Targeted temperature management using the "Esophageal Cooling Device" after cardiac arrest (the COOL study): A feasibility and safety study.

BACKGROUND: Targeted temperature management (TTM) between 32 and 36°C is recommended after out-of-hospital cardiac arrest (OHCA). We aimed to assess the feasibility and safety of the "Esophageal Cooling Device" (ECD) in performing TTM. PATIENTS AND METHODS: This single-centre, prospective, interventional study included 17 comatose OHCA patients. Main exclusion criteria were: delay between OHCA and return of spontaneous circulation (ROSC)>60min, delay between sustained ROSC and inclusion >360min, known oesophageal disease. A TTM between 32 and 34°C was performed using the ECD (Advanced Cooling Therapy, USA) connected to a heat exchanger console (Meditherm III®, Gaymar, France), without cold fluids' use. Primary endpoint was feasibility of inducing, maintaining TTM, and rewarming using the ECD alone. Secondary endpoints were adverse events, focusing on potential digestive damages. Results were expressed as median (interquartiles 25-75). RESULTS: Cooling rate to reach the Target Temperature (33°C-TT) was 0.26°C/h [0.19-0.36]. All patients reached the 32-34°C range with a time spent within the range of 26h [21-28] (3 patients did not reach 33°C). Temperature deviation outside the TT during TTM-maintenance was 0.10°C [0.03-0.20]. Time with deviation >1°C was 0h. Rewarming rate was 0.20°C/h [0.18-0.22]. Among the 16 gastrointestinal endoscopy procedures performed, 10 (62.5%) were normal. Minor oeso-gastric injuries (37.5% and 19%, respectively) were similar to usual orogastric tube injuries. One patient experienced severe oesophagitis mimicking peptic lesions, not cooling-related. No patient among the 9 alive at 3-month follow-up had gastrointestinal complains. CONCLUSION: ECD seems an interesting, safe, accurate, semi-invasive cooling method in OHCA patients treated with 33°C-TTM, particularly during the maintenance phase.

Parental origin of the X-chromosome does not influence growth hormone treatment effect in Turner syndrome.

CONTEXT: The parental origin of the intact X-chromosome has been reported to affect phenotype and response to GH treatment in Turner syndrome (TS). OBJECTIVE: Our objective was to evaluate the influence of the parental origin of the X-chromosome on body growth and GH treatment effect in TS. DESIGN AND SETTING: We conducted a population-based cohort study of TS patients previously treated with GH. PARTICIPANTS: Participants included patients with a nonmosaic 45,X karyotype; 556 women were identified as eligible, 233 (49%) of whom participated, together with their mothers. Data were analyzed for 180 of these patients. MAIN OUTCOME MEASURES: We performed fluorescence in situ hybridization analysis to exclude mosaicism and microsatellite analysis of nine polymorphic markers in DNA from the patients and their mothers. The influence on growth and effect of GH were analyzed by univariate and multivariate methods. RESULTS: The X-chromosome was of paternal origin (X(pat)) in 52 (29%) of 180 and of maternal origin (X(mat)) in 128 (71%) of 180 patients. Height gain from the start of GH treatment to adult height was similar in X(mat) and X(pat) patients (+2.1 ± 0.9 vs. +2.2 ± 0.8 TS sd score, P = 0.45). The lack of influence of parental origin of the X-chromosome was confirmed in multivariate analysis. Parental origin of the X-chromosome also had no effect on the other growth characteristics studied, including growth velocity during the first year on GH treatment. Patient height was correlated with the heights of both parents and was not influenced by the parental origin of the X-chromosome. CONCLUSION: In this, the largest such study carried out to date, the parental origin of the X-chromosome did not alter the effect of GH treatment or affect any other features of growth in TS.