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Biomedical subjects

A Cattani

Publications and source records attributed to A Cattani.

13 recordsLinked to original sources
PubMed1993

[3 beta-hydroxysteroid dehydrogenase defect: frequency of presentation in a sample of Chilean hirsute women].

The defect of 3 beta hydroxysteroid dehydrogenase (3 beta HSD) is frequent among hirsute women and clearly dependent on the ethnic composition of the studied population. Our aim was to study the frequency of 3 beta HSD deficit in a group of Chilean hirsute women. Basal and post ACTH concentrations of cortisol, 17 hydroxyprogesterone and 17 hydroxypregnenolone were measured by RIA in 40 hirsute post puberal women and in 15 normal age matched female volunteers. Criteria for considering a 3 beta HDS deficit were 17 hydroxypregnenolone values and 17 hydroxypregnenolone/17 hydroxyprogesterone and 17 hydroxypregnenolone/cortisol ratios after ACTH stimulation over the 95% confidence intervals of normal women. Basal dehydroepiandrosterone sulphate and testosterone levels were also measured in hirsute women. All samples were obtained during the follicular phase of the menstrual cycle. ACTH stimulated hormone values and ratios were diagnostic for 3 beta HDS deficit in 7.5% of hirsute women. Basal testosterone was over 80 ng/dl in 47.5% and dehydroepiandrosterone sulphate over 3.9 micrograms/ml in 52.5% of these women. There was no correlation between dehydroepiandrosterone or testosterone values and ACTH stimulated hormone values. It is concluded that 3 beta HSD is frequent in hirsute women and that its diagnosis requires the determination of ACTH stimulated 17 hydroxypregnenolone values and 17 hydroxypregnenolone/17 hydroxyprogesterone ratio.

17-alpha-Hydroxypregnenolone↗
PubMed1989

The paradoxical response of growth hormone (GH) to thyrotropin-releasing hormone (TRH) in constitutionally tall children involves a cholinergic pathway.

To investigate whether or not a cholinergic pathway is involved in the paradoxical response of GH to TRH in constitutionally tall children, we studied 8 healthy prepubertal children aged 4 2/12-7 10/12 yr, whose heights were over the 95th percentile of the NCHS tables. We defined as "paradoxical" a GH increment greater than 5 ng/ml in response to TRH. Five out of 8 children showed a paradoxical response of GH to TRH (mean GH peak after TRH of 10.7 +/- 1.1 ng/ml). Pretreatment with atropine (0.01 mg/kg IM 30 min prior to the TRH administration) abolished the TRH induced GH rise (peak GH after TRH of 1.5 +/- 1.0 ng/ml, p less than 0.01) but did not modify the TSH response (peak TSH after TRH: basal conditions 8.7 +/- 0.8 microU/ml, post atropine: 9.5 +/- 1.4 microU/ml, p greater than 0.05). Our results demonstrate that a cholinergic pathway is involved in the paradoxical response of GH to TRH in constitutionally tall children.

Acetylcholine↗
PubMed1978

[Damages of malfunction of the electrostimulating system (author's transl)].

In this study we describe the damages, or the ill-functioning of the electrostimulating system due to failure or bad functioning of the catheter electrode, of the electronic circuits and of the energy sources. Complications due to iatrogen causes or to clinical pathology have not been dealt with. Defects of electrostimulation are described in their clinical, electrocardiographic, oscilloscopic and electrophysiologic aspects, and in the operative report, through the study of 1455 cases. In the differential diagnosis of the defects of electrostimulation we point out their biological causes. The sheath interruption, observed in 31 cases, causes defects in electrostimulation, depending on the extension and on the position of the unsheathing. The circuit variations can be compared with the effect produced by a shunt capacitor. The sheath interruption causes a current reduction which reaches stimulating surface and the differential diagnosis concerns the electronic failure of the generator, the battery discharge, the organic liquid infiltration in the insertion point, the position of the catheter, and the tip perforation of it. The breaking of the spiral (in 6 cases) can be partial or total, and may be compared to the forming of a series capacitor between the electrodes which may sham the increase of the myocardic threshold. The stimulating surface, too wide respecting the intensity supplied by the electrostimulator, brings about a low current density and failures in electrostimulation; the difference between such condition and the one caused by a high myocardiac threshold is shown by determining the safety factor. A very small stimulating surface increases the electrode impedance and may cause a defect of the perception function, if the generator input impedance (4 cases) is reduced. The fall of the output voltage may be caused by a battery discharge, and is the most frequent cause of electrostimulation disturbances; it has been observed in 432 cases. Other causes of the fall of the output voltage (30 cases) are the outflow of mercury from the cells, or mycotic formations. The ill-functionning or the loss of perception (9 cases) caused by defects of the electrostimulator must be distinguished from the ones caused by the endocavitarian potential reduction (myocardiac infarction, conduction disturbances: 2 cases). Variations of the stimulating cycle can be caused by ageing, humidity on resistances and on oscillator condensers (9 cases). Accelerated stimulating was observed in 1 case, plate corrosion in 3 cases, high density of anodic current in 9 cases, generator turnover in 3 cases. Finally we give the chief points of electrical stimulating disturbances due to interferences of electromagnetic radiation.

Cardiac Pacing, Artificial↗
PubMedDate not supplied

[Di George syndrome].

Two patients with Di George syndrome are presented. Diagnosis was done at ages 4 months and 16 days respectively. Their main clinical symptoms were hypocalcemic convulsions, unusual facies (hyperthelorism, low set prominent ears, micrognathia, short philtrum) and cardiac malformations (vascular ring with right aortic arc, aberrant left innominated artery and ligamentum arteriosus in one of them and Tetralogy of Fallot with pulmonary valve atresia in the other). The first patient is now a 3.5 year old boy, his vascular ring was repaired and he has hypoparathyroidism but no clinical nor laboratory evidence of cellular immunodeficiency. The other patient had evidence of heart failure at her second week of life, she died at age sixteen days and, at necropsy, Fallot's tetralogy with pulmonary valve atresia, closed ductus arteriosus, histologically normal ectopic thymus and absent parathyroid glands were demonstrated. We postulate that these cases correspond to partial forms of Di George syndrome.

Antibodies, Monoclonal↗