Dr Ganda argues that insulin deficiency, rather than glucagon excess, was the major factor in the genesis of ketoacidosis in our patient. However, diabetic ketoacidosis results from a spectrum of metabolic derangements, and it is unlikely that any single factor causes its occurrence. Insulin lack, by and of itself, in the maturity-onset diabetic has not clearly been shown to result in ketoacidosis.^1-3 Alternatively, we did not mean to imply that the hyperglucagonemia in our patient was the only factor causing ketoacidosis, but rather an important contributing factor. Glucagon has established hyperglycemic effects, and its secretion in the diabetic state may increase the severity of the disease.^1,4

A genetic basis for the relative insulin deficiency in our patient can only be speculative in view of the negative family history. Other factors (eg, destruction of the beta cells by the tumor itself) could have been operative.⁴

Finally, the