Weber-Christian disease is characterized by recurrent inflammation in the fat layer of the skin. We report a boy, aged 2 years and 9 months, with Weber-Christian disease who presented with tender rounded swelling on the dorsum of both hands and chest wall with mild erythema in overlying skin associated with high grade continuous fever.

Background: Recurrent pneumonia is a challenge for pediatric pulmonologists. There are limited data on the underlying causes of recurrent pneumonia in children in the developing countries. Aim: To identify the underlying causes of recurrent pneumonia in children with undiagnosed etiology. Patients and Methods: The study was conducted in Pulmonology Units, Pediatric Departments Tanta and Ain-Shams Universities Hospitals from 2017 to 2019. Fifty-six cases children with a diagnosis of recurrent pneumonia were included to identify the etiologies. The underlying causes were confirmed in each case according to the clinical features and the diagnostic tests. Results: Uncontrolled bronchial asthma was the commonest cause of recurrent pneumonia (23.2%), followed by congenital heart diseases (12.5%) and aspiration syndromes (12.5%). Conclusion: Uncontrolled bronchial asthma was the most common underlying cause of recurrent pneumonia in children, so early diagnosis and proper controller therapy may decrease the risk of occurrence of recurrent pneumonia.

Introduction. Vigabatrin (VGB) is an antiepileptic drug that acts to irreversibly inhibit the γ-aminobutyric acid (GABA) transaminase enzyme, elevating GABA levels. Broad studies have established that long-term treatment and/or high doses of VGB lead to variable visual defects. However, little attention has been paid to its other side effects, especially those demonstrating cerebellar involvement. Sodium glucose-linked co-transporter 2 (SGLT2) inhibitors are antidiabetic agents with protective effects far greater than expected based on their anti-hyperglycemic effect. Method. Our study herein was designed to investigate the possible ameliorative effect of empagliflozin, the SGLT2 inhibitors, in VGB-induced cerebellar toxicity. A total of 40 male Wistar rats were allocated equally into 4 groups: Group I: control group; Group II: VGB group; Group III empagliflozin treated VGB group; and Group IV: empagliflozin treated group. All groups were subjected to the detection of cerebellar messenger RNA gene expression of silent mating type information regulation 2 homolog 1 (SIRT1) and Nucleoporin p62 (P62). Mammalian target of rapamycin (mTOR), adenosine monophosphate-activated protein kinase (AMPK), and beclin1 levels were assessed by the ELISA technique while malondialdehyde (MDA) level and superoxide dismutase (SOD) activity were detected spectrophotometrically. Immuno-histochemical studies, focusing on glial fibrillary acidic protein (GFAP) and S100 were performed, and the optical color density and the mean area percentage of GFAP positive astrocytes and the number of S 100 positive cells were also counted. Results. Following empagliflozin treatment, we documented significant upregulation of both SIRT1 and P62 mRNA gene expression. Additionally, AMPK, Beclin1 levels, and SOD activity were significantly improved, while both mTOR and MDA levels were significantly reduced. Conclusions. We concluded for the first time that empagliflozin efficiently ameliorated the VGB-induced disrupted mTOR/AMPK/SIRT-1 signaling axis with subsequent improvement of the autophagy machinery and mitigation of the oxidative and inflammatory cellular environment, paving the way for an innovative therapeutic potential in managing VGB-induced neurotoxicity.