Acute Gastrointestinal Graft-versus-Host Disease in Pediatric Patients: Serum Albumin on Day 5 from Initiation of Therapy Correlates with Nonrelapse Mortality and Overall Survival

Abstract

The aim of the present study was to identify factors associated with the risk of development of gastrointestinal acute graft-versus-host disease (GI-aGVHD), as well as to evaluate the impact of various baseline parameters on response to treatment, nonrelapse mortality (NRM), and overall survival (OS) in pediatric patients with GI-aGVHD after allogeneic hematopoietic stem cell transplantation (allo-SCT). We retrospectively analyzed 300 pediatric patients who underwent allo-SCT from HLA-matched related or volunteer unrelated donors in our institution. GI tract involvement was observed in 46 out of 133 patients with aGVHD grade II-IV. Severe aGVHD (grade III-IV) was more frequently observed among patients with GI-aGVHD in comparison with patients without GI involvement (P < .001). Treatment with steroids resulted in durable responses in 22/46 patients; 14 additional patients responded to salvage therapy, whereas 10 were refractory to all treatments administered. Using Cox regression analysis, we observed that serum albumin level ≥ 3 mg/dL on day 5 after the initiation of therapy with steroids was statistically significantly associated with decreased hazard of NRM and improved OS (P = .021 and P = .026, respectively). In our study, serum albumin level, early (+ day 5) after the onset of steroids in patients with GI-aGVHD, was a predictor of treatment outcome. Prospective randomized trials need to be performed to verify the predictive significance of serum albumin and the need for early intensification of immunosuppressive treatment.

Nutritional risk factors predict severe acute graft‐versus‐host disease and early mortality in pediatric allogeneic hematopoietic stem cell transplantation

“…One study demonstrated that a >0.5 g/dl decrease in serum albumin level from pretransplantation to the onset of aGVHD predicts the development of grade III–IV disease . In addition, low albumin levels at day +5 after transplant were predictive of lower overall survival among patients with gut GVHD . Although both malnutrition and inflammation are known to decrease serum albumin levels, its relationship with GVHD is poorly understood and warrants additional investigation .…”

“…11 In addition, low albumin levels at day +5 after transplant were predictive of lower overall survival among patients with gut GVHD. 7 Although both malnutrition and inflammation are known to decrease serum albumin levels, its relationship with GVHD is poorly understood and warrants additional investigation. 12 We had relatively few patients with low baseline serum albumin, and it was not an independent risk factor for TA B L E 5 Adjusted longitudinal analysis of nutritional status and risk of GVHD within the subsequent 30-day period aGVHD or mortality.…”

“…Graft‐versus‐host disease (GVHD) risk was not assessed in this study. Other studies have demonstrated that low levels of another marker of poor nutrition, albumin, are associated with lower overall survival in both children and adults …”

“…Other studies have demonstrated that low levels of another marker of poor nutrition, albumin, are associated with lower overall survival in both children and adults. 6,7 Although the data are limited, studies have not demonstrated a consistent relationship between pretransplant BMI and the incidence of acute GVHD (aGVHD). [8][9][10] Other studies investigating the role of serum albumin level have demonstrated that a >0.5 g/dl decrease from pretransplantation predicts the development of grade III-IV disease.…”

“…11 Goussetis et al also demonstrated that low albumin levels at the time of diagnosis of aGVHD of the gut were predictive of lower overall survival. 7 Although both malnutrition and inflammation are known to decrease serum levels, the relationship between albumin and aGVHD is poorly understood and warrants additional investigation. 12 Vitamin D may also suppress the Th1-type response of aGVHD and prevent activation of alloreactive T cells, which mediate aGVHD.…”