Growth hormone effects on hypertrophic scar formation: a randomized controlled trial of 62 burned children

The hypercatabolism after massive pediatric burns has been effectively treated with recombinant human growth hormone, an anabolic agent that stimulates protein synthesis and abrogates growth arrest. While experimental studies have shown increased potential for fibrosis induced by growth hormone therapy, adverse effects on human scars have not been investigated. Our aim was to evaluate hypertrophic scar formation in 62 patients randomized to receive injections of 0.05 mg/kg/day of recombinant human growth hormone or placebo, from discharge until 1 year after burn. Scar scales were used to evaluate scar-severity at discharge, 6, 9, 12, and 18-24 months after burn, by three observers blinded to treatment. Computer-assisted planimetry allowed quantification of percentage of hypertrophic scar formation. Types I and III collagens were localized and quantified in scars and normal skin of patients from both groups, using immunohistochemistry with confocal laser microscopy analysis. Insulin-like growth factor-1 blood levels helped assess compliance. Statistical analysis showed that scar hypertrophy significantly increased from 6 to 12 months after injury in both groups, while decreasing at 18-24 months postburn. Types I and III collagens were statistically increased in the reticular layer of scars from both groups when compared to paired normal skin. Insulin-like growth factor-1 was significantly increased in the recombinant human growth factor-treated group. No differences were seen when recombinant human growth factor and control groups were compared using the scar scales, planimetry, or immunohistochemistry. We concluded that recombinant human growth hormone therapy did not adversely affect scar formation and should not contraindicate the administration of recombinant human growth hormone as a therapeutic approach to severely burned children.     

Percutaneous absorption of 2,6-di-tert-butyl-4-nitrophenol (DBNP) in isolated perfused porcine skin.

DBNP (2,6-di-tert-butyl-4-nitrophenol) has been reported as a potential contaminant in submarines. This yellow substance forms when lubrication oil mist containing the antioxidant additive 2,6-di-tert-butylphenol passes through an electrostatic precipitator and is nitrated. Percutaneous absorption of 14C-DBNP was assessed in the isolated perfused porcine skin flap (IPPSF). Four treatments were studied (n=4 flaps/treatment): 40.0 microgram/cm(2) in 100% ethanol; 40.0 microgram/cm(2) in 85% ethanol/15% H(2)O; 4.0 microgram/cm(2) in 100% ethanol; and 4.0 microgram/cm(2) in 85% ethanol/15% water. DBNP absorption was minimal across all treatment groups, with the highest absorption detected being only 1.08% applied dose in an aqueous ethanol group. The highest mass of 14C-DBNP absorbed was only 0.5 microgram. The majority of the applied dose remained on the surface of the skin. This suggests that there is minimal dermal exposure of DBNP when exposed topically to skin.     

Normal pressure hydrocephalus and cerebral blood flow: a PET study of baseline values.

Regional cerebral blood flow (CBF) was studied with O(15)-water positron emission tomography and anatomic region-of-interest analysis on co-registered magnetic resonance in patients with idiopathic (n = 12) and secondary (n = 5) normal pressure hydrocephalus (NPH). Mean CBF was compared with values obtained from healthy volunteers (n = 12) and with clinical parameters. Mean CBF was significantly decreased in the cerebrum and cerebellum of patients with NPH. The regional analysis demonstrated that CBF was reduced in the basal ganglia and the thalamus but not in white matter regions. The results suggest that the role of the basal ganglia and thalamus in NPH may be more prominent than currently appreciated. The implications for theories regarding the pathogenesis of NPH are discussed.     

Life-threatening asthma and anaphylaxis in schools: a treatment model for school-based programs.

BACKGROUND: Pediatric asthma is the No. 1 chronic disease in childhood and is responsible for significant morbidity and mortality. In Nebraska, the number of asthma-related deaths is greater than the national average, and in 1998, 2 students died of acute asthma attacks while attending school in the Omaha public schools (OPSs). In response, we designed and implemented a program to respond to this problem. OBJECTIVE: To implement and study a school-based program for the treatment of life-threatening asthma and anaphylaxis in the OPSs. METHODS: The Emergency Response to Life-Threatening Asthma or Systemic Allergic Reactions (Anaphylaxis) Protocol was designed and evaluated in 78 OPSs from 1998 to 2003. Nurses and school staff were trained in the protocol, which required the use of nebulized albuterol and/or intramuscular epinephrine in conjunction with an emergency response procedure. Outcomes were measured by improvement in acute care in schools and survival of students. Results: In the 5 years of evaluation, 98 students were treated successfully. One student died. Of those treated with the protocol, equal numbers had at school both asthma action plans (AAPs) and metered-dose inhalers (MDIs), MDIs only, or neither AAPs nor MDIs. As a result of the program, there has been an increased awareness from parents, teachers, and physicians about the necessity of an emergency response program. In 2002, an outcome of the OPS program resulted in the formation of Attack on Asthma Nebraska to ensure that Nebraska schools have the education, training, and medications to respond to anyone experiencing a life-threatening asthma or anaphylaxis attack at school. The following year, a revised protocol was approved by the Nebraska State Board of Education for use in all Nebraska schools. CONCLUSIONS: Emergency response protocols provide protection for children while in school. This program should serve as a national model for other school-based programs for children and adolescents with asthma and anaphylaxis.