[Behavior of testicular androgenic and adrenocortical hormones in obesity. Physiopathological and clinical considerations].
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Biomedical subjects
Publications and source records attributed to D Scavo.
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The possible role of the renin-angiotensin system and ACTH in controlling the temporal organization of circadian rhythm of aldosterone was studied in patients with mesor-hypertension (MH) by simultaneous radioimmunological determinations of within-day changes in plasma renin, aldosterone and cortisol. Thirty-nine uncomplicated, untreated mesor-hypertensive patients, divided in subtypes, were examined. The interrelationship between the rhythm components revealed that the circadian cyclicity of aldosterone in both mesor-normotensive and mesor-hypertensive subjects, with either normal or high renin patterns, has a similar timing in acrophase with renin periodicity, which leads the circadian cortisol rhythm. In low-renin mesorhypertensive subjects a circadian rhythm of aldosterone and cortisol, but not of renin, remains demonstrable. The confidence limits of the estimated acrophase for circadian cortisol rhythm do not, however, overlap the confidence arcs of the aldosterone phase. These findings suggest that in normal or high renin MH subjects the aldosterone rhythmicity is mainly controlled by the renin-angiotensin system. Conversely in low-renin MH subjects the temporal organization of the aldosterone circadian sequences seems to be completely independent of renin-angiotensin control.
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To investigate whether inappropriate LH secretion in Polycystic Ovary Syndrome (PCO) was related to a reduction of inhibitory opioid control on the GnRH-LH system, 23 women affected by PCO (12 obese, BMI: 37.1 +/- 3.9 and 11 non obese, BMI: 21.5 + 2.4) and 19 fertile women (10 obese, BMI: 38.8 + 1.8 and 9 non obese, BMI: 20.1 + 1.5) were studied. Plasma levels of Beta-Endorphin (B-Ep) in basal condition and LH and FSH serum levels following acute administration of naloxone (0.1 mg/kg e.v.) were evaluated in the PCO and control groups. Moreover, in order to investigate whether the neuroendocrine abnormalities in PCO are a primary hypothalamic defect or secondary to an inappropriate feedback of gonadal steroids, the LH response following Naloxone administration was evaluated again after two months of clomiphene therapy (50 mg p.os ones a day for 5 days). The women affected by PCO had increased LH/FSH ratio, testosterone levels (P < 0.001, P < 0.01) and significantly decreased T/E2 ratio, SHBG levels compared to the normal women (P < 0.01, P < 0.001). B-Ep plasma levels in PCOs OB and PCOs nOB (6.13 + 1.2 Pmol/L, 4.8 + 0.4 Pmol/L) were similar to those observed in obese and non obese control women (7.2 + 2.5 Pmol/L, 4.2 + 1.3 Pmol/L), respectively. In the PCO and control groups naloxone induced a significant increase of FSH and LH levels. Thus the area under the curve of LH and FSH was significant higher after naloxone, than following saline infusion both in PCO (P < 0.01, P < 0.05) and controls (P < 0.001, P < 0.001). However, in PCO the post naloxone FSH increase was similar to that found in fertile women, while the LH increase post naloxone was lower than that observed in controls (50 + 32.4% vs 101.6 + 36.7%; P < 0.01). Particularly in PCO with LH/FSH ratio equal or higher than 3, no significant variation of LH levels was found after naloxone. Moreover the LH increase post naloxone was similar in PCO OB (46 + 19.8%) and in PCO nOB (49.9 + 13.1%), correlated negatively with LH basal levels (P < 0.02), LH/FSH (P < 0.005), E1/E2 (P < 0.005) and was independent of T/E2, BMI and duration of the disease. Following clomiphene treatment, the LH response after naloxone was significantly higher than that observed before treatment (from 9.4 + 4.2 mUI/ml to 16.5 + 3.9 mUI/ml, P < 0.001).(ABSTRACT TRUNCATED AT 400 WORDS)
This study was carried out in order to investigate serum changes of osteocalcin (BGP) and angiotensin converting enzyme (SACE) activity in a group of patients with hyperthyroidism. We studied 20 hyperthyroid patients (F 14, M 6; age mean 37.5 +/- 16.8 years) and 13 control subjects (F 11, M 2; age mean 40.3 +/- 7.5 years). In both patients and controls we measured: FT3, FT4, T3, T4, TSH, BGP, SACE. Finally, in patients with hyperthyroidism a TRH test and functional investigations were also performed. We observed that mean SACE levels were significantly increased in hyperthyroid patients (32.06 +/- 10.3 nmol/ml/min) in respect to control subjects (14.66 +/- 3.88 nmol/ml/min) (p = 2.02 E-6). Similarly serum BGP levels were significantly increased in hyperthyroid patients (5.94 +/- 2.55 ng/ml) than in control subjects (2.89 +/- 1.58 ng/ml) (p = 5.66 E-4). There was a significant linear correlation between SACE and T4 levels (r = 0.48; p < 0.05), between serum BGP and T4 (r = 0.50; p < 0.02) and furthermore between SACE and BGP (r = 0.57; p < 0.01). In conclusion both serum BGP and SACE levels are increased in patients with hyperthyroidism and are directly correlated between than and with indexes of thyroid function; therefore, they may be regarded as peripheral indexes of hyperthyroidism.
This case reports deals with a male patient, white, aged 51, bricklayer, tobacco smoker. At 43 years old a tubercular epididimite was surgically treated with orchiectomy. Recently, the reports marked weakness, weight loss, headache, vertigo, hypotension. On admittance to the hospital, hyperpigmentation was also present. Previous therapy (cortisone acetate 40 mg/die), was suspended, clinical investigations showed impaired adrenal and thyroidal functions; antimicrosomal antibodies were also present. Therefore therapy with cortisone acetate (25 mg x 2/die, 9-alpha-fluorohydrocortisone 0.1 mg/die and L-thyroxine 100 mcg/die) was instituted with marked improvement of the patient's conditions. This case reports highlights the importance of proceeding with complete investigations on the system, even when dealing with a tubercular Addison's disease.
This investigation is devoted to explore the 24-h patterns of serum angiotensin converting enzyme (ACE) activity in clinically healthy subjects and migraine patients taking as reference the adrenal cycle. Time data series have been analyzed by means of chronobiologic procedures. The biostatistical approach has documented that the enzymatic activity of serum ACE in clinically healthy subjects changes with a circadian periodicity. The chronobiologic approach has additionally revealed that the enzymatic activity of serum ACE activity is circadianly aperiodic in migraine patients, while plasma cortisol shows a preserved cyclicity along 24-h scale. The aperiodicity suggests that the enzymatic degradation of the ACE-dependent substrate is inappropriate over the 24-h span.
We describe a case of prolonged spontaneous remission of Cushing's disease lasting since 1986 and documented both clinically and biochemically. This case confirms previous sporadic observations based mainly on clinical findings and indicates that spontaneous remission of Cushing's disease, although rare, may exist. The Authors outline that in some cases of Cushing's disease it could be convenient to adopt a conservative policy with frequent outpatient reviews in order to observe the natural course of the disease, particularly when the clinical findings are mild and the original lesion is not recognized with the available technology.
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Five male and 5 female clinically healthy volunteers, 17-37 years of age, gave systemic venous blood at 0600, 0800, 1200, 1800, 2000 and 0000 for RIA of (supine values) plasma renin-angiotensin (PRA) and aldosterone (PA) under 4 conditions: a. unrestricted sodium intake, no treatment; b. unrestricted sodium intake and 40 mg propranolol per os every 6 h; c. sodium restriction, no treatment; d. propranolol loading on sodium deprivation. Cosinor methods were used for data analysis. Sodium restriction amplifies the circadian rhythms of PRA and PA, whereas propranolol loading inhibits these same rhythms on a unrestricted sodium intake, but much less so under conditions of sodium deprivation. The propranolol-induced inhibition of the circadian rhythms investigated on a unrestricted sodium intake suggests that the beta-adrenergic system is an effective mechanism coordinating the circadian rhythmic functions investigated. The persistence of the rhythms in sodium-depleted subjects under pharmacological blockade of beta-adrenoreceptors is in keeping with the concept that a second mechanism of the circadian rhythms examined is located in the sodium-sensitive macula densa cells of the renal distal tubule.
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