SummaryThe biological disappearance rate of coagulation factors II, VIT, IX and X from plasma is decreased in myxoedema and increased in thyreotoxicosis. In patients with elevated body temperatures, an increase of up to three times the normal rate was observed. The clinical implications of these findings are briefly discussed.

Aims/hypothesis IRS-1 serine phosphorylation is often elevated in insulin resistance models, but confirmation in vivo in humans is lacking. We therefore analysed IRS-1 phosphorylation in human muscle in vivo. Methods We used HPLC-electrospray ionisation (ESI)-MS/MS to quantify IRS-1 phosphorylation basally and after insulin infusion in vastus lateralis muscle from lean healthy, obese non-diabetic and type 2 diabetic volunteers. Results Basal Ser323 phosphorylation was increased in type 2 diabetic patients (2.1±0.43, p≤0.05, fold change vs lean controls). Thr495 phosphorylation was decreased in type 2 diabetic patients (p≤0.05). Insulin increased IRS-1 phosphorylation at Ser527 (1.4±0.17, p≤0.01, fold change, 60 min after insulin infusion vs basal) and Ser531 (1.3±0.16, p≤0.01, fold change, 60 min after insulin infusion vs basal) in the lean controls and suppressed phosphorylation at Ser348 (0.56±0.11, p≤0.01, fold change, 240 min after insulin infusion vs basal), Thr446 (0.64±0.16, p≤0.05, fold change, 60 min after insulin infusion vs basal), Ser1100 (0.77±0.22, p≤0.05, fold change, 240 min after insulin infusion vs basal) and Ser1142 (1.3±0.2, p≤0.05, fold change, 60 min after insulin infusion vs basal). Conclusions/interpretation We conclude that, unlike some aspects of insulin signalling, the ability of insulin to increase or suppress certain IRS-1 phosphorylation sites is intact in insulin resistance. However, some IRS-1 phosphorylation sites do not respond to insulin, whereas other Ser/Thr phosphorylation sites are either increased or decreased in insulin resistance.

SummaryIn 20 patients suffering from bleeding complications during long-term treatment with phenprocoumon, the depression of the activity of Factors II, VII, IX and X, on the average, was found to be stronger than in so-called adequately treated patients, whereas no statistically significant differences could be demonstrated between the average activity of the 4 factors. The individual variations between the 4 factors were higher than those found in normal individuals and adequately treated patients.Thrombotest activity appeared to be considerably lower than the average factor activity. This discrepancy is mainly caused by the action of the recently discovered circulating anticoagulant occurring in coumarin-treated or vitamin K-deficient patients.