Vitamin D and Acute Cellular Rejection in Liver Transplant
Vitamin D and Acute Cellular Rejection in Liver Transplant
Out of 262 LT patients, 149 were eligible for inclusion in the final analysis. Of the excluded patients, 46 were treated with an IL-2 antagonist, 34 patients were prior solid organ transplant recipients, 1 patients did not have a pre LT 25(OH)D level, while 7 had vitamin D treatment prior to LT. Five patients had a serum creatinine above 2.0 mg/dL, 2 patients died within 3 days of surgery, and 6 were lost to follow-up within 12 months of transplantation. The study population had a median age of 54 years (IQR 49–62) and was predominantly male and Caucasian. The cause of the participants' underlying liver disease was categorized as viral hepatitis (B or C), Laennec's cirrhosis, autoimmune hepatitis (AIH) or "other" (Table 1). The median MELD score was 16 (IQR: 13–19). Fewer than half of the patients had diabetes or prediabetes prior to transplant. The median 25(OH)D level was 16 ng/mL (IQR 10–21), indicating that most patients had vitamin D deficiency according to the Endocrine Society's practice guidelines.
While no significant associations were observed between the development of ACR, AIH, and age (P = .067), patients with AIH were estimated to have 2.9 times greater odds of having ACR than those with other diagnoses (95% CI: 0.93–9.12). Older patients (P = .074) appeared to have lower odds of developing rejection within 1 year posttransplant. For every 10-year increase in age at transplant, the estimated odds of experiencing ACR decreased multiplicatively by 0.72 (95% CI: 0.51–1.03), which corresponded to a 28% decrease in the estimated odds of ACR.
After adjusting for age, MELD score, and an AIH diagnosis, there was no evidence for an association between ACR and baseline 25(OH)D levels (P = .24). For every doubling of the baseline 25(OH)D level, the estimated odds of ACR decreased multiplicatively by 0.75 (95% CI: 0.46–1.22). This corresponded to a nonsignificant 25% decrease in the estimated odds of ACR per doubling of 25(OH)D level. Table 2 summarizes the associations with ACR within the first year of LT.
In our cohort study, 92% (137 of 149 subjects) had a 25(OH) D level <30 ng/mL. Vitamin D deficiency (<20 ng/mL) was noted in 77% (108 subjects), while insufficiency (20–30 ng/mL) was noted in 19% (29 subjects). There was no statistically significant association between PTH and 25(OH)D levels. Furthermore, there was no statistically significant association between low 25(OH)D levels and the diagnosis, number, or severity of ACR episodes within the first year after LT. 25(OH)D levels were 16.1 ± 6.8 ng/mL for 48 subjects with no rejection, 16.1 ± 8.2 ng/mL for those with a mild first bout of ACR (n = 58), and 18.4 ± 12.4 ng/mL for those who experienced a moderate/severe first episode of ACR (n = 39). However, in a subgroup analysis of patients who had 25(OH)D levels <30 ng/mL, there was a statistically significant negative correlation (P = .0252) between 25(OH)D level and the rate of ACR (Table 3).
Results
Out of 262 LT patients, 149 were eligible for inclusion in the final analysis. Of the excluded patients, 46 were treated with an IL-2 antagonist, 34 patients were prior solid organ transplant recipients, 1 patients did not have a pre LT 25(OH)D level, while 7 had vitamin D treatment prior to LT. Five patients had a serum creatinine above 2.0 mg/dL, 2 patients died within 3 days of surgery, and 6 were lost to follow-up within 12 months of transplantation. The study population had a median age of 54 years (IQR 49–62) and was predominantly male and Caucasian. The cause of the participants' underlying liver disease was categorized as viral hepatitis (B or C), Laennec's cirrhosis, autoimmune hepatitis (AIH) or "other" (Table 1). The median MELD score was 16 (IQR: 13–19). Fewer than half of the patients had diabetes or prediabetes prior to transplant. The median 25(OH)D level was 16 ng/mL (IQR 10–21), indicating that most patients had vitamin D deficiency according to the Endocrine Society's practice guidelines.
While no significant associations were observed between the development of ACR, AIH, and age (P = .067), patients with AIH were estimated to have 2.9 times greater odds of having ACR than those with other diagnoses (95% CI: 0.93–9.12). Older patients (P = .074) appeared to have lower odds of developing rejection within 1 year posttransplant. For every 10-year increase in age at transplant, the estimated odds of experiencing ACR decreased multiplicatively by 0.72 (95% CI: 0.51–1.03), which corresponded to a 28% decrease in the estimated odds of ACR.
After adjusting for age, MELD score, and an AIH diagnosis, there was no evidence for an association between ACR and baseline 25(OH)D levels (P = .24). For every doubling of the baseline 25(OH)D level, the estimated odds of ACR decreased multiplicatively by 0.75 (95% CI: 0.46–1.22). This corresponded to a nonsignificant 25% decrease in the estimated odds of ACR per doubling of 25(OH)D level. Table 2 summarizes the associations with ACR within the first year of LT.
In our cohort study, 92% (137 of 149 subjects) had a 25(OH) D level <30 ng/mL. Vitamin D deficiency (<20 ng/mL) was noted in 77% (108 subjects), while insufficiency (20–30 ng/mL) was noted in 19% (29 subjects). There was no statistically significant association between PTH and 25(OH)D levels. Furthermore, there was no statistically significant association between low 25(OH)D levels and the diagnosis, number, or severity of ACR episodes within the first year after LT. 25(OH)D levels were 16.1 ± 6.8 ng/mL for 48 subjects with no rejection, 16.1 ± 8.2 ng/mL for those with a mild first bout of ACR (n = 58), and 18.4 ± 12.4 ng/mL for those who experienced a moderate/severe first episode of ACR (n = 39). However, in a subgroup analysis of patients who had 25(OH)D levels <30 ng/mL, there was a statistically significant negative correlation (P = .0252) between 25(OH)D level and the rate of ACR (Table 3).
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