Earlier onset of puberty in girls: relation to increased body mass index and race.

OBJECTIVE: A recent study conducted by the Pediatric Research in Office Settings network provided evidence that girls in the United States, especially black girls, are starting puberty at a younger age than earlier studies had found, but the reasons for this are not known. Because nutritional status is known to affect timing of puberty and there is a clear trend for increasing obesity in US children during the past 25 years, it was hypothesized that the earlier onset of puberty could be attributable to the increasing prevalence of obesity in young girls. Therefore, the objective of this study was to reexamine the Pediatric Research in Office Settings puberty data by comparing the age-normalized body mass index (BMI-ZS; a crude estimate of fatness) of girls who had breast or pubic hair development versus those who were still prepubertal, looking at the effects of age and race. RESULTS: For white girls, the BMI-ZS were markedly higher in pubertal versus prepubertal 6- to 9-year-olds; for black girls, a smaller difference was seen, which was significant only for 9-year-olds. Higher BMI-ZS also were found in girls who had pubic hair but no breast development versus girls who had neither pubic hair nor breast development. A multivariate analysis confirms that obesity (as measured by BMI) is significantly associated with early puberty in white girls and is associated with early puberty in black girls as well, but to a lesser extent. CONCLUSIONS: The results are consistent with obesity's being an important contributing factor to the earlier onset of puberty in girls. Factors other than obesity, however, perhaps genetic and/or environmental ones, are needed to explain the higher prevalence of early puberty in black versus white girls.

Pediatric research in office settings (PROS): a national practice-based research network to improve children's health care.

OBJECTIVES: To describe the establishment of a national pediatric primary care research network to improve children's health care-Pediatric Research in Office Settings (PROS), and to evaluate the network's progress toward achieving its objectives. SETTING: Pediatric practices in all 50 states and Puerto Rico. PARTICIPANTS: Approximately 1400 pediatric practitioners from more than 470 practices. RESULTS: Beginning in 1986, a core of volunteer pediatrician coordinators from participating American Academy of Pediatrics chapters were identified to oversee local PROS efforts, represent practitioners, and inform the development of proposed research studies. PROS subsequently recruited practitioners from around the country, building a research infrastructure and a system of collaboration between the practitioners, research staff at the AAP, and investigative teams at academic institutions. This PROS collaboration has developed and conducted 10 primary care research studies that have added to the knowledge base of pediatric primary care. CONCLUSIONS: PROS has accomplished two of its initial objectives-development of a structure and process for pediatric practice-based research and provision of research experience to practitioners. Successful and consistent achievement of a third objective-meaningful dissemination of study results to relevant audiences-will depend on meeting several challenges.

Premedication with clonidine does not attenuate suppression of certain lymphocyte subsets after surgery.

UNLABELLED: Sixty-four patients undergoing elective major surgery were randomly assigned into a double-blinded, placebo-controlled, clinical trial to test the hypothesis that premedication with clonidine would attenuate postoperative reductions in circulating lymphocytes. The treatment group (n = 28) received a clonidine skin patch (0.3 mg/d) and a 0.6-mg oral loading dose 60-90 min before surgery. The control group (n = 36) received placebo patches and pills. Absolute blood levels of the following lymphocyte subsets were measured before induction of a standardized general anesthetic (baseline) and the morning after surgery: CD2, CD3, CD4, CD8, CD20, CD56, and the CD4:CD8 ratio. Significant decreases in lymphocyte subsets CD2, CD3, and CD4 were found in both groups; CD56 was significantly decreased only in the placebo group. However, the extent of lymphocyte depletion from baseline to Postoperative Day 1 between the clonidine and placebo groups was not different. Plasma concentrations of epinephrine, norepinephrine, and cortisol were measured from blood samples drawn at 8:00 AM on Postoperative Day 1. Plasma norepinephrine levels were significantly lower among patients who received clonidine. However, no significant differences were found in plasma epinephrine or cortisol levels between the clonidine and placebo groups. With a clinical dose, clonidine did not prevent postoperative lymphocyte depletion. alpha2-Agonists may not suppress adrenocortical stress responses sufficiently to prevent postoperative immune suppression. IMPLICATIONS: Lymphocyte (white blood cell) counts often decrease after major surgery. We hypothesized that clonidine would reduce hormonal stress and blunt reductions in lymphocytes after major surgery. In a randomized trial, we found no differences from placebo in cortisol levels or lymphocyte changes. Lymphocyte levels did not predict infectious complications.

Premedication with oral and transdermal clonidine provides safe and efficacious postoperative sympatholysis.

We studied 61 patients undergoing elective major non-cardiac surgery in a randomized, double-blind, placebo-control clinical trial to test the hypothesis that the addition of clonidine to a standardized general anesthetic could safely provide postoperative sympatholysis for patients with known or suspected coronary artery disease. Patients were allocated randomly to receive either placebo (n = 31) or clonidine (n = 30). The treatment group received premedication with a transdermal clonidine system (0.2 mg/d) the night prior to surgery, which was left in place for 72 h, and 0.3 mg oral clonidine 60-90 min before surgery. Clonidine reduced enflurane requirements, intraoperative tachycardia, and myocardial ischemia (1/28 clonidine patients vs 5/24 placebo, P = 0.05). However, clonidine decreased heart rates only during the first five postoperative hours; the incidence of postoperative myocardial ischemia (6/28 clonidine vs 5/26 placebo) did not differ between the two groups. Patients who experienced postoperative myocardial ischemia tended to have higher heart rates after surgery. Clonidine significantly reduced the plasma levels of epinephrine (P = 0.009) and norepinephrine (P = 0.026) measured on the first postoperative morning. There were no differences in the need for intravenous fluid therapy or antihypertensive therapy after surgery. The number of hours spent in an intensive care setting and the number of days spent in hospital were not different between the two groups. These results suggest that larger doses of clonidine should be investigated for their ability to decrease postoperative tachycardia and myocardial ischemia.