INTRODUCTION Hyperthyroidism is associated with a reduction in bone mineral density (BMD). Suppressive doses of thyroxine (T4), inducing subclinical hyperthyroidism, have been reported by some investigators to reduce BMD. Little work has been done on replacement doses of T4. AIM The aim was to investigate the effect of replacement doses of T4 on BMD. STUDY DESIGN Cross‐sectional study of hypothyroid patients on long‐term T4 replacement doses, comparing those who had primary hypothyroidism with those who were previously hyperthyroid. PATIENTS Fifty women on replacement doses of T4 for more than 5 years were recruited. Twenty‐five were treated for primary (group 1) and 25 for radioiodine‐induced hypothyroidism (group 2). They were well matched for age, menstrual status, smoking history, body mass index (BMI), dose and duration of T4 replacement as well as thyroid status. MEASUREMENTS BMD was assessed by dual energy X‐ray absorptiometry. Free T4 (FT4), FT3 as well as ultrasensitive TSH assays were used to assess thyroid status. RESULTS The two groups showed no difference in BMD (g/cm2) of the lumbar spine (1.008 vs. 0.957, P  =  0.25), femoral neck (0.745 vs. 0.735, P  =  0.79) and total hip (0.878 vs. 0.837, P  =  0.24). When the two groups were pooled, there was no significant difference between the patients and a reference population with femoral neck and total hip BMD expressed as a standard deviation (Z) score. However, the lumbar spine mean Z score was significantly greater than zero. For each site, there was a negative correlation of BMD with age in at least one group but, in general, BMI, FT4, FT3 and duration of T4 replacement did not correlate with BMD. T4 dose, however, had a consistent positive correlation with BMD in the spine, femoral neck and the hip (P  =  0.01, 0.04 and 0.02, respectively) in group 2 but not group 1. CONCLUSION In this study, there is no evidence for a difference in bone mineral density in patients receiving replacement doses of thyroxine irrespective of the aetiology of their hypothyroidism. The reduced bone mineral density associated with hyperthyroidism appears to be restored, maintained and in some cases possibly improved while on long‐term thyroxine replacement post‐radioiodine.

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Surgical repair of an acute, distal, tendo Achillis rupture in a 59-year-old diabetic male is described in which the Mitek Anchor System was used. The injury described is a distal tear of the insertion of the tendon into the calcaneus without avulsion fracture of the calcaneus. Sixteen months of postoperative follow-up care, including casting for equinus deformity, progressive weightbearing, range of motion exercises, and physical therapy, have been free of complications. The authors include a brief overview of historical and current reparative techniques for comparison. The authors conclude that the use of the Mitek Anchor System affords the surgeon a simple and effective method for the repair of acute, distal, tendo Achillis rupture when other methods cannot be used because of the location of the rupture.

Membrane cofactor protein (MCP; CD46) is a 50-60 000 MW glycoprotein, expressed on a wide variety of cells and tissues in man, which plays an important role in regulating complement activation. Human MCP has also been shown to be the receptor for measles virus. We have recently identified the pig analogue of MCP and demonstrated that pig MCP has cofactor activity for factor I-mediated cleavage of C3b when these components are derived either from pig or human. As a consequence, pig MCP is an efficient regulator of the classic and alternative pathways of human and pig complement. In order to define the potential importance of MCP in protecting against complement activation in the pig, we have conducted a comprehensive survey of its distribution in pig cells and organs. As in humans, MCP in the pig is broadly and abundantly distributed. Pig MCP is highly expressed on all circulating cells, including erythrocytes, in contrast to its absence on human erythrocytes. Multiple isoforms of MCP are found on cells and in tissues, probably representing products of alternative splicing analogous to those found in man. MCP is abundantly expressed throughout all tissues examined with particularly strong staining on the vascular endothelium. Connective tissue elements within liver and testis are also strongly stained by anti-pig MCP antibodies. Pig MCP is expressed only weakly on skeletal muscle cells and expression is absent from smooth muscle cells in the lung and vessel walls, sites at which human MCP is expressed. Of particular note, MCP is not expressed in B-cell areas of the germinal centres of lymph nodes.

Background: Peripheral nerve grafts (PNGs) in the spinal cord support axonal regeneration and functional recovery. Chondroitinase ABC (ChABC) has been used to break down chondroitin sulfate proteoglycans (CSPGs) that inhibit axonal regeneration. If ChABC is effectively delivered to the injury site, CSPGs can be broken down so axons can pass through the distal interface between the graft and the spinal cord before CSPG accumulation has an adverse impact on recovery.