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Biomedical subjects

A Bellastella

Publications and source records attributed to A Bellastella.

At least 73 records · Page 4Linked to original sources

Control of adrenergic overactivity by beta-blockade improves the quality of life in patients receiving long term suppressive therapy with levothyroxine.

Several symptoms and signs of hyperthyroidism are frequently shared by patients receiving L-T4 suppressive therapy. The aim of this study was to evaluate whether a beta-adrenergic blocking drug could reduce the severity of these symptoms and signs in these patients, as previously reported in patients with hyperthyroidism. Eleven patients (mean age, 42 +/- 11 yr; 10 females and one male) affected with differentiated thyroid carcinoma or nontoxic goiter were selected from a more numerous group of patients receiving suppressive therapy based on the presence of palpitations, increased heart rate, left ventricular systolic function, and other symptoms mimicking exaggerated beta-adrenergic activity. In these patients the cardioselective beta-blocking drug bisoprolol was added to the L-T4 suppressive therapy at a dose of 2.5-5 mg/day. Blood samples were collected for the determination of thyroid hormones and TSH concentration during L-T4 therapy and after 3 and 6 months of associated L-T4 plus bisoprolol therapy. Cardiac function was assessed by clinical evaluation, standard and Holter electrocardiogram, as well as one- and two-dimensional echocardiography. Furthermore, we applied the symptom-rating scale previously used by Klein et al. in hyperthyroid patients to assess the quality of life in our group of patients. Our findings show that the addition of bisoprolol to L-T4 suppressive therapy produces a normalization of heart rate, which was significantly increased during TSH suppressive therapy, and the disappearance of atrial arrhythmias with considerable reduction of palpitations. Furthermore, bisoprolol produced an effective improvement in measures of the hyperthyroid symptom scale, with significant reduction of the mean score. The echocardiographic data showed an increased left ventricular mass index with significantly enhanced systolic function at the basal evaluation. After 6 months of combined L-T4 plus bisoprolol therapy, left ventricular mass index normalized, and the indices of left ventricular systolic function were reduced, with a tendency to normalize. Further studies conducted on a larger series of patients are required to verify the long term implications of cardiac parameter variations on cardiovascular morbidity and mortality. Our results, however, show that the addition of bisoprolol to L-T4 suppressive therapy improves the quality of life in those patients with clinical features of enhanced adrenergic activity.

Adult↗

Effects of lithium treatment on hypothalamic-pituitary-thyroid axis: a longitudinal study.

Lithium carbonate, widely used in the treatment of bipolar patients, is well known to induce thyroid alterations. In this longitudinal study the thyroid function was investigated during lithium treatment over a period of 12 months in 12 euthymic bipolar patients with a normal thyroid function and absence of thyroid antibodies. Nine of the 12 patients were further studied on the 15th month, 5 of these 9 on the 18th month and 4 of the last-mentioned 5 on the 24th month. The mean basal and TRH-stimulated TSH values during lithium therapy were significantly higher as compared to those at the beginning of the treatment. More particularly, during lithium therapy, a significant increase of basal TSH over the normal range was found in 10 out of the 12 patients. A rise of TRH-stimulated TSH was found in 11 out of the 12 patients. The impairment of the hypothalamic-pituitary-thyroid (HPT) axis was transitory in the majority of cases. Two patients developed a nodular goiter during the treatment. Plasma T3, T4, FT3 and FT4 levels did not change during the treatment. Thyroid antibodies remained undetectable. The conclusions of the study are twofold: 1) Subclinical hypothyroidism during lithium therapy is much more frequent than previous cross-sectional studies suggest; 2) Thyroxine replacement in lithium-treated patients is advisable in order to prevent subclinical hypothyroidism and the risk of a subsequent goiter.

Adult↗

Prevalence of antisperm antibodies by SpermMARtest in subjects undergoing a routine sperm analysis for infertility.

To evaluate the prevalence of antisperm antibodies (ASA) attached to the sperm plasma membrane in male partners of infertile couples, the binding of latex particles to spermatozoa was investigated using SpermMARtest, included routinely in semen analysis. A total of 860 men were examined, who were referred consecutively for semen analysis. Of these, 750 men were referred because of infertility (0.6-10 years in duration) whereas 110 were volunteers with a history of previous fertility. Samples were assessed by the SpermMARtest kit using latex particles sensitized with human IgG. Sperm-latex binding was read after 3 min and samples scored as negative, positive or highly positive when < 10, > 10-40, or > 40% binding occurred, respectively. Of the samples 132 (17.3%) were excluded because of azoo- or severe oligo-asthenozoospermia. IgG attached to spermatozoa were detected in nearly 13% of semen samples from the infertile population and in one of 110 fertile men (0.9%). From the infertile group, 6.2% of samples showed > 40% binding, and 6.7% intermediate binding, with an overall ASA prevalence of 12.9% in subjects undergoing semen analysis for infertility.

Adult↗

Remission of subclinical adrenocortical failure in subjects with adrenal autoantibodies.

Idiopathic Addison's disease is a chronic organ-specific autoimmune disorder with a long subclinical period characterized only by the presence of adrenal autoantibodies (AA) with or without adrenal function failure. The aim of this longitudinal study was to evaluate the behavior of AA using, an indirect fluorescence method, and adrenal function in 20 AA-positive and 50 AA-negative patients screened by an investigation of a large population of organ-specific autoimmune disease patients without clinical Addison's disease. As controls, 100 normal age-matched subjects were tested only once. In the 20 AA-positive and 50 negative patients, AA and adrenal functional tests were evaluated every 4 months for 5 yr. The AA-positive patients were grouped into 5 adrenal functional stages, specifically: stage 0, normal adrenal function; stage 1, high PRA and low (or normal) aldosterone levels alone; stage 2, along with impaired cortisol response to ACTH, stage 3, along with increased ACTH levels; and stage 4, clinically overt Addison's disease. On the basis of the behavior of AA, the 20 positive patients were grouped as follows: group A, 11 patients with AA titer of 1:8 or higher at the first observation and persistently AA positive in subsequent observations, with titers ranging from 1:8 to 1:64; group B, 6 patients with initial AA titers of 1:8 or lower and AA disappearance in subsequent observations; and group C, 3 patients with AA titer of 1:32 or higher, undergoing corticosteroid therapy after the start of the study and showing AA disappearance in subsequent observations. With respect to adrenal function in group A, 2 patients initially in stage 1 and 1 patient initially in stage 2 did not progress to the upper stages, whereas 5 patients initially in stage 0 and 3 initially in stage 1 progressed subsequently to the upper stages, in 2 cases reaching overt clinical Addison's disease (stage 4). On the other hand, all of the patients of group B showed both a spontaneous disappearance of AA and recovery of adrenal function during the study span. Also, the 3 patients of group C showed disappearance of AA after corticosteroid therapy with recovery of adrenal function. None of the 50 patients who were initially AA negative became AA positive subsequently or showed impairment of adrenal function. We reached the following conclusions. 1) AA, even if present initially in some subjects without clinical Addison's disease, can subsequently disappear. 2) Restoration of adrenal function after disappearance of AA indicates that a spontaneous remission of subclinical adrenocortical failure can occur.(ABSTRACT TRUNCATED AT 400 WORDS)

Addison Disease↗

Cardiac effects of long term thyrotropin-suppressive therapy with levothyroxine.

To investigate the effects of long term thyroid hormone suppressive therapy on the heart, 20 patients were evaluated by noninvasive techniques. Of them, 10 were athyreotic after surgery for differentiated thyroid cancer, and 10 had diffuse or nodular goiter. The mean age of the group was 39 +/- 11 yr. Twenty age- and sex-matched subjects served as controls. The mean dose of levothyroxine was 163 +/- 34 micrograms daily. Plasma TSH was undetectable in all patients. Mean serum T4, free T4, and sex hormone-binding globulin were significantly higher (P < 0.001), whereas mean serum T3, free T3, and osteocalcin did not differ from control levels. Cardiac evaluation consisted of a standard 12-lead electrocardiogram, an ambulatory electrocardiographic monitoring (Holter), and an echocardiographic study. Two patients showed abnormal electrocardiograms for left ventricular hypertrophy. Holter demonstrated an increase in average heart rate (84 +/- 7 vs. 70 +/- 6 beats/min; P < 0.01). Prevalence of atrial premature beats was higher in the patient group than in the control group (100% vs. 60%; P < 0.006). The echocardiogram showed an increased left ventricular mass index in the patient group (97 +/- 24 vs. 80 +/- 18 g/m2; P < 0.02). Furthermore, left ventricular systolic function was enhanced, with higher values of fractional shortening (38 +/- 7% vs. 34 +/- 4%; P < 0.05) and rate-adjusted velocity of shortening (1.2 +/- 0.13 vs. 1.05 +/- 0.14 circumferences/sec; P < 0.01). These findings indicate that long term levothyroxine therapy at suppressive doses markedly affects cardiac function.

Adult↗

Body composition, bone metabolism, and heart structure and function in growth hormone (GH)-deficient adults before and after GH replacement therapy at low doses.

The effects of recombinant GH doses (10 micrograms/kg.day, 3 times a week for 6 months) lower than those previously used in the treatment of GH-deficient adults (GHDA) on body composition, bone mineral content, and heart structure and function were investigated in seven (six males and one female, aged 25-27 yr) GHDA. They were studied before treatment, after treatment, and 6 months after stopping therapy, and findings were compared with those for 20 sex-, age-, and body mass index-matched healthy controls. Before treatment, GHDA showed a significant reduction in insulin-like growth factor-I levels, an increase in bioimpedance and fat mass percentage, a reduction of bone density at both distal and proximal sites, a decrease in bone Gla-protein and procollagen III levels, and significant cardiac impairment supported by a reduction of left ventricular mass index and left ventricular systolic function with decreased fractional shortening and rate-adjusted mean velocity of circumferential fiber shortening. GH treatment normalized insulin-like growth factor-I levels, body composition and echocardiographic findings, but not bone density. Six months after stopping therapy, all parameters investigated returned to the pretreatment conditions. Our results suggest that prolonged GH deficiency induces alterations in body composition and bone metabolism and density, and impairment of cardiac structure and function in adult life. GH replacement therapy for 6 months, despite the low doses used by us, is able to improve all previously impaired biochemical and clinical features, except for bone density. This improvement disappears 6 months after the withdrawal of therapy.

Adult↗

HLADR5 and C4BQO high frequency and antinuclear antibodies positivity in patients with 21 hydroxylase deficiency from Campania region.

HLA haplotypes, complement C4 factor and factor B immunochemical concentrations and autoantibodies titer have been studied in six patients with mild congenital adrenal hyperplasia (MC-AH), in two patients with classical congenital adrenal hyperplasia (CCAH) and in their parents. A high frequency of DR5 and C4BQO alleles have been found in MCAH patients. Moreover, C4BQO allele is carried out in three out of four cases associated with DR5. In the two CCAH patients we found a B51 and a B14 allele, the last one usually described in the non classical form of the disease in population of different ethnic origin. Signs of autoimmunity in some patients and parents have been found. C4 null alleles were several-fold more frequent among our patients with respect to the same ethnic control group and the autoantibody positivity could be the result of an altered immune regulation. The presence of a positive correlation between cortisol basal levels and C4 and Bf concentrations in the six MC-AH patients suggests an interrelationship between hormonal factors and immunological findings in this disease. Our finding about HLA antigens not previously described in this syndrome may stimulate more profound studies by genomic and cDNA probes.

17-alpha-Hydroxyprogesterone↗

Evaluation of GH paradoxical responses to TRH and LHRH in acromegalic patients during long-term treatment with octreotide.

In some acromegalics, GH release can be induced by TRH and/or LHRH administration. The pathogenesis of these GH paradoxical responses was supposed to be a somatotroph-reduced sensitivity to somatostatin, somatotrophin release-inhibiting factor (SRIF), or an hypothalamic derangement of the SRIF release. In this study, this hypothesis was investigated by means of GH suppression during chronic therapy with octreotide [Somatostatin analogue (SMS)] in order to evaluate the possible correlation between GH and insulin-like growth factor 1 (IGF-1) normalization and the disappearance of these paradoxical responses in 15 acromegalic patients: 15/15 with a paradoxical GH rise after TRH and 7/15 with a paradoxical GH rise after LHRH. SMS therapy was administered subcutaneously at the dose of 150-450 micrograms/day. During the treatment, GH and IGF-1 levels normalized in 12 patients and were reduced in the remaining 3 others. The GH response to TRH disappeared in 7 patients, while the GH response to LHRH disappeared in 4 patients. chi 2 analysis failed to show any significant correlation between GH and IGF-1 normalization and the disappearance of GH response to TRH and LHRH (chi 2 = 0.00686). No linear correlation existed between GH/IGF-1 decrease and GH peak or area under the curve at any time ('r' values: TRH test, GH -0.47, IGF-1 -0.48; LHRH test, GH -0.50, IGF-1 -0.49). The absence of any significant correlation between GH/IGF-1 normalization and the disappearance of GH paradoxical responses during chronic octreotide administration suggests that other factors apart from SRIF sensitivity are involved in the genesis of these responses.

Acromegaly↗

Thyroid hormone inhibition of intermediary metabolism in dog thyroid slices stimulated by different agonists.

The role of thyroid hormones in a short loop feedback in the thyroid is controversial. This process was studied in dog thyroid slices stimulated by TSH, carbachol and phorbol esters. Incubation of thyroid slices with T3 and T4 for 1 hour inhibited the subsequent stimulation of glucose oxidation induced by carbachol and phorbol esters but not by TSH. T3 also inhibited the stimulation of 32P incorporation into phospholipids stimulated by these two agonists. Glucose oxidation stimulated by TSH, carbachol and 12-0-tetradecanoyl-phorbol-13-acetate (TPA) was inhibited by rT3 and the inhibition was not reversed by methimazole, which did abolish the inhibition induced by iodide, MIT and DIT. TSH stimulation of cAMP was not blocked by T3 or T4 but was by rT3 and MIT- and DIT. The mechanism of such inhibition appears to be complex, possibly involving formation of iodide from rT3, MIT and DIT but also dependent on the intact iodothyronine. Moreover, our data suggest that T3 and T4 exert their inhibition on the thyroid through the phospholipids cascade and this mechanism is probably independent on the release of iodide from these iodocompounds.

Animals↗

Height and weight of nursery and primary school population from Torre del Greco, a Campania town, Italy.

Height and weight were measured in 7902, 3.5-11-year-old children from Torre del Greco nursery and primary school and arranged in centiles by cumulative frequencies calculation after sorting into ascending order measurements and counting up from the bottom. Our population height and weight measurements were compared to Tanner's by chi-square test. Our population seems to be taller and fatter with respect to Tanner's. Two possible explanation can be suggested: 1) British data are findings published several years ago; 2) Modified conditions of life in South-Italy in the last 30 yr, especially increased feeding availability can explain both increased height and frequent weight excess observed. These data suggest that for a correct auxological evaluation it seems useful to compare children not only to Tanner's standards but to centiles derived from the same population.

Age Factors↗

Blindness impairs plasma growth hormone response to L-dopa but not to arginine.

To investigate how blindness influences GH secretion, we studied the GH response to L-dopa and arginine in 8 blind adult males and 10 normal age-matched control males. Arginine and L-dopa tests were performed in random order at least 1 week apart at 0800 h, and plasma GH was measured by RIA. The blind subjects showed GH responses to arginine similar to those in normal subjects [peak, 22.1 +/- 1.3 vs. 20.5 +/- 1.3 micrograms/L (+/- SE)], but their GH response to L-dopa was significantly reduced [peak, 5.4 +/- 1.3 vs. 20.3 +/- 2.4 micrograms/L (+/- SE); P less than 0.01]. Because L-dopa is believed to release GH by stimulating endogenous GHRH, whereas arginine may act by suppressing endogenous somatostatin secretion, we propose that blindness may impair GH release by inhibiting GHRH secretion.

Adult↗

Plasma and urinary growth hormone and insulin-like growth factor I in children with chronic renal insufficiency.

We investigated the plasma and urinary growth hormone (GH) levels, and plasma insulin-like growth factor (IGF-I) in 15 (8 prepubertal and 7 pubertal) subjects with chronic renal insufficiency. Four of our 7 pubertal patients had a short stature (standard deviation score from -2.7 to -4.0). Significantly increased plasma GH and IGF-I levels were found in pubertal subjects alone (p less than 0.05). The urinary GH levels was significantly increased in prepubertal and pubertal subjects (p less than 0.001 and 0.05, respectively). A significantly inverse correlation between urinary GH excretion and creatinine clearance was found (r = -0.55; p less than 0.05). Increased plasma GH, IGF-I and urinary GH levels seem to suggest a complex alteration of GH and somatomedin metabolism in central and peripheral (receptor) cells.

Adolescent↗

Blindness influences the growth of institutionalized prepubertal subjects.

To investigate if blindness influences the growth rate of young subjects we measured height and weight of 71 prepubertal blind subjects (33 females and 38 males) aged 7-10 yr, in Tanner stage one puberty, living at the Institute "Martuscelli" for young blind individuals in Naples, Italy. They were divided into two groups: group 1 consisting of 27 subjects (14 females and 13 males) with total blindness; group 2 consisting of 44 subjects (20 females and 24 males) having only a light perception. The distribution in quintiles of their height and weight was compared by X2 test for trend to that of an age-matched large population (7902 subjects: 3808 females and 4094 males) of primary school from the same district. A stature significantly lower than controls was evidenced in both group 1 (p = 0.0006) and in group 2 (p = 0.008). When the comparison is performed taking into account the sex of subjects, the girls of both group 1 (p = 0.0014) and group 2 (p = 0.0004) show a stature significantly lower than female controls, whereas the stature of boys of both groups did not differ from that of male controls. No statistically significant differences in weight distribution were found between controls and either group 1 and group 2. Our results suggest that total or partial blindness could influence negatively the growth of prepubertal subjects; in particular it can cause short stature or growth delay especially in female sex.

Blindness↗

Prepubertal endocrine follow-up in subjects with Wilms' tumor.

Twenty-three prepubertal subjects treated for Wilms' tumor (10 males and 13 females) were endocrinologically evaluated off therapy from 0.5 to 4.08 years. They were divided into two groups: 11 subjects (6M, 5F) who had received chemotherapy only (group 1) and 12 (4M, 8F) who had in addition received abdominal radiation (1,500-3,000 rads) (group 2). Follicle-stimulating hormone (FSH), luteinizing hormone (LH), prolactin (PRL), thyroid-stimulating hormone (TSH), free thyroxine (FT4), free tri-iodo thyronine (FT3), testosterone (T), estradiol-17 beta (E2), and cortisol (F) were measured by radioimmunoassay (RIA). Plasma levels of TSH, PRL, FT4, FT3, and F were normal in both groups, as were FSH, LH, T, and E2 in group 1. In group 2, female subjects showed FSH levels significantly higher than controls, while LH and E2 were normal; male subjects showed significantly higher LH levels, while FSH and T levels were normal. These results indicate that in the treatment protocol used by us for Wilms' tumor (WT), chemotherapy does not affect endocrine function, whereas abdominal radiation seems to damage gonadal function directly. The present findings indicate that gonadal damage may be revealed in WT before puberty not only in females, as has been previously reported, but also in male subjects.

Antineoplastic Combined Chemotherapy Protocols↗

Plasma thyrotropin, thyroxine, triiodothyronine, free thyroxine, free triiodothyronine, and cortisol levels in blind prepubertal boys.

Findings on thyroid function in blind subjects are lacking. The aim of this study was to investigate the thyroid hormonal pattern in prepubertal blind subjects. Six healthy and 8 blind males, aged 7-10 yr, in Tanner stage one puberty, living at Institute "Martuscelli" for blind young subjects, Napoli, Italy, were studied. Each had a TRH (200 micrograms) test at 08:00 h after nocturnal rest. Plasma TSH, T4, T3, free T4(FT4), free T3(FT3) and cortisol (F) were measured by RIA. Our blind subjects show levels of TSH (basal values and absolute peak after TRH), T4, T3 and F normal but FT4 levels significantly higher than controls (39 pg/ml +/- 4.7 vs 12 +/- 0.6, p less than 0.001; 14 pg/ml +/- 1.3 vs 4.7 +/- 0.2, p less than 0.001, respectively). Our results, similar to those found in some patients with euthyroid hyperthyroxinemia, suggest that the prolonged inability to receive light signal could influence the metabolism of thyroid hormones and/or cause a tissue resistance to their action, even if this hypothesis must be verified by future more extensive investigations.

Blindness↗

Dysgerminoma in 45,X Turner syndrome: report of a case.

Here we report the fourth case of dysgerminoma in a patient with the syndrome of gonadal dysgenesis and 45,X karyotype. Typical Turner's syndrome features were unusually associated with breast development, menarche and secondary amenorrhoea. Exaggerated basal and GnRH stimulated gonadotrophin and low oestradiol levels were typical of post-pubertal Turner's syndrome. Detailed (standard) chromosome and banding analysis excluded the presence of Y chromosome material. This case suggests that the presence of a Y chromosome is not necessary for abnormal differentiation of germ cells and the occurrence of a gonadoblastoma.

Adolescent↗