[Nonfunctional pituitary adenoma and pulmonary sarcoidosis--a case report]. / Wspólistnienie nieczynnego hormonalnie gruczolaka przysadki i sarkoidozy--opis przypadku.

A case of the coexistence of nonfunctional pituitary adenoma and pulmonary sarcoidosis is reported. 39 years old female presented symptoms of a pituitary-gonadal axis insufficiency, visual deficit and dizziness. CT pituitary imaging revealed large intra and extrasellar tumour. Histological examination of the tissue obtained at transsphenoidal surgery showed chromophobic adenoma. Hypopituitarism and transient diabetes insipidus occurred after the surgery. The adequate replacement therapy with hydrocortisone and sex steroids was introduced. At the time of the pituitary tumour diagnosis enlargement of pulmonary lymph nodes was also observed. Based on histological examination of tracheal and bronchial epithelium specimens obtained during bronchoscopy the diagnosis of pulmonary sarcoidosis was made. No other systemic sarcoidosis localisation was confirmed. Histological re-evaluation of adenoma showed no noncaseating granuloma tissue. The overlapping symptoms of pituitary adenoma and other intrasellar masses may result in diagnostic difficulties, particularly in the presence of systemic disorders in which this gland may be involved.

In vitro study of the effect of photodynamic therapy on pituitary adenomas.

Photodynamic therapy (PDT) has been employed in the management of recurrent cerebral gliomas, but its activity against pituitary adenomas has not been specifically studied. An in vitro study of the effects of PDT against a variety of pituitary adenomas was conducted. It was found that PDT using haematoporphyrin derivative as a photosensitizer showed dose dependent activity against a variety of pituitary adenomas. The activity of PDT against pituitary adenomas should be investigated further and may hopefully provide a useful form of adjuvant therapy for preventing recurrence of micro-invasive pituitary adenomas or dealing with established recurrence after surgery and radiotherapy.

Oculomotor nerve repair using interposed nerve graft.

A case of interposed nerve graft repair of an oculomotor nerve damaged during surgery for a laterally growing retrosellar pituitary adenoma is reported. The patient showed partial but functionally useful recovery of nerve function and was able to resume professional work. Only a few reports of end-to-end repair have been published, and they indicate that partial return of nerve function can be expected in such cases.

Follicle stimulating hormone-secreting pituitary adenoma: inappropriate secretion and effect of pulsatile luteinizing hormone releasing hormone analogue (buserelin) administration.

A patient with an FSH secreting pituitary adenoma is reported. Elevated FSH and serum free alpha-subunit (SU) with low levels of LH and testosterone (T) were found. Immunostaining showed the presence of alpha-SU, FSH-beta and LH-beta subunits. LHRH analogue (buserelin) was administered in a pulsatile manner, by portable computerized infusion pump sc for ten days. During the first 24 h of treatment FSH, LH (p less than 0.001) and T (p less than 0.01) rose significantly. Ten days later, the expected desensitization phenomenon did not occur, but further increases of T (8.4 +/- 2.6, mean +/- SD, vs 17.4 +/- 4.1 nmol/l, p less than 0.001) and FSH (58.9 +/- 9.6 vs 70.7 +/- 3.8 mlU/ml, p less than 0.001) were registered. LH decreased (12.5 +/- 2.4 vs 7.1 +/- 0.6 mlU/ml, p less than 0.001) at day 10, but remained higher than basal level (5.0 +/- 0.6, p less than 0.001). Free alpha-SU also rose (2.8 +/- 0.4 vs 4.4 +/- 1.7 mlU/ml, p less than 0.001) after ten days of treatment. The chronic stimulatory effect of analogue on LH with a lack of desensitization suggests tumorous secretion despite a partially preserved negative feedback of testosterone. Low basal LH levels, in some patients with FSH secreting tumors may not be due to tumor mass effect, but rather may be the consequence of altered LH production and/or secretion by the tumor. Although buserelin may not have a therapeutic effect, it is of use in differential diagnosis of hypergonadotropinemia.

A bromocriptine-responsive corticotroph adenoma secreting alpha-MSH in a patient with Cushing's disease.

Clinical and in-vitro investigations have been performed on a corticotroph adenoma removed from a patient suffering from Cushing's disease. Prior to surgery, the patient's Cushing's disease had been successfully controlled, clinically and biochemically, by long term administration of bromocriptine. After selective adenomectomy, tumour tissue was investigated by a perfused isolated cell column technique. It was shown that the tumour cells secreted immunoreactive- (IR)- ACTH and IR-alpha-MSH and that the release of both peptides was promptly suppressed by dopamine. Chromatographic analysis of the secreted IR-alpha-MSH revealed a high proportion of acetylated alpha-MSH; smaller amounts of desacetyl alpha-MSH and diacetyl alpha-MSH were present. The relevance of these findings to the proposal that certain corticotroph adenomas are derived from the intermediate lobe of the pituitary is discussed. It is concluded that there is little direct evidence for involvement of the residual zona intermedia of the adult human pituitary in the development of Cushing's disease.

[Effect of tamoxifen on the treatment of pituitary adenomas with bromocriptine].

Administration of 2-Br- alpha-ergocryptine (bromocriptine = CB-154) in combination with an estrogen-receptor blocking agent tamoxifen were performed in two patients with prolactinoma and non-functioning adenoma, respectively. Case 1 was a 50-year-old male with hyperprolactinemia, impaired pituitary function and visual disorders, in whom a large invasive sellar mass lesion was disclosed by CT scans, which extended supra- and parasellarly and extracranially into paranasal sinuses and pterygopalatine fossa on the left side. As the effect of bromocriptine therapy was partial in tumor size reduction and decrease of serum PRL level and it could not be gained further improvement except for the well recovered visual acuity, tamoxifen was used together with bromocriptine resulting further reduction of tumor size and normalization of serum PRL level. Unexpectedly the medication was ceased during and after a couple of bypass surgery for angina pectoris, and it was followed by elevation of serum PRL level and regrowth of the sellar tumor as well as impairment of vision. By tamoxifen therapy the visual acuity showed some improvement, but the serum PRL level and the tumor size remained as before. Then the combination therapy with bromocriptine and tamoxifen was started again. Case 2 was a 38-year-old female with three children, who had secondary amenorrhea, galactorrhea, borderline level of serum PRL with impaired pituitary function and visual disorders. Under the diagnosis of a non-functioning pituitary adenoma with supra-sellar extension, a craniotomy was done and intracapsular partial removal of the tumor was made, revealing a chromophobe adenoma in light microscopy and undifferentiated cell adenoma in electron-micrographs.(ABSTRACT TRUNCATED AT 250 WORDS)

Rapid improvement in visual field defects following bromocriptine treatment of patients with non-functioning pituitary adenomas.

The role of bromocriptine in the treatment of non-functioning pituitary tumours is not yet defined. Patients with these tumours who present with visual field defects usually undergo immediate surgery. Three consecutive patients are reported: each had rapid improvement in their visual field defects following bromocriptine 7.5 mg/d before surgery. Histological and immunohistochemical examination confirmed that their tumours were non-functioning chromophobe adenomas. Their responses indicate that bromocriptine may have a role in the management of some patients with non-functioning pituitary tumours.

Cyproheptadine-mediated inhibition of growth hormone and prolactin release from pituitary adenoma cells of acromegaly and gigantism in culture.

The effect of cyproheptadine on growth hormone (GH) and prolactin (Prl) secretion from cultured pituitary adenoma cells of acromegaly and pituitary gigantism was studied. When varying doses of cyproheptadine ranging from 0.01 to 1 microM were added to the incubation media, GH secretion was consistently inhibited and a dose-response relationship was observed between the cyproheptadine concentrations and the amounts of GH released into the media. In pituitary adenomas which concurrently produced and secreted Prl, cyproheptadine likewise suppressed Prl release in a dose-related manner. This effect of cyproheptadine was not blocked by coincubation with serotonin. Similarly, coincubation with a dopaminergic antagonist, haloperidol, failed to reverse the inhibitory action produced by cyproheptadine. When coincubated with dopamine, cyproheptadine further inhibited GH and Prl secretion. These results suggest that cyproheptadine possesses a direct action on human somatotroph adenoma cells to inhibit GH and Prl secretion by an unknown mechanism that is different from serotonergic and dopaminergic systems.

The effect of dopamine agonist therapy on large functionless pituitary tumours.

Fifteen patients (12 male) with large pituitary tumours and serum prolactin levels below 1000 mU/l were given dopamine agonist therapy (bromocriptine, mesulergine or pergolide) for a mean of 9 months (range 3-36 months). Serum prolactin became undetectable in all. Despite this, significant suprasellar extensions and any associated neurological defect remained in 14 patients, who therefore were referred for surgery. In one patient there was evidence of spontaneous pituitary infarction unrelated to dopamine agonist therapy. At operation 12 patients had apparently functionless pituitary adenomas which failed to immunostain for prolactin, one had an epidermoid cyst and one a Rathke's pouch cyst. We conclude that patients with large pituitary tumours and only a mildly elevated serum prolactin are unlikely to have prolactinomas, and that such tumours are not likely to show significant tumour shrinkage with medical treatment with dopamine agonists.

Effective bromocriptine treatment of a pituitary macroadenoma during pregnancy.

A 32-year-old woman with 5 years of oligomenorrhea and 2 years of amenorrhea became pregnant after ovulation induced by clomiphene citrate, human menopausal gonadotropin, and human chorionic gonadotropin. Although there were no neurologic or ophthalmologic symptoms before pregnancy, ptosis and diplopia developed progressively from 14 weeks' gestation. Physical, radiologic, and laboratory examinations revealed hyperprolactinemia with pituitary macroadenoma. In an attempt to delay surgery, 7.5 mg bromocriptine was administered daily. The serum prolactin level was lowered and clinical symptoms improved with bromocriptine treatment. The pregnancy continued uneventfully and normal twins were born at 39 weeks' gestation. Two weeks after delivery, a transsphenoidal hypophysectomy was performed.

Rapid resolution of visual field defects and reduction in macroprolactinoma size with bromocriptine therapy. A case report.

Therapy for large prolactinomas depends very much on the treatment modalities available at a particular institution. Surgery is often unsuccessful in restoring endocrine function to normal. Previous reports have demonstrated evidence of tumour regression after 3 or more months' therapy with bromocriptine (Parlodel; Sandoz). More recently, objective evidence of rapid reduction in the size of large prolactin-secreting pituitary tumours, in patients who have had no prior therapy, has been reported. We describe a patient presenting with a chiasmal syndrome and amenorrhoea due to a pituitary macro-adenoma with suprasellar extension i whom rapid tumour regrowth to its pre-operative size occurred 3 months after surgery and irradiation. Administration of bromocriptine (up to 7.5 mg/d) resulted in complete resolution of the visual field defects, radiographic evidence of tumour regression and normoprolactinaemia within 12 days of commencing bromocriptine. Further significant tumour size reduction and improved anterior pituitary function were found after another 5 weeks of therapy.

Bromocriptine treatment of seven women with primary amenorrhoea and prolactin-secreting pituitary tumours.

Seven women with primary amenorrhoea and hyperprolactinaemia were treated with bromocriptine. All the women had started to develop secondary sex characteristics at normal age but pubertal development stopped and menarche did not occur. Radiological signs of a pituitary tumour were found in all the women. Before the pituitary tumour was diagnosed, four women had been given longterm cyclical oestrogen replacement therapy. Three women had received primary tumour therapy with surgery and/or irradiation but had persistent hyperprolactinaemia. The basal luteinizing hormone (LH) levels were low in four of the women while all the women had normal basal levels of follicle-stimulating hormone (FSH) and normal or exaggerated gonadotrophin responses to luteinizing hormone-releasing hormone (LHRH). None of the women had evidence of endogenous oestrogen production before treatment. Bromocriptine treatment normalized the raised serum prolactin levels (46-2900 microgram/l) in all but one woman, in whom the prolactin level decreased from 160 to 38 microgram/l. Regular ovulatory menstrual cycles appeared in four women, one of whom had previously been treated by transsphenoidal adenomectomy followed by external irradiation. Two other women with persistent hyperprolactinaemia after previous surgical and/or irradiation treatment of large pituitary tumours did not menstruate after more than one year of treatment with bromocriptine. One infertile patient with a microadenoma conceived at the first ovulation on therapy and developed symptoms and signs of tumour growth during pregnancy.

Methylprednisolone treatment in patients with brain tumors.

A study was made in 10 patients with brain tumors of the effect of methylprednisolone sodium succinate (Solu-Medrol) on clinical neurological status, intracranial pressure, and periventricular elastance. Significant clinical improvement and reduction in periventricular elastance both ocurred within 24 hours of starting treatment, whereas intracranaial pressure was not significantly reduced until the 2nd day of therapy.