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Biomedical subjects

G Romanelli

Publications and source records attributed to G Romanelli.

At least 55 records · Page 3Linked to original sources
PubMed1989

Effects of intranasal calcitonin administration on pituitary GH response to hGHRH (1-29)NH2 in normal adult subjects.

Studies in man demonstrated that intramuscular salmon (s) calcitonin (CT) administration blunted pituitary GH response to hypothalamic stimuli such as arginine infusion and insulin-induced hypoglycaemia. However, the mechanisms underlying this inhibiting action of CT are still unclear. The aim of our study was to investigate the effects of intranasal (i.n.) and i.m. sCT administration on GH secretion elicited by direct pituitary stimulation in man with human GH-releasing hormone (GHRH) (1-29)NH2. Seven healthy non-obese volunteers (five men, two women; mean age +/- SDM 25 +/- 2) underwent a bolus intravenous injection of GHRH, 100 micrograms, alone or associated with sCT, administered either i.n., 300 IU, or i.m., 100 IU. Our data demonstrate a significant decrease in GH secretion after GHRH when either i.n. or i.m. sCT is administered. GH peak (mean +/- SDM); GHRH alone 22.9 +/- 2.5 vs GHRH plus i.n. sCT, 8.9 +/- 1.5 micrograms/l, P less than 0.001; or vs GHRH plus i.m. sCT 12.3 +/- 2.5 micrograms/l, P less than 0.001. Area under the curve of GH secretion: GHRH alone 1211 +/- 196 vs GHRH plus i.n. sCT 551 +/- 116 micrograms 120 min/l. P less than 0.001; or vs GHRH plus i.m. sCT 700 +/- 167 micrograms 120 min/l, P less than 0.001. We conclude that sCT is able to inhibit GHRH-stimulated GH secretion in man.

Administration, Intranasal↗
PubMed1989

Growth hormone deficiency in patients with idiopathic adrenocorticotropin deficiency resolves during glucocorticoid replacement.

Glucocorticoids (GC) have stimulatory effects on GH secretion in vitro and suppressive effects when administered in pharmacological amounts in vivo. We studied six patients with ACTH deficiency and severely impaired serum GH responses to insulin tolerance tests and arginine infusion tests. All patients underwent the same tests during GC replacement while receiving cortisone acetate in doses ranging from 12.5-25 mg/day. The three patients with idiopathic ACTH deficiency and no evidence of pituitary mass lesions had impaired GH secretion, which returned to normal during GC replacement. In contrast, the three patients with ACTH deficiency and hypothalamo-pituitary mass lesions detected by a computed tomography scan had impaired GH secretion during GC replacement therapy. Our data indicate that in patients with idiopathic ACTH deficiency, an impaired GH response to stimuli reversible during GC replacement therapy may be the functional consequence of the low levels of circulating cortisol. We conclude that physiological serum cortisol levels are necessary for normal serum GH responses to provocative stimuli in man.

Adrenocorticotropic Hormone↗
PubMed1989

[Salmon calcitonin nasal spray in the treatment of Paget's disease].

Salmon calcitonin (sCT) is biologically effective when intranasally (i.n.) administered. CT is the treatment of choice for Paget's disease; however, the chronic nature of the disease makes parenteral administration uncomfortable due to the high incidence of adverse reactions occurring after CT injection. The aim of our study was to investigate the efficacy, safety and tolerability of a sCT i.n. spray in the long-term treatment of Paget's disease. Ten pts (4M,6F; age between 58-74 years) with radiological lesions characteristic of Paget's disease, serum alkaline phosphatase (sALP) levels at least 50% above the normal range and never treated for their disease before, were given 200 IU/day of sCT nasal spray for 6 months. sALP levels were measured at month 3 and 6 of therapy; clinical data were recorded every month. sALP levels significantly dropped after 3 months of treatment (72 +/- 6% of basal level, p less than 0.01). After 6 months of therapy sALP levels were similar to the 3 month levels. Pain and functional impairment self-evaluated by the patients decreased after 6 months of therapy: pain index from 5.5 +/- 2.2 to 2.1 +/- 1.1, p less than 0.01; functional impairment index from 2.2 +/- 0.5 to 0.7 +/- 0.5, p less than 0.01. Side-effects were not observed during the entire period of the study. In conclusion, the 200 IU daily regimen of the i.n. spray of sCT without absorption enhancer was, for our patients, effective, safe, and well tolerated in the long-term therapy of Paget's disease.

Administration, Inhalation↗
PubMed1988

Relation between cardiac hypertrophy and forearm vascular structural changes before and during long-term antihypertensive treatment.

In patients with hypertension, structural changes develop in the heart and in the systemic arteries that have a significant role in the maintenance and gradual worsening of the hypertensive disease. Blood pressure, basal and post-ischemic "maximal" forearm blood flow (strain-gauge venous occlusive plethysmography), and echocardiographic left ventricular mass index were measured in 28 hypertensive patients (WHO class I or II, 23 men and five women, aged 26 to 59 years). Minimal vascular resistance (mean arterial pressure/peak blood flow) was taken as an index of vascular structural changes. The same measurements were made in a group of 14 patients before and after long-term antihypertensive treatment: in eight patients after six and 12 months of treatment with captopril (50 mg twice a day, plus 25 mg of hydrochlorothiazide per day if necessary) and in six patients after six months of treatment with nitrendipine (20 mg per day, plus 50 mg of atenolol per day if necessary). A significant but weak direct correlation was found between the degree of left ventricular hypertrophy and mean arterial pressure (r = 0.41) or minimal vascular resistance (r = 0.31). Thus, patients were categorized according to whether they had left ventricular hypertrophy or impaired blood flow; the results suggested that left ventricular hypertrophy may be detected earlier than increased minimal vascular resistance. After six months of treatment, both captopril and nitrendipine significantly reduced left ventricular mass index and minimal vascular resistance. Left ventricular mass index was normalized in 50 percent of the patients, whereas minimal vascular resistance was normalized in one patient only. After 12 months of treatment, left ventricular mass index was normalized in all patients; minimal vascular resistance was on the average further reduced but normalized in only one additional patient. Thus, regression of cardiovascular structure also seems to occur earlier in the heart.

Adult↗
PubMed1988

Beneficial effects of one year's treatment with captopril on left ventricular anatomy and function in hypertensive patients with left ventricular hypertrophy.

This study evaluated by echocardiography (M-mode tracings, two-dimensional-guided) the effects of captopril administration for one year (25 to 50 mg twice a day, alone or in combination with hydrochlorothiazide when necessary) on left ventricular mass index, on systolic function at rest and during stress (hand grip for three minutes and cold pressor test for three minutes), and on diastolic function in 15 patients with essential hypertension (13 men and two women, aged 30 to 67 years) with left ventricular hypertrophy. In addition, supine and standing plasma catecholamine concentrations, plasma renin activity, and plasma aldosterone levels were measured. Examinations were performed during a placebo period and after three, six, and 12 months of captopril treatment. Blood pressure was significantly reduced (p less than 0.001), but heart rate did not change. Left ventricular hypertrophy was progressively reduced during treatment, mainly through reduction of left ventricular wall thickness. After one year, all patients had a normal left ventricular mass index (less than 120 g/m2). Before and during treatment, left ventricular systolic function, at rest and on maximal hand grip and cold pressor testing, evaluated on the basis of fractional shortening as related to end-systolic stress, was within the 95 percent confidence limits (calculated in a group of 25 normal subjects) in all 15 patients with essential hypertension. The percent increase in left ventricular dimensions during the diastolic rapid filling phase was significantly increased by treatment (p less than 0.05), indicating improvement of left ventricular relaxation. As expected, plasma renin activity was increased, plasma aldosterone levels were decreased, and plasma catecholamine concentrations did not change. These results indicate that long-term treatment with captopril has beneficial effects on left ventricular anatomy and function in patients with essential hypertension.

Adult↗
PubMed1988

Development of isolated ACTH deficiency in a man with type I diabetes mellitus.

A 45-year-old man with type I diabetes mellitus of 25-yr duration and well controlled by conventional insulin therapy developed an isolated adrenocorticotropic hormone (ACTH) deficiency. He presented with a 3-month history of weight loss, weakness, anorexia and persistent tendency to hypoglycemia that he had never experienced before. Basal and dynamic endocrine testing disclosed absent cortisol secretion caused by an isolated ACTH deficiency due to a primary pituitary defect. Corticosteroid replacement therapy allowed again a good glycometabolic control. The possible causes of hypoglycemia in insulin-treated diabetes and the pathogenetic basis of the reported association are discussed.

Adrenocorticotropic Hormone↗
PubMed1988

Long-term antihypertensive treatment may induce normalization of left ventricular mass before complete regression of vascular structural changes: consequences for cardiac function at rest and during stress.

In 14 essential hypertensive patients, aged 26-59 years, blood pressure, left ventricular mass index (LVMI), systolic function (M-mode echo, two-dimensionally guided), post-ischaemic 'maximal' forearm blood flow (strain gauge venous occlusion plethysmography), plasma renin activity, plasma catecholamines and aldosterone were measured before and after 6 and 12 months of treatment (eight patients were given captopril, 100 mg/day, + hydrochlorothiazide 25 mg/day in five patients, and six patients were given nitrendipine, 20 mg/day, + atenolol 50 mg/day in four patients). Minimal vascular resistance (mean blood pressure/peak forearm blood flow) was taken as an index of arterial structural changes. After 6 months of treatment significant reductions in blood pressure (P less than 0.001), LVMI (P less than 0.001) and minimal vascular resistance were observed. After 12 months of treatment blood pressure, LVMI and minimal vascular resistance were further reduced. The LVMI was normalized in nine cases and the minimal vascular resistance in two cases only. Aldosterone and plasma catecholamines did not change, whereas plasma renin activity was increased during captopril only. Before and during treatment the left-ventricular shortening fraction in relation to end-systolic stress in each patient at rest, and at peak of handgrip and cold pressor tests, fell within the 95% confidence limits of correlation obtained in normals. Thus, in essential hypertensives long-term treatment can induce normalization of LVMI before complete regression of arterial structural changes in the forearm. Left ventricular systolic function is preserved after normalization of LVMI, both at rest and during stress.

Adult↗
PubMed1988

Left ventricular systolic function in relation to withdrawal of different pharmacological treatments in hypertensives with left ventricular hypertrophy.

We evaluated the left ventricular mass index (LVMI) and the functional response to cold pressor and handgrip tests in 74 untreated essential hypertensive patients and 26 age and sex-matched normals. The same measurements were repeated in 22 essential hypertensives after 6 and 12 months of treatment (captopril or nitrendipine, plus diuretic or beta-blocker in a few cases) and in 21 essential hypertensives after withdrawal of treatment, a reduction in the LVMI and a further increase in blood pressure. Left ventricular systolic function was evaluated by the relationship between left ventricular end-systolic stress and fractional shortening. Highly significant negative correlations, with similar slopes and intercepts, were found between end-systolic stress and fractional shortening under basal conditions, after regression of left ventricular hypertrophy and after withdrawal of treatment, both at rest and at the peak of stress tests. An examination of each point of the relation between end-systolic stress and fractional shortening showed that very few points were beyond the 95% prediction limits of the correlation obtained in normal volunteers. These results indicate that left ventricular systolic function is normal in most untreated essential hypertensives, and is usually well maintained after regression of left ventricular hypertrophy during long-term treatment as well as after withdrawal of treatment, both at rest and during an acutely induced afterload increase.

Adult↗
PubMed1988

Reversal of cardiac hypertrophy by long-term treatment with calcium antagonists in hypertensive patients.

The aim of this study was to assess the effects of chronic antihypertensive treatment with verapamil and nifendipine on left ventricular (LV) anatomy and function, also in relation to adrenergic activity and beta-adrenergic sensitivity. In fact, it is known that, during antihypertensive treatment, changes of LV mass and function may be affected also by the level of adrenosympathetic tone. Blood pressure (BP), heart rate (HR), plasma catecholamines (pCA), beta-adrenergic responsiveness to isoproterenol (dose that increased HR by 25 beats/min = CD25), LV mass as well as systolic function (2D-guided M-mode echo), at rest and during stress (handgrip test [HG], 30% max, for 3 min), were measured on placebo, after 1 and 6 months of monotherapy with verapamil (VER, 240 mg/day, 9 patients) or nifedipine (NIF, 40 mg/day, 10 patients). Both treatments significantly reduced BP (p less than 0.05 at least). HR, pCA, and cardiac output did not change during treatment with VER, whereas they were slightly but significantly increased during treatment with NIF (p less than 0.05 at least). CD25 was significantly increased during treatment with VER (p less than 0.05) but not during treatment with NIF. Both treatments induced a significant reduction of LV mass after 6 months (p less than 0.01 with VER and p less than 0.05 with NIF).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Bacteriological and clinical evaluation of cefotetan in the treatment of severe infections in hospitalized patients.

The authors studied 302 hospitalized patients, 164 males and 138 females aged 15-88 years (average 66 years), with severe infections. Cefotetan was administered to 278 of them at the dose of 1 or 2 g, b.i.d. or a single daily dose i.m. Other patients [24] were treated with a continuous intravenous infusion of cefotetan (3 g daily in 5% dextrose). Of these patients 121 were treated for urinary tract infections (UTI); 114 for respiratory tract infections (RTI); 41 for liver biliary duct infections (BDI); 17 for skin or skin structure infections (SKI); 6 for fever of unknown origin and 3 for sepsis. The following Gram-positive organisms [156] were isolated: Streptococcus pneumoniae, Staphylococcus aureus and Streptococcus group D; and the following Gram-negative organisms [122]: Escherichia coli, Proteus vulgaris, Proteus mirabilis, Serratia spp., Klebsiella spp., Haemophilus influenzae and Pseudomonas aeruginosa. The overall eradication rate for Gram-positive organisms was 74% and for Gram-negative organisms it was 88%. The clinical response was satisfactory in 87.7% of patients (specifically, cefotetan was effective in 90% of UTI, 84.2% of RTI, 97.5% of BDI and 82.3% of SKI). The drug was well tolerated and side-effects (such as skin rash, diarrhoea, purpura and pain at the site of injection) occurred in only 4% of patients treated with cefotetan. In conclusion, cefotetan appears to be safe and highly effective for the treatment of severe infections in hospitalized patients.

Adolescent↗
PubMed1987

Effects of infusing alpha-atrial natriuretic peptide in primary hypertension during converting enzyme inhibition.

The effect of atrial natriuretic peptide (ANP), before and after converting enzyme (CE) inhibition, was investigated in six primary hypertensive patients taking a constant diet. In this placebo-controlled, single-blind, randomized study, the patients received, on three different days, i.v. infusions of (a) placebo, or (b) alpha-human ANP, 150 micrograms over 30 min, or (c) alpha-human ANP after acute CE inhibition by enalapril (EN) 20 mg P.O., 4 h before ANP infusion. ANP infusion increased urinary sodium (p less than 0.001) and volume excretion. Blood pressure (BP), heart rate, stroke volume and shortening fraction (echocardiography), plasma renin activity (PRA), and plasma aldosterone did not change significantly. Urinary norepinephrine and dopamine were significantly increased (p less than 0.05) after ANP infusion. BP was significantly reduced after EN in every patient (p less than 0.05). ANP infusion during CE inhibition induced a more sustained increase of sodium excretion and diuresis with respect to ANP infusion alone (p less than 0.05). PRA was significantly reduced while no further reduction of BP was observed. These data suggest that CE inhibition may increase the natriuretic and diuretic effect of ANP in hypertensive patients.

Adolescent↗
PubMed1987

Cardiac function as related to adrenergic activity in hypertensive left ventricular hypertrophy.

Studies in experimental animals and in hypertensive patients have shown that changes in cardiac anatomy and function are not just a simple consequence of the increased pressure load. The activity of the sympathetic nervous system is one of the factors that may influence cardiac performance and also, possibly, the cardiac anatomy of hypertensive patients. Animal studies have strongly suggested a possible role of adrenergic factors in the development of left ventricular hypertrophy. In man, plasma catecholamines are usually higher in hypertensive patients with left ventricular hypertrophy, and a correlation between left ventricular mass and plasma noradrenaline has also been observed. The decrease of cardiac performance after acute beta blockade has been found to be directly related to basal plasma noradrenaline concentration. An impaired response to beta-adrenergic stimulation has been reported in hypertensive animals and has been confirmed in hypertensive patients with left ventricular hypertrophy.

Adult↗