Galactosemia is an inborn metabolic disorder caused by a deficient activity in one of the enzymes involved in the metabolism of galactose. The first description of galactosemia in newborns dates from 1908, ever since complex research has been performed on cell and animal models to gain more insights into the molecular and clinical bases of this challenging disease. In galactosemia, the newborn appears to be born in proper health, having a window of opportunity before developing major morbidities that may even be fatal following ingestion of milk that contains galactose. Galactosemia cannot be cured, but its negative consequences on health can be avoided by establishing precocious diagnosis and treatment. All the foods that contain galactose should be eliminated from the diet when there is a suspicion of galactosemia. The neonatal screening for galactosemia can urge early diagnosis and intervention, preventing complications. All galactosemia types may be detected during the screening of newborns for this disorder. The major target is, however, galactose-1-phosphate uridyltransferase (GALT) deficiency galactosemia, which is diagnosed by applying a combination of total galactose and GALT enzyme analysis as well as, in certain programs, mutation screening. Most critically, infants who exhibit symptoms suggestive of galactosemia should undergo in-depth testing for this condition even when the newborn screening shows normal results. The decision to enroll global screening for galactosemia among the specific population still faces many challenges. In this context, the present narrative review provides an updated overview of the incidence, clinical manifestations, diagnosis, therapy, and prognosis of galactosemia, questioning under the dome of these aspects related to the disease the value of its neonatal monitoring.

An adequate vitamin D level is essential for optimal bone mass formation during growth. The present study aimed to assess (i) the sex-specific, age-specific, and potential seasonal (spring, summer, winter) influences on the pediatric circulating levels of 25-hydroxyvitamin D (25(OH)D); (ii) determine the frequency of pediatric patients with vitamin D deficiency (VDD) or insufficiency (VDI); and (iii) quantify the association between age category, sex, and season types and susceptibility to VDD and VDI, respectively. Laboratory data were collected on serum 25(OH)D levels in children aged between 2 and 18 years (n = 1674) who underwent blood sampling following admission to a university pediatric hospital in Cluj-Napoca (Romania) between January and June 2023. VDD (<20 ng/mL) was observed in 27% of pediatric patients. Among toddlers and preschoolers (2–5 years), VDD was 11%, while it was 33% among school-aged children (6–11 years) and 39% among adolescents (12–18 years). We found a significant difference in the frequencies of vitamin D status between females and males (p = 0.006). Also, we found significant associations of vitamin D status with age categories (p < 0.0001) and seasonal variations (p = 0.03). After adjusting for season of blood collection, the multinomial logistic regression model showed that children aged 6–11 years old (adjusted OR = 7, 95% CI: (4.9, 9.4)), children aged 12–18 years old (adjusted OR = 14, 95% CI: (9.3, 19.6)), and females (adjusted OR = 1.43, 95% CI: (1.10, 1.86)) were significantly associated with higher odds of VDD. In conclusion, the study revealed a significant difference in the frequency of VDD and VDI among pediatric patients older than six years, with a significant difference according to sex and season, being more pronounced among girls and during the winter and spring seasons.

Physiological calcification occurs in bones and epiphyseal cartilage as they grow, whereas ectopic calcification occurs in blood vessels, cartilage, and soft tissues. Although it was formerly thought to be a passive and degenerative process associated with aging, ectopic calcification has been identified as an active cell-mediated process resembling osteogenesis, and an increasing number of studies have provided evidence for this paradigm shift. A significant association between vascular calcification and cardiovascular risk has been demonstrated by various studies, which have shown that arterial calcification has predictive value for future coronary events. With respect to cartilaginous calcification, calcium phosphate or hydroxyapatite crystals can form asymptomatic deposits in joints or periarticular tissues, contributing to the pathophysiology of osteoarthritis, rheumatoid arthritis, ankylosing spondylitis, tendinitis, and bursitis. The risk factors and sequence of events that initiate ectopic calcification, as well as the mechanisms that prevent the development of this pathology, are still topics of debate. Consequently, in this review, we focus on the nexus of the mechanisms underlying vascular and cartilaginous calcifications, trying to circumscribe the similarities and disparities between them to provide more clarity in this regard.

Adverse effects of chemotherapeutic agents remain a significant clinical challenge in the management of gastric cancer. Across the literature, discussions of chemotherapy consistently document a range of toxicities, underscoring that even when treatment halts disease progression, it can leave substantial clinical sequelae. Chemotherapy can impact virtually every organ system, producing multiorgan toxicity with meaningful implications for patient quality of life and treatment feasibility. When initiating a new chemotherapy regimen, prior lack of therapeutic benefit is often associated with difficult recovery or inability to tolerate subsequent chemotherapy, thereby constraining future therapeutic options. Given these considerations and the current absence of universally personalized treatment, a multidisciplinary team—comprising a medical oncologist, gastroenterologist, and internist—is essential to the planning and execution of chemotherapy regimens. We recommend that these chemotherapy regimens be administered within internal medicine departments, in collaboration with the medical oncologist and gastroenterologist, because in many cases the adverse effects outweigh the potential benefits of chemotherapy.

Obesity is a complex, multifactorial chronic disease characterized by excessive and/or aberrant adiposity that requires interventions beyond conventional calorie-restriction models. Current clinical guidelines converge on behavioral modification, encompassing nutritional therapy, physical activity, stress reduction, and sleep improvement, as the cornerstone of obesity management, with psychological therapy, pharmacotherapy, and bariatric procedures as adjunctive or escalating options. While traditional “one-size-fits-all” dietary approaches frequently yield suboptimal long-term outcomes, precision nutrition has emerged as a promising strategy for individualized obesity care. This review critically appraises the evidence underlying each pillar of precision nutrition: genetic profiling shows clear utility in monogenic obesity but variable benefit when diet is matched to common polygenic variants; microbiome-targeted studies reveal that the Bacillota to Bacteroidota ratio shows inconsistent associations with obesity across studies, with genus-level and functional alterations offering more reproducible targets; and metabolomic profiling of postprandial glycemic responses has progressed from foundational predictive algorithms to large-scale clinical validation. It also highlights chrono-nutrition, the alignment of food timing with individual chronotype, as an emerging pillar of personalization. Beyond dietary composition, the review addresses how personalized nutrition can mitigate the adverse effects of incretin-based pharmacotherapy and discusses how artificial intelligence can integrate multi-omics and behavioral data into real-time dietary guidance. Future clinical implementation will require overcoming challenges related to data integration, predictive accuracy, and accessibility, paving the way for more effective, evidence-based obesity management.

Background/Objectives: Vitamin D is essential for calcium and phosphorus homeostasis and bone mineralization in infancy; serum 25-hydroxyvitamin D [25(OH)D] is its main biomarker. In Romania, data on vitamin D status among infants younger than six months remain limited, despite evidence of suboptimal status in other Romanian pediatric and perinatal populations. This study aimed to assess vitamin D status in infants aged 1–5 months in northwestern Romania and its associations with supplementation dose, feeding type, and season of blood sampling. Methods: This single-center observational study included infants aged 1–5 months. Serum 25(OH)D was interpreted as deficient (<12 ng/mL), insufficient (12–100 ng/mL). Statistical analyses used parametric or non-parametric methods as appropriate to data distribution. Results: The cohort included 124 girls (56.6%) and 95 boys (43.4%; median age 4 [3–5] months). Median serum 25(OH)D was 61.24 [49.53–75.32] ng/mL; 94.5% of infants had sufficient concentrations, deficiency and insufficiency each occurred in 0.9%, and 3.7% had potentially excessive concentrations. Serum 25(OH)D increased progressively with reported supplementation dose (p < 0.0001) and differed by feeding type (p = 0.0279), with breastfed infants having higher concentrations than formula-fed infants. No significant seasonal difference was observed (p = 0.4218). Conclusions: In this hospital-based cohort, most infants had sufficient 25(OH)D concentrations, in a context of near-universal supplementation. Higher reported doses were associated with higher 25(OH)D concentrations, and concentrations >100 ng/mL occurred almost exclusively in infants receiving 2000 IU/day. Without data on calcium metabolism, these concentrations do not indicate vitamin D toxicity, but they support adherence to recommended prophylactic doses.