Search Results (117)

The prevalence of vitamin D deficiency has been noted to be of great concern to the population due to its association with multiple chronic ailments, such as those that affect the cardiovascular system, diabetes, bone diseases, and the immune system, and even some cancerous forms. The underlying mechanics are not well understood, but epidemiological and clinical research demonstrates notable correlations, correlated to different degrees by population, based on genetic, environmental, and lifestyle differences. The use of advanced machine learning methods in this study aimed to examine the association between serum vitamin D levels and chronic disease risk using the de-identified electronic health records from Intensive Care Unit (ICU) patients in the MIMIC-III database. A final cohort of 38,712 unique patients was selected after applying predefined inclusion and exclusion criteria, the data being used for machine learning model development and evaluation. To predict the status of chronic diseases based on vitamin D levels, supervised machine learning models were used: Logistic Regression (LR), Support Vector Machines (SVM), Random Forest (RF), and K-Nearest Neighbors (KNN). Data preprocessing involved strategies such as missing data imputation, normalization, and feature engineering to improve model training. The accuracy, precision, recall, F1-score, and receiver operating characteristic curve (ROC-AUC) were used to assess model performance. LR performed the best with the ROC-AUC of 92.5% and accuracy of 85.2%, and SVM was close behind the ROC-AUC: 90.9 percent. The chronic disease was associated with 2.1 times higher risk of chronic disease among people with severe vitamin D deficiency (p < 0.001), which was in agreement with earlier observational data. RF did not work as well (ROC-AUC: 87.7%) because it required higher dimensionality data, e.g., genetic and lifestyle parameters. The study shows the possible use of AI-based diagnostics in preventive medicine. As an example, presented vitamin D testing of high-risk population (e.g., increasing tests in old age, obesity, or dark-skinned population) adapted to ML-based risk assessment as well as supplementation plans could enhance this prevention. Full article

Leukemia represents a heterogeneous group of hematologic malignancies characterized by the dysregulated proliferation, differentiation, and survival of hematopoietic cells. Vitamin D (VD), a fat-soluble secosteroid hormone, is increasingly recognized not only as a regulator of calcium–phosphate metabolism but also as an important immune–metabolic modulator involved in hematopoietic homeostasis, inflammatory signaling, and cellular fate determination. Growing evidence suggests that VD deficiency may influence leukemogenesis, disease progression, treatment responsiveness, and supportive-care outcomes in patients with leukemia. Mechanistic studies indicate that the active metabolite, 1,25-dihydroxyvitamin D₃ (calcitriol), modulates leukemic cell biology by activating the vitamin D receptor (VDR) and regulating genomic and non-genomic signaling pathways, including MAPK, PI3K/AKT/mTOR, JAK/STAT, NF-κB, and β-catenin. Through these pathways, VD may affect transcriptional programs governing proliferation, differentiation, apoptosis, autophagy, immune regulation, and treatment resistance. Clinical and observational studies suggest that low 25-hydroxyvitamin D levels may be associated with adverse outcomes in selected leukemia subtypes, including poorer treatment responses, shorter overall survival and relapse-free survival, and shorter time to treatment. However, the available data remain heterogeneous, and causality has not been established. This review provides an integrated translational synthesis of VD deficiency in leukemia, linking molecular mechanisms with subtype-specific clinical evidence and supportive-care implications. Although VD supplementation should not be considered an independent anti-leukemic therapy, individualized assessment and correction of deficiency may represent a rational, low-toxicity component of supportive care. Further prospective and interventional studies are needed to define optimal supplementation strategies, identify responsive patient subgroups, and clarify the clinical relevance of VD status in leukemia. Full article

Background: Osteoporotic vertebral compression fractures (OVCFs) are the most prevalent manifestation of osteoporotic skeletal disease, associated with severe pain, functional decline, and elevated risk of subsequent fractures. Conservative management remains the first-line approach for stable fractures, yet pain control is often suboptimal, and vertebral collapse progresses in up to 37% of patients. Bio-activated orthosilicic acid combined with vitamins D3 and K2 (BioSi-DK) may support fracture healing through complementary mechanisms acting on osteoblast differentiation, collagen synthesis, osteocalcin carboxylation, and mineralization, but its clinical efficacy in OVCFs has not previously been investigated. Methods: A retrospective, multi-center comparative cohort study was conducted in patients aged >50 years with DXA-confirmed osteoporosis and acute thoracolumbar OVCFs (AO Spine OF1-OF2) managed conservatively. Patients receiving BioSi-DK supplementation (two capsules daily for two months, then one capsule daily for four months) in addition to standard conservative treatment were compared with controls receiving conservative treatment alone. Propensity score matching (1:1, sex-exact constraint, caliper 0.3 SD) was applied across twelve pre-specified baseline covariates. The primary outcome was pain intensity at six months, assessed by numerical rating scale (NRS). Secondary outcomes included NRS change, analgesic use, Patient Global Impression of Change (PGIC), requirement for vertebral augmentation (kyphoplasty), MRI marrow edema score (MES), and Genant grade change. Results: After propensity score matching, 38 patients (19 per group) with balanced baseline characteristics were analyzed (mean age 71.2 ± 6.5 years; 89.5% female; mean T-score −2.61 ± 0.32; mean baseline NRS 8.26 ± 0.95). The BioSi-DK group achieved a significantly lower post-treatment NRS score compared with controls (2.05 ± 2.17 vs. 3.84 ± 2.83; p = 0.015; Cohen’s d = −0.71) and a significantly greater mean NRS reduction (−6.21 ± 1.90 vs. −4.42 ± 2.12 points; p = 0.005; d = −0.89). Analgesic discontinuation was more frequent in the BioSi-DK group (68.4% vs. 36.8%; p = 0.068). Kyphoplasty was required in 5.3% of BioSi-DK patients versus 21.1% of controls (p = 0.340; OR = 0.21), and vertebral compression grade remained stable in 100% of supplemented patients versus 84% of controls. At two months, MES improvement by at least one category was more frequently observed in the BioSi-DK group than in controls, suggesting an earlier edema resolution effect; at six months, MES distribution was comparable between groups (p = 0.620). Conclusions: BioSi-DK supplementation as an adjunct to conservative management was associated with a statistically significant and clinically large reduction in pain at six months, with favorable trends in analgesic burden, kyphoplasty requirement, and edema resolution. The safety profile was excellent. These findings support the conduct of prospective, randomized, placebo-controlled trials to confirm BioSi-DK as an effective adjunct therapy for OVCFs. Full article

Background: Vitamin D is involved not only in calcium–phosphate homeostasis but also in immune and endothelial regulation. Vitamin D deficiency has been suggested to worsen disease activity in systemic lupus erythematosus (SLE). Environmental and lifestyle factors, including seasonal sun exposure, smoking, diet, and supplementation, may influence vitamin D status and disease manifestations. This study aimed to evaluate the association between serum 25-hydroxyvitamin D [25(OH)D] levels, disease activity, and anti-double-stranded DNA (anti-dsDNA) antibody titers in patients with SLE, taking selected lifestyle and environmental factors into account. Methods: Serum 25(OH)D concentrations, SLE disease activity assessed by the Systemic Lupus Erythematosus Disease Activity Index 2000 (SLEDAI-2K) score, and anti-dsDNA antibody titers were measured in patients with SLE and healthy controls. Blood samples were collected during sunny (April–September) and non-sunny (October–March) months. Information on vitamin D supplementation, smoking status, and dietary habits was obtained using a structured questionnaire. Associations between vitamin D status, disease activity, anti-dsDNA seropositivity, season of blood collection, supplementation, smoking, and diet were analyzed statistically. Results: Patients with SLE had significantly higher mean serum 25(OH)D levels than controls, mainly due to frequent vitamin D supplementation. No significant associations were observed between serum 25(OH)D levels and SLEDAI-2K scores or anti-dsDNA antibody positivity. Seasonality, smoking status, and adherence to special diets were not significantly related to disease activity or anti-dsDNA seropositivity. Vitamin D supplementation was strongly associated with sufficient 25(OH)D levels but did not translate into reduced disease activity or lower anti-dsDNA prevalence. Conclusions: Serum 25(OH)D concentration was not associated with clinical or immunological activity of SLE in this cross-sectional study, despite effective correction of deficiency through supplementation. These findings likely reflect the heterogeneity of SLE and the limitations of single time-point assessments, although regular monitoring and individualized vitamin D supplementation may still be considered in SLE care, particularly in the context of recommended photoprotection. Full article

The number of patients who require endoprosthetic treatment related to osteoporosis has increased in recent years. Vitamin D3 supplementation has long been standard practice in osteoporosis treatment, while vitamin K2 has gained importance. Using our in vitro model, we compared the osteogenic behaviour of primary healthy human osteoblasts (hOBs) and primary osteoporotic human osteoblasts (hopOBs) under unchanged conditions, with vitamin K2, vitamin D3 and the combined addition. Fluorescence microscopy examinations on a plastic surface and a rough titanium surface structure revealed morphological differences. A quantitative analysis of mineralisation and differentiation was performed using an alizarin red S assay and analysis of alkaline phosphatase activity. It was shown that the hopOBs behave differently morphologically on the titanium surface, while hopOBs are particularly noticeable due to the higher number of cell–cell interactions with vitamin K2. The rough surface led to more pronounced mineralisation of the hopOBs. This effect was pronounced under vitamin K2. Vitamin D3 had an effect in the initial phase of hopOB differentiation. Overall, vitamin K2 had a greater influence on the mineralisation of hopOBs than expected. It must be assumed that vitamin K2 plays a significantly greater role in the metabolism of hopOBs than previously assumed. Full article

Background/Objectives: Obesity in young adults is a major public health concern and a key contributor to cardiometabolic risk. Vitamin K2 (VK2) has been proposed as a potential adjuvant therapy; however, evidence from randomized controlled trials remains limited. This study evaluated the effect of VK2 supplementation on cardiometabolic risk factors in young adults with overweight or obesity. Methods: In this 12-week randomized, double-blind, placebo-controlled trial (NCT05995522), men and women aged 18–35 years with overweight or obesity (BMI 25–40 kg/m²) were assigned to receive VK2 (menaquinone-4, 100 µg/day) or placebo. Both groups received standardized nutritional counseling. Body composition, blood pressure, glucose homeostasis, lipid profile, and vitamin K-dependent proteins were assessed at baseline and post-intervention. Between-group differences were analyzed using ANCOVA adjusted for baseline values. Results: Forty-six participants completed the study (placebo n = 24; VK2 n = 22). VK2 supplementation significantly reduced total cholesterol (−10.64 mg/dL, p = 0.038) and LDL cholesterol (−6.12 mg/dL, p = 0.005) compared with placebo. A reduction in systolic blood pressure showed a trend toward significance (−5.56 mm Hg, p = 0.067). No significant effects were observed on body composition, glucose metabolism, or vitamin K-dependent proteins. Conclusions: VK2 supplementation resulted in improvements in total and LDL cholesterol levels, with no significant changes in vitamin K-dependent proteins, and may represent a safe and potentially beneficial adjunct to nutritional strategies aimed at early cardiometabolic risk modulation. Full article

Background/Objectives: Mild cognitive impairment (MCI), the prodromal stage of Alzheimer’s disease, may be influenced by nutritional status and genetic susceptibility. This systematic review synthesised evidence on how nutritional biomarkers interact with genetic variants, particularly APOE ε4, to influence cognitive outcomes in individuals with MCI. Methods: Following PRISMA 2020 guidelines, seven studies were included (three longitudinal, two randomised controlled trials, and two cross-sectional) involving adults aged ≥55 years with MCI. Nutritional exposures comprised plasma or serum concentrations of vitamins A, D, E, the vitamin B group, lipids, selenium, and ketogenic medium-chain triglycerides. Genetic risk was assessed primarily through APOE ε4 status. Risk of bias was assessed using RoB 2 and ROBINS-I, and certainty of evidence using GRADE. Due to heterogeneity in biomarkers, cognitive tools, and study designs, findings were synthesised narratively. Results: Across nutrient categories, higher concentrations of vitamin D, selenium, and antioxidants were associated with better cognitive outcomes. kMCT supplementation improved episodic memory and brain energy metabolism. Evidence for nutrient–gene interactions was mixed: APOE ε4 modified responses to vitamin B group and selenium but showed limited influence on vitamin D, lipids, or kMCT effects. Heterogeneity in biomarker assays, cognitive tools, and genetic stratification limited comparability across studies. Conclusions: Nutritional biomarkers appear to influence cognitive trajectories in MCI, and some associations may differ by APOE ε4 status. However, small samples and limited genetic stratification constrain interpretation. Future research should prioritise standardised biomarker measurement, genetically stratified cohorts, and individual participant data meta-analyses to clarify nutrient–gene interactions in MCI. Full article

Vitamin D, traditionally regarded as a nutrient, is increasingly recognized as a pharmacologically active secosteroid with pleiotropic effects extending beyond calcium homeostasis and bone integrity. Together with vitamin K2, it participates in the fine-tuning of mineral metabolism and vascular health, potentially modulating cardiometabolic risk through intertwined endocrine and paracrine pathways. Despite widespread fortification and supplementation, vitamin D deficiency remains a major global health concern, driven by limited sun exposure, obesity, and metabolic dysfunction. Observational and mechanistic studies consistently link low serum 25(OH)D concentrations with hypertension, insulin resistance, heart failure, and increased cardiovascular mortality. At the molecular level, vitamin D exerts pharmacological actions—modulating the renin–angiotensin–aldosterone system, exerting anti-inflammatory and antifibrotic effects, and influencing endothelial and cardiomyocyte signaling. While experimental and epidemiological evidence suggests potential cardiovascular benefits, large randomized controlled trials (RCTs) provide conflicting results, particularly regarding hypertension and heart failure. However, these often-neutral results do not preclude a targeted action. On the contrary, clinical efficacy is strongly dependent on baseline deficiency status and the presence of metabolic cofactors. In this context, high-dose supplementation of Vitamin D, in combination with Vitamin K2 to prevent vascular calcification, elevates the supplement to a genuine pharmacological agent, with a distinct therapeutic potential for modulating cardiometabolic risk in selected patient subgroups. Emerging evidence supports the concept that vitamin D, when appropriately dosed and combined with K2, may act more as a low-potency pharmacological modulator than a simple nutritional supplement. This review synthesizes current mechanistic, observational, and interventional evidence, aiming to clarify whether vitamin D should be reclassified—from a micronutrient to a pharmacologically relevant agent—in cardiometabolic prevention and therapy, proposing a paradigm shift toward personalized and targeted dosing strategies, characteristic of precision pharmacology. Full article

This study aimed to investigate the effects of dietary manganese deficiency and compare the impact of manganese macroparticles (MnCO₃) and nanoparticles (Mn₂O₃NPs) on bone remodeling and metabolism. Twenty-seven male Wistar rats were divided into three groups (n = 9): control (standard MnCO₃, 65 mg Mn/kg), manganese-deficient, and Mn₂O₃NPs-supplemented (65 mg Mn/kg). After a 12-week feeding period, bone-related markers and gene expression were analyzed in the femur and blood. Mn-deficient rats showed reduced plasma levels of bone-specific alkaline phosphatase (BALP), tartrate-resistant acid phosphatase 5b (TRAP5b), interferon-β (IFN-β), RANKL glycoprotein, 1,25-dihydroxyvitamin D₃ (1,25-(OH)₂D₃), vitamin K₂, and collagen turnover markers (PINP, CTX-1, NTX). Femur levels of BALP, TRAP5b, interferon-γ (IFN-γ), osteonectin, calcitonin, PICP, PINP, and CTX-1 were also decreased. Replacing MnCO₃ with Mn₂O₃NPs increased IFN-γ but lowered IFN-β and 1,25-(OH)₂D₃ levels in plasma. This treatment also decreased the femur level of BALP and calcitonin, and the RANKL:OPG ratio, while increasing the expression level of Sp7 and Ctsk genes. To conclude, our results suggest that manganese deficiency is associated with suppressed bone turnover and altered mineral metabolism. Furthermore, replacing MnCO₃ with Mn₂O₃ nanoparticles did not yield the anticipated benefits for bone remodeling, as evidenced by the observed imbalances in osteogenic and resorptive markers, indicating a need for cautious evaluation of nanoparticle-based supplementation. Full article

Background/Objectives: Vitamin D deficiency is highly prevalent worldwide and is associated with multiple comorbidities and pharmacological treatments that may interfere with its metabolism. Evidence on the effect of supplementation across different drug user groups remains limited. Methods: A prospective study was conducted across community pharmacies over twelve months. Baseline socio-demographic, serum 25(OH)D concentration, quality of life (QoL), lifestyle habits, and medication use were collected. Participants received vitamin D supplementation for 12 months. Changes in vitamin D status and QoL were analyzed according to medication use. Logistic regression identified predictors of achieving adequate serum vitamin D levels (>30 ng/mL). Statistical significance was set at p < 0.05. Results: At baseline, 87.2% of 210 participants had insufficient or deficient vitamin D levels. After supplementation, mean serum vitamin D increased significantly from 21.3 ± 8.2 to 32.1 ± 12.6 ng/mL (p < 0.001), and QoL scores improved from 68.6 ± 18.7 to 77.8 ± 18.5 (p < 0.001). Dietary intake of vitamin D–rich foods and outdoor activity also increased. Supplementation improved vitamin D status among users of benzodiazepines, proton pump inhibitors, beta-blockers, statins, levothyroxine, metformin, and angiotensin-converting enzyme inhibitors, but not among corticosteroid, nonsteroidal anti-inflammatory drugs, or vitamin K antagonist. Multivariate analysis confirmed adherence as a strongest predictor of vitamin D adequacy (OR = 15.31, 95% CI = 2.90–80.75), while corticosteroid therapy, diabetes, and hypercholesterolemia were negatively associated. Conclusions: Vitamin D supplementation effectively corrected deficiency and improved QoL, but its efficacy varied according to comorbidities and medication use. Personalized supplementation strategies, emphasizing adherence and considering pharmacological profiles, may optimize outcomes. Further studies should explore mechanistic drug–nutrient interactions and long-term clinical implications. Full article

Objective: Studies show a high prevalence of vitamin D deficiency in Greece and Cyprus despite an abundance of sunlight. We investigate the vitamin D status of Greeks and Cypriots living in the UK, where sunlight availability is more limited. Design: Cross-sectional study of serum 25-hydroxyvitamin D (25(OH)D) using the UK Biobank cohort. Setting: The UK Biobank is a study of over 500K UK dwelling participants, with baseline measurements from 2006–2010. Participants: A sample of 325 Greek/Cypriot and 4158 British/Irish participants (aged 40–69 years). Results: The Greeks/Cypriots had statistically significantly lower median serum 25-hydroxyvitamin D (25(OH)D) (40.3 nmol/L) compared to the British/Irish (47.6 nmol/L). Eleven percent of British/Irish and 22.8% of Greeks/Cypriots had serum 25(OH)D < 25 nmol/L. Being exposed to summer sunlight for >30 min/d, as well as having a blood draw in summer or autumn, was statistically significantly associated with lower odds of 25 (OH))D < 50 nmol/L. Living in Scotland, having a winter blood draw, and not using a vitamin D-containing supplement were associated with increased odds of 25(OH)D < 50 nmol/L. Ethnicity was not a predictor of 25(OH)D < 50 nmol/L after confounder adjustment (Greek/Cypriot OR = 1.18 (95% CI 0.85, 1.63; British/Irish OR = 1.0). Conclusions: UK dwelling Greeks/Cypriots have a higher prevalence of vitamin D deficiency (<25 nmol/L) compared to the British/Irish population, but evidence from the literature is mixed as to whether they have a higher prevalence than when living in their country of origin. Public health interventions are required to improve 25(OH)D status in UK ethnic minority groups. Full article

Multiple sclerosis (MS) is a chronic autoimmune neurodegenerative disorder characterized by progressive demyelination and axonal degeneration within the central nervous system, driven by complex genomic and epigenomic dysregulation. Its pathogenesis involves aberrant DNA methylation patterns at CpG islands of numbers of genes like OLIG1 and OLIG2 disrupting protein expression at myelin with compromised oligodendrocyte differentiation. Furthermore, histone modifications, particularly H3K4me3 and H3K27ac, alter the promoter regions of genes responsible for myelination, affecting myelin synthesis. MS exhibits chromosomal instability and copy number variations in immune-regulatory gene loci, contributing to the elevated expression of genes for pro-inflammatory cytokines (TNF-α, IL-6) and reductions in anti-inflammatory molecules (IL-10, TGF-β1). Vitamin D deficiency correlates with compromised immune regulation through hypermethylation and reduced chromatin accessibility of vitamin D receptor (VDR) dysfunction and is reported to be associated with dopaminergic neuronal loss. Vitamin D supplementation demonstrates therapeutic potential through binding with VDR, which facilitates nuclear translocation and subsequent transcriptional activation of target genes via vitamin D response elements (VDREs), resulting in suppression of NF-κB signalling, enhancement of regulatory T-cell (T_reg) responses due to upregulation of specific genes like FOXP3, downregulation of pro-inflammatory pathways, and potential restoration of the chromatin accessibility of oligodendrocyte-specific gene promoters, which normalizes oligodendrocyte activity. Identification of differentially methylated regions (DMRs) and differentially expressed genes (DEGs) that are in proximity to VDR-mediated gene regulation supports vitamin D supplementation as a promising, economically viable, and sustainable therapeutic strategy for MS. This systematic review integrates clinical evidence and eventual bioinformatical meta-analyses that reference transcriptome and methylome profiling and identify prospective molecular targets that represent potential genetic and epigenetic biomarkers for personalized therapeutic intervention. Full article

Background: Hypophosphatemia is a frequently underestimated metabolic disorder, yet it can be one of the first biochemical findings in primary hyperparathyroidism (PHPT). Current diagnostic and surgical criteria for PHPT do not include serum phosphate, despite its potential value as an early marker. Methods: We report the case of a 79-year-old woman with type 2 diabetes mellitus, hypertension and osteoarthritis, followed since 2015 for persistent hypophosphatemia (0.8 mg/dL) and stress fractures. Results: Initial calcium and vitamin D levels were normal, but PTH was elevated. Bone scintigraphy revealed multiple stress fractures, while ultrasound and sestamibi scan were inconclusive. Despite cholecalciferol and calcitriol supplementation, hypophosphatemia persisted. From 2023, progressive hypercalcemia developed (10.9 mg/dL), with sustained hypophosphatemia (1.7 mg/dL), persistently high PTH (121 pg/mL) and markedly elevated FGF-23 (1694 kRU/L). Renal phosphate wasting was demonstrated, with reduced tubular reabsorption. An 18F-fluorocholine PET-CT performed in 2024 identified two right parathyroid adenomas, establishing the diagnosis of PHPT. The patient was referred for parathyroidectomy. Conclusions: Hypophosphatemia may serve as a complementary biomarker in the diagnostic and therapeutic approach to PHPT, but only after other potential causes of low phosphate levels have been excluded, as illustrated in this case. Its consideration could facilitate the early identification of PHPT and improve clinical decision-making, particularly in patients who do not meet classical surgical indications. Full article

We investigated gene regulatory relationships in the neonatal liver to identify potential mechanisms by which maternal vitamin and mineral supplementation during gestation influences developmental programming in heifer calves. Liver transcriptomes were profiled by RNA-Seq in calves collected 30 h after birth from dams fed either a basal diet (CON; n = 6) or the basal diet plus a vitamin and mineral premix (VTM; n = 6; 113 g·heifer⁻¹·d⁻¹), starting 60 days pre-breeding and continuing through gestation. Using DESeq2, we identified 630 DEGs between treatment groups (p ≤ 0.05 and |log2FC| ≥ 0.5). Over-represented pathways included oxidative phosphorylation, AMPK, PI3K/Akt, and FoxO, key regulators of energy homeostasis. We also identified 58 transcription factors (TFs) and 435 differentially connected genes (p ≤ 0.05), suggesting maternal diet induced a regulatory rewiring of TFs and histone deacetylating genes. Gene set enrichment analysis revealed genes positively ranked, such as LRAT and LMBRD1, underlying the vitamin digestion and absorption pathway, indicating coordinated upregulation in the VTM group. Conversely, 23 DEGs associated with the OXPHOS KEGG pathway were downregulated in the VTM calves. Further research should explore whether these transcriptional changes are linked to epigenetic modifications established at birth, persist throughout postnatal development, and potentially contribute to multigenerational inheritance. Full article

Background: Children with cystic fibrosis (CwCF) are at increased risk of fat-soluble vitamin (FSV) deficiency due to fat malabsorption. In France, children were usually supplemented with multiple individual vitamin preparations but have recently converted to DEKAs Plus Liquid (DPL), an absorption-enhanced, CF-specific, multivitamin formulation that includes vitamins D₃, E, K₁, A (beta-carotene and retinol), B, C, zinc, and selenium. We evaluated the impact of this change on FSV levels, treatment satisfaction, and compliance. Methods: Young CwCF (n = 39, mean age 2.3 ± 1.1 years) were analyzed retrospectively. Serum FSV levels, prothrombin time, treatment satisfaction, and compliance were assessed at baseline (M0) and after 12 months (M12). Results: Paired data analysis was performed on the 34 who completed 12 months. After 3 months, the initial daily dose was adjusted in nine cases. Median (interquartile range) serum levels of vitamin E (19.3 (17–27) vs. 26.3 (20–31) µmol/L, p = 0.0002) and 25-hydroxyvitamin D (80.2 (68–91) vs. 88.5 (79–108) nmol/L, p = 0.04) increased. Prothrombin time and vitamin A levels showed no significant change (p = 0.7, p = 0.4, respectively). The total number of FSV deficiencies decreased from 10 to 1, vitamin D deficiency was eliminated, and vitamin K₁ supplementation increased from 76% to 100% (p = 0.008). The median treatment satisfaction score (VAS_1–10) improved from 7 (5–9) to 9 (9–10) (p = 0.0006). Patient compliance remained high (9.5 (8.5–10) vs. 10 (9–10), p = 0.4). Conclusions: Switching from individual vitamins to DPL reduced vitamin deficiencies and improved FSV levels and patient satisfaction. Full article