The objective of this study was to evaluate the vitamin status, inflammatory markers, and oxidative stress markers in adult patients up to 3 days after thermal injury. This prospective study was conducted with 11 patients 24 to 72 hours after thermal injury (Burn Group), total surface area ranging from 10 to 41%, 34.3 ± 9.3 years, 82% of males, body mass index of 22.3 ± 2.9 kg/m2. We included 11 healthy adults (Control Group), 36.5 ± 7.6 years, 73% of males, and body mass index of 23.8 ± 2.5 kg/m2. Laboratory data were measured (plasma total protein, albumin, transferrin, lymphocyte counts, zinc, and iron), as well as serum vitamins (folic acid, vitamin B12, and vitamins A, C, and E), inflammatory stress markers (C-reactive protein, ferritin, and acid α1-glycoprotein) and oxidative stress markers such as glutathione peroxidase (GPx) and thiobarbituric acid reactive substances. The inflammatory stress was characterized by lower levels of total protein (median difference 1.2 g/dL, 95% CI: 0.4–2.1) and albumin (median difference 0.9 g/dL, 95% CI: 0.5–1.5), and higher levels of C-reactive protein (median difference −8.12 mg/dL, 95% CI: −11.62 to 4.61) and α-1 glycoprotein acid (median difference −28.56 mg/dL, 95% CI: −51.57 to −5.07) in burn patients. Decreased serum levels of vitamin A (median difference 1.10 μmol/L, 95% confidence interval [CI]: 0.42–1.66) and vitamin C (median difference 0.82 mg/dL, 95% CI: 0.50–1.04) were also detected. There was no statistical evidence of difference in the serum levels of glutathione peroxidase and thiobarbituric acid reactive substances between burn patients and controls, respectively. Even though there is an inflammatory stress, the obtained data showed that oxidative stress markers are normal 24 to 72 hours after burn injury. The decrease in negative acute phase protein may account for the diminished serum levels of vitamin A, which seems to be related to inflammatory stress. The marked decrease in the serum levels of vitamin C can be justified by augmented cutaneous loss and consumption in the regeneration of vitamin E.