Thrombosis of leg arteries after prolonged travelVenous thrombosis and subsequent pulmonary embolism after prolonged sedentary travel have been reported.'-3 We describe three cases of thrombosis of leg arteries after prolonged travel. Case reportsCase 1-A 68-year-old man presented with pain in his right calf similar to cramp after a flight lasting at least 20 hours from Australia to England. After arriving home his calf became more painful and the foot cold and numb. There was gradual improvement over the next few days, but seven days after arrival in England he sought hospital treatment. He was fit, blood pressure 140/80 mm Hg, in sinus rhythm, with no ankle oedema or calf tenderness. All pulses in the left leg were present and normal. The right common femoral pulse was present, but all pulses below this in the right leg were absent. There was reduced sensation in the right foot, which was cool. He had a block of his right superficial femoral artery. He was given intravenous heparin and subsequently warfarin. A right femoral arteriogram taken six days after admission (see figure) showed a complete block of his right superficial femoral artery, and there were signs of thrombosis. Interestingly there were multiple collateral channels suggesting

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In 13 nondiabetic acromegalic patients glucose homeostasis was studied by use of the hyperglycaemic clamp technique and compared to a group of sex and age matched and a group of sex, age and weight matched controls. When compared to a control group of normal weight glucose stimulated insulin release (I) was significantly increased and tissue sensitivity to insulin (M/I) significantly decreased. However, no significant differences were observed when the parameters were compared with a weight matched group. Glucose stimulated insulin release correlated positively with growth hormone (GH) and somatomedin-C levels, whereas no such a correlation could be obtained for M/I. Thus, chronic growth hormone excess seems to induce hyperinsulinaemia which in turn leads to obesity and metabolic changes comparable to those of obesity.

1. It has been shown that sodium bicarbonate has no effect or could even be detrimental in various forms of metabolic acidosis. Dichloroacetate, a stimulator of the pyruvate dehydrogenase complex, might offer an alternative treatment. The present study therefore examines the metabolic and haemodynamic effects of dichloroacetate and sodium bicarbonate in healthy volunteers. 2. On 2 different days, sodium dichloroacetate (50 mg/kg body weight) or sodium bicarbonate (1.5 mmol/kg body weight) was given intravenously as a single bolus in 10 healthy volunteers. Haemodynamic parameters were measured using a microprocessor-controlled system. Measurements were performed before and 30 and 60 min after infusion. 3. After administration of dichloroacetate, cardiac index increased from 2.3 +/- 0.03 to 2.7 +/- 0.1 1 min-1 m-2 (P less than 0.05), peripheral vascular resistance decreased from 266 +/- 9.7 to 240 +/- 1.7 kPa s l-1 (2662 +/- 97 to 2398 +/- 169 dyn s cm-5, P less than 0.05), oxygen availability increased from 442 +/- 16 to 535 +/- 30 ml min-1 m-2 (P less than 0.05) and serum lactate concentration fell from 1.4 +/- 0.14 to 0.6 +/- 0.1 mmol/l (P less than 0.05). With infusion of sodium bicarbonate there were no significant effects on any of these variables. 4. Our results show that dichloroacetate administered intravenously reduces the serum lactate concentration. The main effects of dichloroacetate itself are on the haemodynamic variables. Dichloroacetate increases cardiac index and oxygen availability and decreases peripheral vascular resistance, whereas sodium bicarbonate has no effect on haemodynamic or metabolic parameters. These data give some further insights in the actions of dichloroacetate and support the use of dichloroacetate as alternative therapy in various forms of metabolic acidosis.

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