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Biomedical subjects

D B Allen

Publications and source records attributed to D B Allen.

At least 55 records · Page 3Linked to original sources
PubMed1994

A meta-analysis of the effect of oral and inhaled corticosteroids on growth.

This analysis summarizes studies comparing attained heights with expected heights of children with asthma treated with inhaled or oral corticosteroids. The possible moderating effects of treatment duration, and dosage and asthma severity are also examined. A preliminary database of 95 articles rendered 21 includable studies representing 810 patients with asthma, which yielded 29 tests of the corticosteroid-growth effect. Statistical integration of the results of these studies revealed a significant but small tendency for corticosteroid therapy in general to be associated with diminished final height (Z = 2.328, p = 0.01, mean r = -0.023). However, this effect varied for the specific drugs under consideration. As expected, significant weak growth impairment was observed for prednisone (Z = 2.137, p = 0.0164, mean r = -0.295) and "other oral corticosteroids" (Z = 9.107, p = 2.44E-18, mean r = -0.260). On the other hand, a significant moderate tendency was observed for inhaled beclomethansone dipropionate therapy to be associated with attaining normal stature (Z = 7.395, p = 2.17E-13, mean r = +0.432). There was no statistical evidence for beclomethasone dipropionate therapy to be associated with growth impairment at higher doses, for longer therapy durations, or among patients with more severe asthma. This meta-analytic integration indicates that available studies of inhaled beclomethasone dipropionate therapy do not show an association between its use and the adverse effect of diminished stature.

Administration, Inhalation↗
PubMed1993

Defective aldosterone synthesis associated with hyperkalemic periodic paralysis.

OBJECTIVE: To describe defective aldosterone biosynthesis (corticosterone methyl oxidase type II [CMO-II] deficiency) in a kindred with hyperkalemic periodic paralysis. SETTING: Tertiary care hospital in Madison, Wis. PATIENTS: Individuals studied included a female infant with failure to thrive, hyponatremia, and hyperkalemia; the infant's asymptomatic mother and father; and a maternal aunt and grandmother with hyperkalemic periodic paralysis. INTERVENTIONS: Mineralocorticoid synthetic pathways were analyzed with synthetic adrenocorticotropin stimulation. In one patient with hyperkalemic periodic paralysis, acetazolamide sodium therapy was discontinued and replaced with fludrocortisone acetate therapy. MEASUREMENTS/MAIN RESULTS: Impaired aldosterone synthesis with marked accumulation of mineralocorticoid precursors 18-hydroxycorticosterone and corticosterone indicated severe CMO-II deficiency in the infant. In her relatives and parents, baseline aldosterone levels (74 to 111 pmol/L) were low (reference range, 194 to 830 pmol/L, a nonstricted sodium diet). Serum 18-hydroxycorticosterone levels (442 to 1021 pmol/L) were normal (reference range, 138 to 1270 pmol/L), but ratios of 18-hydroxycorticosterone to aldosterone were abnormally elevated (4.5 to 13.7; reference range, 2.65 +/- 1.86), indicating deficient CMO-II enzyme activity. Acetazolamide therapy was substituted with fludrocortisone therapy in the maternal aunt without return of paralytic symptoms. CONCLUSION: This association of hyperkalemic periodic paralysis with CMO-II deficiency and resolution of paralytic episodes with fludrocortisone therapy suggests a contribution of defective mineralocorticoid-mediated potassium homeostasis to the pathogenesis of hyperkalemic periodic paralysis.

Aldosterone↗
PubMed1993

Effects of nightly clonidine administration on growth velocity in short children without growth hormone deficiency: a double-blind, placebo-controlled study.

Children with short stature, slowed linear growth velocity, and delayed skeletal maturation may secrete growth hormone (GH) normally in response to provocative stimuli but may also have spontaneous undersecretion of GH. Orally administered clonidine, an alpha 2-adrenergic agonist, is a potent acute stimulator of growth hormone releasing hormone-mediated pituitary GH release. We performed a double-blind, placebo-controlled crossover study of nightly oral clonidine therapy (0.1 mg/m2) in 10 short, slowly growing, non-GH-deficient (stimulated GH level > 15 micrograms/L) prepubertal boys (range, 6.1 to 12.2 years; mean height standard deviation score, -2.3 +/- 0.4). Results of 6 months of clonidine therapy were compared with the results of 6 months of placebo therapy; GH responsiveness was subsequently assessed in 7 of 10 patients. Growth velocity (4.9 +/- 0.6 cm/yr baseline) was not improved by clonidine (4.6 +/- 1.2 cm/yr) or placebo (5.2 +/- 1.2 cm/yr), but it increased (p < 0.001) with GH therapy (8.2 +/- 1.3 cm/yr). Clonidine therapy similarly did not significantly affect plasma levels of insulin-like growth factor I or bone age maturation. Diminution in clonidine-stimulated peak GH levels was not observed after long-term oral clonidine therapy. Thus, in contrast to previous non-placebo-controlled studies, nightly clonidine therapy did not increase growth velocity or plasma insulin-like growth factor I levels. Subsequent acceleration in growth velocity during GH therapy suggests that a proposed increase in clonidine-induced endogenous GH secretion does not result in an effective growth-promoting stimulus.

Administration, Oral↗
PubMed1993

Newborn screening for congenital adrenal hyperplasia in Wisconsin.

Beginning in February 1993, newborn screening for 21-hydroxylase deficiency congenital adrenal hyperplasia (21OH-D-CAH) will begin in Wisconsin. This brief review summarizes the pathophysiology of 21OH-D-CAH, its clinical presentation, and the rationale for screening during the neonatal period. An algorithm for interpretation and follow-up of screening results is provided for Wisconsin health care providers.

Adrenal Hyperplasia, Congenital↗
PubMed1992

Can general surgeons perform colonoscopy safely?

The purpose of the current study was to review the safety of colonoscopy performed by nonfellowship-trained general surgeons. To address this issue, we reviewed more than 1,000 consecutive diagnostic and therapeutic colonoscopies and recorded the complications. This was a multi-institutional study involving seven general surgeons, none of whom had had formal fellowship endoscopic training. Perforation was confirmed by laparotomy, bleeding was defined as that requiring hospitalization and/or transfusion, and cardiopulmonary arrest was self-explanatory. There was one perforation in the diagnostic group and none in the therapeutic group, for a rate of 0.10% overall and 0.12% in diagnostic colonoscopy. There were no instances of bleeding or cardiac arrest. This complication rate of 1 per 1,025 colonoscopic procedures by general surgeons compares favorably with that previously reported by other specialties (p less than 0.001). We conclude that postgraduate endoscopy fellowship is not necessary for general surgeons to become safe colonoscopists.

Clinical Competence↗
PubMed1992

Effects of prolonged growth hormone administration in rats with chronic renal insufficiency.

Recombinant hGH (rhGH) augments short-term linear growth in experimental animals and children with chronic renal failure. Significant augmentation of final height, however, requires prolonged growth hormone therapy during years of growth. The effects of prolonged rhGH treatment on linear growth, progression of renal dysfunction, and longevity in the setting of renal insufficiency are unknown. We examined at 9, 15, and 25 wk growth in length and weight, glomerular filtration rate measured by inulin and creatinine clearance, food efficiency (g ingested/weight gained), and survival in treated (U-GH) and untreated (U) 75% nephrectomized uremic rats and in treated (S-GH) and untreated (S) sham-operated rats. We also measured kidney weight to body weight ratios at the time the rats were killed. Treatment was rhGH 1.0 mg s.c. three times a week during wks 4-12 of life. Length of U-GH rats was greater than that of U rats (p less than 0.05) at 15 and 25 wk (but not at 9 wk) and equal to that of S rats throughout the study. Length of S-GH rats exceeded that of S rats. At 9 wk, weight was diminished in both U and U-GH rats (p less than 0.05) versus S and S-GH rats; by 15 wk, U-GH rat weight was equal to S rat weight. Glomerular filtration rate measured by creatinine was markedly reduced in U and U-GH rats and did not increase in response to prolonged rhGH in either U-GH or S-GH rats. Diminished food efficiency of U rats versus S rats (p less than 0.05) was not improved significantly by rhGH.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Diabetes mellitus and exercise.

Physical exercise is traditionally considered beneficial in the treatment of IDDM. Attainment and maintenance of ideal body weight, improvement in self-image, and decreases in hypertension and lipid-related cardiovascular risk factors can all be achieved by the diabetic patient who exercises. Although the value of exercise in improving long-term glycemic control remains controversial, athletic participation by individuals with IDDM is encouraged to achieve the same health benefits enjoyed by exercising nondiabetic individuals. Knowledge of the metabolic responses to exercise in IDDM patients is required for appropriate guidance and management. Careful monitoring and adjustment of insulin doses and nutrition plans can then make possible the safe and successful participation of IDDM patients in virtually any athletic activity.

Diabetes Mellitus, Type 1↗
PubMed1992

Stimulation of collagen synthesis and linear growth by growth hormone in glucocorticoid-treated children.

Impaired linear growth and skeletal maturation associated with chronic glucocorticoid therapy may result from (1) inhibited insulin-like growth factor 1 (IGF-1) activity; (2) impaired type 1 collagen synthesis; or (3) suppressed growth hormone (GH) secretory response to growth hormone-releasing hormone. Each mechanism could potentially be improved by exogenous GH treatment. Seven slowly growing glucocorticoid-treated children received recombinant DNA human GH (0.3 mg/kg/per week) for 6 to 21 (mean 13.1 +/- 4.9) months. Height, weight, IGF-1 activity, glycosylated hemoglobin level, and C-terminal type 1 procollagen level were measured every 3 months and growth velocity was calculated. Skeletal maturation and 2-hour postprandial serum glucose and insulin levels were assessed every 6 months. All patients showed increased growth velocity during treatment with GH. Mean growth velocity increased from 3.43 +/- 0.65 cm/y to 6.72 +/- 0.84 cm/y with GH therapy (P less than .005). Growth velocity standard deviation scores corrected for bone age (P less than .005), IGF-1 levels (P less than .05), and C-terminal type 1 procollagen levels (P less than .005) also increased with GH therapy. C-terminal type 1 procollagen levels correlated well with growth velocity (r = .652) while IGF-1 levels did not (r = .17). Glycosylated hemoglobin levels remained unchanged, but 2-hour postprandial glucose levels rose during GH treatment. Slowly growing glucocorticoid-treated children receiving GH therapy increased growth velocity for 6 to 21 months. Initially diminished C-terminal type 1 procollagen levels rose with GH therapy, a change which corresponded with growth acceleration.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1991

Correlation of glycosylated hemoglobin measured by affinity vs ion exchange chromatography with mean blood sugar in pediatric IDDM patients.

Affinity chromatography provides a more specific estimate of glycosylated hemoglobin (GlyHb) than does ion exchange chromatography (HbA1). However, whether GlyHb correlates closer than HbA1 with mean blood glucose has not been established. GlyHb and HbA1 were measured in pediatric IDDM patients attending a clinic (n = 285 visits) over a one year period and correlated with the mean of a patient's blood glucose measurements from records of home blood glucose monitoring. Mean GlyHb was higher than mean HbA1 (10.8% vs 9.6%) as was its standard deviation (2.2% vs 1.5%). While both GlyHb (r = 0.75) and HbA1 (r = 0.65) were strongly correlated with estimates of mean blood glucose, the correlation with GlyHb was significantly stronger than with HbA1 for the entire spectrum of metabolic control (P = 0.03), as well as for a segregated group of 'poorly controlled' patients with mean blood glucose greater than 150 mg/dl (P = 0.04). The results suggest that GlyHb is more accurate than HbA1 for estimating metabolic control and that GlyHb shows greater discriminating power than HbA1, especially at high concentrations of blood sugar. The mean blood glucose can be estimated from the equation: mean blood glucose (mg/dl) = (11.3 x GlyHb) + 32.

Adolescent↗
PubMed1990

Growth hormone therapy for short stature: panacea or Pandora's box?

Increased availability of growth hormone (GH) because of increased production using recombinant DNA technology has led to increased demand. Many children who do not have classic GH deficiency may respond to GH therapy. These observations require rethinking of the medical indications for GH therapy, and raise two central ethical questions: (1) Is it justified to discriminate on the basis of GH deficiency? (2) Whatever the indication for GH treatment, at what height should GH therapy be considered an entitlement? We argue, first, that GH responsiveness, not GH deficiency, should be the criterion for GH treatment, and that prior arguments emphasizing GH deficiency are based on vague or faulty notions of disease, handicap, or potential. Second, we argue that children who are handicapped (arbitrarily defined as including those whose height is below the 1st percentile) and GH responsive are entitled to treatment. Children above that height, whether GH deficient or not, may permissibly be treated, but there is no societal obligation to do so. Such an approach would reduce, though not eliminate, some of the more severe burdens of short stature without aggravating the pernicious effects of "heightism" in American society.

Attitude↗