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Background The aim of this study was to determine ovarian reserve using serum anti‐Müllerian hormone (AMH) level in children who had undergone either ovarian‐preserving surgery or oophorectomy because of ovarian torsion. Methods Patients aged > 10 years who had undergone surgery for unilateral ovarian torsion were contacted for the study with ethics committee approval. Seventeen patients agreed to be included. Results A total of 10 patients had undergone ovarian detorsion and seven had undergone oophorectomy. Mean age at operation was 11.6 ± 2.23 years (range, 8–15 years) and 13.2 ± 2.17 years (range, 10–16 years), respectively (P = 0.46). Ovarian torsion was isolated in four patients in the first group, and in three in the second. The remainder had associated benign masses. At the time of this study, mean patient age was 18 ± 2.11 years (range, 14–21 years) with a mean postoperative follow up of 5.9 ± 2.8 years (range, 2–10.5 years). Echogenicity of all preserved ovaries was normal on pelvic Doppler ultrasonography, with presence of antral follicles in six. Three ovaries were smaller than expected for age, although two of these had antral follicles. Mean AMH was 5.54 ± 2.25 ng/mL in the detorsion group and 2.70 ± 2.11 ng/mL in the oophorectomy group (P = 0.04). Conclusions The presence of follicles in preserved ovaries after detorsion has been reported previously. AMH is expressed in granulosa cells of growing follicles and its serum level is valuable in assessing the quantitative aspects of ovarian reserve. Preservation of the ovary in children with torsion is justified in terms of future ovarian reserve.

Aim This study presents a single institutional experience with H-type tracheoesophageal fistula (H-TEF). Methods Esophageal atresia (EA) patients who underwent primary surgery in a single center between 2006 and 2018 were retrospectively evaluated. Results Among 110 EA patients, 7 (6.4%) had H-TEF. There were 5 males and 2 females. The primary complaints were choking, cyanosis, and/or apnea with feeding, swallowing difficulty, recurrent bronchopneumonia, or bile in endotracheal tube. The relevant symptoms began during neonatal period with varying degrees of severity in all. The initial diagnosis was proximal esophageal web as demonstrated by contrast swallow and endoscopy in one patient; H-TEF was diagnosed during the course of treatment for the web. Hydrocephalus with severe neurological sequela unrelated to H-TEF and cardiac malformation were present in one. Contrast esophagography was employed in three patients for diagnosis two of which were diagnostic. All underwent diagnostic bronchoscopy. Delayed diagnosis (after 30 days of life) occurred in five (71%). The median age at operation was 3.8 months (11 days–33 months). The level of the fistulas was between C5 and T3. Preoperative bronchoscopic cannulation was successful in all but one. The operation was done via a right cervical approach in six patients and thoracotomy in one. All patients were followed up for at least one year and there was one recurrence detected five months after the first operation. She underwent a secondary surgery with a successful outcome. Right vocal cord paralysis was detected postoperatively in the patient with hydrocephalus. Conclusions H-TEF is a rare subtype of EA malformations with a delay in diagnosis in most cases. Suggestive clinical findings, especially neonatal respiratory symptoms should always be regarded as an indication for further investigations. Although contrast esophagograms may reveal the diagnosis, bronchoscopy is the gold standard diagnostic test in our practice. It should be done preoperatively in every patient not only for diagnostic confirmation but also for cannulation of the fistula to ease the operation. H-TEF might be considered a relatively innocent EA variant but its surgery is not devoid of complications. The patients should be followed up for recurrence and recurrent laryngeal nerve injury on the long term.

Introduction Bosentan is an endothelin-1 receptor antagonist with anti-inflammatory, antioxidant, and antiproliferative effects. We aimed to evaluate its effects on lung tissue in a pulmonary contusion (PC) model. Materials and Methods The rats were randomly divided into five groups: PC3: PC evaluated on the 3rd day (n = 8), PC-B3: PC enteral bosentan 100 mg/kg/day, for 3 days (n = 8), PC7: PC evaluated on the 7th day (n = 7), PC-B7: PC 7 days bosentan 100 mg/kg/day, for 7 days (n = 8), C: control (n = 6). Unilateral lung contusion was created by dropping a metal weight onto the chest. The rats were sacrificed on the 3rd or the 7th days. The lung tissue was evaluated histopathologically for alveolar edema, congestion, and leukocyte infiltration, biochemically for malondialdehyde (MDA), superoxide dismutase (SOD), and nitric oxide (NO) levels, and immunohistochemically for inducible nitric oxide synthase (iNOS), endothelial nitric oxide synthase (eNOS), and apoptosis scores. Results Alveolar edema, congestion, and leukocyte infiltration scores were increased in all groups compared with the control group (p < 0.05) and decreased in bosentan-treated groups compared with the relevant nontreated groups (p < 0.05). Fibrosis was observed only in PC7 and PC-B7 groups. Bosentan did not have any effect on fibrosis development. iNOS and eNOS levels were higher in all groups compared with the control (p < 0.05) without a difference in the nontreated versus treated groups (p > 0.05). Bosentan treatment caused decreased MDA and increased SOD levels in comparison to the nontreated groups (p < 0.05). Tissue NO levels did not show any significant difference among groups. PC groups had higher levels of apoptosis compared with the control group (p < 0.05). The degree of apoptosis decreased in bosentan-treated groups compared with the nontreated groups (p < 0.05). Conclusion PC causes progressive lung tissue damage. Bosentan reduced leukocyte infiltration and alveolar edema and congestion caused by PC. It also decreased MDA levels and increased SOD levels. Bosentan prevents tissue damage by inhibiting acute inflammatory response and reduces oxidative stress secondary to inflammation. It has therapeutic effects on apoptosis.