A unique presentation of destructive shoulder arthropathy in the chronic phase of chronic myeloid leukaemia.

We present a previously unreported case of rapidly progressing, destructive shoulder arthropathy as an initial presentation of chronic phase chronic myeloid leukaemia. This patient initially presented to clinic for consideration of an arthroplasty for symptom relief; however, her loss to follow-up yielded a rapid progression of her symptoms. Bone marrow aspirate and targeted biopsy of the humeral head excluded blast cell crisis, in contrast to previously reported cases. She was treated conservatively with medical management of her underlying disease. Although leukaemic arthritis is a recognized phenomenon, chronic myeloid leukaemia is not known to cause bone destruction of this kind, particularly in the absence of blast crisis. Medical treatment with a tyrosine kinase inhibitor provided a dramatic improvement in our patient's pain, without the risk of attempted arthroplasty in unknown bone quality. We describe a unique presentation of severe bone destruction as a manifestation of chronic myeloid leukaemia in the absence of blast crisis. This should be considered as a rare differential diagnosis in joint arthropathy and may be appropriately managed initially with medical therapy, whereas future arthroplasty comprises uncharted territory in unknown bone quality.

Irreducible anterior dislocation of the shoulder due to soft tissue interposition of subscapularis tendon.

The shoulder joint is the most unstable joint in the body and is easily dislocated. Anterior shoulder dislocation is the commonest and can be associated with glenoid and humeral fractures. Anterior shoulder dislocations are not infrequently associated with cuff tendon tears; however, anterior shoulder dislocation is easily reducible. Irreducible anterior dislocation of the glenohumeral joint is uncommon, and this could be due to bony as well as soft tissue causes. Persistent anterior dislocation due to torn subscapularis interposition in the glenohumeral joint is very rare, and only a few operative cases have been reported in the literature. We present MR features of one such case and a literature review.

Changes underlying the dynamic contrast-enhanced MRI response to treatment in rheumatoid arthritis.

OBJECTIVE: Dynamic contrast-enhanced MRI of patients with rheumatoid arthritis has shown a decrease in the early enhancement rate (EER) of synovitis after treatment. The purpose of this work was to investigate the underlying changes. METHODS: 3D dynamic contrast-enhanced images were acquired from 13 patients before and 1-2 weeks after anti-TNF alpha treatment. The EER of the inflamed synovium was measured. The T1 relaxation time of the synovitis was calculated from images at different flip angles. The time course of the arrival of gadolinium at the radial artery was determined. The gadolinium enhancement of the inflamed synovium was modeled to calculate the fractional plasma volume (vp), the fractional extravascular, extracellular fluid volume (ve), and the volume transfer constant (Ktrans). Pre- and post-treatment values were compared and the dependence of the EER on each parameter was assessed. RESULTS: There was a decrease in the EER measured over 26 s after treatment (29%, p = 0.002). Reductions in T1 (12%, p = 0.001), Ktrans (31%, p = 0.002), and vp (43%, p = 0.01) contributed to this; however, the EER was relatively insensitive to changes in ve. CONCLUSIONS: The decrease in EER after anti-TNF alpha treatment is largely caused by reductions in the volume transfer constant Ktrans, the fractional plasma volume vp, and the T1 relaxation time. Only the contributions from Ktrans and vp directly reflect synovial vascularity.

Pharmacokinetic modeling of dynamic contrast-enhanced MRI of the hand and wrist in rheumatoid arthritis and the response to anti-tumor necrosis factor-alpha therapy.

Dynamic contrast-enhanced MRI (DCE-MRI) of the hand and wrist was performed in 11 patients with rheumatoid arthritis twice before and once 2 weeks after treatment with anti-tumor necrosis factor (TNF)-alpha therapy. A rapid, T1-weighted 3D spoiled gradient echo (SPGR) sequence was used for the dynamic imaging. T1 estimation was performed using similar images obtained at different flip angles. The relative radiofrequency field was estimated from the known T1 of the periarticular fatty marrow. The arterial input function (AIF) was measured at each examination, and normalized to the expected plasma concentration to reduce partial volume effects. Synovial enhancement was modeled to yield values for Ktrans, ve, and vp. Ktrans and ve showed good reproducibility. There was a significant decrease of about 20% in Ktrans after 2 weeks of treatment. This study demonstrates the potential of DCE-MRI and pharmacokinetic modeling to study early changes in inflammatory activity in rheumatoid arthritis following treatment.