Addition of sufentanil to bupivacaine in caudal block effect on stress responses in children

BACKGROUND: The aim of the present randomized study was to determine the effect of adding sufentanil to bupivacaine, compared with bupivacaine alone in caudal block, on the surgical stress response in children. METHODS: The children were premedicated with midazolam 0.5 mg/kg. All children received induction with nitrous oxide and sevoflurane. Anesthesia was maintained with the same volatile agents in the both groups. The children were randomly allocated to two groups. Group I received bupivacaine alone (n = 17) and group II received bupivacaine + sufentanil (n = 16). Caudal block was performed with 0.25% bupivacaine 2 mg/kg (group I) or 0.25% bupivacaine 2 mg/kg with sufentanil 0.5 microg/kg (group II) after induction of anesthesia. Blood samples were obtained after induction of anesthesia (T(0)) to measure baseline concentrations of cortisol, prolactin, glucose and insulin. Additional samples were obtained 30 min after the start of surgery (T(1)), and 60 min after the end of surgery (T(2)). RESULTS: All of the basal values (T(0)) were within the normal ranges of the authors' laboratory for children of this age group and there were no differences between the groups (P > 0.05). In both groups, glucose concentration increased at T(1), compared with T(0) and T(2) (P < 0.05). The glucose concentration was unchanged at T(2) compared with T(0) in both group (P > 0.05). In both groups, prolactin concentration increased at T(1), compared with T(0) and decreased at T(2), compared with T(1) (P < 0.05). Cortisol decreased at T(1) and T(2), compared with T(0) in both groups. (P < 0.05). Insulin concentration remained unchanged at T(0) and T(2), but increased slightly at T(1) in both groups (P > 0.05). There were no significant differences in plasma prolactin, cortisol, glucose and insulin levels between the two groups at T(1) and T(2) (P > 0.05). CONCLUSION: There is no advantage in adding 0.5 microg/kg sufentanil to bupivacaine over bupivacaine alone in the caudal block, with regard to the surgical stress response in children.     

Response of the ENPP1-Deficient Skeletal Phenotype to Oral Phosphate Supplementation and/or Enzyme Replacement Therapy: Comparative Studies in Humans and Mice

Inactivating mutations in human ecto-nucleotide pyrophosphatase/phosphodiesterase-1 (ENPP1) may result in early-onset osteoporosis (EOOP) in haploinsufficiency and autosomal recessive hypophosphatemic rickets (ARHR2) in homozygous deficiency. ARHR2 patients are frequently treated with phosphate supplementation to ameliorate the rachitic phenotype, but elevating plasma phosphorus concentrations in ARHR2 patients may increase the risk of ectopic calcification without increasing bone mass. To assess the risks and efficacy of conventional ARHR2 therapy, we performed comprehensive evaluations of ARHR2 patients at two academic medical centers and compared their skeletal and renal phenotypes with ENPP1-deficient Enpp1^asj/asj mice on an acceleration diet containing high phosphate treated with recombinant murine Enpp1-Fc. ARHR2 patients treated with conventional therapy demonstrated improvements in rickets, but all adults and one adolescent analyzed continued to exhibit low bone mineral density (BMD). In addition, conventional therapy was associated with the development of medullary nephrocalcinosis in half of the treated patients. Similar to Enpp1^asj/asj mice on normal chow and to patients with mono- and biallelic ENPP1 mutations, 5-week-old Enpp1^asj/asj mice on the high-phosphate diet exhibited lower trabecular bone mass, reduced cortical bone mass, and greater bone fragility. Treating the Enpp1^asj/asj mice with recombinant Enpp1-Fc protein between weeks 2 and 5 normalized trabecular bone mass, normalized or improved bone biomechanical properties, and prevented the development of nephrocalcinosis and renal failure. The data suggest that conventional ARHR2 therapy does not address low BMD inherent in ENPP1 deficiency, and that ENPP1 enzyme replacement may be effective for correcting low bone mass in ARHR2 patients without increasing the risk of nephrocalcinosis. © 2021 American Society for Bone and Mineral Research (ASBMR).