Preliminary data suggesting production of interleukin-12 by rat Leydig cells cultured in vitro.
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Animals↗
Biomedical subjects
M Giusti
Publications and source records attributed to M Giusti.
Nitric oxide modulates Leydig cell function in vitro: is this a way of communication between the immune and endocrine system in the testis?
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Animals↗
Serum leptin levels in males with delayed puberty during short-term pulsatile GnRH administration.
Leptin may be a possible trigger for puberty. In normal males, it has been shown that leptin increases from the pre-pubertal to the early pubertal stage, and then declines in the late pubertal stage. We examined leptin levels in six male adolescents (mean age 16.3+/-0.6 yr; range 14.2-17.6 yr) with delayed puberty (constitutional delay of puberty no.=2; idiopathic hypogonadotropic hypogonadism no.=4) during 120 days of subcutaneous pulsatile GnRH administration. A group of subjects in pre-puberty (no.=11), early-puberty (n=10) and mid-puberty (no.=7) were evaluated as controls. Morning blood samples were taken for determination of leptin, testosterone, LH and FSH levels. In delayed puberty subjects blood samples were taken every 30 days after the start of GnRH administration. At each examination BMI and testicular volume were evaluated. A follow-up examination was performed in the 6 patients 1.3-7.5 yr after the end of the 120 days of GnRH therapy. At baseline evaluation in delayed puberty mean leptin levels were 11.3+/-2.0 microg/l (median 11.3 microg/l; range 4.7-17.3 microg/l) and were higher than those found in pre-puberty (p=0.04) and mid-puberty (p=0.001). During GnRH administration there was no change in BMI and leptin levels but there was an increase in gonadotrophin levels, testosterone and testicular volume. One hundred and twenty days after, mean serum leptin were 10.1+/-2.1 microg/l (median 9.1 microg/l; range 3.4-16.8 microg/l). At the end of the study, leptin levels were higher in delayed puberty than in mid-puberty (p=0.002). At the follow-up examination leptin levels were 4.3+/-1.3 microg/l (median 3.4 microg/l; range 1.4-9.1 microg/l) (p=0.03 vs end of 120 days GnRH therapy) while testosterone and BMI were not changed. In conclusion 120-day pulsatile GnRH administration induced in males with delayed puberty physiological-like pubertal changes but not the decline in leptin levels reported during the progression of puberty. Therefore, in males with delayed puberty an impairment in the phenomenon of leptin decline associated with progression of puberty could be suggested. However after retrospective diagnosis of pubertal delay and long-term therapy in subjects with idiopathic hypogonadotropic hypogonadism leptin levels declined. These data seem to indicate that time more than increase in testosterone levels and testicular volume is the determinant of leptin decline at puberty.
Adolescent↗
Biphasic effect of nitric oxide on testosterone and cyclic GMP production by purified rat Leydig cells cultured in vitro.
Nitric oxide (NO) biphasically modulates osteoclast function and sperm motility by exerting a positive effect at low concentrations and a negative effect at high concentrations. We therefore tested whether NO exerts a comparable effect on testosterone secretion by cultured rat Leydig cells. Three NO-donors, S-nitroso-N-acetylpenicillamine (SNAP), diethylamine/nitric oxide complex sodium salt (DEA/NO) and diethylenetriamine nitric oxide adduct (DETA/NO) were administered in a wide range of concentrations (10(-8)-10(-3) M for 3 h) to Percoll-purified Leydig cells from adult rats. These drugs raised testosterone and cGMP secretion when used at low concentrations (10(-8)-10(-5) M); however, they inhibited testosterone, but did not affect cGMP, secretion at concentrations higher than 10(-5) M. Administration of the NO scavenger haemoglobin (160 micrograms/mL) prevented both the stimulatory and the inhibitory effect of these drugs. Nitrite accumulation was measured as a marker of NO released by the drugs in our in vitro system; it fell within the range of control media in the presence of NO-donor concentrations lower than 10(-5) M, but was several-fold higher in the media of cells treated with concentrations of the NO-donors greater than 10(-5) M. These data show that (1) NO exerts a biphasic effect on testosterone secretion, which is stimulatory at low and inhibitory at high concentrations; (2) the stimulatory effect of NO is mediated by cGMP, the classic second messenger for NO action.
Adult↗
The role of rDNA genes in X chromosome association in the aphid Acyrthosiphon pisum.
Silver staining of mitotic metaphases of the aphid A. pisum reveals the presence of argentophilic bridges connecting the two X chromosomes. The presence of nucleolar material connecting sex chromosomes seems to be quite a common phenomenon in organisms belonging to very different phyla, and suggests a role of nucleolar proteins in chromosome association and disjunction. In somatic cells of A. pisum, bridges connecting X chromosomes are detectable not only after silver staining but also after CMA3 staining. This finding suggests that GC rich DNA is involved in this type of association. Molecular analysis of rDNA intergenic spacers shows several 247 bp repeats containing short sequences having a high level of homology with the chi sequence of Escherichia coli and with the consensus core region of human hypervariable minisatellites. Moreover, each 247 bp repeat presents a perfect copy of a promoter sequence for polymerase I. These aphid repeats show structural homologies with a 240 bp repeat, which is considered to be responsible for sex chromosome pairing in Drosophila, not only in view of their common presence within rDNA spacers but also for their length and structure. The presence of chi sequences in the IGS of A. pisum, by promoting unequal crossing-over between rDNA genes, could thus give rise to the nucleolar organizing region (NOR) heteromorphism described in different aphid species. Although X pairing at NORs is fundamental in aphid male determination, the presence of heteromorphism of rDNA genes does not inhibit male determination in the A. pisum clone utilized for our experiments.
Animals↗
Somatostatin and its analog lanreotide inhibit the proliferation of dispersed human non-functioning pituitary adenoma cells in vitro.
OBJECTIVE: Somatostatin is a powerful inhibitor of hormone secretion and cell proliferation. Treatment with somatostatin analogs in humans causes a reduction in size and secretory activity of some endocrine tumors, including somatotropic pituitary adenomas. Less studied are the effects of somatostatin agonists on non-functioning pituitary adenomas (NFPAs). In this study we characterized the effects of somatostatin and its analog lanreotide on the proliferation of NFPAs in vitro and the intracellular mechanisms involved. DESIGN: Twenty-three NFPA post-surgical specimens were analyzed for somatostatin receptor (SSTR) expression and 12 of them were cultured in vitro to study somatostatin's effects on cell proliferation, assessed by means of [(3)H]thymidine uptake, and the intracellular signaling. RESULTS: One or more SSTR subtypes were expressed in 90% of the adenomas tested. Somatostatin and lanreotide treatment inhibited phorbol myristate acetate (PMA)-induced cell proliferation. Vanadate pretreatment reversed somatostatin and lanreotide inhibition of PMA-induced DNA synthesis suggesting an involvement of tyrosine phosphatase in this effect. In the only adenoma tested, somatostatin directly induced a tyrosine phosphatase activity. Somatostatin and lanreotide caused also a significant inhibition of voltage-sensitive calcium channel activity induced by 40mmol/l K(+) depolarization in microfluorimetric analysis. CONCLUSIONS: These data show that somatostatin and lanreotide inhibit human NFPA cell proliferation in vitro, and suggest that activation of tyrosine phosphatases and inhibition of the activity of voltage-dependent calcium channels may represent intracellular signals mediating this effect.
Adenoma↗
A novel mechanism for the melatonin inhibition of testosterone secretion by rat Leydig cells: reduction of GnRH-induced increase in cytosolic Ca2+.
The site of inhibition, by melatonin, of GnRH-dependent testosterone secretion was investigated in adult rat Leydig cells cultured in vitro. The various effects downstream of the binding of GnRH to its own receptor were isolated and mimicked by specific drugs. Testosterone secretion was then evaluated after 3 h stimulation with GnRH, thapsigargin (1 microM), phorbol-12-myristate-13-acetate (100 nM), arachidonic acid (20 microM), and ionomycin (1 microM) in the presence or absence of melatonin (215 nM). The effect of melatonin on the GnRH-induced changes in cytoplasmic calcium concentration ([Ca(2+)](i)) was also studied, using Fura-2 as fluorescent Ca(2+) indicator. Melatonin attenuated the increase in [Ca(2+)](i) and inhibited the testosterone secretion induced by GnRH, but not that induced by ionomycin. Both ionomycin and thapsigargin potentiated GnRH-induced testosterone secretion; however, ionomycin, but not thapsigargin, partially prevented the inhibitory effect of melatonin on cells stimulated with GnRH. The effect of melatonin was probably dependent on the binding of melatonin to its Gi-protein-coupled receptor, as the inhibitory effect on GnRH-induced secretion was supressed in cells pretreated with pertussis toxin in a concentration of 180 ng/ml for 20 h. Assay of 17-hydroxy-progesterone showed that, irrespective of the treatment, cells cultured with melatonin secreted greater amounts than controls. We conclude that melatonin reduces GnRH-induced testosterone secretion by 1) decreasing [Ca(2+)](i), through impairment of the GnRH-dependent release of Ca(2+) from intracellular stores and 2) blocking 17-20 desmolase enzymatic activity, an effect that occurs irrespective of changes in [Ca(2+)](i).
17-alpha-Hydroxyprogesterone↗
[Gonadotropin response to GnRH and seminal parameters in low grade varicocele].
The pathogenetic role of varicocele in male infertility is still controversial. Although epidemiological data have clearly shown a higher incidence of varicocele in the population of subfertile and infertile patients, the real effectiveness of the surgical repair of varicocele, expressed as increase in the pregnancy rate, is still debated. The presurgical gonadotropin releasing hormone (GnRH) test is the most reliable predictive index of successful surgical outcome in terms of fertility. Only patients with an increased gonadotropin response (in particular FSH) to GnRH will benefit from the surgery. The aim of the present study was to evaluate the gonadotropin response to GnRH 50 micrograms i.v. in a group of patients with low-medium grade varicocele. At the beginning of the test, a fine needle was inserted into the forearm and kept patent by a saline solution. Blood samples were collected at the following experimental times: 0, +15, +30, +60, +90, +120 min. The stimulus was administered i.v. as bolus at time 0. The gonadotropin response to the stimulus and baseline levels of testosterone, PRL, 17 beta oestradiol and SHBG were compared with those of a control group. Moreover, all the patients underwent semen analysis after 3-7 days' abstinence and to ultrasound-doppler of the testis. Finally, we preliminarily looked for the presence of microdeletions on the Yq chromosome by polymerase chain reaction. No difference in baseline hormonal levels was found between the patients with varicocele and the controls; the LH response to GnRH was also similar in the two groups. The patients with varicocele showed a significantly (p = 0.03) higher FSH response (13.6 +/- 5.9 mUI/ml) to GnRH than controls (3.8 +/- 0.5 mUI/ml). A significant positive correlation (r = 0.6, p = 0.05) was found between LH peaks after GnRH testing and varicocele grade. Nine of 11 patients with varicocele showed significant seminal abnormalities (i.e., oligoasthenospermia): all patients showed a normal karyotype and no microdeletions were detected on the Yq chromosome. The authors underline the importance of presurgical GnRH testing in patients with low grade varicocele, given the close correlation between gonadotropin-stimulated peaks and varicocele grade found in the study. The presence of significant seminal abnormalities, even in patients with low grade varicocele, suggests the use of molecular genetic techniques to detect possible microdeletions on the Yq chromosome, which may be responsible for the infertility.
Adolescent↗
[An increased prevalence of thyroid echographic and autoimmune changes in hyperprolactinemic women on therapy with dopaminergic drugs].
Prolactin (PRL) possesses mitogenic and immunomodulatory properties. We evaluated the prevalence of ultrasonographic thyroid alterations and thyroid autoimmunity in hyperprolactinaemic (HPRL) women and correlated these with PRL levels. Furthermore, we studied the PRL binding in human benign nodular thyroid tissues. 133 HPRL patients (16-63 years) and 103 healthy female controls (16-63 years) with no known history of thyroid disease were studied. Blood samples were collected for PRL, FT3, FT4, TSH, thyroid peroxidase auto-antibodies (TPO Ab) and thyroglobulin auto-antibodies (Tg Ab) assays. All subjects underwent thyroid ultrasonography. PRL binding to thyroid membranes was determined by in-vitro radioreceptor assay in 5 human benign nodular thyroid fragments obtained from female patients. No difference in TSH levels was found, while FT3 (4.5 +/- 0.1 pmol/L) and FT4 (16.2 +/- 0.4 pmol/L) levels were significantly higher in controls than in HPRL (FT3: 3.8 +/- 0.1 pmol/L, p = 0.01, FT4: 15.4 +/- 0.2 pmol/L, p = 0.04). The prevalence of thyroid ultrasonographic alterations (simple goitre, uni-multinodular goitre, chronic thyroiditis) was significantly higher in HPRL (30.8%) than in controls (15.5%, p = 0.01) but did not correlate with mean initial and actual PRL levels or duration of the disease. The prevalence of autoantibodies was significantly higher in HPRL (29.6%) than in controls (14.3%, p = 0.04) but did not correlate with PRL levels. Very low specific PRL binding to thyroid membranes was detected. The high prevalence of thyroid ultrasonographic alterations and autoimmunity in HPRL suggests a possible role of PRL in the development of thyroid diseases. Clinical and instrumental thyroid screening may therefore be advisable in these patients.
Adolescent↗
Assessment of quality of life in recently post-menopausal women on dopaminergic therapy for pathological hyperprolactinaemia.
BACKGROUND: Psychological distress has been reported in pre-menopausal hyperprolactinaemic women. The aim of this study was to assess quality of life in a group of recently post-menopausal women with a long-term history of hyperprolactinaemia. METHODS: Thirty-one recently post-menopausal hyperprolactinaemic women (age range 46-59 years) and 37 control women matched for age and menopausal status. Hyperprolactinaemia had been diagnosed 2-22 years before the study. All hyperprolactinaemic women were on dopaminergic therapy. The self-rating Kellner Symptom Questionnaire (KSQ) and the Hamilton Depression Scale (HDS) were used to evaluate psychiatric profile. Evaluation of climacteric symptoms was performed with the ad-hoc self-rating 21-item Menopausal Rating Scale (MRS). Serum PRL, E2, LH, FSH, and free-thyroid hormones were evaluated. RESULTS: Hyperprolactinaemic women showed normal PRL on dopaminergic therapy. No difference was noted in PRL, LH, FSH, free-T4, and E2 levels between groups. Free-T3 was significantly (p = 0.001) lower in hyperprolactinaemic than in control women. There was no difference in overall scores on the MRS between the groups. Only the item "rapid and strengthened heart-beat" was significantly (p = 0.04) lower in hyperprolactinaemic than in control women. Control women showed a significant correlation between the score for this item and free-thyroid hormone levels. Overall KSQ scores and subsection analysis of items did not show significant differences between groups. On HDS evaluation, depressive symptoms were similar in hyperprolactinaemic and control women. CONCLUSIONS: Quality of life seems unchanged in recently post-menopausal women with a long-term history of hyperprolactinaemia currently on dopaminergic therapy. The present study does not therefore support the differences in psychological profile reported in literature between untreated hyperprolactinaemic and control women unselected for age.
Dopamine Agents↗
Hypothalamic-pituitary-adrenocortical axis function in premenopausal women with rheumatoid arthritis not treated with glucocorticoids.
OBJECTIVE: To assess hypothalamic-pituitary-adrenocortical axis function in patients with rheumatoid arthritis (RA) not previously treated with glucocorticoids in relation to their inflammatory condition and in comparison to healthy controls. METHODS: We evaluated, in 10 premenopausal patients with RA and 7 age matched controls, plasma dehydroepiandrosterone (DHEA), its sulfate (DHEAS), and cortisol concentrations, together with inflammatory cytokine levels [interleukin 6 (IL-6) and IL-12], both in basal conditions and after stimulation with ovine corticotropin releasing hormone (oCRH) and with low dose intravenous (5 microg) adrenocorticotropic hormone (ACTH). RESULTS: DHEA and DHEAS basal concentrations were found to be significantly lower (p<0.05) in premenopausal patients with RA than in controls. As expected, significantly higher basal levels of IL-6 and IL-12 (p<0.05) were found in patients with RA. After the low dose ACTH testing, the DHEA area under the curve value was found to be significantly lower (p<0.01) in patients than controls. Similar results, but without statistical significance, were observed after oCRH stimulation. DHEA levels at basal time showed a significant negative correlation with the erythrocyte sedimentation rate and platelet count, as well as with the Steinbrocker class of the disease (p<0.05). Normal plasma cortisol levels during oCRH and ACTH testing were found in patients with RA in spite of their inflammatory condition. After ACTH testing, IL-6 levels decreased significantly (p<0.05), whereas IL-12 levels were unchanged. No significant changes in IL-6 and IL-12 levels were found after oCRH testing. CONCLUSION: The abnormal androgen concentrations observed during testing in patients with RA might support the implication of adrenal androgens in the immune/inflammatory cytokine mediated mechanisms involved in the pathophysiology and clinical aspects of RA.
Adrenocorticotropic Hormone↗
Frequency of recovery from anorexia nervosa of a cohort patients re-evaluated on a long-term basis following intensive care.
The need to treat the acute onset of anorexia nervosa in a specialty unit is well known, but nevertheless, even "clinically recovered" patients show a high rate of relapse. The aim of our study was to re-evaluate various clinical (hemoglobin, transferrin, insulin-like growth factor I, TSH, PRL, gonadotropins and 17 beta-estradiol) and psychiatric [semistructured interview, Eating Disorder Inventory (EDI) Test] parameters in 19 female anorexic patients hospitalized in our department from 1983 to 1993 (with a 9-year median prior to the present study) for the treatment of anorexia nervosa, and to compare these results with those of a previous follow-up performed on the same subjects in 1993. In the present evaluation, no significant variation was found among the clinical, nutritional and hormonal parameters when compared to those of the first follow-up in which all parameters had improved with the exception of the PRL levels, which were significantly low. Meanwhile, the percentage of patients with spontaneous menses increased significantly from 50% to 70%, while the number of patients on psychopharmacological therapy decreased significantly throughout the study. Furthermore the percentage of patients with altered (severe or mild) EDI profiles decreased to 50%. This study emphasizes the positive prognostic role of hospitalization and intensive care in a cohort of anorexic patients. The present study, in addition to demonstrating both a general maintenance of body weight acquired over the years, albeit in the lower normal range, and an increase in the percentage of patients with a regular menstrual cycle, also highlights the persistence of psychiatric abnormalities in a large number of patients, even in those diagnosed as "clinically recovered", thus suggesting the need for long-term psychiatric care.
Adolescent↗
Increased prevalence of Helicobacter pylori infection in females treated with dopaminergic drugs for hyperprolactinaemia.
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Adolescent↗
Impact of recombinant human growth hormone treatment on psychological profiles in hypopituitary patients with adult-onset growth hormone deficiency.
BACKGROUND: We examined the effect of growth hormone (GH) administration on the psychological capacity and sense of well-being in 25 patients with adult-onset GH-deficiency (GHD). METHODS: Very low dosages [0.5-1.0 UIday(-1) s.c. at bed-time] of recombinant human (rh)-GH (n = 13; aged 50+/-15 years, mean+/-SD) or placebo (n = 12, 53+/-14 years) were given at random for a 6-month period. Quality of life was assessed by using the Italian version of the self-rating Kellner Symptom Questionnaire (KSQ) and the Hamilton Depression Scale (HDS). RESULTS: No difference in insulin-like growth factor I (IGF-I) levels was noted between groups on entry to the study. A significant increase in IGF-I [month 0 56.2+/-10.4 microg L(-1) vs. month 6 125.7+/-16.7 microg L(-1); P < 0.001] levels was noted only in the rh-GH-treated group. There was no difference in overall scores on the KSQ between the rh-GH-treated and control groups on entry. A slight, non-significant, decrease in overall scores was noted in both groups of subjects. Subsection analysis of items from the KSQ did not show significant differences in either group during the 6-month period. A significant decrease (month 0 28+/-1 vs. month 6 25+/-1; P = 0.02) in the HDS score was noted in rh-GH-treated but not in placebo-treated patients. There was a significant correlation (rs, -0.56, P = 0.05) between increase in IGF-I levels and decrease in HDS scores in rh-GH treated patients. CONCLUSION: The data demonstrate that low rh-GH dosages significantly improve psychological profiles as rated by HDS evaluation in adult-onset patients with GHD. On the other hand, a 6-month period of treatment does not produce any significant differences in quality of life as measured by KSQ between treated patients and placebo controls.
Adult↗
Cilia-associated respiratory (CAR) bacillus infection in conventionally reared rabbits.
This study was designed to investigate the prevalence of Cilia-associated respiratory (CAR) bacillus infection in rabbits reared for meat production in Italy and to correlate the presence of CAR bacillus with inflammatory lesions of the respiratory tract. Seventy health, 3-month-old, New Zealand White rabbits, raised in 10 different rabbitries in Northern Italy were randomly selected at slaughter. No gross lesions were found at necropsy in any rabbit. In each animal, the trachea and lungs were sampled, fixed in 10% formalin, embedded in paraffin and stained with the Warthin-Starry method to evaluate the presence of CAR bacillus, and with haematoxylin and eosin to evaluate the presence of inflammatory lesions. CAR bacillus was present in 50 out of 70 rabbits (71.4%) with a prevalence of the infection that varied from 30% to 100% in the seven rabbitries. CAR bacillus was present both in the trachea and bronchi in 23 cases (32.8%), only in the trachea in 24 cases (34.3%) and only in the bronchi in three cases (4.3%). Inflammatory lesions were found in the trachea (22 cases, 31.4%) and the bronchi (58 cases, 82.8). There was a strong, statically significant correlation between the presence of CAR bacillus in the bronchi and bronchial inflammatory lesions (P < 0.0001). This study indicates that CAR bacillus infection is widespread in conventionally reared rabbits in Italy and that a possible correlation exists between the presence of CAR bacillus and bronchial inflammatory lesions.
Animals↗
Desmopressin and low-dose ACTH test in rheumatoid arthritis.
OBJECTIVE: To ascertain whether a different regulation and sensitivity of the hypothalamic-pituitary-adrenal axis exists and whether a type of cortisol resistance is present in rheumatoid arthritis (RA) patients, a chronic disease in whose pathogenesis modifications of the steroid milieu are involved. DESIGN: We studied the basal and dynamic response of ACTH and adrenal steroids to various stimuli acting on the hypophysis or directly on the adrenal gland. METHODS: We studied ten RA patients (39.8 +/- 7.4 (S.D.) years), defined according to the American Rheumatism Association, and seven healthy control patients (34.1 +/- 9.6 (S.D.) years). All subjects underwent testing, in random order, with placebo, desmopressin (DDAVP) (10 microg i.v.), ovine corticotropin-releasing hormone (oCRH) (1 microg/kg body weight) and low-dose ACTH (5 microg i.v.), during the follicular phase of two different menstrual cycles. Blood samples were collected at different times for ACTH and adrenal steroids assay. Baseline estradiol (E2), testosterone and IGF-I levels were also evaluated. All subjects collected urine specimens for 24 h urine free cortisol (UFC). RESULTS: No difference in E2, testosterone or UFC was found between RA patients and controls. IGF-I levels were significantly (P < 0.01) lower in RA patients (110.6 +/- 6.4 microg/l) than in controls (207.0 +/- 37.9 microg/l). Mean baseline dehydroepiandrosterone (DHEA) and delta4-androstenedione levels of the four tests were significantly (P < 0.05) lower in RA patients than in controls. In RA, a negative correlation was found between mean DHEA levels, class of disease (r = -0.67, P < 0.05) and erythrocyte sedimentation rate (r = -0.63, P < 0.05). After placebo no difference in ACTH and cortisol area under curves (AUCs) was found between RA patients and controls. After DDAVP no cortisol or ACTH response was found in RA patients, while a significant (P < 0.05) ACTH release was found in controls. Only in RA patients was DDAVP able to induce a significant (P < 0.01) DHEA increase. After oCRH a similar significant response in ACTH (P < 0.05), cortisol (P < 0.01), and DHEA (P < 0.01) was found in both groups. After low-dose ACTH, a similar significant (P < 0.01) cortisol response was found in both RA patients and controls; indeed in RA patients DHEA AUC (2196.0 +/- 321.8 nmol/l per 90 min) was significantly lower (P < 0.01) than DHEA AUC (4280.8 +/- 749.0 nmol/l per 90 min) in controls. A similar significant (P < 0.01), though not abnormal, 17-hydroxyprogesterone response to ACTH was found in both groups. CONCLUSIONS: Our study underlines reduced adrenal steroid and IGF-I levels, but not the previously described cortisol resistance in RA patients; it shows that baseline and dynamic cortisol levels are 'normal' but inadequate in the setting of a sustained inflammatory disease like RA. The reduced basal and low-dose ACTH-induced DHEA levels could reflect both a reduced sensitivity of the adrenal gland to exogenous corticotropin and a decreased steroid synthesis due to a partial adrenal enzymatic defect (P450 17,20 lyase).
Adrenocorticotropic Hormone↗
Dopaminergic modulation of hexarelin-induced GH and PRL secretion in hyperprolactinemia.
Hexarelin (Hex), a synthetic GH-releasing peptide, has recently been found to possess a weak PRL-releasing effect in normals. The aims of this study were to investigate the effect of Hex on GH and PRL secretion in 10 hyperprolactinemic women (HPRL) and 7 controls (C). All subjects underwent stimulus testing with placebo, bromocriptine (Br) (2.5 mg po at time -60), Hex (2 micrograms/kg/bw i.v.), and Br plus Hex. During placebo, HPRL showed a higher (p < 0.01) PRL area under curve (AUC) than C. Br significantly (p < 0.01) reduced PRL AUC both in HPRL and in C. Hex was able to induce a slight but significant (p < 0.05) PRL release in both groups. PRL response to Hex was abolished (p < 0.01 vs Hex) by Br priming in HPRL, while it was only blunted (p < 0.05 vs Hex) in C. Br induced a significant (p < 0.01) GH increase in both groups. However, GH AUC after Br was significantly higher (p < 0.01) in C than HPRL. Hex induced a significant (p < 0.01) GH release both in HPRL and in C. Br priming did not modify GH response to Hex in HPRL while it slightly (p < 0.05) increased GH response to Hex in C, suggesting that neuroendocrine modifications present in HPRL might, per se, be able to impair GH response to Br plus Hex, thus giving rise to receptor competition. Hex had a weak PRL-releasing effect in both groups studied, this was only blunted by Br priming in C but was abolished in HPRL, suggesting that oversensitivity to DA-ergic agents present in HPRL could be able to antagonize completely Hex action.
Adult↗
Magnetic resonance evaluation of autonomous thyroid nodules treated by percutaneous ethanol injection.
Magnetic resonance (MR) imaging was used to evaluate the effect of ultrasound-guided percutaneous ethanol injection (PEI) of autonomous thyroid nodules (ATNs). Nine patients affected with ATN (3.7-32.2 mL volume) underwent PEI (4-19 mL ethanol, subdivided in 3-6 weekly procedures). MR imaging (1.5 T) was performed before each alcoholization and 1 month after the last PEI procedure with the following parameters: T1- (550/12) and T2-weighted (2200/160) spin-echo images; 4-mm slices, 10% gap; coronal planes. A further seven patients with normal thyroid function, who had undergone PEI 6-18 months before, underwent an MR examination with the same parameters. The signal-to-noise ratio (S/N) of ATN and extranodular gland, as well as ATN volume, were evaluated on the T2-weighted images. On T1-weighted images, ATNs appeared mostly hypointense before treatment, with hyperintense areas during treatment, and were lightly hyperintense 6-18 months after treatment. S/N on T2-weighted images: extranodular gland 3.5-9.2; ATNs, before treatment 13.2-19.7, before the last procedure 7.7-11.6, 1 month after the last procedure 5.6-10.9; previously treated ATNs, 4.3-8.2. No significant volume reduction was observed with MR 1 month after the last procedure. The MR examination time was about 15 minutes. In conclusion, the effect of PEI on ATNs can be evaluated with an MR examination that is not very time consuming.
Administration, Cutaneous↗