[Evaluation of adrenocortical function in children with severe and critical enterovirus 71 infection].

OBJECTIVE: To evaluate the adrenocortical function in children with severe and critical enterovirus 71 infection by using a high-dose (250 µg) adrenocorticotropic hormone (ACTH) stimulation test. And to at provide experimental basis for glucocorticoid in the treatment of hand-foot-and-mouth disease (HFMD). METHOD: This was a prospective multi-center study which was carried out in PICUs of Beijing Children's Hospital, Zhengzhou Children's Hospital, Kaifeng Children's Hospital and Linyi People's Hospital in Shandong province. Children with severe and critical hand-foot-mouth disease admitted to PICUs of the four hospitals from June 2009 to April 2010 were enrolled in this study, and EV71 virus nucleic acid test and high-dose (250 µg) ACTH stimulation started at the same time. EV71 virus nucleic acid positive 51 cases were eventually enrolled in the study. Cortisol test was performed at baseline (T0) and after high-dose (250 µg) ACTH stimulation at 30 minutes (T30), 60 minutes (T60) in the first 6 hours after admission, but before glucocorticoid was given. The adrenocortical function was evaluated according to ΔTmax [ΔTmax=(T30, T60 maximum)-T0]. Diagnostic criteria of adrenal insufficiency (AI) is increment (ΔTmax)≤9 µg/dl. RESULT: The incidence of AI in 51 cases was 52.94% (27/51). The incidence of AI in severe group was 44.74% (17/38), which was significantly higher in critical group 76.92% (10/13), P<0.05. Of the cases with a pediatric critical illness score (PCIS)≤70, 81.82% (9/11) had adrenal insufficiency, and it was 28.57% (4/14) when PCIS≥90. The incidence of AI was 75% (6/8) and 48.84% (21/43) in death and survivor group respectively, but there were no significant difference between the two groups (P>0.05). Baseline (T0) cortisol in death group was higher than survivor group (P<0.05). CONCLUSION: AI may occur in children with enterovirus 71 infection. The critical enterovirus 71 infection had a high incidence of AI. AI may affect the prognosis of patients with severe and critical enterovirus 71 infection. Exogenous glucocorticoids administration may be considered when AI is identified or highly suspected. The timing, dosage and regimen of glucocorticoid are still unclear. Further animal experiments and clinical trials are needed.

Histologic analysis of acellular dermal matrix in the treatment of anal fistula in an animal model.

BACKGROUND: Human acellular dermal matrix (ADM) has been used successfully for the treatment of severe burns, ureter support, and abdominal wall reconstruction. This study was designed to evaluate the mechanism of ADM in the closure of anal fistula in an experimental porcine model. STUDY DESIGN: The fistula-in-ano model was created in the porcine model and treated with ADM in 14 animals. Fistula specimens were obtained at hours 12 and 24 and on days 3, 7, 14, 28, 60. Hematoxylin and eosin staining, Masson trichrome staining, and immunohistochemical staining for alpha smooth muscle actin and matrix metalloproteinase 9 were performed. RESULTS: The cell density increased from hour 12 to day 7 and decreased from day 7 to day 28 (p < 0.001). Mature vessels stained with alpha smooth muscle actin were identified at day 7. Alpha smooth muscle actin-positive myofibroblasts were found in clusters at the edge of the ADM at day 7. The density of vessels (p < 0.001) and myofibroblasts (p < 0.001) increased from day 7 to day 14. The density of matrix metalloproteinase 9 increased from hour 12 to day 7 and decreased from day 14 to day 60 (p < 0.001). Partially organized bundles of muscle were found by day 60. CONCLUSIONS: We suggest that ADM is a reasonable new option for closure of anal fistulas. Anal fistulas begin to heal as early as 12 hours, and day 7 may be an important time point to judge whether the fistula healed preliminarily or not. The ability of ADM to become vascularized and remodeled by autologous cells may be advantageous for anal fistula healing.