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S Della Casa

Publications and source records attributed to S Della Casa.

18 recordsLinked to original sources
PubMed1992

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.

Adult↗
PubMed1992

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)

Adolescent↗
PubMed1992

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)

Adolescent↗
PubMed1991

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.

Acute Kidney Injury↗
PubMed1991

Influence of naloxone infusion on prolactin and growth hormone response to growth hormone-releasing hormone in anorexia nervosa.

Anorexia nervosa (AN) is frequently associated with anomalies of growth hormone (GH) and prolactin (PRL) secretion. We studied the GH and PRL responses to GHRH1-44 (50 micrograms IV) and the effect of a naloxone infusion (1.6 mg/hr), started 1 hr before GHRH administration, on this response in 12 female patients with AN, aged 15-30 yr, and in seven normal women, aged 19-27 yr, during the follicular phase as controls. In AN, GHRH induced an increase in GH levels similar to that observed in normal subjects. A significant inhibition of the GH response to GHRH was observed during naloxone infusion, similar to the inhibition in normal female subjects during the follicular phase. PRL levels showed a significant increment after GHRH alone and a slight, nonsignificant, PRL increment after GHRH during naloxone infusion in AN patients. In contrast a slight PRL decrease was observed after GHRH, both before and during naloxone infusion, in the normal subjects. Our study demonstrates that endogenous opioids play a role in influencing PRL secretion in patients with AN different from their role in normal subjects.

Adolescent↗
PubMed1991

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.

Adult↗
PubMed1990

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.

Adult↗
PubMed1990

[The role of autoimmune mechanisms in the hyperthyroidism-viral hepatitis syndrome: a possible noncausal association. A review of the literature and the authors' own cases].

Several patients with both Basedow-Graves' hyperthyroidism and viral hepatitis were observed and it was hypothesised that this association could be explained by the individual genetic pattern in which an immunological fragility conditioned a predisposition to autoimmune diseases. This paper reports on the cases observed, the patients' histocompatibility antigen profile and the experimental data found in the literature on autoimmune involvement in the two diseases, whose association may not be coincidental.

Antibody Formation↗
PubMed1989

Corticotropin-releasing hormone inhibition of gonadotropin secretion during the menstrual cycle.

To determine whether corticotropin-releasing hormone (CRH) exerts an inhibitory action on gonadotropin secretion in normal fertile women, the effects of CRH on luteinizing hormone (LH), follicle-stimulating hormone (FSH), and cortisol secretion were studied during the menstrual cycle. CRH had no effect on LH release during the midfollicular phase of the cycle. By contrast, IV injection of 100 micrograms CRH elicited significant decreases in LH concentrations during late follicular (-50%) and midluteal (-52%) phases of the cycle. LH concentrations decreased during the four-hours following injection of CRH and returned to those observed during the control period five hours after injection. Similarly, CRH elicited a significant decrease in FSH secretion during the midluteal phase of the cycle. CRH injection induced an increase in cortisol release during all phases of the cycle. These data demonstrate that exogenous CRH administration results in inhibition of gonadotropin secretion in late follicular and midluteal phases of the cycle. These results suggest that elevated endogenous CRH levels resulting in increased cortisol secretion could contribute to decreased gonadotropin secretion and, thus, disruption of reproductive function during stressful conditions in women.

Adult↗
PubMed1989

Corticotropin-releasing hormone inhibition of gonadotropin release and the effect of opioid blockade.

We studied the inhibitory effect of exogenous CRH on pulsatile gonadotropin secretion and the role of endogenous opioid peptides in this phenomenon in normal women. To do so, we infused human CRH (100 micrograms/h for 3 h) into 15 normal women during the midluteal phase of their menstrual cycle and studied its effect on both basal (10 women) and GnRH-stimulated (5 women) plasma gonadotropin levels. CRH infusion induced a significant decrease in plasma LH and FSH levels in all women. The decline in plasma LH (62%) was greater than that in FSH (36%). Plasma LH and FSH concentrations returned to basal levels within 30 min after the end of the CRH infusion. CRH infusion did not alter the gonadotropin response to GnRH. We also infused naloxone plus CRH in the 10 women who had received CRH alone during the midluteal phase of a different cycle. Addition of naloxone to CRH (5 women) reversed the LH and FSH inhibition when naloxone was started 1 h after the start of the CRH infusion. When naloxone was started 1 h before CRH infusion (5 women), plasma LH and FSH concentrations did not change. Plasma cortisol increased similarly during both the CRH and CRH plus naloxone infusions; the mean cortisol levels at the end of the CRH and CRH plus naloxone infusions were 497 +/- 40 (+/- SE) and 484 +/- 41 nmol/L, respectively, compared to 240 +/- 14 nmol/L after saline infusion (P less than 0.001). These results demonstrate that in normal women during the midluteal phase of the menstrual cycle, CRH inhibits the secretion of both LH and FSH. The CRH-induced inhibition of gonadotropin secretion is primarily mediated by endogenous opioid peptides, and this effect is not dependent on glucocorticoid levels. We suggest that the disruptive effect of stress on reproductive function in the women could be, at least in part, dependent on decreased gonadotropin secretion induced by elevated endogenous CRH levels.

Adult↗
PubMed1987

A clinical study of Addison's disease.

Fifty-four patients affected by primary adrenocortical insufficiency have been retrospectively studied. Eighteen were affected by a tuberculous Addison's disease, 24 by an idiopathic Addison's disease and 12 by an unclassifiable form. Modality of arise, clinical presentation and association with other diseases are reviewed. The most useful laboratory and instrumental tests for the diagnosis are discussed and a diagnostic flow-chart is proposed.

Addison Disease↗
PubMed1987

Autoimmune polyglandular syndrome, primary empty sella, and acute lymphocytic leukaemia.

A young man is reported with an autoimmune polyglandular syndrome (APS) characterized by Addison's disease, primary hypothyroidism, primary hypogonadism, vitiligo, associated with primary empty sella and partial impairment of pituitary hormone secretion. Two years later the patient showed a null cell type acute lymphocytic leukaemia, immediately after surgery for an inguinal hernia. Pathogenetic mechanisms are postulated on the basis of HLA studies and lymphocytic typing.

Addison Disease↗
PubMed1987

Treatment of undescended testes with hMG and hMG plus hCG: clinical, hormonal and sonographic evaluation.

20 children (mean age 4, 6 yrs), of whom 13 had unilateral and 7 had bilateral cryptorchidism were treated with hMG: 40 I.U. three i.m. injections per week for six or eight weeks. Where there was no descent of testis, treatment was continued with hMG at the same dosage plus hCG 500 I.U. one i.m. injection per week for an additional four weeks. The children were tested for FSH, LH and Testosterone serum levels at the beginning of treatment and after 6, 8 and 14 weeks. We obtained testicular descent in 10 out of 20 cases treated. Ultrasonography enabled us to locate the undescended testes in all cases and to follow the response to treatment.

Child↗
PubMed1983

Endocrine study of anorexia nervosa.

The main objective of the study was to evaluate the endocrinological picture of anorexia. The sample consisted of 23 anorectic patients (20 females, 3 males) with a control group of 10 normal females and 5 normal males. All participants underwent a work-up which included testing for hypothalamic, hypophyseal, thyroidal, adrenal, gonadal functioning and glucose metabolism. Our results revealed a reduced urinary output and low serum levels of gonadotropins with different responses to LHRH correlating with the stage of the illness. We found reduced urinary estrogens and elevated testosterone levels in females. Males demonstrated a reduction of testosterone. While basal prolactinemia was normal in both sexes, males showed an exaggerated response to TRH. The thyroid function study in anorectic patients revealed a decrease in T3 and in free T3 and an increase in reverse T3. Free T4 was slightly increased with normal T4 levels. Basal TSH was normal with a delayed peak after TRH. We also noticed in the anorectic population reduced basal glucose levels with a flat glucose curve; reduced insulin levels with a slight increase after glucose administration; elevated basal GH with a fair response to L-Dopa; elevated serum cortisol with loss of circadian rhythm and slightly inhibited by dexamethasone. In addition, both noradrenalin and VMA were reduced. We concluded that the multiple endocrine abnormalities found are consistent with hypothalamic dysfunction. The etiology of this dysfunction remains for the endocrinologist highly controversial.

Adolescent↗
PubMed1983

Thyroid function in altered nutritional state.

We studied plasma concentrations of TSH (basal and after TRH), thyroxine (T4), 3,5,3'-triiodothyronine (T3), 3,3',5'-triiodothyronine (reverse T3; rT3), free T4 and free T3 in thirty obese subjects, twenty patients with anorexia nervosa, fifteen malnourished subjects and twenty normal weight subjects. Total serum T4 values were similar for the four groups of subjects while serum free T4 values were slightly increased in anorexia nervosa and normal in the other groups. Serum total and free T3 levels were both significantly decreased in anorexia nervosa and malnutrition, and within normal limits in obesity. The mean serum rT3 level was increased in anorexia nervosa and malnutrition while was reduced in obesity. A delay in peak response of TSH to TRH stimulation (30' rather than 20') was noted in anorexia and malnourished patients. The results suggest that these alterations of serum iodothyronines are due to a different peripheral conversion of T4 to T3 according to nutritional status.

Adolescent↗
PubMed1983

Effect of somatostatin on the pituitary-thyroid axis.

We studied the effect of Somatostatin on the pituitary-thyroid axis of 37 volunteer subjects. 17 were euthyroid, 12 hypothyroid, 7 hyperthyroid and one had a TSH secreting pituitary adenoma. We measured by radioimmunoassay plasma iodothyronines T4, T3, rT3, FT4 and FT3, as well as TSH in basal conditions and after TRH stimulation. Somatostatin (as an initial bolus of 250 micrograms i.v. followed by an infusion of 500 micrograms/h) was given in short-term infusion (3 h) or long-term infusion (12 h). The results obtained showed that during short-term infusion Somatostatin: does not influence TSH in normal subjects; reduces significantly basal TSH in hypothyroid patients; reduces significantly the TSH response to TRH both in normal and in hypothyroid subjects as well as in the case with a TSH secreting pituitary adenoma. During long-term infusion Somatostatin: does not change TSH levels in normal or hyperthyroid subjects; does not change the values of T4, FT4, T3, FT3 and rT3 in normal subjects; does not change the values of T4 and FT4 in hyperthyroid subjects but reduces significantly the values of T3 and FT3 and produces a marked rise in rT3 in the same ones. In conclusion, the inhibiting effect of exogenous Somatostatin is evident whenever TSH levels are high for pathological conditions or for drug stimulation. The findings of T3 and FT3 reduction with a marked rise in rT3 in hyperthyroid subjects during the long infusion indicate an extrathyroidal effect of Somatostatin on the peripheral metabolism of iodothyronines.

Adolescent↗
PubMedDate not supplied

[Evaluation of the testicular function using the HCG test in normal and cryptorchid children].

The testicular function has been evaluated by a single dose hCG-test in normal and cryptorchid prepubertal boys using three different protocols. No remarkable difference has been observed using different posologic protocols. Testicular function in boys affected by cryptorchidism was similar to the testicular function in normal controls. However cryptorchid boys older than 6 years of age showed a significant reduction in testicular response to hCG-test in comparison to cryptorchid boys younger than 6 years of age.

Adolescent↗