A case of malignant pheochromocytoma, with a recurrence 17 years after the initial diagnosis of benign pheochromocytoma, was presented. The autopsy revealed multiple metastases of pheochromocytoma to the bone marrow of the thoracic and lumbar vertebrae. Of particular note is the fact that the patient was associated with paralytic ileus, polyuria and hypercalcemia and that he died of hypercalcemia crisis. Cases like this appear to be very rare.

An unusual case of coexisting acromegaly and Cushing's syndrome is reported in a 34-yr-old female. There was no biochemical or morphological evidence to suggest the presence of other endocrinopathies. She did not have any family history to suggest a hereditary tendency to endocrine disorders. Her acromegaly and Cushing's syndrome were proven to be due to a pituitary somatotroph adenoma and a cortisol-producing adenoma in the right adrenocortex, respectively. Surgical removal of both tumors led to a marked biochemical improvement of the two endocrinopathies. To account for the simultaneous occurrence of the two endocrine tumors, at least two endocrine syndromes may be considered. One of them is Carney's complex. However, Cushing's syndrome in this complex is unexceptionally due to primary pigmented nodular adrenocortical disease, differing from the adrenal pathology of our patient. In addition, a lack in this case of any other characteristic suggestive of this syndrome appears to speak against this possibility. A second possibility is multiple endocrine neoplasia type 1. The absence of a parathyroid or pancreatic islet cell tumor does not strongly support this possibility, but adrenocortical lesions are not rare in this syndrome although they are only rarely functional. However, existence of similar case reports, although very few, in the literature leaves the possibility that she represents another rare variant of sporadic multiple endocrine neoplasia type I syndrome.

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We report an extremely unusual case of prolactinoma which emerged at recurrence as a null cell adenoma. A 53-year-old woman sought medical attention for progressive visual loss and headache. A pituitary tumour was detected by a computed tomographic scan, and hyperprolactinemia was noted. The tumour, removed by a transfrontal surgery, was a chromophobe adenoma, and immunohistochemically the adenoma cells were selectively positive for PRL, which indicated a prolactinoma. Postoperatively, her plasma PRL level was normalized. Seven years later, she noted blurred vision and again sought medical attention. A CT scan demonstrated recurrence of a pituitary tumour. On this occasion, however, she was not hyperprolactinemic. She underwent again a transfrontal resection of the pituitary tumour. Its histology was again a chromophobe adenoma, but the adenoma cells showed no positive immunostaining for any anterior pituitary hormone including PRL, which indicated a null cell adenoma. We have no clear explanation of the pathogenesis underlying her very unusual course. However, null cells (assuming that the original tumour was a mixed adenoma) left behind at the first surgery, or unidentified hypothalamic and/or pituitary derangements might possibly have been responsible for the recurrence. We learned from this patient that recurrent pituitary adenomas may not necessarily have the same endocrine features as did the original tumours. This information appears to make a valid clinical point, because if hormone levels alone are followed after pituitary surgery, recurrent pituitary tumours may be overlooked.Pituitary tumours may recur, mostly within the first 10 years after the initial treatment (1-5). Recur¬ rence rate following surgery alone has been re¬ ported to be 16-30% (1-3); a combined surgery and radiation therapy reduces the rate to 3-15% (1-5).It is known that irradiation of the pituitary fossa may induce the development of a sellar or parasellar tumour of non-pituitary origin, such as an osteogenic sarcoma (6), fibrosarcoma (7,8) or glioma (9). Apart from such radiation oncogenesis, it is commonly held that most, if not all, recurrent pi¬ tuitary tumours are expected to show the same histopathological and endocrine features as did the original tumours. This observation is clinically im¬ portant in the follow-up of patients with function¬ ing pituitary tumours, because re-increases in hor¬ mone levels may suggest tumour regrowth.In this context, a previous case report by Teramoto et al. (10) appears extremely unusual. Their patient was initially diagnosed to harbour a GHproducing adenoma and was operated on, but 7.5 years later it recurred as a null cell adenoma. Re¬ cently, we have experienced a similar case of pitu¬ itary tumour. Our patient was initially diagnosed to have a prolactinoma and operated on, but it re¬ curred 7 years later as a null cell adenoma. We attempted to explain the pathogenesis of this un¬ usual transformation. MethodsHormone assays Determinations of PRL, LH, FSH, TSH, ACTH, GH, cortisol and IGF-I w...

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