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Biomedical subjects

M Angulo

Publications and source records attributed to M Angulo.

At least 37 records · Page 2Linked to original sources
PubMed1990

[Evaluation of oral health status of a preschool group with a predictive test based on mutans group and clinical studies].

A children's population, aged from 2 to 5 years, was studied for three years. Bacteriological and clinical criteria were followed, with a determination of the M. st level in non-stimulated saliva in the age-groups of 3, 4 and 5 years. We found, as Alaluusua did, a correlation between the M. st level in saliva and the number of caries. With this study, a large number of caries-free children had a low M. st level. The largest amount of caries appears in children with a high M. st level. The highest caries incidence in this population appears at the 4 year children group. It has to be remembered that this is an age-group with specific characteristics. Caries is a disease depending on many factors and the M. st level would be very significant to an early detection of risks, but should be evaluated considering all the parameters as a whole. Its predictive value is not sufficient by itself but it has an unquestionable value when detecting risk patients of an early age. Therefore, treatment has to be the result of an etiological diagnosis addressed to prevention after an evaluation of all the factors related with the caries disease.

Child, Preschool↗
PubMed1989

Leukocyte alkaline phosphatase in hypothyroidism and hyperthyroidism. Response to initiation of thyroxine replacement therapy.

Leukocyte alkaline phosphatase (LAP) activity was determined in normal subjects, and in untreated, symptomatic patients with primary hypothyroidism or thyrotoxicosis. The means +/- 1 SD of (n) subjects were, respectively: 61.7 +/- 27.5 (16), 149.9 +/- 56.3 (9) and 96.9 +/- 27.7 (9). The mean LAP values of the hypothyroid and thyrotoxic groups were significantly different from that of the normal group (P less than .01). Values were above the normal range (20 to 120) in seven of the nine hypothyroid patients. LAP values were in the upper half of the normal range in eight of the nine thyrotoxic patients. In the two hypothyroid patients studied at 24-hour intervals, LAP activity was altered markedly within 48 hours of initiation of thyroxine therapy, 25 micrograms daily. In five hypothyroid patients followed for several months after initiating thyroxine replacement, LAP levels were essentially normal within 1 to 2 months. In the thyrotoxic patients, LAP values declined within the first month of medical management, but tended to remain within the normal range.

Alkaline Phosphatase↗
PubMed1988

Hypothalamic-pituitary gonadal axis in boys with primary hypothyroidism and macroorchidism.

Nine of 15 boys with severe long-standing primary hypothyroidism were found to have macroorchidism. All 15 patients had elevated thyroid-stimulating hormone levels. However, only those patients with testicular enlargement had striking elevations of serum prolactin and gonadotropin values. The response to gonadotropin-releasing hormone in our patients was blunted, in contradistinction to that of children with true precocious puberty. In spite of the elevated levels of luteinizing hormone, the serum testosterone levels were in the prepubertal range, explaining the lack of peripheral manifestations of androgenic effect. Improvement of testosterone secretion followed decreasing prolactin levels with bromocriptine administration, suggesting an inhibitory effect of prolactin on luteinizing hormone action at the Leydig cell. We conclude that testicular enlargement is the result of continuous follicle-stimulating hormone stimulation and that the term "true precocious puberty" is not appropriate in children with hypothyroidism and macroorchidism unless the hypothalamic-pituitary gonadal axis is shown to be at the pubertal stage.

Adolescent↗
PubMed1986

Effect of prolonged clonidine administration on growth hormone concentrations and rate of linear growth in children with constitutional growth delay.

Sixteen prepubertal children with constitutional growth delay (10 boys and six girls, mean age 7.2 +/- 2.1 years) were administered a daily dose of clonidine (0.15 mg/m2) for a period of 1 year. Growth hormone levels, plasma somatomedin C, and linear growth rate were significantly increased at the end of the treatment. Six of the children maintained the higher growth rate even 6 months after treatment. These and other studies suggest that prolonged stimulation of the hypothalamus by clonidine may ameliorate the impairment of growth hormone release seen in some children with constitutional growth delay. Because of the low cost and the convenience of the oral route, administration of clonidine could be a mode of treatment in some children with poor growth.

Administration, Oral↗
PubMed1984

Growth hormone inhibition causes increased selenium levels in Duchenne muscular dystrophy: a possible new approach to therapy.

Nine children with Duchenne muscular dystrophy were given Sanorex (mazindol), a growth hormone inhibitor, daily for 6 months. There was no significant change in their muscle function, but there was a significant reduction in weight gain and in levels of growth hormone, somatomedin C, hair zinc, serum zinc, and serum LDH. Selenium and glutathione peroxidase in the serum increased significantly. Thirteen other children with growth hormone deficiency had a significant reduction in hair selenium following growth hormone administration. These results show a significant relationship between growth hormone and selenium nutritional status and confirm our previous reports indicating an effect of growth hormone on zinc nutritional status. It is possible that prolonged therapy with a growth hormone inhibitor would attenuate the course and improve the longevity of patients with muscular dystrophy.

Adolescent↗
PubMed1983

Septo-optic dysplasia and median cleft face syndrome in a patient with isolated growth hormone deficiency and hyperprolactinemia.

A pituitary evaluation was carried out in a 12-year-old girl who had early puberty, short stature, optic nerve hypoplasia, and agenesis of the corpus callosum. Her growth hormone (GH) response to insulin-induced hypoglycemia and arginine infusion was blunted. Basal and stimulated levels of prolactin were elevated. The association of GH deficiency and hyperprolactinemia suggests a disruption of the dopaminergic modulation of these hormones. The facial features seen in our patient, such as hypertelorism, V-shaped frontal hairline, and cleft nose and upper lip, are enough to justify the diagnosis of median cleft face (MCF) syndrome. However, the optic nerve hypoplasia and the GH deficiency are characteristics of septo-optic dysplasia, and, to our knowledge, they have never been described in patients with MCF syndrome. Our case fulfills the diagnostic criteria of both, representing a link between both ends of this spectrum.

Abnormalities, Multiple↗
PubMed1983

Synergistic effects of growth hormone therapy on plasma levels of 11-deoxycortisol and cortisol in growth hormone-deficient children.

We have studied the response of blood levels of progesterone, 17-hydroxyprogesterone, 11-deoxycortisol, and cortisol to acute ACTH stimulation in children with isolated GH deficiency. Patients with isolated GH deficiency had generally higher levels of 11-deoxycortisol and lower levels of cortisol than controls both before and after ACTH stimulation. The steroid levels were almost completely restored to control levels after 3 months of treatment with GH. The pre-ACTH treatment levels of 11-deoxycortisol and cortisol were low in patients with both GH and ACTH deficiencies before and during GH therapy. Therefore, GH alone did not appear to have any effect on the hydroxylation of 11-deoxycortisol to cortisol. Before GH therapy, ACTH increased the concentrations of the two steroids. After GH therapy was started, the increase in 11-deoxycortisol was much smaller, but the increase in cortisol was much larger than before therapy. These results suggest a synergistic effect of GH on ACTH action on the biosynthesis of cortisol in the adrenals. Variations in the levels of 11-deoxycortisol and cortisol during hormonal manipulations lead to the identification of the mitochondrial hydroxylation of 11-deoxycortisol as one of the possible sites of action of GH.

17-Hydroxycorticosteroids↗
PubMed1981

Transient adrenogenital syndrome due to exposure to danazol in utero.

We describe a premature female infant exposed in utero to danazol during the first trimester of pregnancy. She was first observed in the newborn period with marked degree virilization and clinical findings suggestive of salt-losing congenital adrenal hyperplasia. This was supported by the high plasma levels of 17 alpha-hydroxyprogesterone and adrenocorticotropic hormone and low plasma cortisol level. Levels of testosterone, androstenedione, 11-deoxycortisol, and renin were also elevated. An excessive increase in the levels of 17 alpha-hydroxyprogesterone and 11-deoxycortisol to corticotropin administration associated with impaired increase in plasma cortisol level strongly suggests a partial block in the 21-hydroxylation of 17 alpha-hydroxyprogesterone. However, the high levels of 11-deoxycortisol also suggest a block of the steroid 11 beta-monooxygenase. A year later she was found to have normal basal levels of the adrenal steroids and normal response to corticotropin administration, pointing out the transitory nature of these abnormalities. It may be hypothesized that danazol produced a transitory block of the steroid 21- and 11 beta-monooxygenases in this child.

Adrenal Hyperplasia, Congenital↗