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Biomedical subjects

A Loviselli

Publications and source records attributed to A Loviselli.

47 records · Page 3Linked to original sources
PubMed1988

Radioactive iodine thyroid uptake in patients with amiodarone-iodine-induced thyroid dysfunction.

Amiodarone, an iodine-rich drug, represents at the present, at least in Europe, one of the most common sources of iodine-induced thyroid dysfunction. The drug may induce both hypothyroidism and thyrotoxicosis. In spite of the large iodine intake occurring during amiodarone therapy, 131I thyroid uptake is detectable in patients with amiodarone-iodine-induced hypothyroidism, irrespective of the presence or absence of underlying thyroid disease. In contrast, in patients with amiodarone-iodine-induced thyrotoxicosis, 131I thyroid uptake is normal or even elevated in those with co-existent underlying thyroid disorders, whereas it is very low in those with an apparently normal thyroid gland. Perchlorate discharge test was performed in 8 patients with hypothyroidism and in 5 patients with hyperthyroidism induced by amiodarone: a positive test was found in all hypothyroid patients and a negative test in all hyperthyroid patients.

Adult↗
PubMed1987

The effect of androgen blockade on pulsatile gonadotrophin release and LH response to naloxone.

In order to clarify the effects of androgen blockade on the hypothalamic-pituitary-testicular axis in man, four patients with advanced prostate cancer, not previously treated, were given oral flutamide, 250 mg three times daily for 9 days. Before, and 7, 8 and 9 days after starting flutamide treatment, on separate days, the following tests were performed: a gonadotrophin pulsatility study, with 20 min interval blood sampling for 12 h, a naloxone test and a GnRH test. Flutamide induced a significant increase in both LH and FSH pulse frequency, while pulse amplitudes and plasma integrated concentrations (IC) of LH and FSH were unaffected. Plasma integrated concentrations of testosterone and oestradiol rose significantly, while that of prolactin was unaffected. The increase in plasma LH concentration induced by naloxone injection was abolished by flutamide treatment. On the other hand, the small FSH response to naloxone was unaffected by flutamide treatment. Response to GnRH was unaffected by flutamide. These results suggest that flutamide exerts effective androgen blockade at the hypothalamic level, since, despite increased plasma testosterone concentrations, gonadotrophin pulse frequency increased and the LH response to naloxone was abolished.

Anilides↗
PubMed1980

Failure of ketamine to interact with opiate receptors.

Ketamine, an anesthetic agent endowed with several morphine-like effects, failed to displace 3H-dihydromorphine or 3H-methionine-enkephalin from opiate receptors in the rat brain synaptosomal-mitochondrial membrane preparations. Furthermore, ketamine-induced analgesia in rats was not antagonized by naloxone, suggesting that this effect is not mediated by opiate receptors.

Animals↗
PubMedDate not supplied

Enhanced susceptibility to amiodarone-induced hypothyroidism in patients with thyroid autoimmune disease.

BACKGROUND: The iodine-rich antiarrhythmic drug, amiodarone, can induce both thyrotoxicosis and hypothyroidism, the former being more frequent in iodine-deficient areas, the latter in iodine-sufficient areas. In this study we evaluated prospectively thyroid function in amiodarone-treated patients with positive or negative baseline thyroid autoantibody test results who resided in a moderately iodine-deficient area of Italy. SUBJECTS: Two groups of patients received long-term amiodarone treatment: Group 1 included 13 patients with negative thyroid autoantibody test results. Group 2 consisted of seven patients with positive thyroid autoantibody test results and thyroid ultrasound patterns compatible with Hashimoto's thyroiditis. The control group (group 3) included 16 untreated euthyroid patients with Hashimoto's thyroiditis. All subjects resided in a mildly iodine-deficient area of Italy (Southern Sardinia) and had low urinary iodine values. Patients in groups 1 and 2 had markedly elevated urinary iodine excretion during treatment. The follow-up period ranged from 6 to 29 months in group 1, from 4 to 9 months in group 2, and from 12 to 55 months in group 3. RESULTS: Two (15%) of 13 patients in group 1 with nodular goiter developed thyrotoxicosis. No patient in this group developed circulating thyroid autoantibodies. Five (71%) of seven patients in group 2 became hypothyroid after 4 to 9 months of amiodarone treatment associated with a rise in serum thyroid autoantibody levels. No patient in group 3 became hypothyroid. CONCLUSIONS: (1) Amiodarone administration can cause both thyrotoxicosis and hypothyroidism. (2) Hypothyroidism is far more frequent in patients with preexisting thyroid autoimmune disease. (3) Amiodarone can modify the natural history of Hashimoto's thyroiditis. (4) Circulating thyroid autoantibodies do not appear in amiodarone-treated patients who have negative test results prior to therapy.

Adult↗
PubMedDate not supplied

Diagnostic usefulness of thyroid ultrasonography in atrophic thyroiditis.

An abnormal thyroid echographic pattern, characterized by a diffuse low thyroid echogenicity associated with a reduced thyroid volume, was found in 53 of 55 (96%) patients with atrophic thyroiditis. In 10 of these patients, the ultrasound examination was diagnostic for thyroid atrophy, whereas the scintiscan had no abnormality. In only two cases was the reverse observed, ie, absent thyroid radioiodine uptake and no evidence of abnormality in the ultrasound examination. Six out of 24 (25%) patients with thyroperoxidase antibody titers < or = 1:1600 and 4 of 31 (13%) patients with titers > or = 1:6400 had a normal thyroid scintiscan in the presence of an abnormal thyroid echographic pattern. Thus, thyroid echography can be considered the first morphological procedure in patients with hypothyroidism due to atrophic thyroiditis, and thyroid scintiscan can be used to confirm the diagnosis when other results are not definitive.

Atrophy↗
PubMedDate not supplied

[Myxedema coma].

Myxedema coma, an extreme expression of hypothyroidism, represents a medical emergency with high mortality. Hypothermia and cerebro-vascular accidents should be taken into account for correct differential diagnosis. The treatment of myxedema coma is based on prevention of the precipitating factors and on the administration of generous doses of L-thyroxine and/or triiodothyronine, associated with steroids and drugs for respiratory and cardio-vascular complications.

Coma↗