Early life represents a critical developmental programming window during which nutrition and microbial exposures shape long-term physiological function. Feeding mode is a major determinant of infant gut microbiota assembly and metabolic activity. This narrative review synthesizes current evidence comparing breastfeeding (BF) and formula feeding in relation to microbial composition, functional capacity, and immune programming during the preweaning and early postweaning periods. BF may support a relatively stable, bifidobacteria-dominated microbiota enriched in pathways involved in carbohydrate utilization, vitamin biosynthesis, and immune modulation. Human milk oligosaccharides, secretory IgA, lactoferrin, and milk-associated microbes collectively guide microbial succession, enhance barrier integrity, and support immune tolerance. In contrast, formula-fed infants typically exhibit greater microbial diversity, earlier transition toward adult-like profiles, and increased abundance of facultative anaerobes, alongside the enrichment of pathways related to bile acid and amino acid metabolism. Microbiota patterns in formula-fed infants are further influenced by formula composition, including protein load, lipid structure, and supplementation with prebiotics, probiotics, and human milk oligosaccharide analogues. Although advances in formula design have reduced compositional gaps, functional differences in microbial stability and immune programming persist. Recognizing early infancy as a sensitive programming window underscores the need for microbiome-informed nutritional strategies and longitudinal, multi-omics research to clarify causal mechanisms and optimize early-life interventions.

Parathyroid carcinoma (PC) associated with primary hyperparathyroidism (PHPT) has been well investigated in recent years. Data regarding PC evolution in secondary hyperparathyroidism (SHPT) due to chronic kidney disease (CKD) are, however, scarce. Most features that raise the suspicion of PC in PHPT are part of the usual SHPT evolution in CKD, mirroring the natural changes undergone by the parathyroid glands. Therefore, pre-surgically establishing the malignant or benign character of the lesions is cumbersome. We present two cases of PC in end-stage renal disease, one of which was bilateral, diagnosed after total parathyroidectomy in a high-volume parathyroid surgery center. A literature review of the data was also performed. A systematic search of the PubMed/MEDLINE database until January 2024 identified 42 cases of PC associated with SHPT. Understanding the PC features in CKD might improve associated bone and mineral disease management, and reduce the risk of metastasis, parathyromatosis, or recurrence. Irradiation, prolonged immunosuppression, long dialysis vintage, and genotype may predispose to the malignant transformation of chronically stimulated parathyroids. Despite postsurgical diagnosis, favorable outcomes occurred when distant metastases were absent, even without “en bloc” resection. Further research is warranted to delineate specific diagnostic and therapeutic approaches tailored to this particular patient subpopulation.

Linear growth is traditionally attributed to the growth hormone (GH)/insulin-like growth factor-1 (IGF-1) axis, yet “growth without GH” is documented. We report five patients with severe GH deficiency—one congenital and four acquired, who reached normal or tall stature despite persistently low IGF-1. All patients had obesity and metabolic complications (insulin resistance, dyslipidemia, and/or fatty liver). Catch-up or sustained growth occurred before or independent of sex-steroid replacement in most cases. One patient with lifelong hypogonadism showed slow, prolonged growth with delayed epiphyseal fusion. Three patients also received recombinant human GH (rhGH), without a significant impact on overall growth velocity, but with favorable metabolic outcomes. Findings support multifactorial drivers of linear growth beyond the GH/IGF-1 pathway. Likely contributors include insulin signaling associated with adiposity, permissive thyroid hormone action, local growth-plate paracrine pathways, and, in hypogonadism, delayed epiphyseal closure. Genetic modifiers that enhance chondrogenesis or delay growth-plate fusion may contribute. We also reviewed the published literature on “growth without GH,” integrating single-case reports and series to contextualize these mechanisms and outcomes. In conclusion, profound GH deficiency does not preclude near-normal or accelerated growth. In “growth without GH,” therapeutic priorities should pivot from stature to cardiometabolic risk reduction. rhGH may be considered to improve metabolism when individualized and closely monitored, recognizing that height velocity is often adequate. Notably, rhGH consistently improved lipid profiles and steatohepatitis in two patients, suggesting a primarily metabolic benefit. Lifelong follow-up from childhood into adulthood is essential.

Background: Chronic kidney disease (CKD) is associated with systemic microvascular dysfunction, yet the relationship between retinal changes and mineral metabolism disturbances across CKD treatment modalities remains incompletely characterized. Methods: We performed a baseline cross-sectional analysis of 77 participants (29 hemodialysis [HD] patients, and 48 kidney transplant recipients [KTR]) who underwent 7 × 7 mm structural optical coherence tomography (OCT) and 6 × 6 mm OCT angiography (OCTA) imaging. Structural parameters included central macular thickness (CMT), ganglion cell layer plus inner plexiform layer (GCL+), ganglion cell complex (GCL++), and subfoveal choroidal thickness (SCT). Microvascular parameters included superficial and deep capillary plexus vessel density (SVPD, DVPD), choriocapillaris density (CCD), and foveal avascular zone (FAZ) area. Serum mineral metabolism markers were correlated with retinal findings. Eyes were analyzed separately as the primary approach, while generalized estimating equation (GEE) models adjusted for age, sex, body mass index, diabetes, and hypertension (HTN) were used for confirmation. Results: FAZ area, SVPD, DVPD, CCD, GCL+, GCL++, and CMT did not differ significantly between cohorts in either per-eye analyses or adjusted GEE models. SCT was lower in HD patients than in KTR in the right eye (p = 0.019) and remained significantly higher in KTR in the adjusted GEE models (p = 0.016), a difference that persisted after excluding participants with diabetes and after adjustment for HTN grade. HTN grade was associated with FAZ area in HD and SCT in KTR. Serum magnesium was inversely associated with FAZ area in HD (B = −95.27, p = 0.034) and positively associated with GCL+ in KTR (B = 10.55, p = 0.048). Conclusions: Retinal microvascular and inner-retinal structural parameters were largely comparable between HD patients and KTR, with SCT the only parameter showing a consistent between-cohort difference (higher in KTR). Serum magnesium and HTN grade were the metabolic and clinical variables most consistently associated with retinal measures.

Obesity can conceal nutritional impairment and compromised muscle health in metabolic dysfunction-associated steatotic liver disease (MASLD). This critical narrative review examines the potential role of eating behaviors in nutritional impairment and muscle health in MASLD, focusing on adults with overweight or obesity while considering the limited findings in lean MASLD and, separately, pediatric evidence. Altered eating behaviors are associated with prevalent MASLD, but their contribution to malnutrition, myosteatosis, and sarcopenic obesity remains unproven. Nutritionally adverse dietary patterns and appetite loss may increase vulnerability, although evidence linking these factors to muscle outcomes derives predominantly from aging and general obesity populations. Total daily protein intake is better supported than specific meal-level distribution targets, while resistance exercise offers more consistent functional benefits than protein supplementation alone in the limited direct MASLD evidence. Restricting eating windows has not demonstrated additional hepatic benefit over usual care. Incretin-associated lean-mass loss does not by itself establish sarcopenia or disproportionate muscle harm and requires interpretation alongside muscle strength and function. Physical inactivity, socioeconomic circumstances, multimorbidity, and reverse causation complicate attribution to eating behavior. These findings support assessment beyond body mass index, integrating eating behaviors, nutritional risk, and muscle health. We propose an adult assessment framework; however, prospective studies are needed to validate it and clarify the independent contribution of eating behaviors to nutritional and muscle deterioration in MASLD.

Background/Objectives: Multidrug-resistant tuberculosis (MDR-TB) remains a major public health challenge in the WHO European Region, which reports the highest global proportion of rifampicin-resistant and MDR-TB cases. Whole-genome sequencing (WGS) has emerged as a key tool for improving drug-resistance detection and supporting molecular surveillance. However, the level of genomic implementation across Central and Eastern Europe (CEE) remains insufficiently characterized. This scoping review aimed to evaluate the use of WGS for MDR-TB in CEE countries and to classify implementation maturity using a predefined framework (L0–L4). Methods: A structured search of PubMed/MEDLINE and Web of Science identified original studies published in English between 2015 and 2026 reporting genomic applications in MDR-TB across 13 predefined CEE countries. Data were extracted on sequencing approaches, resistance prediction, transmission analysis, monitoring of new or repurposed drugs, bioinformatic pipelines, and programmatic integration. Countries were categorized according to a five-level maturity model based on documented capacity, scope of application, and integration into national tuberculosis programs (NTPs). Results: Twenty-eight studies were included. WGS was used in 23/28 studies (82.1%), predominantly for genomic resistance prediction (25/28). Transmission analysis was reported in 19/28 studies, with heterogeneous single nucleotide polymorphism (SNP) thresholds and clustering methodologies. Monitoring of resistance to new or repurposed drugs was described in 8/28 studies. No country achieved Level L4 (formally integrated genomic surveillance). Four countries were classified as L3 and nine as L2, while no L0 or L1 settings were identified. Conclusions: Countries in Central and Eastern Europe demonstrate increasing operational use of WGS for MDR-TB, primarily driven by clinical resistance prediction. However, the lack of formal integration into national surveillance systems highlights a persistent gap between technological adoption and structured public health implementation. Strengthening programmatic integration and methodological standardization is essential for advancing genomic surveillance of MDR-TB in the region.