Lateral neck masses (LNM) often present a diagnostic challenge in the practice of pediatric plastic surgeon. The aim of this study is to investigate the clinical and ultrasound (US) characteristics of pediatric LNM in order to make mutual comparison between their entities and enable the most accurate preoperative diagnosis. A cross-sectional study was conducted among 250 pediatric patients treated by surgical excision or sclerotherapy in our institution in the period from July 2009 to June 2019. Lymphatic malformation was the most frequent congenital LNM (60.9%), while reactive or granulomatous lymphadenitis was the most frequent acquired LNM (47%). Congenital anomalies were significantly more often localized in the upper half of the sternocleidomastoid (SCM) muscle region, and had more often soft consistency than acquired ones. Congenital LNM had a 32.37 (3.44–304.63) times higher likelihood of incorrect (p = 0.002) and 5.86 (1.35–25.48) times higher likelihood of undetermined (p = 0.018) than correct US findings, respectively. Acquired LNM were significantly more often localized in the region behind the SCM muscle and more often had solid US appearance in comparison to the congenital ones. Association of the clinical and US findings is very important in determining the most accurate preoperative diagnosis without exposing the children to unnecessary utilizing ionizing radiation or anesthesia. Although they are mostly benign, extreme caution is necessary due to malignancies which were found in 16.4% of all our patients.

This study aimed to evaluate the general, hepatoprotective and renoprotective effects of amifostine (AMI) in rats treated with a large, single dose of doxorubicin (DOX), assessed at 7 and 56 days after administration. Rats were divided into six experimental groups: Control (0.9% NaCl intraperitoneally (ip)), amifostine (AMI300, 300 mg/kg (ip)), doxorubicin (DOX6, 6 mg/kg (ip)), doxorubicin (DOX10, 10 mg/kg (ip)), doxorubicin (DOX6, 6 mg/kg (ip)) + amifostine (AMI300, 300 mg/kg (ip) 30 min before DOX6), and doxorubicin (DOX10, 10 mg/kg (ip)) + amifostine (AMI300, 300 mg/kg (ip) 30 min before DOX10). Absolute liver and kidney weights were significantly increased in AMI300 + DOX6-treated animals compared to DOX6 only on day 56. In the group of DOX10-treated rats, AMI300 significantly prevented changes in the number of white blood cells during the four weeks after treatment. The severity of hepatic and renal injuries in the DOX6-treated groups was also significantly less in rats pretreated with AMI300 on day 56 (p < 0.01). Our results indicate that hepatic and renal protection significantly contribute to the successful use of AMI against DOX-induced subacute toxicity in rats.

Background/Aim: Orofacial clefts are the most common birth defect of the head. Clefts arise due to a lack of tissue fusion during prenatal development. Various factors can cause the absence of fusion of these structures during 6-8th week of embryonic development. It is proven that the cause of non-syndromic orofacial clefts (NSOFCs) has multifactorial etiology. This review aims to provide a comprehensive summary on etiology and classification of NSOFCs. Material and Methods: Online bibliographic databases were utilized in order to find as many as possible available studies that showed a connection between any environmental factor and genes and NSCL/P, also available studies and books which represented any NSOFC classification system. Results: From the 35 articles and books reviewed, key etiological factors and numerous classification systems that developed over time have been identified. While the multifactorial nature is well-established and proven, specific percentage contributions of individual factors, either environmental or genetic, remain inconclusive. No single classification system is considered perfect, underscoring the need for continued research. Conclusions: Existing classification systems for NSOFCs all have advantages and disadvantages, lacking universal ease of use and comprehensiveness. However, they reflected the evolving understanding of NSOFCs, progressing from anatomical to embryological and developmental perspectives. While several potential etiological factors have been identified, the precise etiology of NSOFCs remain unclear due to complex interplay of factors involved in their occurrence. A definitive cause has not yet been identified.