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Patients with intestinal fat malabsorption and urolithiasis are particularly at risk of acquiring fat-soluble vitamin deficiencies. The aim of the study was to evaluate the vitamin status and metabolic profile before and after the supplementation of fat-soluble vitamins A, D, E and K (ADEK) in 51 patients with fat malabsorption due to different intestinal diseases both with and without urolithiasis. Anthropometric, clinical, blood and 24-h urinary parameters and dietary intake were assessed at baseline and after ADEK supplementation for two weeks. At baseline, serum aspartate aminotransferase (AST) activity was higher in stone formers (SF; n = 10) than in non-stone formers (NSF; n = 41) but decreased significantly in SF patients after supplementation. Plasma vitamin D and E concentrations increased significantly and to a similar extent in both groups during intervention. While plasma vitamin D concentrations did not differ between the groups, vitamin E concentrations were significantly lower in the SF group than the NSF group before and after ADEK supplementation. Although vitamin D concentration increased significantly in both groups, urinary calcium excretion was not affected by ADEK supplementation. The decline in plasma AST activity in patients with urolithiasis might be attributed to the supplementation of ADEK. Patients with fat malabsorption may benefit from the supplementation of fat-soluble vitamins ADEK.

Deposition of amyloid β protein (Aβ) to form neuritic plaques in the brain is the unique pathological hallmark of Alzheimer’s disease (AD). Aβ is derived from amyloid β precursor protein (APP) by β- and γ-secretase cleavages and turned over by glia in the central nervous system (CNS). Vitamin A deficiency (VAD) has been shown to affect cognitive functions. Marginal vitamin A deficiency (MVAD) is a serious and widespread public health problem among pregnant women and children in developing countries. However, the role of MVAD in the pathogenesis of AD remains elusive. Our study showed that MVAD is approximately twofold more prevalent than VAD in the elderly, and increased cognitive decline is positively correlated with lower VA levels. We found that MVAD, mostly prenatal MVAD, promotes beta-site APP cleaving enzyme 1 (BACE1)-mediated Aβ production and neuritic plaque formation, and significantly exacerbates memory deficits in AD model mice. Supplementing a therapeutic dose of VA rescued the MVAD-induced memory deficits. Taken together, our study demonstrates that MVAD facilitates AD pathogenesis and VA supplementation improves cognitive deficits. These results suggest that VA supplementation might be a potential approach for AD prevention and treatment.

Vitamin A is an important regulator of immune protection, but it is often overlooked in studies of infectious disease. Vitamin A binds an array of nuclear receptors (e.g., retinoic acid receptor, peroxisome proliferator-activated receptor, retinoid X receptor) and influences the barrier and immune cells responsible for pathogen control. Children and adults in developed and developing countries are often vitamin A-deficient or insufficient, characteristics associated with poor health outcomes. To gain a better understanding of the protective mechanisms influenced by vitamin A, we examined immune factors and epithelial barriers in vitamin A deficient (VAD) mice, vitamin D deficient (VDD) mice, double deficient (VAD+VDD) mice, and mice on a vitamin-replete diet (controls). Some mice received insults, including intraperitoneal injections with complete and incomplete Freund’s adjuvant (emulsified with PBS alone or with DNA + Fus-1 peptide) or intranasal inoculations with Sendai virus (SeV). Both before and after insults, the VAD and VAD+VDD mice exhibited abnormal serum immunoglobulin isotypes (e.g., elevated IgG2b levels, particularly in males) and cytokine/chemokine patterns (e.g., elevated eotaxin). Even without insult, when the VAD and VAD+VDD mice reached 3–6 months of age, they frequently exhibited opportunistic ascending bacterial urinary tract infections. There were high frequencies of nephropathy (squamous cell hyperplasia of the renal urothelium, renal scarring, and ascending pyelonephritis) and death in the VAD and VAD+VDD mice. When younger VAD mice were infected with SeV, the predominant lesion was squamous cell metaplasia of respiratory epithelium in lungs and bronchioles. Results highlight a critical role for vitamin A in the maintenance of healthy immune responses, epithelial cell integrity, and pathogen control.

Vitamin A (all-trans-retinol) is a fat-soluble micronutrient which together with its natural derivatives and synthetic analogues constitutes the group of retinoids. They are involved in a wide range of physiological processes such as embryonic development, vision, immunity and cellular differentiation and proliferation. Retinoic acid (RA) is the main active form of vitamin A and multiple genes respond to RA signalling through transcriptional and non-transcriptional mechanisms. Vitamin A deficiency (VAD) is a remarkable public health problem. An adequate vitamin A intake is required in early lung development, alveolar formation, tissue maintenance and regeneration. In fact, chronic VAD has been associated with histopathological changes in the pulmonary epithelial lining that disrupt the normal lung physiology predisposing to severe tissue dysfunction and respiratory diseases. In addition, there are important alterations of the structure and composition of extracellular matrix with thickening of the alveolar basement membrane and ectopic deposition of collagen I. In this review, we show our recent findings on the modification of cell-junction proteins in VAD lungs, summarize up-to-date information related to the effects of chronic VAD in the impairment of lung physiology and pulmonary disease which represent a major global health problem and provide an overview of possible pathways involved.

Vitamin A is required for important physiological processes, including embryogenesis, vision, cell proliferation and differentiation, immune regulation, and glucose and lipid metabolism. Many of vitamin A’s functions are executed through retinoic acids that activate transcriptional networks controlled by retinoic acid receptors (RARs) and retinoid X receptors (RXRs).The liver plays a central role in vitamin A metabolism: (1) it produces bile supporting efficient intestinal absorption of fat-soluble nutrients like vitamin A; (2) it produces retinol binding protein 4 (RBP4) that distributes vitamin A, as retinol, to peripheral tissues; and (3) it harbors the largest body supply of vitamin A, mostly as retinyl esters, in hepatic stellate cells (HSCs). In times of inadequate dietary intake, the liver maintains stable circulating retinol levels of approximately 2 μmol/L, sufficient to provide the body with this vitamin for months. Liver diseases, in particular those leading to fibrosis and cirrhosis, are associated with impaired vitamin A homeostasis and may lead to vitamin A deficiency. Liver injury triggers HSCs to transdifferentiate to myofibroblasts that produce excessive amounts of extracellular matrix, leading to fibrosis. HSCs lose the retinyl ester stores in this process, ultimately leading to vitamin A deficiency. Non-alcoholic fatty liver disease (NAFLD) is the hepatic manifestation of metabolic syndrome and is a spectrum of conditions ranging from benign hepatic steatosis to non-alcoholic steatohepatitis (NASH); it may progress to cirrhosis and liver cancer. NASH is projected to be the main cause of liver failure in the near future. Retinoic acids are key regulators of glucose and lipid metabolism in the liver and adipose tissue, but it is unknown whether impaired vitamin A homeostasis contributes to or suppresses the development of NAFLD. A genetic variant of patatin-like phospholipase domain-containing 3 (PNPLA3-I148M) is the most prominent heritable factor associated with NAFLD. Interestingly, PNPLA3 harbors retinyl ester hydrolase activity and PNPLA3-I148M is associated with low serum retinol level, but enhanced retinyl esters in the liver of NAFLD patients. Low circulating retinol in NAFLD may therefore not reflect true “vitamin A deficiency”, but rather disturbed vitamin A metabolism. Here, we summarize current knowledge about vitamin A metabolism in NAFLD and its putative role in the progression of liver disease, as well as the therapeutic potential of vitamin A metabolites.

Vitamin A supplementation (VAS) programs targeted at children aged 6–59 months are implemented in many countries. By improving immune function, vitamin A (VA) reduces mortality associated with measles, diarrhea, and other illnesses. There is currently a debate regarding the relevance of VAS, but amidst the debate, researchers acknowledge that the majority of nationally-representative data on VA status is outdated. To address this data gap and contribute to the debate, we examined data from 82 countries implementing VAS programs, identified other VA programs, and assessed the recentness of national VA deficiency (VAD) data. We found that two-thirds of the countries explored either have no VAD data or data that were >10 years old (i.e., measured before 2006), which included twenty countries with VAS coverage ≥70%. Fifty-one VAS programs were implemented in parallel with at least one other VA intervention, and of these, 27 countries either had no VAD data or data collected in 2005 or earlier. To fill these gaps in VAD data, countries implementing VAS and other VA interventions should measure VA status in children at least every 10 years. At the same time, the coverage of VA interventions can also be measured. We identified three countries that have scaled down VAS, but given the lack of VA deficiency data, this would be a premature undertaking in most countries without appropriate status assessment. While the global debate about VAS is important, more attention should be directed towards individual countries where programmatic decisions are made.

Although broad-scale data might suggest low prevalence, millions of children in India still suffer from Vitamin A and Vitamin D deficiencies despite India's existing guidelines for Vitamin A deficiency. To address the issue, the Government of India has recommended fortification of oil and milk to improve Vitamin A and Vitamin D consumption. However, there is limited information on the health benefits and cost-effectiveness of fortifying oil and milk at scale. To estimate the health benefits and cost-effectiveness of supplementation programme and fortification of milk and oil among children under 5 years, pregnant women, women in the reproductive age group, and the elderly. To measure the health benefits associated with supplementation and fortification of oil and milk, the number of DALYs that are currently lost due to Vitamin A and Vitamin D deficiencies were estimated. For Vitamin A related mortality, a reduction of 4%, 12% and 23% were assumed while the assumptions for estimating morbidity benefits were derived from Global Burden of Disease. For the costing exercise, we considered the following two scenarios: (1) high-dose vitamin A supplementation for children and pregnant women; (2) industrial fortification of oil for children, pregnant women, women in the reproductive age group, and the elderly. Overall, intervention related to Vitamin A could avert 1,119,044 Years of Life Lost (YLLs) at a 23% reduction, 194,616 YLLs at 4%, and 583,849 YLLs at 12% and 28,534 YLDs. Intervention related to Vitamin D could avert 99,219 YLDs. The total cost for supplying supplements to approximately 109,965 thousand children and 26,920 thousand pregnant women is around 26 million USD. The cost to fortify is 7.6 million USD for oil and 9.8 million USD for milk fortification for children and women. The overall cost effectiveness ratio of the fortification programme is 150. Fortification could emerge as a potentially superior long-term solution, considering the widespread consumption of oil and milk, offering a broader reach to the population.

While recent data on vitamin A deficiency (VAD) prevalence is lacking, the 2004 Côte d'Ivoire Nutrition and Mortality Survey reported that 26.7% of children aged 6-59 months were affected by VAD, and approximately 60% were at risk. Since 2016, the government has transitioned from mass campaigns to routine vitamin A supplementation (VAS) delivery integrated into health services. However, evidence on the cost-effectiveness of the routine distribution approaches is limited. This study evaluated the cost, coverage, and cost-effectiveness of three routine VAS delivery strategies across two health districts in northern Côte d'Ivoire. A mixed-methods study evaluated three routine VAS delivery strategies - routine-fixed, advanced community-based, and catch-up - across two health districts, Ferkessédougou and Niakaramadougou, in northern Côte d'Ivoire. The quantitative cost data were collected via a structured tool covering six cost categories: planning, procurement, training, social mobilization, distribution, and supervision. VAS coverage was assessed through a post-event coverage survey (PECS) via a two-stage cluster sampling methodology. A cost-effectiveness analysis determined the cost per child supplemented, the cost per DALY averted, and a sensitivity analysis tested the robustness of the findings under different cost scenarios. The total program cost for July-December 2023 was 25.5 million FCFA, with personnel costs comprising over 70% of expenditures. In Ferkessédougou, the routine advanced community-based strategy was the most cost-effective, at 458 FCFA per child in rural areas (versus 596 FCFA for the routine-fixed facility-based approach in the same area). In Niakaramadougou, the December catch-up was more cost-effective in rural areas (606 FCFA per child) than the routine-fixed approach (714 FCFA). Across both districts combined, the routine-fixed strategy averaged roughly 651 FCFA per child supplemented, and the cost per DALY averted ranged from 30,093 FCFA (advanced strategy in Ferkessédougou) to 89,550 FCFA (catch-up Jul 2023 in Niakaramadougou) - all below Côte d'Ivoire's cost-effectiveness threshold (0.5 x GDP per capita; approximately USD 1,265). All three strategies were cost-effective, though the advanced community-based strategy achieved the best balance of reach and efficiency. Scaling advanced strategies within health system constraints may enhance sustainability and coverage in low-resource settings.

To identify the factors associated with anemia and to document the severity of micronutrient deficiencies, malaria and inflammation, a nationally representative cross-sectional survey was conducted. A three-stage sampling procedure was used to randomly select children <5 years of age and adult women from households in two strata (urban and rural). Household and individual data were collected, and blood samples from children and women were used to measure the prevalence of malaria, inflammation, and deficiencies of iron, vitamin A, folate, and vitamin B12. 839 children and 945 non-pregnant women were included in the survey. In children, the prevalence rates of anemia (76.3%; 95% CI: 71.8, 80.4), malaria (52.6%; 95% CI: 46.0, 59.0), and acute and chronic inflammation (72.6%; 95% CI: 67.5, 77.1) were high. However, the prevalence of vitamin A deficiency (17.4%; 95% CI: 13.9, 21.6) was moderate, and the prevalence of iron deficiency (5.2%; 95% CI: 3.3, 8.1) and iron-deficiency anemia (3.8%; 95% CI: 2.5, 5.8) were low. Malaria and inflammation were associated with anemia, yet they explained only 25% of the population-attributable risk. In women, 44.8% (95% CI: 40.1, 49.5), 35.1% (95% CI: 30.1, 40.4), and 23.6% (95% CI: 20.4, 27.3) were affected by anemia, malaria, or inflammation, respectively. The prevalence rates of iron deficiency (8.3%; 95% CI: 6.2, 11.1), iron-deficiency anemia (6.1%; 95% CI: 4.4, 8.6), vitamin A deficiency (2.1%; 95% CI: 1.1, 3.1) and vitamin B12 deficiency (0.5%; 95% CI: 0.2, 1.4) were low, while folate deficiency was high (79.2%; 95% CI: 74.1, 83.5). Iron deficiency, malaria, and inflammation were significantly associated with anemia, but explained only 25% of cases of anemia. Anemia in children and women is a severe public health problem in Sierra Leone. Since malaria and inflammation only contributed to 25% of anemia, other causes of anemia, such as hemoglobinopathies, should also be explored.

Background: Micronutrient deficiencies are common and play a significant role in the prognosis of many chronic diseases, including heart failure (HF), but their prevalence in HF is not well known. As studies have traditionally focused on causes originating within the intestines, exocrine pancreatic insufficiency (EPI) has been overlooked as a potential contributor. The exocrine pancreas enables the absorption of various (fat-soluble) micronutrients and may be insufficient in HF. We hypothesize that EPI contributes to micronutrient deficiencies in HF. Objectives: To evaluate micronutrient concentrations in HF cases and their association with clinical characteristics and EPI. Materials and Methods: Plasma samples from 59 consecutive hospitalized patients with HF were analyzed for vitamins A, D, and E and the minerals selenium and zinc. EPI was defined as fecal elastase 1 level < 206 μg/g. Results: The mean age of patients was 59 ± 14 years, with 24 (41%) being women, and a median NT-proBNP concentration of 3726 [2104–6704] pg/mL was noted. Vitamin A deficiency occurred in eight (14%) of the patients, and 12 (20%) exceeded the upper limit. More than half (51%) were vitamin D-deficient. No patients showed vitamin E deficiency, but 14 (24%) had elevated levels. Selenium deficiency was common, affecting 36 (61%) patients, while zinc was below the normal range in seven patients (12%). Micronutrient levels did not differ significantly based on the presence of EPI. Conclusions: This study provides novel insights into the micronutrient status of patients with HF. Deficiencies in vitamins A and D, selenium, and zinc are prevalent in HF, but these findings are not associated with exocrine pancreatic function.