Biomedical subjects
A Liuzzi
Publications and source records attributed to A Liuzzi.
[Effects of insulin on RNA and lipid synthesis in embryonal sensitive ganglia].
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[Research on the mechanism of action of testosterone: analysis of RNA induced in the mouse submaxillary gland].
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[Physiopathological and diagnostic significance of urinary pregnanetriolone in Cushing's syndrome].
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Metabolic effects of a specific nerve growth factor (NGF) on sensory and sympathetic ganglia: enhancement of lipid biosynthesis.
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[Determination of delta 5-pregnene-3-beta,17-alpha,20-alpha-triol in human urine].
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Alternative pathways of glucose metabolism in developing chick brain.
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Effectiveness of the dopamine agonist lisuride in the treatment of acromegaly and pathological hyperprolactinemic states.
We have studied the effects of the chronic administration of the dopamine agonist lisuride (L) in 21 acromegalics (group 1) and in 25 patients with pathological hyperprolactinemia (group 2). Before starting the treatment levels of PRL and/or GH were determined during acute tests with L (0.3 mg po) or TRH (0.2 mg iv). L was given in doses ranging between 0.4 and 2.4 mg/day. GH and/or PRL were determined at monthly intervals, TRH (6 patients of group 1 and 10 of group 2) was repeated during L therapy. In 10 patients of group 1 GH levels were reduced below 10 ng/ml by L therapy; in the remaining patients GH levels were reduced by 50% of the pretreatment values or they were unchanged. The correlation (p less than 0.01) found between GH levels during acute and chronic L administration indicates that GH changes after acute test are predictive of the outcome of the treatment. In all patients PRL was reduced during the therapy to at least 50% of the basal values and in most patients PRL fell to the normal range. No correlation was found between PRL levels during acute and chronic L administration. During the therapy TRH still increased GH levels in most patients whereas it failed to raise PRL. The withdrawal of L was followed by a rapid return of GH to the pretreatment values whereas PRL showed a slower increase. In acromegalics whose GH was lowered by L there was also a marked amelioration of clinical and metabolic parameters. The lowering of PRL was accompanied by the resumption of ovulatory menses even in patients with tumoral hyperprolactinemia. Males reported improvement in sexual performance. An improvement of visual field occurred in 1 patient. In 1 patient with a large prolactinoma serial computerized tomography scans performed during 2 yr of treatment showed a marked reduction of the tumor size.
GH regulation in acromegaly.
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[Medical treatment of acromegaly with dopaminergic agents].
The medical treatment of acromegaly with dopaminergic drugs has its physiopathological premise in the observation that agents capable of stimulating dopaminergic receptors directly are capable of determining GH secretion inhibition in a large percentage of acromegalic patients. Chronic administration of 5-20 mg/die of bromocryptin, long acting dopaminergic agonist, leads to a stable reduction in the levels of GH and somatomedin C (SmC) in about 50% of patients. However, these are only normalised in 20%. Treatment induces marked improvement in the clinical and metabolic changes typical of acromegalic disease. The therapeutic effect of dopaminergics may be maintained for periods of treatment lasting years but upon suspension of treatment pH levels return quickly to pretreatment levels. The antitumoral effect of the dopaminergic frequently encountered in prolactinomas is a rarer event in acromegaly and occurs more readily in patients with mixed secreting GH and PRL tumours than in pure GH. Currently octractide, a long lasting somatostatin analogue, is the most effective drug in the medical treatment of acromegaly; however the dopaminergic agonists remain a valid alternative.
[Role of medroxyprogesterone acetate (MPA) on the blood level of STH in 12 patients with acromegaly].
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[STH blood level after metopirone in 12 patients with acromegaly].
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[Behavior of blood somatotropin in states of hyperadrenocorticism].
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[Behavior of blood somatotropin in Turner's syndrome].
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Neuroactive drugs in endocrine diseases: notes on their physiopathological and therapeutical aspects.
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