Impact of serum LDH on clinical outcomes in patients with good-risk metastatic non-seminomatous germ cell-cell tumors (NSGCT).

Abstract

588 Background: In pts with NSGCT, serum AFP, hCG and LDH play an important role in staging, risk stratification and choice of treatment (tx). Given its low specificity, NCCN recommends against systemic tx in pts whos’ only evidence of metastatic disease is an elevated LDH. Pts with serum LDH <1.5x the upper limit of normal (ULN) are considered to have good risk disease while pts with LDH 1.5-10x ULN and >10x ULN are considered to have intermediate (int.) and poor risk disease respectively. In pts stratified into int. or poor risk disease based on LDH levels alone, the optimal tx approach remains unknown; notably, NCCN recommends treating int. risk disease as good risk if the int. classification is based solely on LDH being 1.5-3ULN. Here, we describe clinical outcomes in pts with advanced NSGCT based on their LDH levels. Methods: The prospectively maintained Indiana University testicular cancer database was queried for pts with advanced NSGCT who had elevated LDH but otherwise good risk disease, including AFP and hCG levels. We grouped pts into LDH risk groups defined as: good risk (LDH<1.5x ULN), int. risk (LDH 1.5-10x ULN), and poor risk (>10x ULN). Chemo regimens were also grouped into risk groups defined as: good risk (BEPX3, EPX4, VIPX3) or int/poor risk (BEPX4, VIPX4, BEPX3+EPX1). The Kaplan-Meier method was used to analyze progression free survival (PFS) and overall survival (OS) using the log rank test to compare groups. Results: We identified 101 pts w/ NSGCT with elevated LDH but otherwise good risk disease, including AFP and hCG levels. 60 pts (59.4%) had good risk LDH, 40 (39.6%) had int. risk and 1 (1%) had poor risk LDH. In pts with good risk LDH, 57 (95%) were treated with good risk chemo and 3 (5%) were treated with int. or poor risk chemo. In the 41 pts with int/poor risk LDH, 34 (82.9%) were treated with good risk chemo while 7 (17.1%) were treated with int. or poor risk chemo. The 2y PFS in pts with good risk LDH compared to pts with int. or poor risk LDH was 91.7 vs 89.5% (p=0.67) and the 2y OS was 97.7 vs 94.6% (p=0.87). When evaluating all pts treated with good risk chemo, there was no difference in survival outcomes between LDH risk categories. In pts with LDH 1.5-3x ULN, 2y PFS was 96.3% vs 74.5% in pts with LDH>3ULN (p=0.0274); 2 y OS was 96.3 vs 90.9% (p=0.63). 14 pts had an LDH >3ULN. 9 were treated with good risk chemo and 5 were treated with int/poor risk chemo. 2 y PFS was 91.7% in the good risk LDH cohort vs 74.5% for pts with LDH >3ULN(p=0.026); 2y OS was not significantly different. Conclusions: In pts with NSGCT with elevated LDH but otherwise good risk disease, there was no difference in 2y PFS or OS among pts with good risk LDH vs int/poor risk LDH. In all pts treated with good risk chemo regimens, survival outcomes were not statistically different between LDH levels. PFS was shorter in pts with LDH >3ULN vs pts with good risk LDH but there was no difference in 2 y OS.