Pregnancy induces complex changes in energy metabolism, manifested clinically by insulin resistance, low fasting blood glucose levels, and proneness to ketosis. It is quite unusual for pregnant women who do not have type I diabetes to progress from ketosis to frank ketoacidosis, although this phenomenon is common in larger mammals. In the case described here, glucocorticoid administration in the setting of a prolonged fast triggered a metabolic cascade leading to ketoacidosis in a pregnant woman without type I diabetes. Other details of this illustrative case serve to synthesize several disparate observations regarding the pathogenesis of pregnancy ketoacidosis. Physicians should be aware of the potential for rapidly developing ketoacidosis with atypical biochemical and clinical features in pregnant women who are treated with high doses of glucocorticoids.

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