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Biomedical subjects

P Fossati

Publications and source records attributed to P Fossati.

At least 127 records · Page 7Linked to original sources
PubMed1979

[Orthostatic hypotension in complicated diabetes mellitus: study of the renin-angiotensin-aldosterone system (author's transl)].

Plasma renin activity (P.R.A.) and plasma aldosterone (P.A.) were studied basally and after various stimuli in eight diabetic subjects with orthostatic hypotension and autonomic neuropathy. Five of them had chronic renal failure and proteinuria. On a diet containing 100 mEq Na/24 H, mean P.R.A. was 0,80 +/- 0,32 ng/ml/h in the supine position and 0,95 +/- 0,43 ng/ml/h in the upright position (N.S.); mean P.A. was 111 +/- 77 pg/ml in the supine position and 234 pg/ml in the upright position (p less than 0,01). On a diet containing 10 mEq Na/24 H, mean P.R.A. was 1,54 +/- 0,76 ng/ml/h in the supine position and 2,44 +/- 1,53 ng/ml/h in the upright position (N.S.). There was little stimulation of P. R. A. by low sodium intakes. After furosemide (n = 6), epinephrine + norepinephrine (n = 4) or diazoxide (n = 2), there was no stimulation of P.R.A. and P.A. Thus in diabetic patients with orthostatic hypotension and autonomic neuropathy basal values of P.R.A. and P.A. are in the normal range but there is dysregulation of renin-angiotensin-aldosterone system.

Adult↗
PubMed1978

[Pituitary adenoma with alpha, 17-39 ACTH and beta, MSH cells, without hypercorticism (author's transl)].

In one case of pituitary basophil adenoma, the majority of the cells contains numerous small granulations which, by using immunohistoenzymatic technique, react with alpha, 17-39 ACTH and beta, MSH antisera. The reaction with anti beta, 1-24 ACTH is negative. The radioimmunoassay of ACTH reveals an increase of plasmatic ACTH, but the cortisol cycle stays low. This data suggests that this functional adenoma releases a product of which has an immunological relationship with ACTH, without biological activity.

Adenoma, Basophil↗
PubMed1978

[Emerson-Trinder reaction: study of various chromogens and analyses of the principle interferences (author's transl)].

Several phenolic compounds and aromatic amines were tested with a system consisting of hydrogen peroxide, peroxidase and 4-aminophenazone for their chromogenic activity in the Emerson-Trinder reaction: sulphonated 2,4-diclorophenol had the greatest activity, about 4 times that of unsubstituted phenol. The mechanism of action of serum components (serum proteins, bilirubin and ascorbic acid) which can interfere in the Emerson-Trinder reaction was also investigated by the same analytical system. Binding of phenolic compounds to serum was found to be responsible for protein interference: this can be overcome by increasing the phenolic compounds concentration. The interference by bilirubin and ascorbic acid is due to hydrogen peroxide consumption, in competition with the chromogenic substrate.

Aminopyrine↗
PubMed1978

[Enzymatic determination of uric acid in serum with the trinder reaction (author's transl)].

We describe a direct colorimetric method for the enzymatic assay of uric acid. 50 microliters serum aliquots are incubated for 30 min with a diluted hexacyanoferrate solution, to remove interference by non-specific reducing agents. Uric acid is then oxidized to allantoin in the presence of uricase (Aspergillus flavus), with the simultaneous production of hydrogen peroxide; this is measured by a modified Emerson-Trinder reaction, in which phenol has been replaced by sulphonated 2,4-dichlorophenol, a more sensitive chromogen. The method gives linear results up to 20 mg of uric acid/100 ml.

Colorimetry↗
PubMed1977

[The sella turcica and pituitary function in congenital hypothyroidism due to thyroid ectopia or hypogenesis (author's transl)].

Nine patients suffering from hypothyroidism due to thyroid ectopia or hypogenesis, with a large sella turcica, were examined at adolescence or during adult life. TSH, prolactin and growth hormone function were studied. Basal plasma TSH, evaluated in 5 cases, was raised and responded explosively to stimulation with TRH. The administration of L-dopa was not associated with any notable changes in TSH. In one case, the chronic administration of l-T3 resulted in a fall followed by normalisation in plasma TSH levels. Basal plasma prolactin, explored in 6 patients, was high in 4 females and normal in 2 males. TRH stimulation resulted in a marked increased in prolactin in the female cases and a moderate increase in the male cases. L-dopa caused a fall only in high prolactin values. Stimulation of GH by argininehydrochloride, insulin hypoglycaemia and L-dopa gave variable responses. In one case, substitutive thyroid hormone therapy restored the GH response to L-dopa and arginine hydrochloride to normal. Paradoxically, GH increase following stimulation with TRH.

Adolescent↗
PubMed1977

[Hyperprolactinism and antiprolactin drugs].

After being suspected in the presence of galactorrhoea, it is now easy to prove hyperprolactinism thanks to radioimmunoassay of prolactin. The repercussions of hyperprolactinism on gonad function are now well known, especially in women where they lead to anovulation then amenorrhoea, whereas in man there occurs hypoandrogenism with loss of libido. Hyperprolactinemia may occur in numerous circumstances and may be deduced logically from the mechanism of secretory regulation of this hormone. Among the latter, one cause dominates the others by its therapeutic consequences, I.e. the presence of an adenoma or microadenoma secreting prolactin discovered thanks to tomography of the sella turcica. The treatment of hyperprolactinism has advanced in recent years with the introduction of dopamineric drugs such as bromcriptin which permits one to normalise prolactinemia and thus restore gonad function. It's use requires however certain precautions and neurological and ophthalmic supervision when htere is a microadenoma.

Adenoma↗
PubMed1977

Hypogonadism, galactorrhoea and hyper-prolactinaemia: Evaluation of pituitary gonadotrophins reserve before and under bromocriptine.

Twenty patients with hypogonadism (19 women with amenorrhoea and 1 man with impotence and infertility), galactorrhoea and hyper-prolactinaemia (range: 36 to 344 ng/ml) were studied. The radiological study of the sella turcica, including in all cases hypocycloidal tomograms, allowed classification of the patients into 3 groups: group I (n = 4) had a grossly enlarged sella turcica, group II (n = 12) had localized alterations indicating the probable existence of a prolactin-secreting microadenoma ("microdeformation") while group III patients presented no radiological abnormality. Before treatment, all the patients were submitted to a complete evaluation of the function of their anterior pituitary, including the LH and FSH responses to iv administration of Gn-RH. All the group I patients had low basal LH levels and a blunted response to Gn-RH. The basal LH and in response to Gn-RH were normal in most of the group II patients and in all of the group III patients. An exaggerated FSH response to Gn-RH was observed in 6/12 patients with microdeformation (group II) but not in groups I and III patients. A low LH and a blunted LH response to Gn-RH is highly suggestive of the existence of a pituitary prolactin-secreting adenoma in case of amenorrhoea and hyper-prolactinaemia patients; a normal response does not however rule out such a diagnosis. The reasons for a exaggerated FSH response to Gn-RH in patients with suspected prolactin-secreting microadenoma remain to be investigated though this pattern can also occur in other cases of amenorrhoea. Hence the Gn-RH test might contribute to the assessment of the hypothalamo-pituitary axis of patients with hyper-prolactinaemia. Six patients treated for 4 months with bromocriptine (CB-154) were submitted to re-evaluation of their pituitary gonadotrophins reserve. All the women experienced restoration of menses with 39 days of treatment and the male patient regained potency. It was observed that bromocriptine treatment and subsequent normalized prolactin levels in the 4 group II women tested were associated with normalization of their previously exaggerated FSH response to Gn-RH; LH responses were also diminished in these cases. These data are compatible with the hypothesis that hyper-prolactinaemia per se could interfere with the endogenous secretion of Gn-RH at the hypothalamic level. In one patient with grossly enlarged sella turcica and a previous lack of an LH and FSH response to Gn-RH, bromocriptine treatment restored a normal gonadotrophins response, confirming that, in this case, the alteration of this response was indeed due to a prolonged lack of endogenous Gn-RH secretion.

Adolescent↗