Lateral hip pain: findings from magnetic resonance imaging and clinical examination.

STUDY DESIGN: Prospective cross-sectional study. OBJECTIVES: To examine the radiological and physical therapy diagnoses of lateral hip pain (LHP), and determine the validity of selected clinical variables for predicting gluteal tendon pathology. BACKGROUND: LHP is frequently encountered by clinicians. Further investigation is required to establish the specific pathologies implicated in the cause of LHP, and which clinical tests are useful in the assessment of this problem. METHODS AND MEASURES: Forty patients with unilateral LHP underwent a physical therapy examination followed by magnetic resonance imaging (MRI) studies. Three radiologists analyzed the images of both hips for signs of pathology. Interobserver reliability of the image analyses, the agreement between the physical therapy and radiological diagnoses, and the validity of the clinical tests were examined. RESULTS: Gluteus medius tendon pathology, bursitis, osteoarthritis and gluteal muscle atrophy (predominantly affecting gluteus minimus) were all implicated in the imaging report of LHP. While prevalent in symptomatic hips, abnormalities were also identified in asymptomatic hips, particularly relating to the diagnosis of bursitis. The strength of agreement between radiologists was variable and little agreement existed between the physical therapy and radiological diagnoses of pathology. Nine of the 26 clinical variables examined in relation to gluteal tendon pathology had likelihood ratios above 2.0 or below 0.5, but the associated 95% confidence intervals were large. CONCLUSIONS: The diagnosis of LHP is challenging and our results highlight some problems associated with the use of MRI as a diagnostic reference standard. This factor, together with the imprecise point estimates of the likelihood ratios, means that no firm conclusions can be made regarding the diagnostic utility of the clinical tests used in the assessment of gluteal tendon pathology.

Co-expression of CD21L and IL17A defines a subset of rheumatoid synovia, characterised by large lymphoid aggregates and high inflammation.

OBJECTIVE: To determine whether the expression of IL17A and CD21L genes in inflamed rheumatoid synovia is associated with the neogenesis of ectopic lymphoid follicle-like structures (ELS), and if this aids the stratification of rheumatoid inflammation and thereby distinguishes patients with rheumatoid arthritis that might be responsive to specific targeted biologic therapies. METHODS: Expression of IL17A and CD21L genes was assessed by RT-PCR, qRT-PCR and dPCR in synovia from 54 patients with rheumatoid arthritis. A subset of synovia (n = 30) was assessed by immunohistology for the presence of CD20+ B-lymphocytes and size of CD20+ B-lymphocyte aggregates as indicated by maximum radial cell count. The molecular profiles of six IL17A+/CD21L+ and six IL17A-/CD21L- synovia were determined by complementary DNA microarray analysis. RESULTS: By RT-PCR, 26% of synovia expressed IL17A and 52% expressed CD21L. This provided the basis for distinguishing four subgroups of rheumatoid synovia: IL17A+/CD21L+ (18.5% of synovia), IL17A+/CD21L- (7.5%), IL17A-/CD21L+ (33.3%) and IL17A-/CD21L- (40.7%). While the subgroups did not predict clinical outcome measures, comparisons between the synovial subgroups revealed the IL17A+/CD21L+ subgroup had significantly larger CD20+ B-lymphocyte aggregates (P = 0.007) and a gene expression profile skewed toward B-cell- and antibody-mediated immunity. In contrast, genes associated with bone and cartilage remodelling were prominent in IL17A-/CD21L- synovia. CONCLUSIONS: Rheumatoid synovia can be subdivided on the basis of IL17A and CD21L gene expression. Ensuing molecular subgroups do not predict clinical outcome for patients but highlight high inflammation and the predominance of B-lymphocyte mediated mechanisms operating in IL17A+/CD21L+ synovia. This may provide a rationale for more refined therapeutic selection due to the distinct molecular profiles associated with IL17A+/CD21L+ and IL17A-/CD21L- rheumatoid synovia.