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ABSTRACTDuring the initial half-year of their existence, infants cannot receive the influenza vaccine, yet they face the greatest susceptibility to severe influenza complications. In this study, we seek to determine whether influenza vaccination of maternal and household contacts is associated with a reduced risk of influenza-like illness (ILI) and severe acute respiratory infection (SARI) in infants. This work was prospectively conducted during the influenza season. A total of 206 infants were included in this study. The percentage of infants with only the mother vaccinated is 12.6% (n:26), and the percent of infants with all household contacts vaccinated is 16% (n:33). Among the infants with only the mother vaccinated, the effectiveness of influenza vaccine is estimated as 35.3% for ILI and 41.3% for SARI. Among infants with all household contacts vaccinated, the effectiveness is estimated as 48.9% for ILI and 76.9% for SARI. Based on the results of multivariate logistic regression analysis, all-household vaccination is a protective factor against SARI (OR: 0.07 95% CI [0.01–0.56]), household size (OR: 1.75, 95% CI [1.24–2.48]) and presence of secondhand smoke (OR: 2.2, 95% CI [1.12–4.45]) significant risk factors for SARI in infants. The mother alone being vaccinated is not a statistically significant protective factor against ILI (OR: 0.46, 95% CI [0.19–1.18]) or SARI (OR: 0.3, 95% CI [0.11–1.21]). Along with the obtained results and analysis, this study provides clear evidence that influenza vaccination of all household contacts of infants aged 0–6 months is significantly associated with protecting infants from both ILI and SARI.

Background: Human species does not synthesize vitamin B12. In developing countries, vitamin B12 deficiency in infants due to maternal diet without adequate protein of animal origin has some characteristic clinical and laboratory features. We report our cases that admitted to hospital with different clinical presentations by the need of hospitalization but have the diagnosis of vitamin B12 deficiency in follow-up and evaluation. Material and Methods: Hospital records of infants diagnosed with vitamin B12 deficiency between 2011 and 2013 were evaluated retrospectively. Results: A total of 22 patients were included with a mean age of 6.4 months. All of the mothers had vitamin B12 deficiency. All of the patients were fed with breast milk. Four of the patients’ (18.2%) weight and height were below the third percentile. The most common symptoms of the patients were as follows; infections in 8, pallor in 8, refuse to solid food or to suck in 4, failure to thrive in 4, fatigue in 3, hypotonia and neuro-developmental delay in 1, convulsions in 2, and vomiting in 1. Two of the patients had jaundice at admission and they got the diagnosis of hemolytic anemia as well. Six patients had the neurologic signs and symptoms. Anemia was found in 18/22 patients (81.8%). Three patients (13.6%) had leukopenia, 8 patients (36.4%) had neutropenia, 2 patients (9.1%) had thrombocytopenia. Cyanocobalamine was administered to all patients and mothers. After the treatment, all of patients’ clinical and laboratory findings were improved. Conclusions: Pediatricians must consider nutritional vitamin B12 deficiency due to maternal dietary deficiency in the differential diagnosis of some hematological, neurological, and gastrointestinal disorders of infants with poor socioeconomic status. Delay in diagnosis may cause irreversible neurological damage.

The one of the leading causes of adolescent morbidity and mortality worldwide is motor vehicle accidents (MVA). The use of seat belts significantly lowers MVA fatalities and injuries. The aim of this study is to investigate adolescent seat belt usage patterns and relation with risky behaviors. The study conducted at two medical institutions with non-immigrant and literate adolescents aged 12–18. Demographics, seat belt use, and risk-taking behavior were collected through questionnaires. 726 teenagers (422 girls and 304 boys) with an average age of 176.7 ± 23.37 months participated in the study. Parents’ educational levels and front-seat belt use have been found to be correlated. Comparatively to non-users, seat belt users demonstrated lower risk scores (total, traffic, substance, and social). The use of seat belts was significantly predicted by traffic risk, according to logistic regression. The frequency of seatbelt use was higher among participants from cities with higher socioeconomic status. As a result, it was found that adolescents who exhibited more risky behaviors had a lower frequency of seat belt use and seat belt use was associated with socioeconomic level and parental education level. It is thought that population-based studies to be conducted on this subject are important.

Systemic pseudohypoaldosteronism (PHA) is a rare, salt-wasting syndrome that is caused by inactivating variants in genes encoding epithelial sodium channel subunits. Hyponatremia, hyperkalemia, metabolic acidosis, increased aldosterone and renin levels are expected findings in PHA. Clinical management is challenging due to high dose oral replacement therapy. Furthermore, patients with systemic PHA require life-long therapy. Here we report a patient with systemic PHA due to SCNN1B variant whose hyponatremia and hyperkalemia was detected at the 24th hour of life. Hyperkalemia did not improve with conventional treatments and dialysis was required. He also developed myocarditis and hypertension in follow-up. Challenges for diagnosis and treatment in this patient are discussed herein. In addition, published evidence concerning common features of patients with SCNN1B variant are reviewed.

Hypomagnesemia is a rare cause of seizures in childhood but should be kept in mind in recurrent and intractable seizures and hypocalcemia in communities where consanguineous marriages are common. Familial hypomagnesemia with secondary hypocalcemia is a rare genetic cause of hypomagnesemia, due to variants in the transient receptor potential melastatin 6 (TRPM6) genes. Here, a three year-old boy with a novel variant in this gene and had difficulties with enteral hypomagnesemia treatment is presented. He had recurrent seizures since two years of age and was diagnosed with epilepsy and treated with multiple antiepileptic drugs. Subsequently, he was diagnosed with rickets due to severe hypocalcemia at another center. The patient was hypotonic and neurodevelopmentally poor. The most prominent laboratory finding was of hypomagnesemia with secondary hypocalcemia. The genetic analysis revealed a novel variant in the TRPM6 gene. After parental treatment of intravenous magnesium (Mg2+) sulfate and calcium, the treatment was switched to enteral Mg2+ medications, due to persistent hypomagnesemia and the gastrointestinal side-effects, different oral preparations were used. The patient was stable on an oral maintenance dose of Mg2+ oxide with borderline blood Mg2+ levels and resolution of hypocalcemia. Hypomagnesemia is one of the causes of hypocalcemia. Enteral replacement is the key treatment but the treatment should be individualized for each patient. Normalization of hypomagnesemia is not always easy and should not be the aim of the treatment.

Glycogen storage disease type 2 (Pompe’s disease) is an autosomal recessive, fatal glycogen storage disease presenting with hypotonia and muscle weakness. It is known that deficiency of lysosomal acid alpha-glucosidase (acid maltase) leads to progressive generalised myopathy, cardiomyopathy and death in early infancy because of respiratory muscle weakness. Excessive undegradable intracellular glycogen deposition plays a role in the pathogenesis of the disease. Here we report a 3.5 month-old girl presenting with respiratory failure due to pneumonia and hypotonia, who was later diagnosed as Pompe disease.