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R Lanes

Publications and source records attributed to R Lanes.

62 records · Page 4Linked to original sources
PubMed1979

Sustained effect of human growth hormone therapy on children with intrauterine growth retardation.

Previous studies have not clarified whether human growth hormone (HGH) therapy can significantly increase the height of patients with intrauterine growth retardation (IUGR). To determine whether the initial increase in growth rate is sustained through subsequent treatment, 19 prepubertal patients who had IUGR were treated with HGH. Ten of them received a second treatment course. Growth rates (in centimeters per year) were 4.8 +/- 1.4 (mean +/- SD) for the pretreatment period, 7.6 +/- 2.3 for the first treatment period, 4.2 +/- 2.5 for the interval between treatments, 5.9 +/- 1.4 for the second treatment period, and 4.3 +/- 2.6 for the posttreatment period. Growth rates for the two treatment periods were significantly greater than for the periods before, interval between, and posttreatment. Height expressed as the number of standard deviations below the mean for age increased significantly between the onset of treatment and the most recent measurement. These data indicate that HGH has a sustained positive effect on increasing growth rates in children with IUGR, although the magnitude of the effect may decrease with further treatment. Furthermore, we suggest that it is worthwhile to treat patients who have IUGR with HGH for prolonged periods of time, if supplies exceed those necessary to treat children with growth hormone deficiency.

Adolescent↗
PubMed1978

Evaluation of the growth hormone exercise test in normal and growth hormone-deficient children.

A group of 168 short but otherwise normal children (group A) and 25 children deficient in growth hormone (GH) (group B) wwere studied with an exercise stimulation test to determine the expected error of this method. In group A, 125 (74.4%) had maximum GH responses greater than 15 ng/ml, 23 (13.7%) had responses between 10 and 15 ng/ml, and 20 (11.9%) had responses less than 10 ng/ml. The mean +/- SD values were 8.4 +/- 0.4 ng/ml at 0 time, 26.3 +/- 15.0 at 20 minutes, and 10.7 +/- 8.3 at 40 minutes. The mean maximum response was 27.7 +/- 14.3 ng/ml. In group B, 22 (88%) had maximum responses less than 10 ng/ml and 3 (12%) had responses between 10 and 15 ng/ml. Patients with maximum responses less than 10 ng/ml have a high probability of being GH-deficinet, whereas patients with responses between 10 and 15 ng/ml are less likely to be GH-deficient. No patients with responses greater than 15 ng/ml were GH-deficient.

Adolescent↗
PubMedDate not supplied

Long-term therapy with a single daily subcutaneous dose of growth hormone releasing hormone (1-29) in prepubertal growth hormone deficient children. Venezuelan Collaborative Study Group.

As part of a multicenter study to evaluate the efficacy and safety of one daily subcutaneous dose of 30 micrograms/kg of GHRH, 16 prepubertal GH-deficient children with a mean chronological age of 9.0 +/- 2.3 years were treated for 12 to 24 months. After six months of therapy 11 children (68.7%) were considered good responders in that their growth velocity increased by greater than 2 cm/yr over baseline and were continued on GHRH, while five subjects (31.3%) were regarded as poor responders and switched to recombinant hGH for the following six months. Growth velocity increased significantly in responders from a baseline of 3.4 +/- 0.7 cm/yr (mean +/- SD) to 6.8 +/- 0.1 cm/yr, 6.2 +/- 0.9 cm/yr, 6.6 +/- 1.0 cm/yr and 6.5 +/- 0.7 cm/yr at 6, 12, 18 and 24 months respectively. Bone ages advanced by an amount equivalent to the months of treatment. GHRH antibodies were detected in 4/11 and 6/11 responders at six and 12 months of treatment and in 2/5 non-responders at six months, but seemed not to interfere with growth. No side effects or changes in glucose and lipid levels were noted during therapy. These results suggest that GHRH (1-29) at the dose and schedule used is generally effective in the treatment of GH deficiency.

Body Height↗
PubMedDate not supplied

Effects of two years of growth hormone treatment in short, slowly growing non-growth hormone deficient children.

Thirty-two short, slowly growing prepubertal children with normal GH levels (after clonidine stimulation and overnight sampling) were treated with GH hormone for 2 consecutive years at a dose of 0.1 IU/kg/day s.c. Fifteen similar children were followed for 2 years without therapy (controls). Height velocity increased in our treated group from 3.8 +/- 0.9 cm/yr to 7.3 +/- 1.3 cm/yr and 7.1 +/- 0.9 cm/yr in the first and second years of therapy, with 85.7% and 87.5% of our patients growing > 2 cm/yr above baseline. Height SDS changed from -2.4 +/- 0.4 to -2.0 +/- 0.7 in the first year and to -1.8 +/- 0.5 during the second year of treatment, while bone ages increased at a slightly higher rate than chronological ages. An increase in the final height predictions of our patients during therapy was noted. Height velocity increment in the control group was not significant and height SDS of this group did not change. GH therapy in short, slowly growing non-GH deficient children seems to be effective and safe in the short term; however, its efficacy in increasing the final height of this group of patients is still undetermined.

Adolescent↗
PubMedDate not supplied

Effect of glycemic control on the growth velocity and several metabolic parameters of conventionally treated children with insulin dependent diabetes mellitus.

To determine the effect of glycemic control on the growth velocity and several metabolic parameters of children with insulin-dependent diabetes mellitus (IDDM), 79 patients with IDDM, 45 females and 34 males with a mean chronological age of 8.4 +/- 3.0 years were followed over a 5-year period starting at the onset of diabetes. Glycemic control was assessed by measuring total glycosylated hemoglobin; children were divided into better controlled, GHb < 9%, 30 children (Group A) and worse controlled, GHb > or = 9%, 49 patients (Group B). Growth velocity was significantly lower, in the five years of follow up, in the worse controlled patients when compared to the better controlled subjects (4.8 +/- 1.6 vs 6.7 +/- 2.2 cm/yr after the first year and 5.0 +/- 2.0 vs 6.5 +/- 1.8 cm/yr after the fifth year, in group B and group A, respectively). Higher cholesterol (185.3 +/- 33.7 vs 158.8 +/- 39.5 mg/dl) and triglyceride levels (85.9 +/- 43.5 vs 71.0 +/- 37.4 mg/dl) were apparent in the worse controlled patients, when compared to the better controlled children. Insulin dose was not significantly different in the two groups (0.76 +/- 0.3 vs 0.84 +/- 0.4 U/kg/day in the 1st year and 0.9 +/- 0.3 vs 0.92 +/- 0.4 U/kg/day in the 5th year, in group B and A respectively). Although both groups received the same initial and long term training by our pediatric diabetes team, more frequent blood glucose monitoring, better record keeping and rotation of injection sites and more clinic visits were clearly noted in the better controlled group. Ketoacidotic episodes were more common in the worse controlled patients, while better controlled children had a higher number of hypoglycemic episodes. In conclusion, we have found poor glycemic control, as reflected by higher glycosylated hemoglobin levels, to affect the growth velocity and several metabolic parameters of children with diabetes followed for a five-year period. Other factors besides insulin dose and initial and subsequent diabetic education seem to play a role in their glycemic control.

Blood Glucose↗
PubMedDate not supplied

Acipimox, a nicotinic acid analog, stimulates growth hormone secretion in short healthy prepubertal children.

Recent studies in adult volunteers have demonstrated that the free fatty acid reduction induced by acipimox, a nicotinic acid analog, stimulated GH secretion per se and enhanced in an additive manner the GH secretion elicited by such different stimuli as pyridostigmine, GHRH and GHRP-6. In order to evaluate whether acipimox administration stimulates GH secretion in prepubertal children, we administered a single oral dose of acipimox (100 mg for children weighing <30 kg and 200 mg for those >30 kg) to 14 healthy prepubertal children with a mean age of 8.2 +/- 1.9 years, a mean bone age of 6.2 +/- 3.0 years, growing along the 5-10th percentiles, and with normal thyroid function and IGF-I levels. Acipimox administration elicited a sustained increase in GH from a mean baseline level of 0.6 +/- 0.4 to 6.7 +/- 2.4 microg/l at the end of the test (p<0.05), with a mean GH peak of 10.5 +/- 3.5 microg/l. GH release was delayed so that peak GH levels were achieved 180 minutes after acipimox administration. In order to determine whether acipimox was capable of enhancing the GH secretion elicited by levodopa (L-Dopa), we administered either oral L-Dopa (250 mg for children weighing <30 kg and 500 mg for those >30 kg) or oral acipimox plus L-Dopa to the same children on different days. GH concentrations increased in a similar fashion following either of these tests (from a baseline level of 1.2 +/- 0.4 and 0.7 +/- 0.4 microg/l to 8.4 +/- 2.7 and 9.3 +/- 2.9 microg/l at the end of the test (p<0.001), with peak GH concentrations of 13.1 +/- 4.1 and 11.8 +/- 3.3 microg/l after L-Dopa or acipimox plus L-Dopa, respectively). Although the peak GH concentrations obtained after the combined administration of acipimox plus L-Dopa were similar to those obtained after either acipimox or L-Dopa administration, a larger number of our patients reached a GH cut-off point of >7 microg/l following combined therapy than with either stimulus alone (13/14 patients with combined therapy and 10/14 with acipimox alone). No side effects other than mild facial flushing were noted after acipimox administration. These results indicate that: 1) following the administration of a single oral dose of acipimox, significant GH secretion was elicited in healthy short prepubertal children; 2) the combined administration of acipimox plus L-Dopa did not, however, enhance the GH secretion of this group of children; 3) acipimox was well tolerated with minimal side effects; and 4) further studies in both GH sufficient and GH deficient children are necessary to evaluate acipimox's usefulness in assessing GH reserve.

Body Height↗
PubMedDate not supplied

Epidemiology and inmunogenetics in recently diagnosed Venezuelan children with insulin-dependent diabetes mellitus.

Genetic and immunological markers in children with Type I diabetes have not been studied previously in Venezuela. We evaluated 91 newly diagnosed IDDM children mean age 7.8 +/- 4.5 (range 0.8-20.8 years), 51 females and 40 males. Eleven percent of first degree relatives had a family history of Type I IDDM; 56.7% had had upper respiratory infection prior to diagnosis and 12.7% had had either mumps or varicella. Peak incidence of disease was found in February and March and August to October. Eighty seven percent had HLA-DR3 and/or DR4 vs 36% of the Venezuelan general population; 81.6% were HLA-DQW2 and/or HLA-DQW8. We found 55.9% to have positive islet cell antibodies (ICA) with 4 of these having a positive complement fixation test. Three patients (7.9%) were found to have positive insulin autoantibodies. Only 3 out of 11 HLA-identical siblings had positive ICAs, while none had positive insulin autoantibodies. One of them also had a positive complement fixation test; this subject developed IDDM. No positive serotypes for enterovirus (Coxsackie-B) were found in our patients, but we detected 11 cases with elevated titers for cytomegalovirus antibodies and positive antibodies for measles, mumps, herpes and varicella were found in some children. These data confirm that most of our Type I diabetics carry HLA-DR3 or DR4 and that the heterozygous DR3/DR4 phenotype is markedly increased in this population; they also indicate that DR3QW2 and DR4QW8 are associated with increased risk in our population.

Adolescent↗