Dorina Pjetraj

Background: Picky eating (PE), also termed food selectivity, is one of the most common feeding concerns in childhood. Although often a transient developmental stage, persistent or severe selectivity may lead to nutritional deficiencies, growth impairment, and psychosocial consequences. Methods: This narrative review is based on literature searches conducted in April 2025 across PubMed, Web of Science, Embase, Medline, and Google Scholar. Articles published between 2015 and 2025 were included if they addressed the epidemiology, etiology, assessment, or management of PE in children aged 0–18 years. Additional seminal references predating this period were also considered. Results: Prevalence estimates of PE vary widely (13–50%), with peak incidence between ages two and six. Contributing factors include genetic predisposition, sensory sensitivities, temperament, family feeding practices, environmental influences, and adverse feeding experiences. Distinction from avoidant/restrictive food intake disorder (ARFID) and pediatric feeding disorder (PFD) is essential, as these conditions carry greater risk of nutritional and psychosocial impairment. Assessment relies on caregiver-report instruments, clinical observation, growth monitoring, and targeted nutritional evaluation. Effective management integrates parental education, responsive feeding strategies, repeated exposure to novel foods, and, when indicated, nutritional supplementation or referral to multidisciplinary teams. Sensory-based therapies, behavioral interventions, and psychoeducational programs show particular benefit in persistent cases. Conclusions: While most children outgrow PE without adverse outcomes, a subset remains at risk of long-term nutritional compromise and psychosocial difficulties. Early recognition, family-centered guidance, and evidence-based interventions are essential. Future research should refine diagnostic criteria, develop culturally sensitive assessment tools, and evaluate innovative therapies to improve outcomes.

Background: Methemoglobinemia (MetHb) is a rare and potentially life-threatening condition caused by oxidation of ferrous hemoglobin (Fe2+) to the ferric (Fe3+) state, making it incapable of binding oxygen and resulting in cyanosis and tissue ischemia. Case presentation: This case presentation describes a 1-year-old boy who developed sudden cyanosis and reduced consciousness disorder. An initial assessment showed decreased oxygen saturation (SpO2 85%) despite oxygen therapy, while point-of-care venous blood gas (VBG) analysis assessed high rates of MetHb (72.7%). Methylene blue and ascorbic acid were administered, resulting in in rapid clinical recovery and normalized VBG test results. The trigger for this condition was not identified, however the most likely cause of poisoning was attributed to food oxidants. Conclusion: Starting from the description of a clinical case, this paper discusses the causes and mechanisms of possible poisoning and reviews recent guidelines for methemoglobinemia management.

A new chemiluminescence immunoassay method (CLIA) for detecting IgA anti-transglutaminase (atTG IgA) in celiac disease (CD) has prompted inquiries into its diagnostic performance. We conducted a systematic review and meta-analysis comparing CLIA with traditional enzyme-linked immunosorbent assay (ELISA) and fluorescence enzyme immunoassay (FEIA). We searched PubMed, Medline, and Embase databases up to March 2024. The diagnostic references were intestinal biopsy and ESPGHAN guidelines. We calculated the sensitivity and specificity of atTG IgA assessed by CLIA and the odds ratio (OR) between the assays. Eleven articles were eligible for the systematic review and seven for the meta-analysis. Sensitivity and specificity of atTG IgA CLIA-assay were 0.98 (95% CI, 0.95–0.99) and 0.97 (95% CI, 0.94–0.99), respectively. The sensitivity of atTG IgA antibody detection did not significantly vary across the three assay modalities examined (CLIA vs. ELISA OR: 1.08 (95% CI, 0.56–2.11; p = 0.8); CLIA vs. FEIA OR: 6.97 (95% CI, 0.60–81.03; p = 0.1). The specificity of atTG IgA assessed by FEIA was higher than for CLIA (OR 0.17 (95% CI, 0.05–0.62); p < 0.007). According to the systematic review, normalization of atTG IgA levels in CD patients following a gluten-free diet was delayed when using CLIA compared to ELISA and FEIA methods. Conflicting findings were reported on the antibody threshold to use in order to avoid biopsy confirmation.

Background: Glycogen storage disease type XII is a rare metabolic disease resulting from Aldolase A deficiency that causes muscle glycogen accumulation, with crisis of rhabdomyolysis and hemolytic anemia. In the very few cases described, rhabdomyolysis crises are caused by fever and/or exercise and can accompany acute hemolytic anemia. Although currently there is no therapy available for this disease, the guidelines for the management of other forms of glycogen storage diseases recommend a nutritional therapy in order to avoid hypoglycemia or prevent exercise-induced rhabdomyolysis. Case presentation: In this case report we describe a new phenotype of the disease in a 14-year-old boy, characterized by seizures and rhabdomyolysis. Beside an antiepileptic treatment, we propose a new therapeutic approach based on ketogenic diet in order to supply an energetic substrate for skeletal muscle and neurons. Conclusions: The anti-epileptic therapy and the dietetic approach were well tolerated by the patient who showed good compliance. This led to a deceleration of the disease with no other acute episodes of seizures and rhabdomyolysis, without any side effects observed.