Soluble tissue factor is a candidate marker for progression of microvascular disease in patients with Type 2 diabetes.

OBJECTIVE: To determine the relationship between abnormalities in blood coagulation and prevalent or incident cardiovascular complications in Type 2 diabetes. DESIGN AND METHODS: Prospective cohort study of 128 patients with Type 2 diabetes in whom blood samples were collected at baseline and after 1 year of follow-up. All cardiovascular complications at baseline and follow-up were recorded. Forty-three healthy, age-matched subjects served as a control group. RESULTS: Logistic analysis revealed an independent relationship between soluble tissue factor (TF) and microvascular disease [per pg mL(-1) TF: Exp(B) = 1.008; CI(95%)1.002-1.014], or neurogenic disease [Exp(B) = 1.006; CI(95%)1.001-1.011]. The highest levels of soluble TF were observed in patients with microvascular and neurogenic disease (P < 0.001). Patients with Type 2 diabetes having a soluble TF concentration >300 pg mL(-1) are at a 15-fold higher risk for the presence of microvascular disease and at a 10-fold higher risk for the presence of neurogenic disease compared with the patients with concentrations below 100 pg mL(-1). Soluble TF was correlated with tissue type plasminogen activator, von Willebrand factor antigen, systolic blood pressure and age. Levels of F1' + 2, D-dimer, FVIII activity, t-PA and vWFag were not different among patients with micro-, macro- or neurogenic complications compared with patients without those complications. Forty-eight new micro-, macro- and/or neurogenic complications were diagnosed after 1 year follow-up. With the exception of higher F1 + 2 levels after 1 year all other markers remained unchanged. A trend toward higher soluble TF levels was observed in patients with new microvascular events (P = 0.056). CONCLUSIONS: Soluble TF is associated with existing microvascular and neurogenic complications in patients with Type 2 diabetes and is a candidate marker for progression of microvascular disease.

Post-traumatic avascular necrosis of the humeral head in displaced proximal humeral fractures.

Nineteen patients with displaced four-part fracture or fracture-dislocation of the proximal humerus were retrospectively studied to investigate the incidence of avascular necrosis and its clinical importance. The average followup duration was 23.6 months. No incidence of avascular necrosis of the humeral head with subchondral collapse was found. Four patients were found to have coarse trabeculae suggesting a revascularized humeral head which probably had become necrotic after the trauma. The treatment of choice for displaced four-part fracture or fracture-dislocation of the proximal humeral is early adequate open reduction and internal fixation rather than primary prosthetic replacement. The authors believe that a majority of the humeral heads in this injury develop avascular necrosis, but most of the humeral heads are quickly revascularized with creeping substitution.

Metabolism of arsenic by sheep chronically exposed to arsenosugars as a normal part of their diet. 1. Quantitative intake, uptake, and excretion.

Information on the effects of long-term organoarsenical consumption by mammals is limited despite the fact that foodstuffs, especially seafood, often contain organoarsenicals at very high concentrations. Here we evaluate the intake, uptake, and excretion (urine and feces) of arsenic by sheep that live on North Ronaldsay in the Orkney Islands and naturally consume large amounts of arsenosugars through their major food source-seaweed. The sheep eat a broad variety of seaweed species, and arsenic concentrations were determined in all the species observed eaten by the sheep (5.7-74.0 mg kg(-1) dry mass). Because of preference and availability, they feed mostly on the seaweed species found to contain the highest arsenic concentrations: Laminaria digitata and Laminaria hyperborea (74 +/- 4 mg kg(-1) dry mass). To quantify the arsenic intake by the sheep, a feeding experiment reflecting natural conditions as close as possible was set up. In the feeding trial, the average daily intake of arsenic by 12 ewes was 35 +/- 6 mg (97% of water-extractable arsenic was present as arsenosugars) gained from feeding on the two brown algae. To test the possible influence of microflora on the metabolism of arsenosugars, six of the sheep were adapted to feeding on grass for 5 months before the start of the trial (control sheep), and the remaining six sheep were kept on their normal seaweed diet (wild sheep). No significant difference in seaweed/arsenic intake and arsenic excretion was found between the two groups of sheep. The arsenic excreted in the feces represents 13 +/- 10% (n = 12) of the total consumed, and on the assumption of that, the average urinary excretion is estimated to 86%.The main arsenic metabolite excreted in urine was dimethylarsinic acid (DMA(V)) (60 +/- 22%) and minor amounts of dimethylarsinoylethanol (DMAE), methylarsonic acid (MA(V)),tetramethylarsonium ion (TMA+), and arsenate (As(V)) together with seven unknown arsenic compounds were also excreted. The urinary arsenic excretion pattern showed a lag period (>4 h) before significant quantities appeared in the urine, an excretion rate that peaked between 4 and 28 h after seaweed intake and a relatively slow half-life (17 h) after end of intake.