Your Grandfather’s Typical Gout: Axial Gout as a
Source of Spinal Pain
Melissa MacDonald,
1
MD
and Eric Yanke,
2
MD
1-University of Wisconsin Hospital and Clinics, Department of Internal Medicine; 2-William S-Middleton VA Hospital-Department of Internal Medicine
Introduction
Background Information and Imaging
Discussion
Back pain is a prominent and often debilitating health problem
with a broad differential diagnosis. Gout and crystalarthropathies are not classically thought to affect the axial
skeleton. However, there has been an increasing number of
case reports suggesting that gout does go beyond the
appendicular skeleton and may be a source of back pain.
Gout is due to deposition of monosodium urate monohydrate crystals in the
extracellular fluids of the joint. For typical presentations (ex: recurrent podagra
with hyperuricemia), clinical diagnosis alone is fairly accurate, but definitive
diagnosis requires demonstration of monosodium urate crystals in synovial fluid
or tophus aspirates.
•  Growing evidence suggests that gout can affect the axial
skeleton
•  Presentation of axial gout is variable: asymptomatic, acute
back pain, radiculopathy or signs of cord compression
Case Presentation
Risk factors for gout include: hypertension, obesity, CKD, metabolic syndrome,
type 2 DM and medications (thiazide and loop diuretics). Psoriasis has many of
these similar risk factors and has also been associated with elevated serum uric
acid levels. Additionally, psoriasis itself may be a risk factor for hyperuricemia,
which can lead to gout.
Presentation to the Emergency Department:
A 63 year old male with a history of psoriatic arthritis, crystalproven gout and hypertension presented to the ED with an
acute pain crisis in his lower back and bilateral hips. His pain
had been progressive over the course of days so that he was
essentially bedbound on presentation. His pain was localized to
the center low back, was stabbing in nature, 10/10 severity and
increased with any movement or coughing. He denied fevers,
chills, night sweats, neurologic deficits and other joint pain. He
had no history of trauma, injury, falls or heavy lifting. On exam,
he was afebrile with stable vital signs. He had significant point
tenderness over his lumbar spine with a positive Faber test
(L>R). He had no neurologic deficits on exam. Labs were
pertinent for ESR 83, CRP 10, WBC 11.1. Multiple sets of blood
cultures were negative.
Hospital Course:
The patient was admitted and initial MRI of the spine/pelvis
showed T2 signal abnormality and enhancement of the opposed
endplates/intervertebral disc space at L2-L3. Due to concern for
osteomyelitis, he underwent 2 bone biopsies and an extensive
infectious work-up, with all cultures and infectious studies
negative. The pathology report for the bone biopsies showed
fibrous tissue and hyaline cartilage with no signs of
osteomyelitis. No crystals were identified. Given the negative
infectious evaluation, he was started on Indomethacin and his
back pain began to gradually improve so that he was almost
pain free upon discharge.
Not only is there growing evidence of gout in the axial skeleton, but psoriatic
arthritis and CPPD can also affect the spine. Imaging can assist in the diagnosis
of these conditions, but many findings are nonspecific with similarities to other
conditions such as osteomyelitis.
Gout
Psoriatic
Arthritis
CPPD
MRI Findings in the
Spine
Involved discs and
endplates appear
inhomogenous, low T2
signal due to fibrous
tissue and crystal
deposits. Abnormal
contrast enhancement
in discs, adjacent
endplates, facet joints,
posterior elements and
epidural space
CT Findings in the
Spine
Bone or joint erosions
with sclerotic margins,
facet joint or
intervertebral disc
abnormal bony
neoformation, tophi
Linear calcifications of
discs, calcifications of
ligamenta flava and
facet joints
Radiographic
findings of the
Spine
Nonspecific findings
including disc space
narrowing, end plate
erosions, hyperostosis,
marginal osteophytosis
Densities at margins of
disc spaces due to
calcification of annulus
fibrosis, disc space
narrowing
Inflamed tissue
Crystal deposits in
extending beyond joint
ligamentum flavum and
capsule, thickened
discs with low T1 and
collateral ligaments
T2 signal intensity.
and periarticular soft
Ossified ligamenta flava
tissue, erosions with
appear ovoid or as
break in cortical bone
nodular
over an area of altered
hypointense masses
signal intensity
•  In patients with known peripheral gout who underwent CT
scan of the spine, 28.6% (12/42) had CT evidence of axial
gout with at least lumbar involvement, but there was no clear
association between axial symptoms and imaging findings
•  Signs of axial gout are more likely in aggressive or poorly
controlled disease, longer duration of disease and tophaceous
gout
Osteomyelitis
Nonanatomic T2 signal
in discs, disc height
reduction, high signal on
T2W in vertebral bodies
early, but in late disease
can see decreased T2
signal due to sclerosis,
end plate erosions,
osteophytosis, sclerosis
Nonspecific findings
Nonspecific findingshypodensity of disc and
vertebral body, reduced
disc height
Asymmetric evidence
of sacroilitis
Late findings include
loss of definition and
irregularity of end plates,
reactive sclerosis,
osteophytosis
•  Axial gout can be managed medically similar to appendicular
gout flares, but severe neurologic involvement may require
surgical treatment
•  Given the variability of symptoms, it is unclear what the longterm implications may be or if screening should be performed
in higher-risk patients
•  Axial gout is a rare cause of back pain, but it should be
considered on the differential in those with a known history of
gout as istandard treatments for gout flares can improve
symptoms significantly
References
1. Gisondi, P., Targher, G., Cagalli, A., & Girolomoni, G. (2014). Hyperuricemia in patients with chronic
plaque psoriasis. Journal of the American Academy of Dermatology, 70(1), 127-130.
2. Khanna, D. (2012). 2012 American College of Rheumatology Guidelines for Management of Gout.
Part 1: Systemic Nonpharmacologic and Pharmacologic Therapeutic Approaches to Hyperuricemia.
Arthritis Care & Research, 64 (10), 1431-1446. doi:10.1002/acr.21772
3. Koes, B., Tulder, M., Ostelo, R., Burton, A., & Waddell, G. (2001) Clinical Guidelines for the
Management of Low Back Pain in Primary Care. Spine, 26(22)., 2504-2513.
Follow-up:
One month later, ESR had decreased to 29 and CRP to 2.5. A
follow-up MRI showed decreased enhancement at L2-L3. He
was later seen in Rheumatology clinic and it was suggested that
his pain was likely due to a crystal-induced arthritis of the spine
despite lack of crystals on biopsy. He was started on allopurinol
and colchicine and has been doing well since.
•  Biopsy/aspiration for crystal analysis is often not practical in
the spine, but is required for definitive diagnosis
4. Lumezanu, E., Konatalapalli, R., & Weinstein, A. (2012). Axial (Spinal) Gout. Curr Rheumatol Rep
Current Rheumatology Reports, 14, 161-164. doi:10.1007/s11926-012-0236-8.
5. Mello, F., Helito, P., Bordalo-Rodrigues, M., Fuller, R., & Halpern, A. (2001). Axial Gout is Frequently
Associated with the Presence of Current Tophi, Although Not with Spinal Symptoms. Spine, 39(25),
E1531-E1536.
6. Nadich, T. (2011). Imaging of the spine. Philadelphia, PA.: Suanders/Elsevier.
Presen&ng(MRI:(Post/contrast(sagi3al(view,(
with(enhancement(at(endplates/disc(of(L2/L3(
Follow/up(MRI:((Post/contrast(sagi3al(view(
with(improvement(of(enhancements(of(L2/L3(
7. Zhang, W. (2006). EULAR evidence based recommendations for gout. Part 1: Diagnosis. Report of a
task force of the standing committee for international clinical studies including therapeutics (ESCISIT).
Annals of the Rheumatic Diseases 1301-1311. doi:10.1136/ard.2006.055251