Background Asthma guidelines have recommended continuing treatment with biologics during coronavirus disease 2019 (COVID‐19) pandemic. However, a continuation of treatment with biologics in patients with severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) has been little investigated. Objective To assess the safety of biologics in patients with SARS‐CoV‐2 infection. Methods A pilot, monocentric, prospective study. Patients aged 6 years old and older with severe asthma on treatment with biologics and confirmed SARS‐CoV‐2 infection were enrolled. Patients were followed‐up with periodic calls at different time points up to 3 months to detect any adverse effect and its relationship with biologic treatment according to the Naranjo Adverse Probability Scale (NAPS). The severity of SARS‐CoV‐2 infection and clinical outcome were also assessed. Results Overall, we included 21 patients (10 on therapy with omalizumab, 9 with dupilumab, and 2 with mepolizumab). Only a patient‐reported two local adverse events. No other adverse event was reported. Twenty out of 21 patients had a mild COVID‐19 course, and no adverse outcome was observed. Conclusion We showed that the scheduled dose of the biologic therapy can be administered safely on time in patients with SARS‐CoV‐2 infection, as the treatment did not result in adverse events or outcomes.

Food allergy (FA) is a pathological immune response, potentially deadly, induced by exposure to an innocuous and specific food allergen. To date, there is no specific treatment for FAs; thus, dietary avoidance and symptomatic medications represent the standard treatment for managing them. Recently, several therapeutic strategies for FAs, such as sublingual and epicutaneous immunotherapy and monoclonal antibodies, have shown long-term safety and benefits in clinical practice. This review summarizes the current evidence on changes in treating FA, focusing on monoclonal antibodies, which have recently provided encouraging data as therapeutic weapons modifying the disease course.

Disheveled EGL-10 and pleckstrin domain-containing protein 5 (DEPDC5) is a key member of the GAP activity toward rags complex 1 complex, which inhibits the mammalian target of rapamycin complex 1 (mTORC1) pathway. DEPDC5 loss-of-function mutations lead to an aberrant activation of the mTOR signaling. At neuronal level, the increased mTOR cascade causes the generation of epileptogenic dysplastic neuronal circuits and it is often associated with malformation of cortical development. The DEPDC5 phenotypic spectrum ranges from sporadic early-onset epilepsies with poor neurodevelopmental outcomes to familial focal epilepsies and sudden unexpected death in epilepsy; a high rate of inter- and intrafamilial variability has been reported. To date, clear genotype–phenotype correlations have not been proven. More studies are required to elucidate the significance of likely pathogenic/variants of uncertain significance. The pursuit of a molecular targeted antiepileptic therapy is a future challenge.

FOXG1 is an important transcriptional repressor found in cell precursor of the ventricular region and in neurons in the early stage of differentiation during the development of the nervous epithelium in the cerebrum and optical formation. Mutations involving FOXG1 gene have been described first in subjects with congenital Rett syndrome. They can cause seizure, delayed psychomotor development, language disorders, and autism. FOXG1 deletions or intragenic mutations also determinate reduction in head circumference, structural defects in the corpus callosum, abnormal movements, especially choreiform, and intellectual retardation with no speech. Patients with duplications of 14q12 present infantile spasms and have subsequent intellectual disability with autistic features, head circumference in the normal range, and regular aspect of corpus callosum. Clinical characteristics of patients with FOXG1 variants include growth deficit after birth associated with microcephaly, facial dysmorphisms, important delay with no language, deficit in social interaction like autism, sleep disorders, stereotypes, including dyskinesia, and seizures. In these patients, it is not characteristic a history of loss of acquired skills.

Macrocephaly or Megalencephaly are two synonyms that define the presence of a head circumference measurements two standard deviations above the age-related mean. Usually thee terms include patients characterized by large head associated with possible neurologic features, including neuro developmental impairment, both in motor and in intellective skills, showing intellective disability, together with possible occurrence of epileptic seizures. Despite this possible overlap between the two terms, is actually justified to distinguish the two eventualities due to different possible causal events, presence of specific cerebral anomalies, and clinical management. We selected a total of 10 patients (7 male, 3 female), observed in the period from July 2013 through July 2019, who were affected from non-syndromic MEG followed up at the pediatric and neuropediatric disorders center of Pediatric Unity of the University Hospital Policlinic-Vittorio Emanuele in Catania, Italy. 5 patients (4 males and 1 females) of the sample, presented the simultaneous presence of abnormally large head, mild/moderate developmental delay, and seizures.