Background/Objectives: Preterm infants represent a population group at increased risk for vitamin D deficiency (VDD) and for its negative impact on various outcomes like metabolic bone disease or rickets, respiratory complications like respiratory distress syndrome and the development of bronchopulmonary dysplasia, necrotizing enterocolitis, or retinopathy of prematurity. Methods: Despite the growing interest in vitamin D research, there is still uncertainty regarding clear recommendations for each high-risk category of premature infants concerning the optimal dosage, optimal product, and timing for initiating vitamin D supplementation to prevent VDD. Results: An analysis of the literature suggests that early intervention for the optimal enteral supplementation of vitamin D is not only successful in achieving higher 25-hydroxi-vitamin D (25(OH)D) at one month but is also linked with improved outcomes. Conclusions: The traditional concepts and current recommendations for assessing vitamin D status and optimal supplementation need to be revised. Since parenteral nutrition, fortified mothers’ own milk, and special formula for preterm infants cannot provide adequate vitamin D levels, initiating oral supplementation soon after birth is essential to correct VDD in preterm infants.

Superior ophthalmic vein thrombosis (SOVT) is a rare clinical entity that may be associated with hypercoagulability status. We present a case of a 77-year-old woman who presented to the emergency department complaining of eye ptosis, chemosis and conjunctival congestion in the right eye (RE). The ophthalmological examination revealed best-corrected visual acuity (BCVA) was 0.5 for the right eye (RE) 0.5 and 0.06 for the left eye (LE). Intraocular pressure (IOP) was 25 mmHg in RE and 14 mmHg in LE. Non-contrast computed tomography (CT) of the brain and orbits revealed a hyperreflectivity at the level of the right ophthalmic vein and inferior rectus muscle hypertrophy. An extensive hypercoagulable panel was completed and we found a positive result for Factor V Leiden (heterozygous mutation) and methyl-enetetrahydrofolate reductase (MTHFR-C677T homozygous mutations). Systemic steroidal anti-inflammatory and anticoagulant treatments were started immediately. Gradual resolution of symptoms was noted during the hospitalization, and BCVA in her RE was established at 0.7 at the 10-week follow-up.

Background/Objectives: Neuroretinitis (NR) is a rare inflammatory condition characterized by sudden vision loss, optic disc edema and macular star appearance predominantly affecting individuals in their third and fourth decades of life. Methods: This paper describes the case of 33-year-old Caucasian man with no significant medical history complaining of decreased vision for about a week. Results: The ophthalmological exam revealed best-corrected visual acuity (BCVA) for the right eye (RE) of 0.8 (decimal notation) and of 0.9 for the left eye (LE). Intraocular pressure (IOP) was 20 mmHg in RE and 18 mmHg in LE. Slit-lamp examination of both eyes (OU) showed no evidence of intraocular inflammation in the anterior chamber or vitreous cavity. Examination of the posterior pole of the right eye showed bilateral papilledema with an incomplete macular fan pattern. Conclusions: Despite extensive laboratory tests, including serologic and imaging investigations, a definitive etiology remained unclear. It is very important to differentiate NR from other optic nerve disorders, requiring careful clinical evaluation and observation of the evolution of symptoms.

Food allergy is increasingly recognized across geographic regions and age groups, although temporal trends are difficult to separate from differences in diagnostic criteria and surveillance. This narrative review examines how diet and nutrition interact with the wider exposome to influence food allergy risk, oral tolerance, and clinical phenotypes across the lifespan. We critically synthesize evidence on early-life allergen introduction, dietary diversity, fiber and microbial metabolites, Westernized and ultra-processed dietary patterns, epithelial barrier dysfunction, medication exposures, pollution, and changing food systems. Randomized trials support early peanut introduction and, with greater heterogeneity, early egg introduction as preventive approaches; by contrast, causal evidence linking most other nutritional and environmental exposures to clinically confirmed food allergy remains limited. The diet–microbiome–immune axis offers plausible pathways connecting dietary substrates and microbial metabolites to epithelial integrity and immune regulation, but human mechanistic and longitudinal evidence remains incomplete. Globalization, migration, alternative protein sources, and climate-related exposures may reshape allergen encounters. Adult-onset food allergy, pollen–food allergy syndrome, alpha-gal syndrome, and cofactor-dependent reactions further illustrate how environmental influences may alter clinical expression beyond infancy. We propose an integrated life-course framework linking nutritional and non-nutritional exposures, underlying biological pathways, and emerging allergic phenotypes, while explicitly distinguishing intervention-supported findings from observational associations and mechanistic hypotheses. Future studies should combine standardized clinical outcomes with dietary assessment, environmental exposure measurements, functional microbiome profiling, metabolomics, and immune phenotyping to identify modifiable pathways relevant to food allergy prevention.