Late spontaneous rupture of the extensor pollicis longus tendon after corticosteroid injection for flexor tenosynovitis.

INTRODUCTION: Spontaneous rupture of the extensor pollicis longus (EPL) tendon has been reported after trauma, rheumatoid arthritis and sports. Rupture may also occur as a consequence of the use of anabolic steroids for recreational purposes, or systemic steroids for the treatment of a variety of medical conditions. CASE REPORT: We present a case report of a woman affected with a spontaneous EPL tendon rupture resulted 14 months after a corticosteroid injection for flexor tenosynovitis, "trigger finger," of the thumb. The edges of the tendon were debrided and sutured using figure of eight stitch and a running locked stitch. In addition multiple specimens were sent to Pathology. DISCUSSION: Duplay in 1876 described spontaneous rupture as a problem of mechanical and pressure phenomena. Another cause of EPL rupture is related to the development and persistence of inflammatory processes seen in patients with medical illnesses such as rheumatoid arthritis. There have been no reports in the literature to date of spontaneous EPL tendon rupture in the late period after steroid injection. Tendon ruptures in the hand usually occur one or two weeks after a corticosteroid injection, and the affected tendons are usually in neighbouring areas.

Inflammation-induced up-regulation of ionotropic glutamate receptor expression in human skin.

BACKGROUND: N-methyl-D-aspartate (NMDA), alpha-amino-3-hydroxy-5-methylisoxazolone-4-propionic acid (AMPA), and kainate (KA) receptors are members of the ionotropic glutamate receptor (iGluR) family and are increased in inflamed rat skin. These receptors contribute to inflammatory pain. In this study, we have examined whether there is a similar increase in iGluRs in inflamed human skin in the presence of inflammatory pain. METHODS: Normal and inflamed-skin biopsies were obtained from eight patients undergoing elective wound-debridement surgery. Real-time-polymerase chain reaction (PCR) and western blot analysis were used for quantitation of iGluR mRNA and protein in normal and inflamed human skin. RESULTS: A significant increase in mRNA and protein for NMDA, AMPA, and KA receptor subunits was detected in inflamed compared with normal skin. The amounts of NMDA (NR1 subunit), AMPA (GluR2 subunit), and KA (GluR6 subunit) mRNA in inflamed skin were mean 6 (SD 1.6-fold), 2.5 (0.6-fold), and 3.8 (0.9-fold) (P<0.05), respectively, greater than that measured in normal skin. The ratio of NR1, GluR2, and GluR6 protein in inflamed compared with normal skin was 5.7 (1.2), 2.4 (0.5), and 3.6 (0.9) (P<0.05), respectively. CONCLUSIONS: These results, in human tissue, demonstrate that iGluR mRNA and protein expression are increased during persistent inflammation and that this increased activity may be involved in mediating clinical inflammatory pain in human skin.