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Biomedical subjects

L Bianconi

Publications and source records attributed to L Bianconi.

At least 19 recordsLinked to original sources

Subclinical hypothyroidism, overt thyrotoxicosis and subclinical hypothyroidism: the subsequent phases of thyroid function in a patient chronically treated with amiodarone.

In a patient chronically treated with amiodarone, subclinical iodine-induced hypothyroidism occurred as a result of excess iodine released from the amiodarone molecule. The patient was maintained on amiodarone and developed thyrotoxicosis as a result of a destructive process into the thyroid follicles. Amiodarone was withdrawn and methylprednisolone and methimazole treatment was started with resolution of the thyrotoxic phase. Months later, off therapy, the patient developed subclinical hypothyroidism. This is the first description of hypo- and hyperthyroidism in the same patient caused by amiodarone therapy. This unusual observation suggests that patients treated with amiodarone are at risk to develop hyperthyroidism even if they show laboratory findings consistent with hypothyroidism.

Amiodarone

Efficacy of intravenous propafenone in acute atrial fibrillation complicating open-heart surgery.

Early postoperative atrial fibrillation (AF) is a frequent complication of major cardiovascular surgery. To assess the effectiveness of intravenous propafenone in this setting, we studied 50 patients who developed AF within 48 hours after open-heart surgery. Intravenous propafenone (2 mg/kg in 10 minutes) was administered 15 minutes after the onset of the arrhythmia. Sinus rhythm was restored in 35 patients (70%) after a mean time of 22 +/- 6 minutes after the beginning of the infusion. The conversion was obtained in 28 of 32 patients (88%) who had a coronary artery bypass graft and in 7 of 18 patients (39%) who had valvular or septal surgery (p less than 0.01). In those whose arrhythmia did not convert to sinus rhythm, the ventricular rate was reduced from 142 +/- 14 beats/min to 108 +/- 9 beats/min (p less than 0.01). In patients whose arrhythmia was converted to sinus rhythm, mean cardiac index increased from a mean baseline value of 2.7 +/- 0.4 L/min/m2 to 3.4 +/- 0.1 L/min/m2 (p less than 0.05), while it remained virtually unchanged in those whose arrhythmia did not convert. No significant side effects were observed. We conclude that intravenous propafenone is effective in converting to sinus rhythm the majority of patients with AF complicating open-heart surgery. Heart rate was reduced in those who did not convert to sinus rhythm and no side effects nor hemodynamic deterioration were observed in any case.

Acute Disease

Effects of oral propafenone therapy on chronic myocardial pacing threshold.

The effects of oral propafenone therapy on pacing threshold were studied in 36 patients chronically paced for sick sinus syndrome or AV block. The pacemakers, all unipolar models and with noninvasive threshold measurement facilities, were: 9 VVI, 15 AAI, and 12 DDD. Each patient received an initial propafenone dose of 450 mg/day, that in 18 cases was increased to 900 mg/day. Threshold was tested at baseline and at each dosage after 7 days of therapy. With the lower propafenone dosage the threshold, measured at 2.5 V, rose from 0.14 +/- 0.10 to 0.21 +/- 0.16 msec (+55%) in the atrium (P less than 0.0001) and from 0.10 +/- 0.08 to 0.15 +/- 0.09 msec (+63%) in the ventricle (P less than 0.0001). In the 18 patients who received both dosages, the mean atrial and ventricular threshold increased from 0.12 +/- 0.10 to 0.17 +/- 0.14 msec with the lower dose and to 0.27 +/- 0.22 msec (+125%) with the higher dose (P less than 0.0001 for both increments). With the 900 mg/day dose, a threshold increment greater than or equal to 300% was observed in 15% of the stimulated chambers. A good linear correlation (r = 0.76) was found between the ventricular threshold increment and the drug induced QRS widening. In conclusion, treatment with oral propafenone increases atrial and ventricular stimulation threshold in pacemaker patients. Threshold increment is dose dependent and proportional to the drug induced QRS widening. In the majority of the cases the threshold increment is not clinically significant, but caution must be used in prescribing high doses of the drug to patients with high baseline threshold.

Aged

Iodine-induced subclinical hypothyroidism in euthyroid subjects with a previous episode of amiodarone-induced thyrotoxicosis.

Amiodarone-induced thyrotoxicosis (AIT) occurs most frequently in patients with underlying thyroid disease and is generally believed to be due to the iodine contamination of amiodarone and iodine released by the metabolism of the drug. We and others have suggested that the thyrotoxicosis may also be secondary to amiodarone-induced thyroiditis. To further determine the etiology of AIT, we administered large doses of iodides [10 drops saturated solution of potassium iodide (SSKI) daily] to 10 euthyroid patients long after an episode of AIT believed to be due at least in part to amiodarone-induced thyroiditis. Six of these 10 patients had an abnormal iodide-perchlorate discharge test before SSKI administration, indicating a subtle defect in the thyroidal organification of iodide. During SSKI administration, 6 patients developed marked iodine-induced basal and/or TRH-stimulated serum TSH elevations, 2 had suppressed basal and TRH-stimulated TSH values, and 2 had normal TSH responses compared to SSKI-treated euthyroid subjects with no history of amiodarone ingestion or thyroid disease. Serum T4 and T3 concentrations remained normal and unchanged during SSKI administration in both the AIT patients and control subjects. These results strongly suggest that excess iodine may not be the cause of the hyperthyroidism associated with amiodarone therapy, especially in those patients with probable amiodarone-induced thyroiditis. Furthermore, like patients with a previous history of subacute thyroiditis and postpartum thyroiditis, the present results suggest that some patients with a previous history of AIT may be at risk to develop hypothyroidism when given excess iodine.

Amiodarone

Inhibition by ethanol of the oxytocin response to breast stimulation in normal women and the role of endogenous opioids.

The possible inhibition exerted by ethanol on the oxytocin response to breast stimulation was tested in normal women. The possible role of endogenous opioids in the control of the oxytocin response to breast stimulation and/or ethanol action was also examined. Sixteen normal women were tested four times on the 22nd day of four consecutive regular menstrual cycles. All women underwent mechanical breast stimulation (for 10 min) with the concomitant administration of normal saline, naloxone (2 or 4 mg in an iv bolus plus 5 or 10 mg over 16 min), ethanol (50 ml in 110 ml of whisky po) or the combination of ethanol and naloxone. Plasma oxytocin levels rose about twofold after breast stimulation, with a mean peak response at 10 min. The oxytocin response to breast stimulation was not changed by the treatment with the lower (2 plus 5 mg) or the higher (4 plus 10 mg) dose of naloxone, whereas it was completely abolished by ethanol. However, when ethanol was given together with naloxone, the oxytocin rise induced by breast stimulation was only partially inhibited by ethanol (the mean oxytocin peak was 50% higher than baseline). At both doses naloxone produced similar effects. These data demonstrate that ethanol inhibits the oxytocin response to breast stimulation. Naloxone sensitive endogenous opioids do not appear to be involved in the control of the oxytocin rise induced by breast stimulation. In contrast, since naloxone partially reversed the inhibiting effects of ethanol, a partial involvement of opioid peptides in ethanol action is supposed.

Adult

Prevalence of anti-thyroid peroxidase antibodies in serum in the elderly: comparison with other tests for anti-thyroid antibodies.

Autoimmune thyroid disease, especially chronic thyroiditis, is prevalent in elderly women and is probably the major cause of hypothyroidism in this population. The reported prevalence of chronic thyroiditis is variable, depending on the area of residence and the method(s) used to detect the presence of anti-thyroid antibodies. The recent finding that thyroid peroxidase (TPO) is the antigen for the thyroid anti-microsomal antibody (AbM) has resulted in the development of sensitive radioimmunoassays (RIA) to detect the presence of AbTPO. We have determined the prevalence of AbTPO (by RIA) in sera from 342 elderly subjects, 248 women and 94 men (mean age 80 years) residing in Reggio Emilia, Italy, and compared the results with other methods for detecting anti-thyroid antibodies, including anti-thyroglobulin (AbTg) and AbM measured by passive hemagglutination (PH) of tanned erythrocytes, and AbM measured by RIA. The prevalence of positive AbTPO was 2.3% in the men and 10.2% in the women, only slightly higher than the prevalence of AbM. However, in the antibody-positive sera, the mean value for AbTPO was approximately 20-fold greater than the upper limit of the normal range, whereas the mean value for AbM was only threefold greater. The prevalence of positive titers for AbM and AbTg measured by PH was far lower, 1.2% and 3.2%, respectively, and those sera weakly positive for AbM and AbTg by PH were strongly positive for AbTPO by RIA. AbTPO RIA may be more useful than AbM and AbTg hemagglutination and AbM RIA for detecting the presence of autoimmune thyroid disease.

Aged

Oxytocin does not modify the prolactin response to metoclopramide in normal women.

The present study was undertaken in order to establish whether oxytocin (OT) affects the dopaminergic control of PRL secretion in normal women during follicular, periovulatory and luteal phase of their menstrual cycle. For this purpose, 22 normal women were tested with a lower (1 mg) or higher (10 mg) dose of the dopaminergic antagonist metoclopramide (MCP) with or without the concurrent treatment with OT (2 IU injected plus 0.033 IU/min infused for 2 h). Since OT was found unable to modify the effect of either 1 or 10 mg MCP, in additional experiments the same doses of MCP and OT were administered after dopamine (0.04 micrograms/kg/min for 2 h) infusion. Also in these experimental conditions OT failed to modify the PRL response to MCP. These data argue against a role of OT in modulation of the dopaminergic control of PRL secretion in normal women.

Adult

Postpartum thyroid dysfunction in an Italian population residing in an area of mild iodine deficiency.

We have evaluated the occurrence of postpartum thyroid dysfunction (PPTD) in a group of 372 women residing in area of mild iodine deficiency. Thyroid function and autoimmune status were evaluated by means serum T4, T3, TSH measurement and detecting the presence of positive antithyroglobulin antibodies (AbTg), antimicrosomal antibodies (AbM) and thyroid-peroxidase antibodies (AbTPO) titers in women at parturition, at 1, 3, 6 and 12 months postpartum. New onset transient hypothyroidism occurred in 6.4% of women whereas transient thyrotoxicosis in only 1.8% of women. Transient hypothyroidism was not preceded by thyrotoxicosis as indicated by thyroid function tests and serum Tg concentrations. At parturition, the positivity of AbM and AbTPO titers and the presence of goiter appeared to be a risk factors for the development of PPTD.

Antibodies

Thyroid function evaluation by different commercially available free thyroid hormone measurement kits in term pregnant women and their newborns.

Evaluation of thyroid status by measurement of free thyroid hormone concentrations seems particularly helpful in conditions with altered serum binding proteins. In pregnancy, a condition of increased thyroxine binding globulin, serum free thyroxine (FT4) and free triiodothyronine (FT3) concentrations have been reported to be normal, increased or decreased. In the present study we have measured serum total and free thyroid hormone concentrations in pregnant women, their newborns and nonpregnant women. Serum FT4 and FT3 concentrations have been measured with 10 different commercially available kits and the results obtained have been compared. Serum total thyroid hormone concentrations in pregnant women were significantly higher than in their newborns and in nonpregnant women. Maternal serum FT4 concentrations measured with the different kits were always significantly lower than values in nonpregnant women. Furthermore, with one kit, the mean maternal serum FT4 concentration was below the normal range and with many kits, a large number of maternal serum samples had serum FT4 concentrations below the normal range. With all kits, except two, neonatal serum FT4 concentrations were higher than values in their respective mothers and, in general, lower than values in nonpregnant women. Serum FT3 concentrations in nonpregnant women were in the normal range, except with one kit, in which the mean serum FT3 concentration was below the normal range. Serum FT3 concentrations in newborns resulted markedly lower than in parturient and in non pregnant women. With almost all kits, serum FT3 values were below the normal range in many maternal samples. With one kit, maternal serum FT3 concentrations resulted higher than in nonpregnant women, whereas with the other kits serum FT3 concentrations were lower.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult

Effect of estrogen or insulin-induced hypoglycemia on plasma oxytocin levels in bulimia and anorexia nervosa.

Plasma oxytocin (OT) levels were measured before and after stimulation with estrogens (1 mg ethynylestradiol orally) or with insulin (0.15 IU/kg)-induced hypoglycemia in seven underweight women with anorexia nervosa, eight normal weight bulimic women, and nine normal controls. Anorectic patients were amenorrhoic; they were tested at their first hospitalization (first tests) and again 8 to 9 weeks later (second tests) when they were eating normally, but were still at a low weight. In addition, anorectic women were tested 16 to 17 weeks after the first test (third tests), when their weight was restored to normal. Normal and bulimic women were tested on the fourth days of normal menstrual cycles. Insulin induced similar hypoglycemic responses in all groups. At each time point of the estrogen tests, plasma estrogen levels were similar in bulimic and normal women, whereas they were significantly lower in anorectic subjects. There were no differences in the basal levels of OT among groups. Both insulin-induced hypoglycemia and estrogen treatment produced striking OT increments in bulimic and control women, without significant differences between groups. During the first tests, no significant increase in plasma OT levels was observed in underweight anorectic women in response to both releasing stimuli. After partial weight recovery, the anorectic women showed a slight, but significant, increase in the OT responses to both insulin-induced hypoglycemia and estrogen administration. Both hypoglycemia- and estrogen-induced OT increases observed during the second tests were significantly lower in underweight anorectic patients than in normal controls. Anorectic subjects regained normal OT responsiveness to both stimuli after complete weight recovery.(ABSTRACT TRUNCATED AT 250 WORDS)

Anorexia Nervosa

Reduction of baclofen-, but not sodium valproate-induced growth hormone release in type I diabetic men.

The effects of sodium valproate (a drug enhancing endogenous gamma aminobutyric acid (GABA)-ergic activity) and of the GABA analog baclofen (a GABA B receptor agonist) on serum GH levels was tested in 8 type I diabetic men and 8 normal controls. Sodium valproate (800 mg) or baclofen (10 mg) were given by mouth at 08.30 h on the experimental day. Control tests with a placebo were performed on different occasions. Basal GH levels were similar in controls and diabetic patients. Sodium valproate induced a 7 fold increase in serum GH concentrations in both groups. In contrast, baclofen-induced GH rise was significantly higher in normal controls (mean peak was 3.4 times higher than baseline) than in diabetic patients (mean peak was only 2.1 times higher than basal value). Serum GH levels did not change after placebo administration in any groups. These data suggest the presence of diabetes-induced alterations of a GABAergic pathway mediated by B receptors in the control of GH secretion. Alternatively, the data might indicate a change in diabetic men of other baclofen-sensitive neurotransmissions, different from GABA.

Adult

Abnormal arginine vasopressin response to cigarette smoking and metoclopramide (but not to insulin-induced hypoglycemia) in elderly subjects.

Aging is known to reduce arginine vasopressin (AVP) response to volumetric stimulations and to increase AVP responses to osmotic stimuli and to administration of metoclopramide (MCP). In order to gain a better insight into the effect of age on AVP secretion, we evaluated AVP responses to cigarette smoking, MCP, and insulin-induced hypoglycemia in 30 male subjects aged 22-81 and divided into 3 groups by age. Basal AVP concentrations were similar in all groups. The AVP response during the insulin tolerance test had a similar pattern and magnitude (2.5-fold increase) in all groups. AVP responses to MCP and cigarette smoking were similar in the two younger groups, with plasma AVP levels increased 2 times by MCP and 2.5 times by cigarette smoking. In contrast, both MCP- and cigarette smoking-induced AVP rises were significantly higher in the oldest group, where plasma AVP concentrations increased 2.5 times after MCP and 3.25 times after smoking. When data of the MCP and cigarette smoking tests were combined, regression analyses showed a significant positive correlation between AVP peak responses to MCP and cigarette smoking in the oldest subjects. These data show that elderly humans have increased AVP responses not only to MCP but also to cigarette smoking, suggesting a common disorder for both alterations. In contrast, the lack of age-related changes in AVP response during the insulin tolerance test demonstrates that the mechanism underlying the AVP response to hypoglycemia is not affected by aging.

Adult

Restoration of normal growth hormone responsiveness to GHRH in normal aged men by infusion of low amounts of theophylline.

In order to establish whether the age-related reduced growth hormone (GH) responsiveness to GH-releasing hormone (GHRH) could be improved by treatment with low amounts of theophylline, a drug mainly acting through cyclic adenosine 3', 5'-monophosphate (cAMP), and calcium-mediated mechanisms, eight adult subjects (aged 20-37) and eight elderly men (aged 64-79) were tested with GHRH (50 micrograms in an iv bolus), theophylline (1.67 mg/min for 3 h), or the combination of both drugs. The GH response to GHRH was significantly lower in the older than in the younger group (mean peaks were 4.5 and 7.5 times higher than baseline, respectively). Theophylline did not change basal GH levels in any subjects and GHRH-induced GH rise in the younger group, whereas it restored normal GH responses to GHRH in the older subjects (mean peak responses were eight times higher than baseline in both groups). These data show that in elderly subjects the mechanism underlying the GHRH-induced GH secretion may be fully activated by GHRH during treatment with low amounts of theophylline.

Adult

Restoration of normal gonadotropin responses to naloxone by chronic bromocriptine treatment in elderly men.

Naloxone is unable to stimulate FSH and LH secretion in elderly men, suggesting a reduced endogenous opioid control of gonadotropin secretion in senescence. In the present study, we examined whether in elderly men a chronic dopaminergic stimulation with bromocriptine (5 mg/day for 7 days) modifies the gonadotropin response to naloxone (4 mg as an i.v. bolus plus 10 mg infused in 2 h). Eleven younger men (group 1, 22-40 years old) participated as controls. Twenty-two elderly men were selected from a larger population and were divided into two groups: subjects with compensated gonadal failure (normal blood testosterone and elevated gonadotropin concentrations; group 2, n = 11; 62-80 years old) and men with normal gonadal function (normal blood testosterone and gonadotropin levels; group 3, n = 11; 61-82 years old). Naloxone induced a striking LH and a slight but significant FSH increase in group 1, but was unable to change serum gonadotropin concentrations in elderly subjects of both groups 2 and 3. When experiments were repeated after bromocriptine treatment, no significant differences in LH and FSH responses to naloxone were observed in the younger subjects. On the other hand, bromocriptine restored significant gonadotropin responses to naloxone in elderly men. In fact, after bromocriptine, naloxone-induced FSH and LH increments in groups 2 and 3 were indistinguishable from those observed in group 1. These data suggest that in men age-related dopaminergic alterations may underlie the defective endogenous opioid control of gonadotropin secretion.

Adult

Impaired intrathyroidal iodine organification and iodine-induced hypothyroidism in euthyroid women with a previous episode of postpartum thyroiditis.

Postpartum thyroiditis (PPT) is common and occurs in 1.7 to 16.7% of pregnant women, depending upon the study population. Most of these women develop transient hypothyroidism and thyroid function usually returns to normal. We have studied 11 euthyroid women with a previous history of PPT to determine the incidence of subtle defects in thyroid function measured by iodide-perchlorate (I-ClO4) discharge tests and TRH tests and to determine whether these women would develop iodide-induced hypothyroidism. Seven (64%) had positive I-ClO4 discharge tests and 5 (46%) had an abnormally high TSH response to TRH. Thyroid antimicrosomal and antithyroid peroxidase were positive in 8 women (73%) with a previous episode of PPT. The administration of pharmacological amounts of iodide (10 drops of saturated solution of potassium iodide daily) for 90 days to these 11 women resulted in elevated basal and TRH stimulated serum TSH concentrations in 8 (72.7%) compared to TSH values during iodide administration to women who had never been pregnant. Antimicrosomal and antithyroid peroxidase concentrations did not change during iodide administration. These findings strongly suggest that euthyroid women with a previous episode of PPT have permanent subtle defects in thyroid hormone synthesis and are inordinately prone to develop iodide-induced hypothyroidism, similar to findings previously reported in euthyroid subjects with Hashimoto's thyroiditis, with a previous episode of painful subacute thyroiditis, or previously treated with radioactive iodine or surgery for Graves' disease.

Adult

Chronic treatment with a long-acting somatostatin analogue in a patient with intestinal carcinoid tumor: occurrence of cholelithiasis.

The long-acting somatostatin analogue SMS 201-995 has been used efficaciously in the therapy of metastatic carcinoid tumor, vasoactive intestinal peptide producing islet cell carcinoma, acromegaly, and TSH secreting pituitary tumors. We report the development of a gallstone in a patient treated for 23 months with a long acting somatostatin analogue for a metastatic carcinoid tumor. Symptomatic improvement and a reduction in the urinary excretion of 5-hydroxyindoleacetic acid occurred. There was no evidence of a gallstone on ultrasound and CT scan of the abdomen prior to somatostatin therapy. A progressively enlarging, asymptomatic gallstone developed during therapy.

Carcinoid Tumor

Increase by naloxone of arginine vasopressin and oxytocin responses to insulin-induced hypoglycemia in obese men.

The present study was carried out to establish whether the low arginine vasopressin (AVP) and oxytocin (OT) responses to insulin-induced hypoglycemia observed in obese men was due to alteration of the opioid control of posterior pituitary function. For this purpose, the AVP and OT releasing effect of insulin (0.15 IU/kg bw)--induced hypoglycemia was tested in eight normal weight men and in 10 age-matched obese subjects, without and with the previous treatment with the specific opioid receptor antagonist naloxone (3 mg in an iv bolus). In a control study, naloxone was given alone to the same subjects. Obese men showed similar basal glucose, AVP and OT levels, which remained unmodified after treatment with naloxone alone. Insulin induced a similar decrement of blood glucose levels in all subjects, with a nadir at 30 min. Plasma levels of AVP and OT rose strikingly in normal and obese subjects with mean peak responses at 30 min for AVP and at 45 min for OT. However, both AVP and OT responses were significantly lower in obese than in control subjects. Pretreatment with naloxone did not modify the AVP and OT responses to hypoglycemia in normal weight subjects, whereas it significantly enhanced both hormonal responses in obese subjects. In the presence of naloxone normal controls and obese subjects showed similar responses of both AVP and OT to hypoglycemia. These data indicate that an abnormal activity of endogenous opioids might account for the hypothalamic posterior pituitary dysfunction, which is responsible for the low AVP and OT responses to insulin-induced hypoglycemia in obesity.

Adult