Vitamin E Supplementation in Burn Patients
| Status: | Completed |
|---|---|
| Conditions: | Hospital |
| Therapuetic Areas: | Other |
| Healthy: | No |
| Age Range: | 6 - 70 |
| Updated: | 4/2/2016 |
| Start Date: | August 2011 |
| End Date: | August 2014 |
| Contact: | Jong O Lee, MD |
| Email: | jolee@utmb.edu |
| Phone: | (409) 770-6731 |
Burned patients because of their increased oxidative stress have severely depleted vitamin
E, which is a dietary antioxidant. Oxidative stress is responsible for much of the
pathophysiology seen in burned patients, which leads to acute and chronic morbidity and
mortality, in addition to a decrease in their quality of life. Oral vitamin E will be used
to reverse the oxidative stress of burn injury and, in the process, decrease the secondary
consequences of thermal trauma. This proposal will demonstrate the benefit of maintaining
adequate vitamin E status.
E, which is a dietary antioxidant. Oxidative stress is responsible for much of the
pathophysiology seen in burned patients, which leads to acute and chronic morbidity and
mortality, in addition to a decrease in their quality of life. Oral vitamin E will be used
to reverse the oxidative stress of burn injury and, in the process, decrease the secondary
consequences of thermal trauma. This proposal will demonstrate the benefit of maintaining
adequate vitamin E status.
We have previously demonstrated that thermal injury depletes plasma vitamin E in pediatric
burn patients. However, plasma changes reflect short-term vitamin E changes, whereas adipose
tissue alpha-tocopherol concentrations reflect long-term vitamin E status. We reported last
year that burn injury depleted vitamin E stores in adipose tissue in children by nearly half
within one month following injury. Our long-term goal is to improve the quality of life of
burn patients by preventing pulmonary and hepatic dysfunction that may occur from vitamin E
depletion. The objectives of this application are to a) attenuate alpha-tocopherol depletion
in burned patients by vitamin E supplementation, b) prevent or reverse oxidative stress in
these patients, and c) collect pilot data on the effect of vitamin E supplementation on lung
and liver function. Our central hypothesis is that the administration of high doses of
alpha-tocopherol will prevent or restore levels of vitamin E in adipose tissue and reverse
the oxidative state in burned patients. The rationale of the proposed studies is that in
severe cases of vitamin E depletion, oxidative stress, fatty liver and lung dysfunction have
all been reported in our patients. We will administer vitamin E supplements (300-1200 IU
RRR-alpha-tocopherol) to burn subjects (n= 20 per group, 6-70 years, ≥20% total body surface
burns) for fifteen days. The subjects will be randomly assigned into two groups: an early
treatment group who will receive vitamin E for days 1-15 of the study, and a delayed
treatment group who will receive vitamin E for days 16-30 of the study. Both groups will be
studied for a total of thirty days. We will test the following aims: Aim 1: determine the
degree that supplemental Vitamin E will attenuate alpha-tocopherol depletion. Aim 2:
determine if supplemental Vitamin E reduces markers of oxidative stress in burned patients.
Aim 3: collect preliminary data to establish the relationship between oxidative stress and
pulmonary pathophysiology and fatty liver after burn injury. We will measure plasma and
adipose tissue alpha-tocopherol and urinary and plasma markers of oxidative stress, prior to
supplementation and then weekly. The proposed research is innovative because the oxidative
stress of burn injury causes a severe depletion of an essential nutrient, vitamin E.
Supplementation of vitamin E is a novel concept that may mitigate the complications of
burns, including lung injury, fatty liver and peripheral neuropathy.
burn patients. However, plasma changes reflect short-term vitamin E changes, whereas adipose
tissue alpha-tocopherol concentrations reflect long-term vitamin E status. We reported last
year that burn injury depleted vitamin E stores in adipose tissue in children by nearly half
within one month following injury. Our long-term goal is to improve the quality of life of
burn patients by preventing pulmonary and hepatic dysfunction that may occur from vitamin E
depletion. The objectives of this application are to a) attenuate alpha-tocopherol depletion
in burned patients by vitamin E supplementation, b) prevent or reverse oxidative stress in
these patients, and c) collect pilot data on the effect of vitamin E supplementation on lung
and liver function. Our central hypothesis is that the administration of high doses of
alpha-tocopherol will prevent or restore levels of vitamin E in adipose tissue and reverse
the oxidative state in burned patients. The rationale of the proposed studies is that in
severe cases of vitamin E depletion, oxidative stress, fatty liver and lung dysfunction have
all been reported in our patients. We will administer vitamin E supplements (300-1200 IU
RRR-alpha-tocopherol) to burn subjects (n= 20 per group, 6-70 years, ≥20% total body surface
burns) for fifteen days. The subjects will be randomly assigned into two groups: an early
treatment group who will receive vitamin E for days 1-15 of the study, and a delayed
treatment group who will receive vitamin E for days 16-30 of the study. Both groups will be
studied for a total of thirty days. We will test the following aims: Aim 1: determine the
degree that supplemental Vitamin E will attenuate alpha-tocopherol depletion. Aim 2:
determine if supplemental Vitamin E reduces markers of oxidative stress in burned patients.
Aim 3: collect preliminary data to establish the relationship between oxidative stress and
pulmonary pathophysiology and fatty liver after burn injury. We will measure plasma and
adipose tissue alpha-tocopherol and urinary and plasma markers of oxidative stress, prior to
supplementation and then weekly. The proposed research is innovative because the oxidative
stress of burn injury causes a severe depletion of an essential nutrient, vitamin E.
Supplementation of vitamin E is a novel concept that may mitigate the complications of
burns, including lung injury, fatty liver and peripheral neuropathy.
Inclusion Criteria:
- Age: 6 - 70 years
- >20% TBSA burn
Exclusion Criteria:
- Septic shock
- Bleeding disorders
- Diabetes, or on diabetes medications or anti-lipidemic agents
- Known liver disease, other than hepatic steatosis
- Kidney/renal disease, endocrine disease, cancer, heart disease, osteoporosis
- Congestive heart failure
- Alcohol abuse (>20 g/day; CAGE questionnaire) or drug abuse (amphetamines, cocaine,
opioids, marijuana)
- Positive hepatitis or HIV screens
- Pregnancy (women)
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