dysfunction in males) and could explain minnie's symptoms. experimental evidence and case reports by cushing led to his publication in 1932 on pituitary basophilism as the cause of cushing's disease. in this publication, the clinical symptoms of the disease, named after cushing, were described. out of the 12 cases with hypercortisolism described in cushing's monograph on the pituitary body, 67% died within a few years after symptom presentation, whereas minnie g. survived for more than 40 years after symptom presentation, despite the fact that she did not receive any treatments for a pituitary tumor. the prolonged survival made minnie's case unique at the time. the reason behind this survival remains a mystery since an autopsy of minnie was refused after her death. however, the most likely explanation, proposed by j. aidan carney and based on statistical evidence, was that the basophil adenoma minnie might have harbored underwent partial infarction, leading to symptom regression. the other hypothesis was that minnie might have had primary pigmented nodular adrenocortical disease (ppnad), which when associated with cushing's syndrome (carney complex) can infrequently cause spontaneous symptom regression of the latter. in 1924, the soviet neurologist nikolai itsenko reported two patients with pituitary adenoma. the resulting excessive adrenocorticotropic hormone secretion led to the production of large amounts of cortisol by the adrenal glands. considering this impact, the name of itsenko was added to the title in some east european and asian countries, and the disease is called itsenko-kushing disease.