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Biomedical subjects

M E Street

Publications and source records attributed to M E Street.

27 records · Page 2Linked to original sources
PubMed1997

Girls with virilisation in childhood: a diagnostic protocol for investigation.

AIM: To analyse critically a protocol for the investigation of girls presenting with virilisation in childhood. METHODS: Twenty five girls aged 1.6-8.7 years with features of virilisation were evaluated. Twenty four had presented with pubic hair, eight with auxilliary hair, seven with facial acne, four with clitoromegaly, and 10 with tall stature. They underwent clinical assessment (height, weight, height velocity, staging of puberty, physical examination for acne, body odour, and clitoromegaly) and laboratory assessment comprising basal concentrations of cortisol, 17 OH-progesterone (17 OHP), androstenedione, dehydroepiandrosteronesulphate (DHEAS), testosterone, and oestradiol. The above steroids were also measured during the short synacthen test (0.25 mg intramuscularly) in 16 subjects and low dose dexamethasone suppression tests (0.5 mg at six hourly intervals over 48 hours). Pelvic ultrasound, computed tomography and magnetic resonance imaging of adrenals were carried out when the biochemical findings suggested that there might be an autonomous source of androgen secretion. RESULTS: Clinical and laboratory assessments differentiated the patients into three diagnostic categories: adrenarche (18 cases), congenital adrenal hyperplasia (five cases), and adrenocortical tumour (two cases). The last had elevated concentrations of DHEAS, 1.5 and 19.1 mumol/l (normal value < 0.5 mumol/l), androstenedione, 24.6 and 21.8 nmol/l (normal < 1 nmol/l), and testosterone, 4.5 and 2.4 nmol/l (normal < 0.8 nmol/l), with none suppressing on dexamethasone suppression. Congenital adrenal hyperplasia subjects had elevated basal serum concentrations of 17 OHP (n = 4): 250, 140, 14, and 14.1 nmol/l (normal < 10 nmol/l) and elevated peak values of 17 OHP after synacthen (n = 3): 76, 179.5, and 175 nmol/l. Adrenarche patients had elevated basal concentrations of DHEAS (median: 2.3 mumol/l; n = 17) and androstenedione (median 2.6 nmol/l; n = 17). Nine patients also had elevated basal serum testosterone concentrations (median 0.9 nmol/l). Peak values of 17 OHP after synacthen were significantly different from baseline (n = 12) and were < 50% of the lowest value in congenital adrenal hyperplasia. Serum DHEAS, androstenedione, and testosterone suppressed following dexamethasone suppression (n = 16), thereby distinguishing adrenarche patients from adrenal tumour patients. Clinical details did not distinguish patients, except for clitoromegaly which was present only in the tumour and congenital adrenal hyperplasia patients. CONCLUSIONS: This protocol proved useful and practical in cases of virilisation presenting particular diagnostic difficulty.

Adrenal Cortex Neoplasms↗
PubMed1997

Management of insulin-dependent diabetes mellitus in adolescents.

There are many reasons for a specific management plan for adolescents with insulin-dependent diabetes mellitus (IDDM). Although most new patients can be managed initially on an outpatient basis, as they reach their teenage years, blood glucose control deteriorates and insulin requirements increase. Eating disorders, missing insulin injections, excess of alcohol all contribute to poor glycaemic control. Teenagers who have had diabetes for a number of years may have developed microvascular complications and disturbances of growth can occur, more often in girls than in boys. The transition to adult care continues to be a significant problem both for paediatricians and patients. Diabetes management during adolescence requires a team effort involving nurse educator, dietitian, paediatric diabetologist and, possibly, a social worker, with referral to specialists if necessary. Organizing this type of care requires a Regional Paediatric Diabetes Centre.

Adolescent↗
PubMed1997

Spontaneous thyrotropin and cortisol secretion interactions in patients with nonclassical 21-hydroxylase deficiency and control children.

Both exogenous and endogenous hypercortisolism result in reduced TSH secretion and mild hypothyroidism. However, little is known about the relation between endogenous TSH and cortisol secretion under physiological or slightly disturbed conditions. To examine this, we evaluated the pulsatility and circadian rhythmicity and time-cross-correlated the 24-h secretory patterns of cortisol and TSH in eight prepubertal children with nonclassical congenital adrenal hyperplasia (NCCAH) and eight age-matched short normal children. In both groups, TSH and cortisol were secreted in a pulsatile and circadian fashion, with a clear nocturnal TSH surge. Although no difference in mean 24-h TSH levels was observed between the two groups, daytime TSH levels were lower in the NCCAH group than in control children (P < 0.05). The cross-correlation analysis of the 24-h raw data showed that TSH and cortisol were negatively correlated, with a 2.5-h lag time for both groups, with cortisol leading TSH. This correlation might reflect a negative glucocorticoid effect exerted on the hypothalamic-pituitary-thyroid axis under physiological conditions. A significant positive correlation with TSH leading cortisol was observed at 8.5 and 5.5 h lag times for the control and NCCAH groups, respectively. The substantially shorter lag time of this positive correlation in NCCAH children than in controls suggests that in the latter, the nocturnal TSH peak occurs temporally closer to their compromised morning cortisol peak. These data indicate that the hypothalamic-pituitary-adrenal axis has a primarily negative influence on endogenous TSH secretion and that even mild disturbances in cortisol biosynthesis are associated with slight alterations in TSH secretion.

Adrenal Hyperplasia, Congenital↗
PubMed1997

Ovarian 17 alpha-hydroxyprogesterone responses to GnRH analog testing in oligomenorrheic insulin-dependent diabetic adolescents.

OBJECTIVE: To investigate the pituitary-ovarian function in adolescent girls with insulin-dependent diabetes mellitus (IDDM). DESIGN: Clinical case-control study. METHODS: The GnRH analog leuprolide acetate was administered subcutaneously to 16 adolescents with IDDM (seven eumenorrheic and nine oligomenorrheic) and 13 controls between 0800 and 0900 h. Blood samples were collected at baseline and 0.5, 3, 6 and 24 h after leuprolide to measure levels of gonadotropins, 17 alpha-hydroxyprogesterone (17-OHP), androgens and estradiol. RESULTS: Mean baseline serum LH levels were significantly higher in eumenorrheic compared with oligomenorrheic IDDM patients, while peak LH responses to GnRH analog testing were similar in all subjects. Oligomenorrheic IDDM girls showed, as a group, a distinct 17-OHP response to GnRH analog stimulation, which in five out of nine girls was in the range of functional ovarian hyperandrogenism (> or = 8.6 nmol/l). Androgen and estradiol levels were not significantly altered in any group. No correlation was found between steroid levels and HbA1c levels, although the latter were significantly higher in oligomenorrheic than in eumenorrheic patients. CONCLUSION: About 50% of the oligomenorrheic IDDM adolescents had an increased ovarian 17-OHP response to GnRH analog stimulation in the range of functional ovarian hyperandrogenism. Factors other than metabolic control, such as stress, may play an etiologic role in IDDM ovarian dysfunction.

17-alpha-Hydroxyprogesterone↗
PubMed1996

Pituitary-ovarian responses to leuprolide acetate testing in patients with congenital adrenal hyperplasia due to 21-hydroxylase deficiency.

To assess whether patients with congenital adrenal hyperplasia (CAH) due to 21-hydroxylase deficiency exhibit a steroidogenic response to GnRH agonist consistent with functional ovarian hyperandrogenism (FOH) and elucidate the relationship between adrenal and ovarian hyperandrogenism, the LH, FSH, estradiol, 17-hydroxyprogesterone (17-OHP), androstenedione, total testosterone, dehydroepiandrosterone, and 17-hydroxypregnenolone responses to a sc dose of leuprolide acetate (500 micrograms) were evaluated in 10 patients with classic CAH (mean age, 18.4 +/- 0.95 yr), 7 of whom had oligomenorrhea, pretreated with dexamethasone (2 mg/day for 5 days, including the day of the test). The results were compared with those obtained in 11 patients with FOH (mean age, 18.7 +/- 0.46 yr) and 17 normal women (mean age, 19.68 +/- 0.59 yr) not pretreated with dexamethasone. Leuprolide acetate stimulation caused a significant augmentation of plasma E2, 17-OHP, androstenedione, testosterone, and 17-hydroxypregnenolone concentrations in all CAH patients. However, in only 6 (60%) of them, all with oligomenorrhea, was the 17-OHP response (posttest minus pretest value) similar to that of FOH patients and significantly higher than that in controls. In this subset of CAH patients, LH plasma levels after stimulation were significantly higher than those of CAH subjects with 17-OHP responses in the normal range, controls, and FOH patients, whereas FSH levels were similar to those of controls. In this latter group, plasma FSH concentrations after stimulation were significantly higher than those in FOH. In conclusion, the results of the present study indicate that LH-dependent functional ovarian hyperandrogenism is frequent in patients with classic CAH. As ovarian hyperandrogenism might be partially responsible for the menstrual irregularities that are common complications in such patients, all classic CAH patients with oligomenorrhea should undergo short term stimulation with GnRH agonists to ascertain the presence of ovarian hyperandrogenism and receive appropriate treatment.

17-alpha-Hydroxypregnenolone↗
PubMed1996

Dose-dependent inhibition of growth hormone (GH)-releasing hormone-induced GH release by corticotropin-releasing hormone in prepubertal children.

Previous studies have shown that CRH is capable of inhibiting GH release in response to GHRH in adult subjects, and this effect appeared to be sex dependent and more pronounced in women than in men. To assess whether CRH has an inhibitory action on GH release in children also, the effects of graded doses of CRH on the GHRH-induced GH secretion were studied in three groups of prepubertal children. All subjects underwent a GHRH test (1 microgram/kg), followed, on separate occasions, by the combined administration of GHRH (1 microgram/kg) and CRH (1 microgram/kg, group A, n = 6; 1.5 microgram/kg, group B, n = 6; 2 microgram/kg, group C, n = 7). GH concentrations in response to the single GHRH injection were comparable in the three groups. The combined administration of GHRH and CRH resulted in serum GH concentrations similar to those obtained in the same subjects in response to GHRH alone when 1 and 1.5 microgram/kg CRH were given. In contrast, the administration of 2 microgram/kg CRH together with GHRH led to an increase in GH concentrations significantly lower than those after the GHRH injection alone (GH area under the curve, 1022.18 +/- 106.26 vs. 3109.16 +/- 794.29 microgram/Lx24 h; P < 0.05). No differences in the GH response to GHRH alone or to GHRH plus CRH were detected between male and female subjects. The results of the present study indicate that CRH is capable of inhibiting GHRH-induced GH release in children. Moreover, the inhibitory effect by CRH appears to be dose dependent and not sex related.

Adolescent↗
PubMed1996

Growth hormone treatment in short normal children.

The efficacy of growth hormone (GH) therapy in short normal children (i.e. children without classical growth hormone deficiency [GHD]) is still under debate. This paper presents the preliminary data of a retrospective Italian multicenter study on children treated with GH until adult height was reached. Final adult height (FAH), however, is not significantly different from the predicted adult height (PAH) calculated at the beginning of treatment. This result is in agreement with those reported in the majority of other similar international surveys. In conclusion, GH should be administered to short normal children only within the framework of well designed prospective experimental studies, which should consider several auxological, clinical and biochemical parameters capable of influencing the therapeutic results.

Adolescent↗
PubMedDate not supplied

Blood glucose normalization-induced haemolysis in three adolescents with type 1 diabetes mellitus at onset and unknown G-6-PD deficiency.

We present three adolescents unknown to be G-6-PD deficient who developed haemolytic anaemia after admission for diabetes at onset uncomplicated by ketoacidosis. These patients had no bacterial infections and had not ingested haemolytic drugs. The fall in glucose availability after the correction of hyperglycaemia is proposed as capable of inducing haemolysis in G-6-PD deficiency.

Adolescent↗