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.

The purpose of this retrospective study was to determine the effectiveness of oral iron therapy in breath-holding spells and evaluation of electrocardiographical changes 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. 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 breath-holding 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. Oral iron therapy can be administered in breath-holding seizures irrespective of whether or not the patient is anemic.

OBJECTIVE: In this study, the relationship between the frequency of bronchopulmonary dysplasia, perinatal risk factors and other prematurity comorbidities were evaluated in very low birth weight infants. METHODS: A total of 872 very low birth weight infants' files were retrospectively reviewed. The effects of the clinical parameters, such as type of birth, small for gestational age, gender, antenatal steroids, early membrane rupture, chorioamnionitis, surfactant administration, respiratory distress syndrome, patent ductus arteriosus, apnea, early and late sepsis on the frequency of bronchopulmonary dysplasia, were evaluated by binary logistic regression analysis. RESULTS: The overall mortality rate was 20.9%. After the first 28-day mortality reduction, the total bronchopulmonary dysplasia frequency was found to be 20.1%. The odds ratio and 95% confidence intervals of the factors affecting the development of bronchopulmonary dysplasia were found to be as follows respectively: respiratory distress syndrome (OR 6.2, 95% CI 3.6-10.6, p<0.01), patent ductus arteriosus (OR 4.9, 95% CI 2.4-9.9, p<0.01), apnea (OR 4.1, 95% CI 2.5-6.9, p<0.01), late sepsis (OR 2.7, 95% CI 1.6-4.5, p<0.01), early membrane rupture (OR 2.6, 95% CI 1.2-5.5, p=0.01), and male gender (OR 1.6, 95% CI 1.0-2.7, p=0.04) was found. However, there was no effect of chorioamnionitis, antenatal steroids, small for gestational age, early sepsis and type of birth on bronchopulmonary dysplasia. CONCLUSIONS: Differently from the usual factors which are low birth weight and a gestational week, there was a significant but non-linear risk relationship between respiratory distress syndrome, patent ductus arteriosus, late sepsis, apnea, early membrane rupture, male gender and bronchopulmonary dysplasia.

NARS2 mutations are known to cause various clinical phenotypes such as nonsyndromic hearing loss, Leigh/Alpers syndrome, refractory epilepsy, developmental delay, intellectual disability and myopathy. We presented the first Turkish variant of NASR2 and added type 1 diabetes mellitus (DM), which was not previously described in the phenotype spectrum of this disease. A 4.5-month-old girl presented with hearing loss, hypotonia, refractory myoclonic epilepsy, severe developmental delay and large subdural hemorrhage. In the first year of the follow-up, type 1 DM developed. A homozygous missense mutation, [c.500 A>G, p.H167R] in the NARS2 gene was detected in the trio-based whole-exome sequencing (WES). In this disease, in addition to multi-organ involvement, type 1 DM may also develop, as in our case. Since it is a mitochondrial disease, the decision to treat with valproic acid should be reconsidered. The long diagnostic process can be shortened with WES.