Laparoscopic hemi-hysterectomy in treatment of a didelphic uterus with a hypoplastic cervix and obstructed hemi-vagina.

OBJECTIVE: Maldevelopment of the Müllerian duct system may result in various urogenital anomalies including didelphic uterus with a hypoplastic cervix and obstructed hemi-vagina. CASE REPORT: We report a patient with this anomaly who was treated by laparoscopic hemi-hysterectomy and hysteroscopic resection of hemi-vagina. A 16-year-old patient who had complained of vaginal pus-like discharge on and off for 1 year was diagnosed by MRI to have a double uterus with obstructed right hemi-vagina and ipsilateral renal agenesis. After hysteroscopic identification of hypoplasia of the right uterine cervix, laparoscopic resection of the right uterus and right fallopian tube and hysteroscopic assisted resection of the vaginal septa were performed successfully. CONCLUSION: We think that combined laparoscopy and hysteroscopy may be an effective alternative in the management and diagnosis of Mullerian anomalies.

Preparing for an influenza pandemic in Italy: resources and procedures in paediatric hospital units.

The World Health Organization (WHO) has stated that preparedness for effectively facing a major influenza epidemic should involve the training of physicians in the management of contagious diseases and upgrading hospital resources and procedures [1]. Children would be particularly vulnerable during an influenza pandemic and specific measures are needed to face the threat to them effectively. We performed a national survey to obtain information about the preparedness in facing a major influenza outbreak in Italian paediatric units. In Italy, paediatrics clinics are found in both paediatric wards and paediatric departments. Departments are more complex structures, containing several units with different specialisations and facilities. For this study, we interviewed heads of both departments and units. A structured questionnaire, including 30 items, was submitted to the heads of 150 paediatric hospital departments across the country. Responses were obtained from 123 units; 10% of these had rooms dedicated to infectious diseases, and 4% had experts in infectious diseases available and routinely applied procedures for preventing the spreading of acute infectious diseases. Only 8% of departments have paediatric intensive care facilities. Few paediatric units, usually located in large children's hospitals or in academic paediatric departments, have a sufficient degree of preparedness to face severe influenza pandemics. A structural improvement of the paediatric units and the use specific procedures are essential for effectively care for children hospitalised because of contagious diseases.

Symptomatic efficacy of stabilizing treatment versus laser therapy for sub-acute low back pain with positive tests for sacroiliac dysfunction: a randomised clinical controlled trial with 1 year follow-up.

AIM: Back pain is a highly frequent condition due to many causes, although most of them cannot be established with certainty. It is also the current clinical and scientific belief that sacroiliac joint syndrome can be a specific low back pain cause. Nonetheless the existence of clinical tests aimed at highlighting the responsibility for lumbar pain secondary to sacroiliac dysfunction, it is not easy to diagnose it with either manual or instrumental means. Moreover, uncertainty is diffuse when facing a correct treatment for patients involved. The aim of this study was to verify, in patients with acute or sub-acute low back pain and positive sacroiliac signs, the efficacy of a stabilising therapy (orthosis and exercises, with previous mesotherapy) directly targeted to sacroiliac dysfunction versus a symptomatic usual care such as He-Ne laser therapy. METHODS: Over a period of 14 months, we recruited 22 patients (10 females, mean age 44+/-11) with acute and sub-acute low back pain and symptoms and signs suggesting a sacroiliac dysfunction. They were randomised in a Group laser (GL), 11 patients treated with He-Ne laser therapy targeting the sacroiliac region, and a Group stabilisation (GS), 11 patients treated with mesotherapy, a specific dynamic sacroiliac support (ILSA) and specific exercises. Outcome criteria included VAS, and Mens and Laslett sacroiliac tests. RESULTS: Out of 449 acute and sub-acute low back pain out-patients, 22 (4.9%) had symptoms and signs suggesting a sacroiliac dysfunction. A reduction of pain was achieved only in the GS. All pain-provocation and stability tests were negative both after the end of treatment and at the follow-up only in the GS. CONCLUSIONS: A targeted approach based on mesotherapy, a specific sacroiliac belt and specific stabilizing exercises proved its efficacy in acute and sub-acute low back pain patients with symptoms and signs suggesting a sacroiliac dysfunction. As soon as it will be possible to identify particular spine syndromes in the universe of non specific low back pain, there will also be the possibility to employ specific therapies.

Adrenal insufficiency as the first clinical manifestation of the primary antiphospholipid antibody syndrome.

We describe a 60-year-old man who developed clinical symptoms and signs of Addison's disease, which was subsequently confirmed biochemically; no cause was apparent. Several months later the patient represented with a fit, followed by a large and extensive venous thrombosis in the right iliac vein and in the veins of the right leg. He had strongly positive antibodies to cardiolipin, strongly suggesting a diagnosis of primary antiphospholipid syndrome. While Addison's disease is a well-recognized, albeit rare, manifestation of the antiphospholipid syndrome, the Addison's disease preceded other clinical evidence of the syndrome by several months, in our patient, at variance with previous cases described in the literature. The antiphospholipid syndrome should be considered as a possible pathogenetic process in patients presenting with Addison's disease where the aetiology is not obvious.

Effect of acute and chronic administration of tamoxifen on GH response to GHRH and on IGF-I serum levels in women with breast cancer.

Tamoxifen, an estrogen antagonist, is usually employed in the treatment of breast cancer. Its mechanism of action is not well known because an antiproliferative effect of the drug has been shown also in estrogen receptor negative tumors, most likely mediated by the inhibition of local growth factors and particularly IGF-I. However, the action of tamoxifen on the GH-IGF-I axis is still open to investigation. We have investigated the influence of acute and chronic treatment with tamoxifen on GH response to GHRH and IGF-I serum levels in six postmenopausal women with metastatic breast cancer. A GHRH test (50 microg i.v. at time 0, GH determinations at 0, 15, 30, 60, 90 and 120 min) was performed (a) basally, (b) 3 h after 40 mg oral administration of tamoxifen and (c) after 8 weeks of 20 mg twice a day oral tamoxifen treatment. IGF-I was measured basally and after chronic tamoxifen therapy. No significant modifications in GH response to GHRH were observed after acute or chronic treatment with tamoxifen vs the basal test. On the contrary, chronic tamoxifen treatment induced a significant decrease in serum IGF-I levels. Basal pretreatment levels of 123+/-18 microg/l were suppressed to 65+/-11 microg/l (mean suppression 47%, P < 0.001). These preliminary data confirm the inhibitory effect of tamoxifen on IGF-I production but seem to exclude the possibility that this effect may be due to an inhibition of GH secretion.

Intracranial and spinal dissemination of an ACTH secreting pituitary neoplasia. Case report and review of the literature.

We report a case of a 52-year-old woman presenting with a recurrence of a large pituitary adenoma with suprasellar extension and an overt Cushing's clinical picture, five years after successful transsphenoidal treatment. After transfrontal ablation of the tumour, followed by external radiotherapy, she was asymptomatic for six years before she exhibited epileptic seizures. A left frontal intracranial neoplasm was diagnosed and removed, and at histological examination it was found to be constituted by a localization of the pituitary ACTH secreting neoplasia. One month later she exhibited spinal dissemination of the ACTH secreting neoplasia which was only partially removed. After four months a Magnetic Resonance Image (MRI) revealed recurrence of the intracranial localization and further spinal dissemination. Because of compressive symptoms, spinal masses with the same histologic features, were partially removed again in three successive surgical operations. Several medical treatments for obtaining the control of corticoid excess, caused by the ACTH overproduction, were tried, but none were satisfactory. Finally a bilateral adrenal venous embolization was performed thus obtaining a critical transient fall of serum cortisol. Five months later the patient died. At necroscopy bilateral adrenal enlargement was found, spinal disseminations were confirmed, and no metastatic lesions were discovered.

Membrane receptors and hormones.

The regulation of metabolic processes, cell growth and differentiation is achieved by an interaction between hormones and specific cellular binding sites termed "receptors". These may be located on the cellular surface, in the cytoplasm or in the nucleus. Recently the structure of several membrane receptors in mammalian cells have been elucidated. These consist of peptide chains possessing multiple functional "domains". We describe in details the extracellular, transmembrane and intracellular "domains". In recent years antibodies to many receptors and analogues of some peptide hormones have become available; these can be used in clinical practice to study receptors, their localization and, in some cases, to block their function.

Paroxystic hypertension in a long-term hemodialyzed patient. Successful adrenalectomy for a dopamine-producing pheochromocytoma.

Pheochromocytoma (Pheo) is an uncommon neoplasm producing blood pressure troubles and it may be undiagnosed in chronic dialyzed patients in whom hypertension is a common finding. The symptoms in Pheo syndrome depends on the prevalent catecholamine released, the most common being epinephrine (E) and norepinephrine (NE). Recently, a particular clinical picture has been described for dopamine (DA)-producing Pheos, in whom a normo-hypotensive status is more often observed. The authors report a case of mainly dopamine-producing Pheo in a long-term dialyzed patient, successfully treated with adrenalectomy. The main steps in diagnosis and preoperative management are described and debated also in view of the particular background produced by the end-stage renal failure. The common imaging techniques adopted for adrenal medullary neoplasms (US, CT, MIBG scintiscan) confirmed to be decisive for diagnosis; HPLC assay of plasma catecholamines is the only biochemical test available in these patients although its significance is questionable due to the poor knowledge of catecholamine metabolism in chronic renal failure. The clinical findings observed in this case seem in disagreement with those already reported in DA producing Pheos. Pheo in hemodialyzed patients is a rare event and it may be hidden by other more common causes of hypertension. However, more awareness from the medical staff allows to diagnose the neoplasm correctly by the currently available methods and to plan a safe surgical therapy also in high-risk patients.

Ovarian autoimmunity and corticotherapy in an in-vitro fertilization attempt.

This case report describes a successful pregnancy and delivery in a woman presenting with ovarian autoimmunity who had previously been involved in two unsuccessful in-vitro fertilization (IVF) attempts. Ten days before a third attempt, she began a regimen of 25 mg per day of prednisolone which was continued throughout the whole IVF protocol. Ovulation was induced by human menopausal gonadotrophin. After administration of 5000 IU of human chorionic gonadotrophin, 18 oocytes were collected. At 48 h after insemination with the patient's husband's spermatozoa, four 4-cell pre-embryos were transferred. A singleton pregnancy developed and led to the birth of a girl who is doing well 10 months later.

Dexamethasone inhibition of interferon-alpha 2-induced stimulation of cortisol and growth hormone secretion in chronic myeloproliferative syndrome.

This study investigated the acute effects of interferon-alpha 2 (IFN-alpha 2) on hormonal secretion in adult patients affected by a chronic myeloproliferative syndrome and tried to shed some light on the mechanism by which IFN-alpha 2 stimulates cortisol and GH secretion in humans. We compared the pattern of IFN-alpha 2-induced cortisol and GH release with that elicited after the same challenge given subsequent to pretreatment with dexamethasone (Dex). We studied eight patients affected by a chronic myeloproliferative syndrome (thrombocythemia) who had been selected for treatment with IFN-alpha 2. Four sets of experiments were performed: 1) 2 mL iv saline was given at 0800 h in eight cases; 2) 3 x 10(6) IU iv IFN-alpha 2 was given at 0800 h in eight cases; 3) 3 x 10(6) IU iv IFN-alpha 2 was given at 0800 h after pretreatment with 1.5 mg Dex (1 mg at midnight the previous night and 0.5 mg at 0700 h on the day of the test) in six cases; and 4) 2 mL iv saline was given at 0800 h after the same Dex pretreatment in four cases. Cortisol and GH were measured in plasma samples drawn at 30-min intervals between 0800 and 1300 h. Acute iv administration of IFN-alpha 2 stimulated the release of both cortisol and GH in each patient with a significant increment vs. control values, as assessed by areas under the curve. The administration of Dex significantly decreased basal plasma cortisol secretion and abolished cortisol response to IFN-alpha 2 administration. These data suggest that the stimulatory action of IFN-alpha 2 on cortisol release is mediated via a modulation of the activity of the hypothalamic-pituitary axis rather than through a direct effect at the level of the adrenal cortex. After Dex plus saline administration, no significant effect was observed on plasma GH levels, which remained low. Dex administration significantly decreased GH response to IFN-alpha 2. These data suggest that a hypothalamic or pituitary stimulation (or both) is involved in the mechanism of IFN-alpha 2-induced GH secretion. It remains to be established whether IFN-alpha 2 directly stimulates pituitary somatotropic cells or whether the cytokine exerts a stimulatory action on GH secretion by indirectly modulating the hypothalamic or pituitary activity. In conclusion, acute iv administration of IFN-alpha 2 represents a potent stimulus for cortisol and GH secretion in adult human subjects.(ABSTRACT TRUNCATED AT 400 WORDS)

Thyrotoxicosis due to ectopic retrotracheal adenoma treated with radioiodine.

Ectopic thyroid tissue is rarely found in the cervical retrotracheal region and its functional autonomy with suppression of the normal gland can be considered unusual. We report a case of thyrotoxicosis in a patient who had no palpable goitre in the neck but was found to have a solitary toxic thyroid nodule behind the trachea. US and CT scanning confirmed that the nodule was retrotracheal and apparently was not continuous or contiguous with the normal thyroid gland. The toxic adenoma showed avid uptake of iodine-131 (131I), and using thallium-201-chloride (201Tl)-SPECT the normal thyroid gland together with the retrotracheal autonomous nodule was demonstrated. The patient underwent radiometabolic therapy with 666 MBq of 131I and a 131I scan performed 6 months later showed only the previously suppressed normal thyroid gland.

Incidentally discovered adrenal masses: a functional and morphological study.

In the last two years we have examined 17 consecutive patients (11 females and 6 males, 20-66 years old) in whom an unsuspected adrenal mass was discovered by ultrasonography or computed tomography performed for unrelated reasons. Pathological diagnosis was available in 11 cases based on surgical excision in 9 (2 pheochromocytomas of 5 and 12 cm in diameter; 2 ganglioneuromas of 5 and 6 cm; and 5 benign cortical adenomas between 3 and 5 cm), autopsy in 1 (a disseminated malignant pheochromocytoma of 16 cm) and fine-needle biopsy in 1 (a pseudo-adrenal mass of 6 cm, that was a regenerative hepatic nodule). The remaining 6 non histologically diagnosed masses were less than 3 cm in diameter. Endocrine studies showed elevated urinary excretion of catecholamines, vanillylmandelic acid and metanephrines in the pheochromocytomas and borderline high values in ganglioneuromas. A low plasma renin activity was encountered in 2 operated cortical adenomas and 3 non operated incidentalomas. In 2 of the latters aldosterone serum levels were elevated and the final diagnoses respectively were Conn's adenoma and dexamethasone-suppressible hyperaldosteronism with bilateral nodular hyperplasia. An inappropriate cortisol secretion was documented in a cortical adenoma removed. Radio-cholesterol scintiscan showed unilateral or increased uptake on the side of adrenal mass (concordant uptake) in the 5 benign cortical adenomas removed and in 4 non operated incidentalomas. A decreased uptake on the side of the adrenal mass (discordant uptake) was found in the 2 ganglioneuromas while an indeterminate bilateral uptake was found in the 2 remaining non operated incidentalomas and in the pseudo-adrenal mass.(ABSTRACT TRUNCATED AT 250 WORDS)

Corticotropin-releasing hormone inhibition of paradoxical growth hormone response to thyrotropin-releasing hormone in insulin-dependent diabetics.

A paradoxical growth hormone (GH) response to thyrotropin-releasing hormone (TRH) has been observed in type 1 diabetic patients and was hypothetically attributed to a reduced hypothalamic somatostatin tone. We have previously reported that corticotropin-releasing hormone (CRH) inhibits GH response to growth hormone-releasing hormone (GHRH) in normal subjects, possibly by an increased release of somatostatin. To study the effect of CRH on anomalous GH response to TRH, we tested with TRH (200 micrograms intravenously [IV]) and CRH (100 micrograms IV) + TRH (200 micrograms IV) 13 patients (six males and seven women) affected by insulin-dependent diabetes mellitus. A paradoxical GH response to TRH was observed in seven of 13 patients, one man and six women. In these subjects, the simultaneous administration of CRH and TRH significantly reduced the GH response to TRH, as assessed by both the maximal GH mean peak +/- SE (2.18 +/- 0.67 v 9.2 +/- 1.26 micrograms/L, P less than 0.005) and the area under the curve (AUC) +/- SE (187 +/- 32 v 567 +/- 35 micrograms.min/L, P less than .001). CRH had no effect on TRH-induced thyroid-stimulating hormone (TSH) release. Our data demonstrate that the paradoxical GH response to TRH in patients with type 1 diabetes mellitus is blocked by CRH administration. This CRH action may be due to an enhanced somatostatin release. Our data also show that exogenous CRH has no effect on TSH response to TRH, thus suggesting the existence of separate pathways in the neuroregulation of GH and TSH secretion.

Effects of sex and age on pyridostigmine potentiation of growth hormone-releasing hormone-induced growth hormone release.

Previous studies have shown that pyridostigmine (PD) is capable of increasing the growth hormone (GH) response to GH-releasing hormone (GHRH) in young healthy subjects. In order to investigate the influence of age and sex on the PD potentiation of GHRH-induced GH release, we have studied the GH response to GHRH (50 micrograms i.v.) 1 h after oral administration of placebo or PD (60 mg) in 8 young healthy men (aged 19-28 years) and 8 age-matched young women (aged 18-25 years) during the follicular phase of the menstrual cycle, as well as in 8 postmenopausal women (aged 57-62 years) and 8 age-matched elderly men (aged 56-64 years). In the same subjects the effect of PD alone (60 mg p.o.) was also studied. Furthermore, in 6 postmenopausal women and 6 elderly men, the effect of a 30-mg PD oral dose on GH secretion and GH response to GHRH was evaluated with a similar protocol. The GH responses (mean +/- SE) to GHRH + placebo were similar in young men (peak 20.1 +/- 2 ng/ml, AUC 1,250 +/- 113 ng/ml/min) and women (peak 29.3 +/- 2.3 ng/ml, AUC 1,769 +/- 305 ng/ml/min). PD 60 mg was capable of significantly increasing the GH response to GHRH in young men (peak 43.5 +/- 5.1 ng/ml, AUC 3,734 +/- 472 ng/ml/min, p less than 0.005) but not in women (peak 39 +/- 2.3 ng/ml, AUC 2,479 +/- 205 ng/ml/min).(ABSTRACT TRUNCATED AT 250 WORDS)

Activation of cholinergic tone by pyridostigmine reverses the inhibitory effect of corticotropin-releasing hormone on the growth hormone-releasing hormone-induced growth hormone secretion.

Previous studies have shown that corticotropin-releasing hormone (CRH) is capable of inhibiting growth hormone (GH) secretion in response to GH-releasing hormone (GHRH). In an attempt to clarify the mechanism of the CRH action, we have studied the effect of enhanced cholinergic tone induced by pyridostigmine on the CRH inhibition of the GH response to GHRH in a group of six normal men and six normal women. All subjects presented a normal GH response to 50 micrograms i.v. GHRH administration (mean peak +/- SEM plasma GH levels 20 +/- 2.9 micrograms/l in men and 28.9 +/- 2.9 micrograms/l in women) with a further significant increase after pyridostigmine pretreatment (60 mg orally given 60 min before GHRH) in men (GH peaks 43.1 +/- 6.9 micrograms/l, p less than 0.005) but not in women (GH peaks 39.2 +/- 3.0 micrograms/l). In the same subjects, peripherally injected CRH (100 micrograms) significantly inhibited the GH response to GHRH (GH peaks 8.1 +/- 0.6 micrograms/l in men, p less than 0.005 and 9.9 +/- 0.7 micrograms/l in women, p less than 0.005). Pyridostigmine (60 mg) given orally at the same time of CRH administration (60 min before GHRH) reversed the CRH inhibition of GHRH-induced GH secretion (GH peaks 35.3 +/- 8.2 micrograms/l in men and 35 +/- 3.3 micrograms/l in women) with a response not significantly different to that seen in the pyridostigmine plus GHRH test. Our data confirm that pyridostigmine is capable of potentiating the GHRH-induced GH release in normal male but not female subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute complications in the course of "mild" hyperparathyroidism.

It is generally accepted that some patients affected by mild asymptomatic primary hyperparathyroidism need not be treated with surgery, but may be medically managed without risk. However, our experience regarding 5 of these cases observed in the last two years, suggests a different approach. These patients, initially diagnosed as having mild hyperparathyroidism based on only moderately elevated serum concentrations of calcium and followed medically for years, were referred to us for a sudden worsening of their clinical course. One 35-year-old man presented hemorrhagic gastritis with severe anemia and type II AV block with syncopal attacks. Three women, aged 51, 64 and 65 years, presented with severe hypercalcemia associated with renal failure in two and with marked bone disease in another. In all these cases parathyroid neoplasms were preoperatively localized (by ultrasonography, CT scan and radioactive 201-Tl 99-Tc scan) and surgically removed. Histological examination showed a parathyroid carcinoma in the male patient and single gland enlargements in the three females. A fifth patient, a 65-year-old woman, was referred to us in critical condition: severe hypercalcemia, osteopenia with femur fracture, myocardial infarction and renal failure. She died in a few days, in spite of intensive medical care. These cases suggest that patients with hyperparathyroidism initially diagnosed as "mild" need close medical observation and preferably, in our opinion, should undergo surgery.

Sexual dimorphism of pyridostigmine potentiation of growth hormone (GH)-releasing hormone-induced GH release in humans.

Sex differences in the neuroregulation of GH secretion are not now known in humans. To investigate whether activation of cholinergic tone by pyridostigmine could cause a sex-related difference in the pituitary responsiveness to GH-releasing hormone (GHRH), we have studied the GH response to GHRH in 16 normal subjects (8 men and 8 women) tested after oral placebo or different doses of pyridostigmine (30, 60, and 120 mg). Each subject presented a normal response after iv administration of 50 micrograms GHRH and placebo. In men each dose of pyridostigmine induced a significant increase in the GH response to GHRH, as assessed by both the maximal GH peak and the area under GH curve. In women, on the contrary, the GH response to GHRH was not potentiated by pretreatment with pyridostigmine at any given dose. Only five female subjects were tested with 120 mg pyridostigmine because of the severe side-effects of the drug at this dosage. Our present data strongly suggest that in humans there is a sex-related difference in the neuroregulation of GH secretion and this is probably expressed through a different cholinergic tone.

Corticotropin-releasing hormone inhibition of growth hormone-releasing hormone-induced growth hormone release in man.

Recent studies in the rat have shown that intracerebroventricular administration of CRH inhibited spontaneous pulsatile GH secretion and prevented GH-releasing hormone (GHRH)-induced GH release. We have studied the effect of CRH on GHRH-induced GH release in man. In the first study, CRH was injected iv at three different doses (100, 50, or 25 micrograms) at 0800 h together with 50 micrograms GHRH in six men and six women. In a second study, 100 micrograms CRH were given iv at 0800 h, 1 h before the administration of 50 micrograms GHRH in five men and five women. Each subject demonstrated a normal GH response after the administration of 50 micrograms GHRH plus saline. All doses of CRH administered simultaneously with GHRH significantly inhibited GHRH-induced GH release in women [peak value +/- SE after GHRH plus saline, 28.9 +/- 2.9 micrograms/L; after GHRH plus 100 micrograms CRH, 9.9 +/- 0.7 micrograms/L (P less than 0.001); after GHRH plus 50 micrograms CRH, 8.7 +/- 0.8 micrograms/L (P less than 0.001); after GHRH plus 25 microgram CRH, 9.5 +/- 1.6 microgram/L (P less than 0.001]). In contrast, in men, while a dose of 100 micrograms CRH was capable of suppressing GHRH-induced GH secretion (peak value +/- SE, 8.1 +/- 0.6 vs. 20 +/- 2.9 micrograms/L; P less than 0.001), no inhibition was observed after 50- and 25-micrograms doses. When 100 micrograms CRH were injected 1 h before the administration of 50 micrograms GHRH, it strongly inhibited GHRH-induced GH secretion in both men (peak value +/- SE, 6.2 +/- 2.8 vs. 24.6 +/- 5.9 micrograms/L; P less than 0.02) and women (peak value +/- SE, 14.2 +/- 4.5 vs. 37.8 +/- 6.7 micrograms/L; P less than 0.005), and this inhibition lasted up to 2 h post-CRH administration. These results demonstrate that CRH is capable of inhibiting GHRH-induced GH release in both men and women. Furthermore, the findings suggest that a sexual dimorphism in the neuroregulation of GH secretion may be present in man. In view of the inhibitory action of CRH on GH secretion, simultaneous administration of CRH and GHRH for testing should be avoided in clinical practice.

Prolactin-secreting adenomas--surgical results.

The long-term follow-up of the transsphenoidal microsurgical treatment in 119 consecutively operated women with a PRL-secreting adenoma is presented. An apparent total removal of the tumor was achieved in 98 cases with an enclosed tumor (58 grade 1 and 40 grade II). In the remaining cases the removal was considered partial. The achievement of persistent normal PRL basal levels was verified in 61 patients (44 grade I and 17 grade II) who had an apparent total removal of the adenoma. In the 37 remaining patients who were thought at surgery to have had total removal we have distinguished two groups: 30 patients showed a "relapse" or "persistence" of PRL levels below 200 ng/ml without clinical and radiological signs of tumor regrowth, and 7 patients with a PRL level higher than 200 ng/ml who had evidence of PRL-secreting tumor recurrence.

Cerebrospinal fluid pressure and prolactin in empty sella syndrome.

In 58 female patients with the primary empty sella (PES) syndrome, a study of the CSF dynamics was done by evaluating both the absorptive reserve by a lumbar infusion test at constant rate, and/or the ICP increase occurring during REM phase of nocturnal physiological sleep. In 33, prolactin (PRL) dynamics were also investigated evaluating both the response to sequential stimulating test with thyrotropin-releasing hormone (TRH) and metoclopramide (MCP) and/or the circadian variation of PRL levels. Impairment of CSF dynamics was found in the 84% who had a hormonal pattern characterized by an increase of the PRL response to TRH and MCP and a decrease of the PRL circadian variation. Twenty-one patients with impaired CSF dynamics underwent CSF shunting procedures with disappearance of the signs of intracranial hypertension. They also had restoration of normal PRL dynamics but the endocrine alterations improved only moderately. Altered CSF dynamics play a role in the pathogenesis of the PES syndrome. A correlation between elevated ICP and the hypothalamo-hypophyseal control of PRL secretion may exist.