Introduction
Vitamin E is an essential lipophilic micronutrient, often referred to in the literature as α-tocopherol, the most metabolically active isoform.1,2 Vitamin E has been recognized as having multiple beneficial properties, including action as a free radical scavenger and antioxidant.1,3 With these actions, vitamin E has been established to have a protective effect on the CNS and hypothesized to be protective against ongoing oxidative damage.1,4 Oxidative damage has been linked to multiple critical illnesses, including respiratory disease, reperfusion injury, and organ dysfunction in humans.4–7
Multiple studies5–7 have concluded that a decrease in vitamin E concentration ([vitE]) occurs in hospitalized humans, although similar studies have not been replicated in small animal or equine patients. The reason behind this change is unknown but hypothesized to be secondary to the patient’s underlying pathophysiology and ongoing oxidative damage, an increase in metabolic consumption, deficiency from decreased intake, or a combination of factors.7 Humans have been documented to ingest inadequate amounts of vitamin E during hospitalization because sources that are high in this micronutrient are often fed in low quantities.8
For the horse, [vitE]s vary in different feed sources, even among types of hay and method of harvest.9–11 Daily intake of as little as 120 IU of vitamin E per day has been found to be protective against peroxidation.12–14 Grass provides an important source of vitamin E in the horse but is often not provided or provided minimally in hospitalized cases.15 Previous research16 has shown significant variation in α-tocopherol concentrations in horses being fed controlled diets with varying vitamin E supplementation.
In the horse, vitamin E deficiency has been linked to neuromuscular disorders including equine neuroaxonal dystrophy/equine degenerative myeloencephalopathy, equine motor neuron disease, and vitamin E–responsive myopathy.17 A portion of the pathophysiology of these diseases revolves around periods of vitamin E deficiency. Importantly, a vitamin E deficiency early in life provides the highest risk to the development of neurodegenerative disease.17,18 Maintaining adequate concentrations of this essential micronutrient might aid in disease prevention or provide support in management of these disease states.17 Although deficiency is likely multifactorial on the basis of literature in other species,8,9 the importance of hospitalization, ongoing oxidative damage during time of disease, and changes in nutrition that come with disease status and change in environment remains unknown in the horse.
The objectives of this study were two-fold. The first objective was to determine the prevalence of vitamin E deficiency in horses at the time of emergency admission, and the second was to determine the prevalence of vitamin E deficiency in horses after hospitalization, at the time of discharge. We hypothesized that [vitE] would decrease from the time of admission to discharge in both hospitalized patients and mares or foals admitted as companion animals. This project aimed to provide insight to the vitamin E status of horses admitted to a hospital in the mid-Atlantic region and determine whether vitamin E supplementation might be necessary to avoid deficiency in horses with systemic illness and suspected ongoing oxidative damage.
Methods
Sample population
A convenience sample of client-owned horses admitted as either the patient or companion through the emergency and critical care service at a tertiary referral center in the mid-Atlantic region were enrolled. Ethical approval was provided by the university ethics committee, and written or verbal owner consent was obtained for enrollment and subsequent blood sampling (IACUC protocol No. 807386). Patient signalment, duration of hospitalization, diagnosis, and treatment protocol were recorded. Both adult horses (over 1 year of age) and foals (under 3 months of age) were sampled during the spring of 2023. Exclusion criteria included known vitamin E supplementation within 1 month prior to or during hospitalization including history of vitamin E–selenium injections in foals, age between 3 and 12 months, and improper sample handling.
Sample collection
Samples were obtained at the time of admission for determination of serum [vitE]. Foals had 5 mL of whole blood drawn via jugular venipuncture, and adults had 10 mL of whole blood drawn via jugular venipuncture. Blood samples were stored vertically in a no-additive (red top) tube. Throughout the duration of handling, samples were protected from light and refrigerated immediately after retrieval prior to processing and analysis.19,20 In those horses or foals hospitalized for a minimum of 5 days’ duration, a second sample was obtained on the day of discharge in the same manner for serum [vitE]. Five days was selected on the basis of changes demonstrated in as little as 48 hours in hospital and alteration in [vitE] measured following as little as 5 days of supplementation in critically ill humans.4,6,7
Data collection
Additional information recorded for each patient included sex, age, breed, location of origin, presenting complaint, and immunoglobulin G (IgG) concentrations in foals.
Vitamin E concentration
Reagents—Methanol (Optima grade), 95% n-hexane (Optima grade), and ethanol (American Chemical Society grade) were purchased from Fisher Scientific. Ultrapure water was obtained from an in-house Milli-Q Integral 5 water purification system (EMD Millipore). Butylated hydroxytoluene (BHT), α-tocopherol, δ-tocopherol, and bovine calf serum were purchased from Sigma-Aldrich.
Standards and sample preparation—A 1,000-mg/L ethanol-BHT stock solution was initially prepared by dissolving 30 mg of BHT in 30 mL of ethanol followed by further dilution to a 30-mg/L working solution. Stock solutions of α-tocopherol (500 mg/L) and δ-tocopherol (1,000 mg/L) standards were prepared in 30 mg/L of ethanol-BHT. Apart from 30 mg/L of BHT-ethanol solution, which was stored at room temperature, all stock solutions and standards were stored at –20 °C until use. δ-Tocopherol working solution (10 mg/L) was prepared in BHT-ethanol and used as an internal standard (IS). α-Tocopherol (vitamin E) calibration standards were diluted with IS solutions to the following concentrations: 0, 0.5, 2.5, 5, 10, and 25 mg/L. Both working IS and calibration standards were freshly prepared on the day of analysis.
After collection, the blood was allowed to clot in the refrigerator for at least 30 minutes. The tube was centrifuged at 1,400 X g for 5 minutes prior to transferring 0.5 mL of serum to a 15-mL polypropylene centrifuge tube. Serum was then either analyzed the same day or stored frozen. Sample preparation and extraction were performed under reduced light to prevent vitamin E degradation. On the day of analysis, frozen serum was thawed in the refrigerator before sample extraction. Half a milliliter of bovine calf serum was used as blank and spike serum controls, with 10 µL of 500 mg/L α-tocopherol added to the latter. An equal volume of IS solution was subsequently added to the serum, and the mixture was vortexed for 15 seconds, forming a precipitate. Liquid-liquid extraction was performed as follows: 2 mL of hexane was added to the tube, vortexed for 1 minute, and centrifuged at 1,400 X g for 5 minutes. After centrifugation, the top organic fraction (hexane) was transferred to a 10-mL borosilicate glass tube and extraction was repeated with 2 mL of fresh hexane. The top organic layers were pooled and evaporated to dryness with a nitrogen evaporator under the fume hood at room temperature. The sample was reconstituted in 0.5 mL of ethanol-BHT and transferred to a 1.7-mL microcentrifuge tube before spinning down at 13,000 X g for 3 minutes. The sample was transferred to an autosampler vial prior to injection.
Instrumentation and high-performance liquid chromatography conditions—The determination of [vitE]s in serum was performed on a high-performance liquid chromatography (HPLC) system (Shimadzu Corp) that was equipped with a low-pressure gradient pump (LC-20AT), autosampler (SIL-20AC), and fluorescence detector (RF-10AXL). The analytical column used in this study was the InfinityLab Poroshell 120 EC-C18 (4.6 X 50 mm, 2.7 µm; Agilent Technologies Inc) with a guard column (4.6 X 50 mm, 2.7 µm). Water and methanol were used as mobile phases A and B, respectively, with the gradient condition for mobile phase B set as follows: held for 3.5 minutes at 98%, increased to 100% at 5 minutes, and held to 6 minutes. It then decreased to 98% at 6.5 minutes and was held to 7 minutes for re-equilibration. Prior to injection, the system was equilibrated at this condition at 1 mL/min for 10 minutes, with the injection volume set at 10 µL. The excitation wavelength of the fluorescence detector was set at 290 nm, while 330 nm was selected as the emission wavelength. The calibration curve was constructed with the ratio of the peak area of vitamin E standard to that of the IS. Precision of the HPLC for [vitE] is 20%.
Statistical analysis
All analyses were conducted with Stata/MP (version 16.1; StataCorp LLC), with a 2-sided test of hypotheses and a P value < .05 as the criterion for statistical significance. Descriptive analyses included computation of means and SDs for normally distributed data, medians and IQRs of continuous variables with non-normal distribution, and tabulation of categorical variables. Tests of normal distribution (Shapiro-Wilk test) were performed to determine the extent of skewness of variables. Frequency counts and percentages were used for summarizing categorical variables. Spearman rank correlation analysis was utilized to assess correlation between confounding factors (sex, age, breed, location of origin, presenting complaint, and IgG concentration if applicable) and change in [vitE].
Vitamin E concentration as the main outcome of interest was analyzed with mixed-effects linear regression, with duration of time between sampling as the major fixed effect. Analysis was adjusted for age, patient versus companion, state of origin, sex, and duration of hospitalization (time between admission and discharge). One-way ANOVA was performed to investigate foals that received plasma versus those that did not.
A post hoc power analysis was conducted first with power analysis for a 2-sample means test to compare vitamin E levels across 2 time points. On the basis of study results and α = 0.05, β = 0.8, and δ = 0.056, we estimated we would need a total of 74,192 animals. The main issues here included the small observed δ (δ = 0.056), resulting in an extremely large and unobtainable N that was determined to be clinically irrelevant. A second power analysis was performed with a more clinically relevant δ (δ = 1) for change in [vitE] over hospitalization. This time, the projected number of animals was 92, in line with the number of animals in our study. Analysis was performed for horses and foals together and separately.
Results
A total of 103 adult horses and 54 foals admitted to a tertiary referral center on emergency were sampled initially. For these patients, the mean [vitE] on admission ([vitE]admit) was 3.7 µg/mL (95% CI, 3.3 to 4.2 µg/mL) for adults and 4.6 µg/mL (95% CI, 4.0 to 5.2 µg/mL) for foals (Figure 1). Seventeen of the 103 adults (16.5%) and 3 of the 54 foals (5.5%) were deficient in vitamin E based on documented reference ranges (Table 1). Forty adult horses and 20 foals were hospitalized for a minimum of 5 days, allowing for measurement of [vitE] at a second time interval ≥ 5 days after the first.
A—Vitamin E concentrations in adult horses (n = 103) at the time of emergency admission recorded in micrograms per milliliter. Horizontal lines at 2 and 10 indicate lower and upper extents of the reference range for adults. The horizontal bar represents the mean vitamin E concentration (3.7), with horizontal bars above and below representative of the 95% CI (3.3 to 4.2). B—Vitamin E concentrations in foals (n = 54) at the time of emergency admission. Dots represent individual foals, with horizontal lines representing the lower extent of the reference range. Blue dots are representative of foals sampled at < 1 day of age, with the blue dotted line representative of the lower extent of the reference range at 2.0 µg/mL. Black dots are representative of foals between 1 and 9 days of age, with the lower extent of the reference range at 1.8 µg/mL. Gray dots are representative of foals between 10 and 29 days of age, with the lower extent of the reference range at 1.2 µg/mL. Red dots are representative of foals between 1 and 2 months of age, with the lower extent of the reference range at 1.5 µg/mL. The horizontal bar represents the mean vitamin E concentration (4.6), with horizontal bars above and below representative of the 95% CI (4.0 to 5.2).
Citation: Journal of the American Veterinary Medical Association 2025; 10.2460/javma.24.09.0590
Reported adequate serum vitamin E concentrations for horses (µg/mL).21
| Age (d) | Lower end to upper end of reference range | |
|---|---|---|
| Fetus | < 1 | 2.0 |
| Newborn | 1–9 | 1.8 |
| Infant | 10–29 | 1.2–10.0 |
| Juvenile | 30–300 | 1.5–10.0 |
| Yearling | 301–700 | 1.5–10.0 |
| Adult | > 700 | 2.0–10.0 |
Adults (n = 40)
Of the 40 adult horses, the following breeds were included: Thoroughbred (n = 15), Warmblood (7), Standardbred (5), Quarter Horse (3), Welsh Pony (2), Tennessee Walking Horse (2), Miniature Horse (1), Paint Horse (1), Appaloosa (1), Belgian Draft (1), Gypsy Vanner (1), and Dartmoor (1). Sex distribution included 23 females, 15 castrated males, and 2 males. The average age of adult horses included in the study was 11.8 years (range, 2 to 28 years). The states of origin included the following: Pennsylvania (n = 20), Maryland (11), New Jersey (6), Delaware (2), and Vermont (1). Twenty-six horses presented to the hospital as the primary patient, and 14 presented as a companion to a foal. Primary presenting concerns for the adult horses that were patients (n = 26) included colic (10), limb laceration (3), ataxia (3), pneumonia (2), esophageal obstruction (2), laminitis (1), high-risk pregnancy (1), retained fetal membranes (1), collapse (1), acute kidney injury (1), and fracture (1). Median duration of hospitalization was 6 days (range, 5 to 16 days). Mean [vitE]admit was 3.6 µg/mL (95% CI, 3.0 to 4.2 µg/mL) and [vitE] at the time of discharge ([vitE]discharge) was 3.7 µg/mL (95% CI, 3.2 to 4.2 µg/mL) for adult horses (Figure 2). Median vitamin E was 3.5 µg/mL for [vitE]admit and 3.6 µg/mL for [vitE]discharge.
A—Vitamin E concentrations in adult horses (n = 40) sampled at emergency admission and discharge. Each individual horse is a dot with lines connecting admission and discharge vitamin E concentrations measured in micrograms per milliliter. B—Vitamin E concentrations in foals (n = 20) sampled at emergency admission and discharge (20). Each individual foal is a dot with lines connecting admission and discharge vitamin E concentrations measured in µg/mL.
Citation: Journal of the American Veterinary Medical Association 2025; 10.2460/javma.24.09.0590
Foals (n = 20)
Of the 20 foals, the following breeds were included: Thoroughbred (n = 10), Standardbred (5), Warmblood (3), Quarter Horse (1), and Welsh Pony (1). Sex distribution included 12 females and 8 males. The average age of foals included in the study was 12 days (range, 0 to 60 days). The states of origin included the following: Pennsylvania (n = 11), Maryland (8), and Delaware (1). Eighteen foals presented to the hospital as the primary patient, and 2 presented as a companion to a mare. Primary presenting concerns for the foals that were patients included diarrhea (n = 5), neonatal maladjustment syndrome (4), colic (4), lameness/presumptive septic synovial structure (2), pneumonia (1), prematurity (1), and patent urachus (1). Median duration of hospitalization was 5 days (range, 5 to 11 days). Median IgG concentration was 749 mg/dL (IQR, 486 to 800 mg/dL), with IgG concentrations measured by immunoturbidimetric method and ELISA semiquantitative rapid test, with any IgG measured as > 800 on the semiquantitative test quantified as 800 mg/dL. A total of 17 foals under the age of 30 days (17 of 20) had measured IgG concentrations. Nine foals received plasma transfusions for failure of transfer of passive immunity (FTPI); a total of 6 were diagnosed with partial FTPI and 3 with complete FTPI. Mean [vitE]admit was 4.6 µg/mL (95% CI, 3.2 to 6.0 µg/mL) and [vitE]discharge was 4.8 µg/mL (95% CI, 3.4 to 6.1 µg/mL) for foals (Figure 2). Median [vitE]admit was 3.4 µg/mL, with [vitE]discharge at 4.5 µg/mL.
Duration of hospitalization, which was variable between horses and defined as the time between [vitE]admit and [vitE]discharge, had no significant effect on [vitE] (P = .85). Similarly, breed, sex, age, location of origin, paired mare/foal comparison, and disease state had no significant effect on [vitE]. In foals, IgG concentration was inversely correlated with [vitE]admit (P = .0034). When foals receiving plasma were compared to those that did not, no statistical significance was observed (P = .24).
Out of all horses (adults and foals) admitted on emergency, 12.7% were found to be deficient. Out of the subgroup hospitalized for ≥ 5 days, 16.7% were deficient at admission. Out of the adult horse group, 17 of 103 (16.5%) were deficient at admission, including 7 of 40 (17.5%) of the subgroup hospitalized for ≥ 5 days. One hospitalized adult became deficient, and 4 hospitalized adults achieved adequate [vitE], with a total of 4 of 40 adults (10%) deficient at time of discharge. Out of the foal group, 3 of 54 (5.5%) were deficient at admission, including 3 of 20 (15%) of the subgroup hospitalized for ≥ 5 days. None of the foals (0 of 20 [0%]) were deficient at time of discharge.
Discussion
Vitamin E concentration was not affected by hospitalization in the cohort of horses sampled. Although patients often do not have access to grass during hospitalization, the results of this study revealed that [vitE] was not significantly affected and vitamin E supplementation is not required unless a previously diagnosed deficiency is present. The study does not diminish the importance of vitamin E supplementation in cases diagnosed as deficient or if concern exists for diseases that result from vitamin E deficiency, and individual horses might require supplementation. Supplementation, although not required for every hospitalized horse, should be considered on the basis of the individual’s disease processes. Additionally, this study supports the importance of monitoring the concentration of this micronutrient given the prevalence of vitamin E deficiency in this cohort of horses.
A total of 12.7% of all horses and 16.7% of horses (17 adults and 3 foals included) hospitalized for a minimum of 5 days were presented in a deficient state, similar to a previously reported population of mares and foals in which 13% were deficient.22 Although the majority of horses were determined to have adequate serum [vitE], the fact that a substantial number were deficient is concerning given the geographic location and patient population of the referral hospital. The hospital is in a region with a reputation for adequate grass pasture turnout and nutrient-rich hay for most horses, and referral clientele generally use commercially formulated feeds. We suspect that vitamin E deficiency might be even more prevalent in other patient populations where geography and management styles result in minimal grass pasture turnout or lower hay quality. Mean serum [vitE] of foals in this study were comparable with previous literature in Standardbred foals.22 Mean serum [vitE] of adults in this population were found to be greater in comparison to previously published data9,10; location and dietary differences might account for this change.17,23
It is important to note that those horses that presented with ataxia did not have underlying vitamin E deficiency as a cause. Vitamin E concentrations for the ataxic horses were 5, 3.1, and 3.4 µg/mL, not consistent with an underlying vitamin E–deficient neuromuscular disease. There were a total of 2 horses with admission [vitE]s exceeding the reference range at 20 and 11.8 μg/mL (> 10 μg/mL; Figure 1). The reason for this elevation in these horses is unknown. The horses were not known to be supplemented with vitamin E prior to referral, although it is unknown whether supplements containing vitamin E as an additional product were used in these horses. The horse with the [vitE] of 20 μg/mL was also severely hypertriglyceridemic (1,188 mg/dL; reference interval, 11 to 52 mg/dL). Measurement of vitamin E via HPLC in lipemic human samples can result in unreliable measurements, and hypertriglyceridemic equine samples also might have abnormally increased values.24–26 The other horse was a Morgan mare that presented with colic and was diagnosed with a small intestinal lesion. Given the breed and diagnosis, hypertriglyceridemia might have contributed to the increased vitamin E value, but this remains unknown, as triglycerides were not monitored in this patient.
In the cohort of horses with discharge vitamin E measurements available, [vitE] was found to increase within the reported reference range (Table 1) in 4 of the 7 deficient horses (57.1%), and all foals with low [vitEadmit] were discharged with adequate concentrations of vitamin E without supplementation provided. Rapid increases in serum [vitE] have been recorded in horses provided vitamin E supplementation in controlled settings; significant differences were observed after 3 days of supplementation, with the minimum average difference being 1 μg/mL among groups.9 In humans in the ICU, [vitE] has been reported to decline throughout hospitalization,4,6 with changes observed in vitamin E as early as 48 hours into hospitalization in humans with critical illness.6 These findings provide insight that rapid alteration in this micronutrient is possible, although the reason behind this change is unknown.
Differences in diets may account for the variances in response to hospitalization across species.9 In neonates, the major vitamin E source is through milk.22,23 Because natural sources of vitamin E are not entirely withheld for the duration of hospitalization across all ages, this might explain why horses are able to maintain adequate vitamin E status while hospitalized. In humans, acute alterations in vitamin E status have been reported within 24 hours following onset of the clinical syndrome.5 It is possible that admission samples were not representative of the peak systemic illness in equine cases and that an acute decline corresponding to peak systemic inflammation was missed.
It is unknown why FTPI was significantly correlated with greater [vitE] (P = .0034). In this geographic area, given the proactive referring veterinarians, it is not uncommon for foals to be administered a plasma transfusion on the farm prior to referral, which might contribute to the higher [vitE] in the group of foals with FTPI. Colostrum is unlikely to be the cause of this finding, as those foals with FTPI would be expected to have ingested less, have exposure to poor-quality colostrum, or have consumed immunoglobulins due to systemic sepsis.27 The specific vitamin E components of hyperimmunized plasma are unknown and related to the donor horse’s concentration. The administration of plasma prior to referral might directly contribute to the serum [vitE] of the foals and might explain the higher [vitE] in foals with partial FTPI when compared to those with complete FTPI. No correlation between foal [vitE] was found when comparing those that received plasma and those that did not. No correlation was identified between mare and foal vitamin E status to explain the findings in the population of foals.
Previous studies investigating [vitE] in foals of varying ages have varied in their defined reference range, with values between 1.5 and 2 µg/mL used as the reference for deficiency.17,28,29 In each manuscript, the discussion as to the importance of age in what is considered a normal [vitE] for foals is emphasized. For the purpose of this study, age-specific reference ranges (Table 1) were used because of the lack of consensus across the literature and laboratory reference ranges provided. In the authors’ experience, < 2 µg/mL is likely deficient, but it is recognized that this is a poorly defined area in the literature. When 2 µg/mL was used as the reference range for foals of all ages, there were 4 foals instead of 3 defined as deficient. This changed the prevalence of vitamin E deficiency in foals presenting to the hospital to 7.4% from 5.5% and the total percent of horses found to be deficient in vitamin E on admission to 13.4% from 12.7%, which might be more accurate.
Despite the findings of this study, supplementation of vitamin E during prolonged hospitalization might be beneficial on the basis of what we know about vitamin E deficiency and development of disorders such as equine neuroaxonal dystrophy/equine degenerative myeloencephalopathy.18 It is unknown at what time during life the insult that might contribute this disease process occurs, or what concentration is protective for any given animal. Studies investigating the development of equine neuroaxonal dystrophy/equine degenerative myeloencephalopathy in neonatal foals found that affected foals had significantly lower [vitE] throughout the initial 120 days of life.28 The specific time frame that vitamin E deficiency might perpetuate this disease process remains unknown. Additionally, many sick patients or those expected to be hospitalized over 5 days might benefit from vitamin E supplementation given its antioxidant properties.1,3,4,12,30 Horses that are supplemented at home should continue supplementation in hospital, since most horses remained stable throughout hospitalization and withdrawal of supplementation would likely precipitate a decrease in concentration.9
The limitations of this study included the small sample size when horses and foals were separated out for analysis on the basis of age. Horses and foals with a history of vitamin E supplementation or supplementation being provided to the dam were excluded. Therefore, there might have been an inclusion bias for horses that tended to have adequate vitamin E status, with horses requiring supplementation to maintain adequate concentration excluded. Five days of hospitalization was selected as an inclusion criterion on the basis of similar studies of humans.7 This duration of hospitalization excluded many horses, some with less severe or quickly resolving disease that permitted discharge within 4 days, and some with severe disease that were euthanized within the first 4 days. This study was of a specific population of horses in the mid-Atlantic region, and regional differences in serum [vitE] cannot be overlooked. The results of this study might not be applicable in other climates, locations, or seasons on the basis of previous studies.10,31 Based on the post hoc power analysis and established δ of 1 and the results from this study, including a larger number of horses would not provide different results. Therefore, we feel confident that our results accurately reflect vitamin E dynamics in this patient population. Additionally, the hay fed in hospital was not analyzed for [vitE]. It is possible that the hay fed in hospital might be different in quality than that fed in the patient’s natural environment, impacting the individual patient’s [vitE], whether positively or negatively. This could have occurred in some deficient patients whose serum [vitE] was found to increase during hospitalization. Additionally, history of supplementation aside from vitamin E is unknown. Some supplements containing vitamin E might have been administered to the patients prior to referral and could have affected the results of this study. In neonates, type of diet, percent body weight being fed, and type of milk being fed (whether solely mare’s milk or milk replacer) in combination with plasma transfusion was not analyzed; therefore, the explanation behind the elevation in [vitE] in foals at discharge remains unknown and is likely multifactorial. This study quantified [vitE] through serum measurements. Serum concentrations are a small portion of the entire body’s stores of vitamin E but have been documented as a comparable measure to concentrations in tissue.32 It is likely that measurement of tissues would not have yielded differing results from those obtained, particularly considering the short course of hospitalization.
Most horses admitted to the hospital do not require vitamin E supplementation to maintain adequate [vitE] during hospitalization, but what was gleaned from this study and supported in previous publications is that vitamin E deficiency is relatively common in horses and [vitE] should be measured in horses being admitted to the hospital.17 Further investigation of a larger sample size of horses with various disease states in comparison to healthy horses admitted for routine procedures or appointments would provide insight to the effect of ongoing oxidative stress and systemic inflammation on this essential micronutrient. It is unknown why foals with FTPI were found to have higher [vitE], as there was no statistical significance or correlation established when the dam’s [vitE] was included in analysis. Vitamin E remains an important antioxidant and micronutrient in horses. Routine measurement of [vitE] and subsequent supplementation is warranted if there is a clinical suspicion of deficiency, concern for ongoing oxidative damage, known poor-quality hay, or lack of exposure to adequate pasture grazing.
Acknowledgments
None reported.
Disclosures
The authors have nothing to disclose. No AI-assisted technologies were used in the generation of this manuscript.
Funding
The authors have nothing to disclose.
ORCID
M. G. Palmisano https://orcid.org/0000-0002-5605-5639
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