In this narrative review, we address the prevention and therapy of iron deficiency anemia (IDA) with oral iron products in pediatric patients. Fortification of complementary foods with iron-containing micronutrient powders is the preferred method for the prevention of IDA in resource-limited settings. In developed countries, the prevention of sideropenia is through the consumption of iron-rich foods of animal origin. Regarding oral iron therapy, ferrous sulfate is the most widely used and cheapest product, but it is less well tolerated due to gastrointestinal side effects compared to complexes of ferric iron with polysaccharides, and complexes of iron with amino acids in casein, such as iron protein succinylate and iron acetyl aspartylate. These latter products are expensive and available only as single-dose vials with a fixed amount of elemental iron. Intermittent administration of ferrous sulfate, once or twice a week, is equally effective to daily therapy, with fewer side effects, and can be used in selected patients. Oral carbonyl iron has excellent bioavailability and the additional advantage of a high safety margin in cases of accidental overdose compared to iron salts, an important consideration given the potentially lethal consequences of iron overdose. Newer liposomal and sucrosomial iron products appear to have better intestinal tolerance and similar efficacy in the treatment of IDA, but limited pediatric data exist. In conclusion, all oral medicinal iron products are effective when prescribed for the treatment of IDA, if well-absorbed and taken consistently for 3 to 6 months. Physicians should be prepared to use alternative oral agents with better tolerance in case of gastrointestinal side effects.

In this narrative review, we address the prevention and therapy of iron deficiency anemia (IDA) with oral iron products in pediatric patients. Fortification of complementary foods with iron-containing micronutrient powders is the preferred method for the prevention of IDA in resource-limited settings. In developed countries, the prevention of sideropenia is through the consumption of iron-rich foods of animal origin. Regarding oral iron therapy, ferrous sulfate is the most widely used and cheapest product, but it is less well tolerated due to gas-trointestinal side effects compared to complexes of ferric iron with polysaccharides, and complexes of iron with amino acids in casein, such as iron protein succinylate and iron acetyl aspartylate. These latter products are expensive and available only as single-dose vials with a fixed amount of elemental iron. Intermittent admin-istration of ferrous sulfate, once or twice a week, is equally effective to daily therapy, with fewer side effects, and should be advocated. Oral carbonyl iron has excellent bioavailability and the additional advantage of a high safety margin in cases of accidental overdose compared to iron salts, an important consideration given the po-tentially lethal consequences of iron overdose. Newer liposomal and sucrosomial iron products appear to have better intestinal tolerance and similar efficacy in the treatment of IDA, but limited pediatric data exist. In con-clusion, all oral medicinal iron products are effective when prescribed for the treatment of IDA, if well-absorbed and taken consistently for 3 to 6 months. Physicians should be prepared to use alternative oral agents with better tolerance in case of gastrointestinal side effects.

Accurate diagnosis of bacterial meningitis is critical, particularly in young febrile infants. Although commercially available multiplex PCR assays enable rapid pathogen detection, these typically do not include Salmonella spp. or other Enterobacteriaceae, which may result in missed diagnoses and/or inappropriate treatment duration. We report the case of a 2‐month‐old female infant with Salmonella enteritidis meningitis and concurrent bacteremia. The patient initially presented with fever, lethargy, and a bulging anterior fontanelle. Cerebrospinal fluid (CSF) analysis was highly suggestive of bacterial meningitis. However, both CSF culture and the FilmArray ME Panel were negative, likely due to prior empirical antibiotic therapy at another hospital. The causative organism was isolated on blood cultures. The infant was treated with intravenous ceftriaxone for 24 days and discharged in excellent clinical condition. Twelve days later, she was readmitted with a relapse of meningitis and bacteremia caused by the same pathogen. She received combination therapy with cefotaxime and cotrimoxazole for 37 days, followed by cefotaxime monotherapy for another 26 days. Immunological evaluation, including assessment of immunoglobulin levels, lymphocyte subsets, and interferon‐γ receptor and Interleukin‐12 receptor expression, was normal. The patient had a favorable outcome with complete clinical and laboratory recovery and a normal neurodevelopmental outcome at follow‐up. Salmonella meningitis is a rare but life‐threatening condition in infants, which may be overlooked when relying on molecular diagnostic panels that do not include this pathogen. Negative CSF PCR results should be interpreted with caution in the presence of typical cytological and biochemical findings of bacterial meningitis. Prolonged antimicrobial therapy of at least 4–6 weeks is essential to prevent relapse and ensure optimal microbiologic and clinical outcomes.

We describe a male toddler with a history of operated posterior urethral valves who developed vitamin D toxicity with hypercalcemia after he was prescribed orally 6,000 IU of cholecalciferol daily for two months for vitamin D deficiency. The disordered calcium metabolism was discovered during hospitalization in our hospital for a urinary tract infection, along with evidence of renal failure. Serum calcium on admission was 4.22 mmol/L, with an ionized calcium level of 2.26 mmol/L. The measured 25(OH)D level was extremely high (3,555 ng/mL), along with a low serum parathyroid hormone, suggestive of severe vitamin D overdose. Despite aggressive hydration, administration of corticosteroids, and a low calcium diet, he required the administration of a single dose of zoledronic acid for resolution of the hypercalcemia. It was later discovered that the patient received an oral solution of vitamin D3 that was recalled due to a higher content of vitamin D3 than stated on its label. Therapy with low-dose bisphosphonates is effective in cases of symptomatic hypercalcemia that does not respond to intravenous hydration, administration of corticosteroids, and elimination of oral calcium intake. Any child presenting with hypercalcemia and low parathyroid hormone should be investigated for the possibility of vitamin D toxicity.