To the Editor.
—Domen et al, in the Archives (140:262-263, 1980), describe an interesting report of a mildly diabetic patient who was discovered to have a metastatic glucagonoma and in whom an episode of diabetic ketoacidosis supervened during the course of an apparent infection. The authors state that glucagon appears to have played an important role in the development of diabetic ketoacidosis in their patient. On the contrary, the data presented in their report indicate that insulin deficiency, rather than glucagon excess, was the major factor in the genesis of ketoacidosis in this patient. This is clearly supported by the subnormal insulin levels in the fasting state, as well as by the markedly attenuated response to oral glucose. Patients with glucagonsecreting islet cell tumors have generally been found to have appropriately elevated insulin levels (60 to 70 μU/ mL, basal),1.2 unlike the patient of Domen et al, thus explaining