Addition of sulfonylurea to insulin treatment in poorly controlled type II diabetes. A double-blind, randomized clinical trial

This study examined the potential beneficial effects of the addition of a second-generation sulfonylurea to insulin therapy for poorly controlled type II diabetes. A randomized, double-blind, crossover experimental design was utilized in 16 type II diabetic patients for a period of eight months. Treatment with glyburide, 20 mg/d (plus insulin), compared with placebo (plus insulin) resulted in a significant reduction in mean basal glucose (232 +/- 12 vs 262 +/- 11 mg/dL [12.8 vs 14.4 mmol/L]) and hemoglobin A1C (10.2% +/- 0.5% vs 10.9% +/- 03%) concentrations. Concomitant with this change, basal C-peptide and free insulin values increased with glyburide therapy, but this pharmacological agent did not alter the ability of the patient's erythrocytes to bind insulin. We conclude that in type II diabetic subjects receiving more than 28 units of insulin per day, the addition of glyburide results in a marginal, but statistically significant improvement in basal glucose concentration, but not in glucose tolerance as assessed by integrated glucose concentration. Whether this small improvement in glycemia is worth the additional cost of sulfonylureas or the risk of drug side effects is not known.     

Failure of intramuscular antivenom in Red‐back spider envenoming

Four cases of Red‐back spider envenoming are reported in which there was minimal response to intramuscular antivenom. Intravenous antivenom was then administered in each case with almost complete resolution of symptoms. All cases were followed up to confirm the effect of treatment. This failure of intramuscular Red‐back antivenom raises the question of its efficacy. There has been no controlled trial to prove that intramuscular Red‐back antivenom is effective and animal work with other antivenoms has demonstrated the intramuscular formulation to have delayed and incomplete effects. Controlled studies should be undertaken to establish the effectiveness of intravenous and intramuscular Red‐back antivenom.     

Reconstruction of mandibular defects with metallic prostheses and microvascular jejunal autografts: an experimental study

A study was undertaken to determine the adequacy of vascularised jejunum to provide stable mucosal cover over a non-biological mandibular substitute. Employing a canine model, composite intra-oral bone-mucosal defects were created and reconstructed with a metal plate covered by a microvascular jejunal patch. These were followed for six months and were assessed clinically, histologically and radiologically. Rapid mucosal healing occurred in all cases. The autografts conformed to the contour of the prosthesis and adequate tongue mobility was preserved. All mandibles remained stable throughout the follow-up period. Histologically, short villi covered the jejunal grafts to three months whilst at six months both normal and abnormal jejunal mucosal morphology was evident.     

The significance of resection length on the patency rate, and the histopathology, of experimentally avulsed and microsurgically repaired blood vessels

The significance of resection length on patency rate, and the histopathology, of microsurgically repaired avulsed blood vessels was examined at 3 weeks in two groups of experimentally avulsed rabbit femoral arteries repaired by different surgeons and in a single series of avulsed and repaired veins. All veins were patent 3 weeks after avulsion and microsurgical repair. Histopathology indicated that the vast majority of lesions in veins were removed at resection. Surgeon A achieved 75% patent arteries and Surgeon B achieved 100% arterial patency (resecting 3.7 mm more on average than Surgeon A). Histopathology revealed numerous luminal circumferential lesions remained in the avulsed artery wall following resection. These lesions were sites of smooth muscle cell proliferation and neointima formation. Although similar arterial damage occurs in human avulsion, considerably lower patency rates are achieved for human arterial avulsion repair than were reported in this experimental study. Factors in addition to vessel wall damage must therefore be involved in thrombosis and occlusion of repaired avulsed arteries. Such factors might be lengthy ischaemia time and severe spasm.     

Beta-adrenergic blockers reduce the risk of fracture partly by increasing bone mineral density: Geelong Osteoporosis Study.

This population-based study documented beta-blocker use in 59/569 cases with incident fracture and 112/775 controls. OR for fracture associated with beta-blocker use was 0.68 (95%CI, 0.49-0.96). Beta-blockers were associated with higher BMD at the total hip (2.5%) and UD forearm (3.6%) after adjusting for age, anthropometry, and thiazide use. Beta-blocker use is associated with reduced fracture risk and higher BMD. INTRODUCTION: Animal data suggests that bone formation is under beta-adrenergic control and that beta-blockers stimulate bone formation and/or inhibit bone resorption. MATERIALS AND METHODS: We evaluated the association between beta-blocker use, bone mineral density (BMD), and fracture risk in a population-based study in Geelong, a southeastern Australian city with a single teaching hospital and two radiological centers providing complete fracture ascertainment for the region. Beta-blocker use was documented for 569 women with radiologically confirmed incident fractures and 775 controls without incident fracture. Medication use and lifestyle factors were documented by questionnaire. RESULTS: Odds ratio for fracture associated with beta-blocker use was 0.68 (95% CI, 0.49-0.96) for any fracture. Adjusting for age, weight, medications, and lifestyle factors had little effect on the odds ratio. Beta-blocker use was associated with a higher BMD at the total hip (2.5%, p = 0.03) and ultradistal forearm (3.6%, p = 0.04) after adjustment for age, anthropometry, and thiazide use. CONCLUSION: Beta-blockers are associated with a reduction in fracture risk and higher BMD.