Office evaluation of urinary tract infections in elderly women.
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Biomedical subjects
Publications and source records attributed to J L Ross.
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We randomly assigned 16 girls with Turner syndrome, age 5 to 15 years, to receive treatment with 100 ng/kg/day ethinyl estradiol or placebo for 6 months, with crossover after a 2-month interim period. We assessed growth by measurement of the 4-week lower leg growth rate and by height velocity. Bone age was determined at the beginning and end of treatment. Growth rate during ethinyl estradiol treatment was approximately 70% greater than during placebo (P less than 0.001), without any bone age advancement relative to that with placebo. The change in predicted height was significantly greater after 6 months treatment with ethinyl estradiol than after treatment with placebo (mean +/- SEM, +0.35 +/- 0.38 cm vs. -0.85 +/- 0.32 cm, P less than 0.03). Breast budding occurred in six patients. We conclude that it may be feasible to begin low-dose estrogen therapy to promote growth at an earlier age than would be conventionally used to induce pubertal development. These data are still relatively short term, however; until long-term data are available, it would be premature to make definitive recommendations regarding the dose and timing of estrogen treatment in Turner syndrome.
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We administered ovine corticotropin-releasing hormone (CRH) as a bolus iv injection (1 microgram/kg) to 21 normal boys and girls, aged 6-15 yr. CRH stimulated release of immunoreactive ACTH and cortisol in all children. The peak plasma ACTH and cortisol levels after CRH were 15.7 +/- 9.4 (SD) pg/ml and 14.3 +/- 3.6 micrograms/dl, respectively, in the girls, and 20.7 +/- 9.7 pg/ml and 16.6 +/- 3.3 micrograms/dl, respectively, in the boys. Plasma ACTH and cortisol responsiveness to CRH did not differ between girls or boys, or between children and adults. Cortisol-binding globulin concentrations in plasma did not change with age. We conclude that CRH provides a safe means of stimulating the pituitary-adrenal axis in children.
The normal ranges for GH responses to GH-releasing hormone (GHRH) have previously been defined for adult men and women. To determine whether the GHRH responses of normal children differ from those of adults and whether children with GH deficiency (GHD) and children who are growing below the first percentile but are otherwise normal (ISS) have GH responses comparable to those of normal children, we studied 90 normal children, 46 girls and 44 boys, with heights between the 10th and 95th percentiles for age, at different pubertal stages. Their responses were compared to those of 24 children with ISS and 32 children with GHD and to values previously measured in young adult men and women. Girls were grouped by Tanner breast stages and boys by testicular volumes. Plasma somatomedin-C, estradiol or testosterone, and bone age were measured in all children. All received a 1 microgram/kg iv bolus dose of GHRH-(1-44)NH2, and GH responses were measured during a 2-h sampling period. Incremental serum GH responses in girls did not change throughout pubertal development and were similar to those of adult women. The responses in boys at midpuberty were somewhat lower (P less than 0.05) than those in either prepubertal boys or adult men. ISS children had mean GH responses [23 +/- 4 (+/- SE) ng/ml] similar to those of normal children. GHD children had significantly lower mean GH responses (11 +/- 3.7 ng/ml) than normal prepubertal children (35 +/- 4.0 ng/ml; P less than 0.01), but the responses of 17 of the 32 GHD children overlapped with the normal range. GH responses to GHRH were not correlated with bone age, weight, height, SmC levels, or estradiol or testosterone concentrations. These results indicate that GH responses to GHRH testing are relatively constant throughout puberty and young adulthood, that ISS children respond normally to GHRH, and that the GHRH test is not a reliable discriminator between individual normal and GHD children.
Short stature is a common feature of Turner's syndrome. We studied the dose-response relationship between short term linear growth and GH dose using the lower leg-measuring device. Three doses of GH (0.05, 0.15, and 0.45 U/kg, three times weekly) were given sc for 1-month treatment periods. Lower leg growth rate increased significantly during treatment with the 0.15 and 0.45 U/kg doses [1.8 +/- 0.2 (+/- SEM) and 1.7 +/- 0.3 mm/4 weeks). The higher dose of 0.45 U/kg was no more effective than the 0.15 U/kg dose. Serum somatomedin-C levels increased after treatment with each of the three doses of GH, but did not differ in any of the three dosage groups. We conclude that 0.15 U/kg GH, three times weekly, stimulates short term growth in patients with Turner's syndrome. Longer term studies are required to determine if this increased growth rate is sustained.
Pelvic sonographic studies were performed on 15 phenotypic females with Turner's syndrome and varying X chromosome abnormalities. In those individuals with the 45XO karyotype, the ovaries were not visible, consistent with the classic description of absent or fibrous streak ovaries. The patients who were chromosomal mosaics showed a range of findings from absent to infantile to normal adult-size ovaries. Turner's syndrome should be suggested in individuals with delayed onset of puberty, primary amenorrhea, and short stature in whom pelvic ultrasonography fails to reveal ovaries. On the other hand, the detection of ovarian tissue by pelvic ultrasonography does not exclude the diagnosis of Turner's syndrome but does suggest that an X chromosomal abnormality other than 45XO is probably present.
We investigated whether a decrease in serum growth hormone contributes to the short stature of adults with Turner syndrome by measuring the 24-hour profile of serum growth hormone in 30 patients aged 2 to 20 years. Growth hormone pulses were defined as a rise from nadir to peak that exceeded three times the intraassay coefficient of variation. Girls with Turner syndrome aged 2 to 8 years did not have statistically different growth hormone levels, peak amplitudes, and peak frequencies compared with those in age-matched controls. By contrast, girls with Turner syndrome aged 9 to 20 years had significantly decreased mean 24-hour growth hormone levels, peak amplitudes, and peak frequencies compared with those in age-matched normal girls. Patients with Turner syndrome of all ages had decreased serum somatomedin-C concentrations and delayed bone ages. We conclude that a relative deficiency of growth hormone in pubertal patients with Turner syndrome may contribute to their adult short stature.
To assess the efficacy of GH-releasing hormone (GHRH) in the treatment of GH deficiency, we measured the effects of pulsatile iv GHRH administration on GH secretion, plasma levels of somatomedin-C (SmC), and short term linear growth (as determined by lower leg measurements) in seven GH-deficient children in a placebo-controlled study. Either GHRH, at a dose of 1 microgram/kg (seven patients), or 0.9% saline (NS; four of these patients) was given iv every 3 h for 9-12 days; all patients also received GH for a similar period. Lower leg length was measured every 3 weeks before and after each treatment. GHRH was more effective than placebo in accelerating linear growth (P less than 0.05). The responses, however, were heterogeneous; four of the children responded with accelerated growth, and three did not. Two of the children who failed to grow had no increase in plasma GH or SmC during GHRH administration, and one had an attenuated GH response. The four children who grew had induction of pulsatile GH secretion [mean peak GH, 10.4 +/- 1.3 (+/- SEM) ng/ml after GHRH vs. 1.5 +/- 0.5 ng/ml after NS; P less than 0.05] and elevation in SmC levels (maximum, 0.5 +/- 0.1 U/ml during GHRH vs. 0.19 +/- 0.05 during NS; P less than 0.01). The lower leg growth velocity during GHRH treatment (2.8 +/- 0.2 mm/3 weeks) was greater than their own basal rate (0.6 +/- 0.2 mm/3 weeks; P less than 0.01) or their growth during placebo treatment (0.4 +/- 0.2 mm/3 weeks; P less than 0.01). Thus, repeated administration of GHRH stimulated increases in GH and SmC in some but not all GH-deficient children. The growth response appears to be related to the magnitude of the GHRH-stimulated rise in GH levels. GHRH increases short term linear growth in some children with GH deficiency and holds promise as an alternative to GH as a form of therapy in these patients.
We previously described a biphasic dose-response curve for ethinyl estradiol on short term growth in patients with Turner's syndrome. To investigate whether there is a similar phenomenon in boys, we measured the 3-week ulnar growth velocity (TUG) after administration of different doses of estradiol to five prepubertal or early pubertal boys. Basal TUG was determined initially. Subsequently, the boys received a 4-day iv infusion of estradiol at each of three doses (4, 20, and 90 micrograms/day) given double blind in a randomized sequence. TUG was determined before and after each infusion and was allowed to return to baseline before giving the second and third infusions. Mean TUG increased from 0.45 +/- 0.11 (+/- SEM) to 1.38 +/- 0.51 mm/3 weeks after the 4 micrograms/day infusion (P less than 0.05), from 0.49 +/- 0.11 to 1.0 +/- 0.4 mm/3 weeks after the 20 micrograms/day infusion (P = NS), and from 0.46 +/- 0.1 to 0.84 +/- 0.12 mm/3 weeks after the 90 micrograms/day infusion (P = NS). The mean serum estradiol level was 10 +/- 2.3 pg/ml during the 4 micrograms/day infusion, 16 +/- 2.3 pg/ml during the 20 micrograms/day infusion, and 96 +/- 12 pg/ml during the 90 micrograms/day infusion. Mean serum somatomedin-C levels were significantly higher only after the 20 and 90 micrograms/day estradiol infusions. We conclude that low dose estrogen can stimulate ulnar growth in boys and may play a role in the male pubertal growth spurt.
Research and statistics have been an integral part of social security program development and administration since the program's beginning. The Office of Research, Statistics, and International Policy (ORSIP) is responsible for developing and disseminating information on the effects of programs operated by the Social Security Administration (SSA) and the interactions among these programs, other tax and transfer programs, and economic, social, and demographic forces. This mission is carried out by collecting and tabulating statistics and by conducting policy research and legislative impact analyses. ORSIP also provides technical assistance to other SSA components. In this overview, each of those functions is outlined and major initiatives to carry out the office's primary objectives for fiscal year 1986 are described.
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We performed complete ophthalmological examinations of 30 consecutive patients with Turner syndrome. Twenty-three had 45XO and 7 had 45XO/46XX karyotypes (mosaicism). Non-familial strabismus was the most prominent ocular abnormality and was present in 33% of the patients. Other eye findings included ptosis (16%), hypertelorism (10%), epicanthus (10%), and antimongoloid slants (10%). Red-green color deficiency was found in 10% of the patients. One patient had congenital periodic alternating nystagmus.