Acute flaccid paralysis (AFP) is a life-threatening clinical entity characterized by weakness in the whole body muscles often accompanied by respiratory and bulbar paralysis. The most common cause is Gullian–Barre syndrome, but infections, spinal cord diseases, neuromuscular diseases such as myasthenia gravis, drugs and toxins, periodic hypokalemic paralysis, electrolyte disturbances, and botulism should be considered as in the differential diagnosis. Human coronaviruses (HCoVs) cause common cold, upper and lower respiratory tract disease, but in the literature presentation with the lower respiratory tract infection and AFP has not been reported previously. In this study, pediatric case admitted with lower respiratory tract infection and AFP, who detected for HCoV 229E and OC43 co-infection by the real-time polymerase chain reaction, has been reported for the first time.
B ronchopulmonary dysplasia (BPD) is a chronic lung disease requiring long-term oxygen support with ≥21% concentration with a variety of modalities in premature infants. Until the 2000s, the diagnosis was made based on whether oxygen requirements continued up to the postnatal 28 th day. However, after this date, diagnosis began to be made based on the severity of the disease as mild, moderate and severe according to gestational week (GW) [1, 2]. Low birth weight (WB) and GW are usual risk factors for BPD, and there is an inverse linear relationship between them. Perinatal risk factors like a cesarean section, male gender, antenatal corticosteroids, EMR, chorioamnionitis, SGA, postnatal surfactant, RDS, early and late-onset sepsis, PDA and apnea are reported to be associated with BPD [3]. According to centers, the incidence of BPD in <32 GW premature infants was reported to be 30% in the United States, 12% in Canada and 14% in Japan [4, 5]. In this study, the relationship of BPD frequency, perinatal risk factors and other prematurity comorbidities were assessed for very low birth weight (VLBW) infants.
Background/aim: The purpose of this retrospective study was to determine the effectiveness of oral iron therapy in breath-holding spells and evaluation of electrocardiographical changes. Materials and methods: Three hundred twelve children aged 1-48 months and diagnosed with breath-holding spells between January 2017 and April 2018 were included. Patients' laboratory findings were compared with 100 patients who had one simple febrile seizure. Results: Cyanotic breath-holding spells were diagnosed in 85.3% (n = 266) of patients, pallid spells in 5.1% (n = 16), and mixed-type spells in 9.6% (n = 30). Sleep electroencephalograms were applied for all patients, 98.2% (n = 306) of which were normal, while slow background rhythm was determined in 1.2% (n = 4). Epileptic activity was observed in only 2 patients (0.6%). The mean hemoglobin (Hb) value in the breathholding spell group was 10.1 mg/dL. Patients' mean corpuscular volume (MCV) was 73 fL. Patients' Hb and MCV values were statistically significantly lower than those of the control group (P < 0.001). The difference between spell burden was not statistically significant (P = 0.691). Spell burden decreased equally in both groups. Conclusion: Oral iron therapy can be administered in breath-holding seizures irrespective of whether or not the patient is anemic.
Background Brain‐derived neurotrophic factor (BDNF) is a noncovalently linked homodimer protein from the neurotrophic growth factor family. Although it is expressed throughout the brain, it is produced more intensively in the entorhinal cortex and hippocampus and can cross the blood‐brain barrier in two directions easily. The aim of this study is to understand, for the first time, whether there is a relationship between febrile seizure (FS) and BDNF. Methods The study included cases diagnosed with FS and febrile illness, of similar age, weight, and height, between 6 months and 6 years. Samples for serum BDNF measurement were taken within the first 24–48 h of admission at the hospital and levels were measured using the commercial enzyme‐linked immunosorbent assay kit and expressed in ng/mL. Results Eighty cases (40 FS, 40 febrile illness) were included in the study. The mean serum BDNF was found to be 6.7 ± 2.4 ng/mL in the FS group and 4.5 ± 2.6 ng/mL in the febrile illness group (P = 0.001). No relation was found between gender, age, body weight, length, and platelet counts and serum BDNF levels. The optimal cut‐off value for serum BDNF was found to be 5.2 ng/mL (75% sensitivity, 62.5% specificity, AUC: 0.723) to distinguish between FS and febrile illness. Conclusions Excluding demographic variables such as gender, age, weight, length, and platelet counts serum BDNF levels have increased in children with FS. Considering the hippocampal origin of FS, we can suggest that the pathophysiology of FS may be related to the BDNF.
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