Sarkar C, Roy S, Kochupillai N, Gupta N, Tandon P N
Department of Pathology, All India Institute of Medical Sciences, New Delhi.
Indian J Med Res. 1990 Oct;92:315-23.
One hundred patients of pituitary adenoma were studied using light microscopy, electron microscopy, immunohistochemistry and serum hormone estimation. Depending on the absence or presence of clinical endocrine manifestation they were divided into 2 groups 'non-functioning' (group I -48 patients) and 'hyper-functioning' (group II- 52 patients). Tumours in group I were chromophobes, some of which (group IA) had no hormone increase in serum nor detection in tissues and ultrastructurally they consisted of secretorily inactive cells (null cell adenomas) while others (group IB) were composed of secretorily active cells with prolactin consistently increased in serum and localized in tissue (lactotroph adenomas). Tumours in group II were chromophobe, acidophil, basophil or mixed adenomas with varying number of secretorily active cells in all. The hormone responsible for the hyperfunction was always raised in serum and localized in tissue. Thus growth hormone was demonstrated in all tumours from patients with acromegaly (somatotroph adenomas), prolactin in all tumours from patients with galactorrhea (lactotroph adenomas) and ACTH in all tumours from patients with Cushing's syndrome (corticotroph adenomas). It was observed, however, that 40 per cent of tumours were pleurihormonal, growth hormone and prolactin being the commonest combination. Interestingly, not all the hormones localized by immunohistochemistry in pleurihormonal adenomas were detected in serum and/or reflected in the clinical picture.
