10/18 Presby report: inflammatory back pain

 

Thanks to Dr. Lan Chen for going through her approach to lower back pain and dropping some awesome rheum pearls!

Your physical exam provides important clues to the diagnosis of AS, its extra-articular manifestations, as well as other rheumatologic conditions

  • FABER/Patrick’s test: can suggest sacroiliitis
  • Lumbar spine exam (although SI inflammation/pain is more common than L-spine pain)
  • Nails: can show pitting suggestive of psoriatic arthritis
  • Skin: psoriatic plaques, erythema nodosum, pyoderma gangrenosum, keratoderma blenorrhagicum (reactive arthritis)
  • Eyes: uveitis
  • Tongue erosions (suggestive of reactive arthritis)

Recall some key features of inflammatory back pain:

  1. Onset of back discomfort before the age of 40 years;
  2. Insidious onset lasting more than 3 months;
  3. Improvement with exercise; No improvement with rest.
  4. Pain at rest or at night
  5. Profound morning stiffness

Presence of four out of five of those features has ~70% sensitivity and specificity for ankylosing spondylitis.

Imaging

Dedicated imaging of the sacroiliac joint is perhaps more useful than general spine or L-spine imaging, since sacroiliitis is more common than L-spine inflammation.

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CT scan: normal SI joint. Note the clean, linear joint space

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CT scan: sacroiliitis. Note the shaggy, narrowed joint space 

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MRI showing marrow edema adjacent to the joint space in a patient with sacroiliitis

In early disease (first few years of symptoms), only MRI is likely to be sensitive enough to pick up SI joint changes; as the disease progresses, CT becomes more sensitive (~5 years into disease course). X-rays are really only useful in advanced disease.

Treatment

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Zochling J, et al. Ann Rheum Dis 2006.

Additionally:

  • Ustekinumab and secukinumab are anti-IL23/IL17 biologics that can be used to treat AS
  • Apremilast is a PDE4 inhibitor that can also be used for AS

There are multiple causes of inflammatory back pain:

  • Primary ankylosing spondylitis
  • Psoriatic arthritis
  • Reactive arthritis
  • Enteropathic arthritis
    • Crohn’s disease
    • Ulcerative colitis
  • Juvenile ankylosing spondylitis
  • Undifferentiated spondyloarthropathies

Other rheum pearls

  • Obesity may be a risk factor for autoimmune disease
  • Gonococcal arthritis tends to more commonly affect upper extremity joints, while reactive arthritis tends to affect lower extremity joints

References

 

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8/24 (HUP) intern report: eosinophilia and migratory polyarthralgia

Late post from last week. Thanks to our excellent sub-I Juan Spinnato for presenting the case of an older man with subacute cough, dyspnea and polyarthralgias who was found to have a marked eosinophilia, and was ultimately diagnosed with a large intrahepatic mass, now favored to be cholangiocarcinoma 😦

Pearls

  • Polyarthralgias have a huge differential, so certain features can help narrow your differential
    • Distribution: pattern (small vs large joints), symmetry, axial involvement
    • Extra-articular manifestations (rash, eye symptoms, muscle weakness)
    • Duration: <6 weeks is often viral, >6 weeks bears further investigation for other causes
    • Periodicity: intermittent (crystalline arthritis) vs constant
    • Demographics (gender, age, race, family hx)

 

We also talked about the utility of inflammatory markers!

Key points

  • What can increase or decrease the ESR?
    • Increase: infection, inflammation (duh), malignancy, trauma
    • Decrease: abnormally shaped RBCs (SCD, spherocytosis, etc), heart failure, extreme leukocytosis
  • There are underlying conditions that can ‘falsely‘ elevate the ESR more than expected
    • Elevate: older age (correction formula: ULN of reference range = age/2 for men and (age + 10)/2 for women), female gender, ESRD, obesity
  • Conditions that can cause a discrepancy between ESR and CRP
    • Elevated ESR, normal CRP
      • monoclonal immunoglobulins
      • SLE (felt to be because type I IFNs produced in SLE inhibit CRP synthesis by liver)
        • Elevated CRP in SLE should raise suspicion for underlying bacterial infection

References

Richie et al. Diagnostic Approach to Polyarticular Joint Pain. Am Fam Phys. 2003.

6/15/17 at HUP: an approach to weakness, HMG CoA reductase Abs

Rheumatologist extraordinaire Mike George was kind enough to help us through a case of a middle-aged woman with weakness who was ultimately diagnosed with a necrotizing myopathy due to HMG CoA reductase antibodies. Along the way we learned how to approach a patient with weakness:

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Take home pearls:

  1. Use a neuroanatomic approach to a patient with weakness
  2. Perform a good neuro exam (including reflexes) on any patient with weakness
  3. Endocrine and toxic/drug myopathies are the most common of any kind of myopathy (including inflammatory myopathies)

References

  1. Chawla J. Stepwise Approach to Myopathy in Systemic Disease. Frontiers in Neurology 2011.
  2. Mammen, A. 2016. Statin-Associated Autoimmune Myopathy. The New England Journal of Medicine. 374, 7 (2016), 664–669.