Diabetologia
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Eight insulin-treated diabetic patients in good glycaemic control were studied as out-patients with frequent determinations of stable glycosylated haemoglobin (HbA1c) before, during and after 1 week of induced poor glycaemic control. Stable HbA1c was determined by cation exchange chromatography after elimination of the labile fraction by incubation in saline (0.15 mol/l). The increase in mean blood glucose was significant on the first day of reduced insulin therapy and greatest after 1 week (6.9 +/- 3.9 mmol/l above basal values). ⋯ The increase represented, on average, 0.009% of total haemoglobin per mmol/l increase in mean blood glucose per 24 h during the period of induced hyperglycaemia. After restoring insulin therapy, a significant decrease in blood glucose was achieved on day 1 and after 2 days, the blood glucose level was similar to before the study. There was no significant decrease in stable HbA1c within the first 2 weeks of improved glycaemia.
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Five hundred and ninety-nine patients with insulin-dependent (Type 1) diabetes mellitus were typed for Bf (factor B) polymorphism, and 318 of them for HLA-A, B and C antigens. Bf and HLA antigen frequencies were compared with those in 536 normal controls. ⋯ This, too was especially pronounced in the juvenile onset cases, in whom it was significantly stronger than in controls (p less than 10(-3)). The known positive associations between Type 1 diabetes and HLA-B8, -B15 and -Cw3 were confirmed.
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Patients with severe diabetic ketoacidosis (pH less than 7.10) were treated according to two protocols. Protocol I consisted of high-dose insulin therapy by intravenous and intramuscular injections and bicarbonate infusion and was used in the first 12 patients; they received an average of 260 U insulin and 167 mmol bicarbonate in the first 6 h of treatment. Protocol II consisted of low-dose continuous intravenous insulin therapy, 8 U/hour, without bicarbonate in a further 12 patients. ⋯ During the low-dose treatment the mean (+/- SD) plasma insulin concentration was 121 +/- 46 microU/ml. The presence of insulin binding antibodies did not result in lower free insulin concentrations. Thus, in the treatment of severe ketoacidosis continuous intravenous therapy with low-dose insulin is as effective as high-dose therapy and bicarbonate-administration is probably unnecessary.
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The prolactin response to 200 microgram thyrotropin-releasing hormone (TRH) IV was studied in seven patients with diabetic ketoacidosis, at the start of the treatment, and again, in the same patients, five days after recovery, when the diabetes was well controlled. Normal basal prolactin concentrations and prolactin responses to TRH were found in both situations. There was no correlation between basal prolactin concentrations, or magnitude of prolactin responses to TRH, and any of the metabolic variables measured. These findings do no suggest a role for prolactin in the development of diabetic ketoacidosis.