OBJECTIVE -Type 2 diabetes is associated with defects in insulin secretion and insulin action. Hyperglycemia may aggravate these defects, a feature known as glucose toxicity. Previous studies have shown that acute correction of hyperglycemia in subjects with long-standing type 2 diabetes gives only short-term improvement in glycemic control after discontinuation of insulin. The current study attempts to identify any characteristics of patients with newly diagnosed type 2 diabetes (fasting glucose Ͼ11.0 mmol/l) who would have a long-term benefit, in terms of glycemic control, from a brief course of insulin therapy. 2 ) with newly diagnosed type 2 diabetes had a 2-3 week course of intensive insulin therapy that was then discontinued. RESEARCH DESIGN AND METHODSRESULTS -Fasting glucose fell from 13.3 Ϯ 0.7 to 7.0 Ϯ 0.4 mmol/l, and this improvement was maintained at the 1-year follow-up (6.7 Ϯ 0.3 mmol/l). The insulin area under the curve for the posttreatment oral glucose tolerance test also improved (8,251 Ϯ 1,880 before therapy, 18,404 Ϯ 4,040 directly after insulin therapy, and 42,368 Ϯ 8,517 pmol ⅐ min at the 1-year follow-up). At 1 year, seven of the subjects maintained good glycemic control on diet therapy alone, eight required oral hypoglycemic agent (OHA) therapy, and one required insulin therapy. The distinguishing features of those who did not require OHA or insulin therapy were that they required less insulin during the active insulin therapy phase (0.37 Ϯ 0.05 vs. 0.73 Ϯ 0.07 units ⅐ kg Ϫ1 ⅐ day Ϫ1 ) and were able to attain a lower fasting serum glucose at the end of the period of insulin therapy (5.9 Ϯ 0.3 vs. 7.7 Ϯ 0.4 mmol/l).CONCLUSIONS -These results demonstrate that in newly diagnosed type 2 diabetes with elevated fasting glucose levels, a 2-to 3-week course of intensive insulin therapy can successfully lay a foundation for prolonged good glycemic control. The ease with which normoglycemia is achieved on insulin may predict those patients who can later succeed in controlling glucose levels with attention to diet alone.

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A maternal history of Graves' disease places the fetus at risk for thyrotoxicosis in utero via the placental transfer of thyroid-stimulating immunoglobulins. Methods for prediction of fetal hyperthyroidism are available, but are not widely used. Clinical assessment of fetal thyroid status by monitoring of fetal heart rate and growth may be inaccurate. This raises some uncertainty in the initial diagnosis of fetal thyrotoxicosis and complicates the assessment of fetal response to maternal propylthiouracil therapy. A case illustrating these pitfalls in the diagnosis and management of fetal hyperthyroidism is presented. The condition was correctly diagnosed, but treatment based on fetal heart rate resulted in biochemical hypothyroidism in the infant at birth. Current recommendations for diagnosis and treatment of fetal hyperthyroidism are reviewed along with recent developments in the field. A modified approach is proposed.

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