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Biomedical subjects

G Moncada

Publications and source records attributed to G Moncada.

13 recordsLinked to original sources
PubMed1998

Subclavian steal syndrome secondary to Takayasu arteritis.

We present a case of 'subclavian steal syndrome' secondary to Takayasu arteritis, in a 32-year-old, Japanese woman, whose clinical manifestations result from severe ocular and brain ischemia, refractory to high dose systemic corticosteroids. Surgical management using two bypass-grafts was carried out. The first one, a GoreTex, 8 mm in diameter, thin wall, stretch type with ring-bypass graft, from the left external iliac artery to the ipsilateral axillary artery. The second one, an autologous reverse saphenous vein graft from the left subclavian artery to the ipsilateral common carotid artery. The result was a remarkable improvement of the patient's general condition and symptoms. Patency of the extra-anatomic conduits was established by digital subtraction angiography (DSA), and transcranial Doppler evaluation, as well as flow velocity assessment revealed an objective improvement of the blood supply to the ischemic areas. The present surgical approach was justified since the inflammatory process extended to the aortic arch. The development of new and efficient operatory techniques, and continuous improvement of the graft-materials provide better expectations for the long-term outcome of refractory syndromes.

Adult↗
PubMed1998

Long-term patency of an aorta-aortic graft bypass in a patient with Takayasu arteritis.

A 39-year-old woman was diagnosed by means of angiography as Takayasu arteritis complicated with severe systemic hypertension due to atypical coarctation of the aorta. Aorta-aortic bypass graft surgery was carried out successfully and hypertension remarkably improved. An evaluation of the graft 23 years later confirmed an almost perfect condition with a very satisfactory clinical status. Extensive long-term follow-up studies have been conducted among young people after surgical repair of aortic coarctation showing encouraging results, however the situation seems to be different for the atypical coarctation in Takayasu patients, since not only the age at the time of intervention affects the outcome, but the different circumstances mainly related to the natural history of the disease. We evaluated the long-term outcome based on similar cases with particular consideration to the extremely rare coexistence of familiar hypercholesterolemia.

Adult↗
PubMed1990

Growth hormone secretion in pubertal age patients with Turner's syndrome.

GH levels were measured every 30 min during sleep over 9 h in 10 patients with Turner's syndrome ranging in age from 10.6-18.9 yr (mean, 15.0 +/- 2.7 yr) and in 12 controls matched for bone age, all of whom had normal GH responses to an orally administered dose of clonidine. We found no significant difference in the mean 9-h overnight GH concentration between groups. The overnight GH concentration was 3.8 +/- 2.2 micrograms/L (mean +/- SD) in Turner's syndrome patients and 4.5 +/- 2.4 micrograms/L in the control group. Total GH output (205.4 +/- 118.7 vs. 251.4 +/- 122.0 U), total number of nocturnal GH pulses (2.4 +/- 0.8 vs. 2.9 +/- 0.7), and mean peak GH response during nocturnal sampling (13.0 +/- 7.4 vs. 13.2 +/- 3.3 micrograms/L) were not different in the children with Turner's syndrome and the controls. We conclude that pubertal age patients with Turner's syndrome secrete GH normally and do not have any abnormality in GH regulation.

Adolescent↗
PubMed1989

The metoclopramide test: a useful tool with the luteinizing hormone-releasing hormone test in distinguishing between constitutional delay of puberty and hypogonadotropic hypogonadism.

To evaluate the effectiveness of intravenous metoclopramide, alone or in combination with luteinizing hormone-releasing hormone (LH-RH), in distinguishing between constitutional delay of puberty and hypogonadotropic hypogonadism, 12 patients with constitutional delay of puberty and 10 patients with hypogonadotropic hypogonadism were studied. All patients received 10 mg/m2 of intravenous metoclopramide and 100 micrograms of intravenous LH-RH on separate days. The mean prolactin (PRL) response following metoclopramide was significantly higher in the constitutional delay of puberty group when compared with the hypogonadotropic hypogonadism patients (P less than 0.01 at 15, 30, 45, and 60 minutes); all patients with constitutional delay of puberty increased their PRL level to greater than or equal to 60 ng/ml, except one who had a peak PRL level of 38 ng/ml. While only 2 of the hypogonadotropic hypogonadism subjects reached a peak PRL concentration of greater than or equal to 60 ng/ml, 4 had peak PRL levels greater than 38 ng/ml. The mean LH and follicle-stimulating hormone (FSH) responses after LH-RH were significantly higher in the constitutional delay of puberty group (P less than 0.01 at 30, 45, and 60 minutes for LH and P less than 0.01 at 45 and 60 minutes for FSH). All constitutional delay of puberty subjects responded to both the metoclopramide and LH-RH tests, while patients with hypogonadotropic hypogonadism responded only to one or to neither of these tests. Therefore, while metoclopramide alone did not allow us to clearly distinguish constitutional delay of puberty from hypogonadotropic hypogonadism, the combined use of both of these stimuli permitted us to detect all subjects with constitutional delay of puberty.

Adolescent↗
PubMed1989

Growth hormone release in response to growth hormone-releasing hormone in term and preterm neonates.

The growth hormone response to a single intravenous dose of human growth hormone-releasing hormone (GHRH) was examined in 23 healthy neonates (12 term and 11 preterm) aged 2-4 days. There were no significant increases in growth hormone concentrations at any point in time studied following GHRH administration in either group of newborns. The mean basal growth hormone levels of term neonates were significantly higher than those of the premature newborns (39.6 +/- 5.3 vs. 23.2 +/- 3.3 ng/ml; p less than 0.01) and this difference in growth hormone remained significant 15 and 30 min after GHRH injection. Gestational age correlated positively with both basal and peak growth hormone concentrations in our patients. In conclusion, first, neonates studied in their first days of life have high basal levels of growth hormone and fail to further secrete any significant amount of growth hormone following a single dose of GHRH, and, second, premature newborns secrete significantly less growth hormone than do term neonates.

Dose-Response Relationship, Drug↗
PubMed1986

Growth hormone secretion in patients with constitutional delay of growth and pubertal development.

Growth hormone levels were measured every 30 minutes during sleep over 9 hours in 20 prepubertal patients with constitutional delay of growth and puberty (CGD) and in 10 age-matched controls, all of whom had had normal GH responses to an orally administered dose of clonidine. We found no significant difference in the mean 9-hour overnight GH concentration between groups (4.5 +/- 1.8 ng/ml (mean +/- SD) in the CGD group, 4.4 +/- 2.8 ng/ml in the control group). Total GH output (258 +/- 99 U vs 222 +/- 135 U), total number of nocturnal GH pulses (3.6 +/- 0.8 vs 3.3 +/- 1.3), mean peak GH response during nocturnal sampling (13 +/- 1.2 ng/ml vs 13.2 +/- 1.3 ng/ml), and basal somatomedin C concentrations were not different in the children with growth delay and controls. We conclude that prepubertal patients with constitutional delay of growth and puberty secrete GH normally and do not seem to have any abnormality in GH regulation.

Adolescent↗
PubMed1986

Facial fractures.

Explore the source record for details and available documents.

Facial Bones↗
PubMed1983

Decreased secretion of cortisol and ACTH after oral clonidine administration in normal adults.

Clonidine, a selective noradrenergic receptor agonist, has been shown to affect various hormones acutely. It increases growth hormone levels in animals and in human adults and children. The effect of clonidine upon ACTH and cortisol levels is not as clear, and both stimulatory and inhibitory effects have been reported. We found a significant decrease in plasma cortisol decreased. No changes in FSH, LH, or prolactin were seen after oral clonidine. Our data are compatible with an inhibitory noradrenergic mechanism modulating ACTH and cortisol secretion in normal adults.

Adrenocorticotropic Hormone↗