Neurological Manifestations of Pediatric Acute COVID Infections: A Single Center Experience.

BACKGROUND: Coronavirus disease 2019 (COVID-19) usually leads to a mild infectious disease course in children, while serious complications may occur in conjunction with both acute infection and neurological symptoms, which have been predominantly reported in adults. The neurological complications in these patients vary based on patient age and underlying comorbidities. Data on clinical features, particularly neurological features, and prognostic factors in children and adolescents are limited. This study provides a concise overview of neurological complications in pediatric COVID-19 cases. MATERIALS AND METHODS: The retrospective study reviewed medical records of all patients who were admitted to our hospital and were diagnosed with COVID-19 by real-time reverse-transcription polymerase-chain-reaction (RT-PCR) assay between 11 March 2020 and 30 January 2021. Patients with a positive PCR result were categorized into two groups: outpatient departments patients and inpatient departments (IPD). RESULTS: Of the 2530 children who underwent RT-PCR during the study period, 382 (8.6%) were confirmed as COVID-19 positive, comprising 188 (49.2%) girls and 194 (50.8%) boys with a mean age of 7.14±5.84 (range, 0-17) years. Neurological complications that required hospitalization were present in 34 (8.9%) patients, including seizure (52.9%), headache (38.2%), dizziness (11.1%) and meningoencephalitis (5.8%). CONCLUSION: The results indicated that neurological manifestations are not rare in children suffering from COVID-19. Seizures, headaches, dizziness, anosmia, ageusia and meningoencephalitis are major neurological manifestations during acute COVID-19 disease. Although seizures were the most common cause of hospitalization in IPD patients, the frequency of meningoencephalitis was quite high. Seizures were observed as febrile seizures for children under 6 years of age and afebrile seizures for those over 6 years of age. Febrile seizure accounted for half of all seizure children.

Antenatal Bartter Syndrome Caused by a Novel Homozygous Mutation in SLC12A1 Gene.

Antenatal Bartter syndrome (BS) is an autosomal recessive hereditary renal tubular disorder caused by mutation in the solute carrier family 12 member 1 (SLC12A1) gene on chromosome 15q21.1. This syndrome is characterized by polyuria, hyponatremia, hypokalemic hypochloremic metabolic alkalosis, and hypercalciuria associated with increased urinary loss of electrolytes. Herein, we report a very low-birth-weight premature newborn with antenatal BS caused by a novel homozygous mutation in the SLC12A1 gene, c.596G>A (p.R199H).

Homozygous congenital factor VII deficiency with a novel mutation, associated with severe spontaneous intracranial bleeding in a neonate.

OBJECTIVE: Herein, a neonate with congenital FVII deficiency is presented. BASIC METHOD: Diagnosis of congenital FVII deficiency was confirmed by genetic analysis using next-generation sequencing method (MiSeq-Illumina). RESULT: Our patient was found to have a novel homozygous mutation. CONCLUSION: Early diagnosis and treatment of congenital FVII deficiency can be crucial.