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We experienced a 41-year-old acromegalic male (Case 1) in whom the basal plasma GH was extremely high (320–450 ng/mL) but plasma IGF-I was only slightly elevated (2.0–2.8 U/mL). His nutritional condition and associated diabetes mellitus did not appear to be responsible for the relatively low IGF-I level, and a GH-autoantibody in the plasma was absent. We thus performed gel filtration analyses of his plasma and somatotroph adenoma to determine elution patterns of immunoreactive (IR) and receptor active (RA) GH. For comparison, the same studies were carried out on plasmas and somatotroph adenomas obtained from three other acromegalics (Cases 2-4) whose basal plasma GH and IGF-I levels were 22-45 ng/mL and 3.5–6.0 U/mL, respectively. IR GH in Case 1’s plasma distributed over an extremely wide range keeping similar titers rather than showing three discernible components (big-big, big, and little GH) as did plasmas and adenomas from Cases 2–4. And, most of the IR GH in Case 1’s plasma was eluted in such fractions that contained low levels of RA GH, indicating a minor proportion of biologically active GH. However, interestingly, the chromatographic profile and total GH content of Case 1’s adenoma were similar to those of Cases 2-4’s adenomas. These results may, at least in part, explain the discrepancy between the plasma GH and IGF-I levels of Case 1. The unexpectedly different GH elution patterns between the plasma and adenoma from this patient, may suggest a contribution of certain plasma factor(s) to the un-usual chromatographic profile of plasma GH.

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.

Accumulating evidence suggests that vasoactive intestinal peptide (VIP) may be a physiological PRL-releasing factor. In the present study, we examined a possible involvement of VIP in the neonatal androgenization (NA)-induced hyperprolactinemia. Twenty-four hours after birth, newborn female rats were injected sc with 1,000 micrograms of testosterone (NA) or with oil vehicle only (control). Both groups were sacrificed at 8 weeks of age. Compared to controls, NA rats showed significantly higher plasma PRL levels (7.3 fold), anterior pituitary (AP) PRL content (2.1 fold) and plasma estradiol levels (2.1 fold). AP VIP content was extremely higher (61 fold) in NA rats than in controls. However, NA did not affect VIP content in the suprachiasmatic nucleus, paraventricular nucleus or median eminence. These results suggest that the NA-induced hyperprolactinemia may be mediated, at least in part, by paracrine and/or autocrine effects of the increased AP VIP on PRL secretion. However, since the potentiation by NA of the AP VIP content was extremely marked compared to those of the other parameters, the possibility was also raised that the increased AP VIP may be involved in other endocrine and/or nonendocrine events occurring in the AP.

The influence of postnatal testosterone on thyrotropin releasing hormone (TRH)-induced prolactin (PRL) response was tested in male rats. Under urethane anesthesia following estradiol pretreatment, neonatally castrated males showed a female-like plasma PRL response 4-fold greater than in adult-castrated males. Substitution of testosterone reversed the NC effect. However, postnatal age-dependent difference was observed in the effect of testosterone. Testosterone produced a marked inhibition on PRL response when given at 2 or 4 weeks of life but not at earlier days. Determinations of adenohypophyseal PRL concentration and TRH receptor density revealed that testosterone inhibition occurred via its detrimental influence not on PRL concentration but on TRH receptor density. These results indicate that (1) the sex-related difference in the rat PRL response to TRH ensues at least partially through inhibition by postnatal testosterone on the adenohypophyseal TRH receptor ontogenesis in male rats, and that (2) there might be a functional dissociation in testosterone-dependent temporal development between two hypothalamic centers which independently regulate cyclic secretability and secretory reserve of PRL.

A case of adrenal carcinoma with Cushing's syndrome was presented. Endocrinological and morphological investigations disclosed the presence of a functional adrenal carcinoma. This case was characterized by its unusual urinary 17-ketosteroid (17-KS) fractionation, i.e. a marked elevation of 17-KS was accompanied by the increments of etiocholanolone, but not of dehydroepiandrosterone (DHEA) or androsterone. Measurements of the plasma adrenocorticosteroids revealed normal DHEA and DHEA-S (sulfate) levels, moderately increased 17-OH-pregnenolone, and markedly increased (less than 100 times the normal) 11-deoxycortisol (cpd S). Therefore, it seems plausible that the normal urinary DHEA level in this patient would have occurred as a result of remarkably low C17-20 lyase activity sufficient to hamper DHEA production, and that markedly increased etiocholanolone might possibly have been converted from cpd S as well as from DHEA and androstenedione through 5 beta-reduction.

A 34-year-old man with acromegaly was observed, and the clinical course and various endocrinological deficiencies occurring before, during and after the development of pituitary apoplexy were evaluated. Following the attack, the patient experienced acute reductions in growth hormone (GH) and other pituitary hormones, adrenohypophyseal insufficiency and transient diabetes insipidus which appeared subsequent to glucocorticoid therapy. The level of growth hormone in serum and cerebrospinal fluid (CSF) was measured synchronously, and the respective regressions of GH levels in serum and CSF were observed. The results demonstrated the utility of measuring hormonal levels in CSF in the clinical evaluation of pituitary apoplexy in a patient with a functioning pituitary tumor.