Endocrine Abstracts

Background: Serum inflammation-based scores can predict clinical outcomes in several cancer types, including adrenocortical carcinoma (ACC). They may also be altered in benign adrenocortical tumours and correlate with cortisol excess. It is unclear whether the inflammation-based score alterations in ACC reflects malignancy, steroid excess, or both.

Methods: A total of 490 patients were included (429 [87.6%] with adrenocortical adenoma [ACA] and 61 [12.4%] with ACC) with available baseline full blood count and hormonal evaluation. We examined the relationship between different inflammation-based scores [neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), lymphocyte-to-monocyte ratio (LMR), systemic immune-inflammation index (SII), and prognostic nutrition index (PNI)] and both malignancy and steroid secretion patterns.

Results: All inflammation-based scores differ between ACC and ACA. Patients with ACC had higher levels of NLR, PLR, SII and lower levels of LMR and PNI compared to patients with ACA (all P values <0.001). This difference remained significant after adjusting for age, tumour size, and cortisol after the 1 mg-overnight dexamethasone suppression test (1 mg-DST). All the inflammation-based scores correlated with cortisol levels after 1 mg-DST in ACA and ACC patients. NLR showed a positive correlation with cortisol levels after the 1 mg-DST, both in ACC and in ACA (P<0.001). Among the inflammation-based scores, NLR demonstrated the highest accuracy in distinguishing ACC from ACA, with an area under the curve of 0.847 (95% CI 0.795–0.894) and an optimal cut-off value of 2.6. A logistic regression analysis showed that NLR >2.6 was independently associated with the presence of ACC, cortisol levels after 1 mg-DST, and age, but not with tumour size. The multivariate analysis showed that both the presence of malignancy (ACC vs ACA, P<0.001) and the presence of cortisol excess (cortisol after 1 mg-DST >50 nmol/l, P<0.001) were associated with higher NLR values. Considering ACC, NLR and SII were higher and PNI was lower in patients with cortisol excess compared to those without cortisol excess (P=0.002, P=0.007, and P=0.044 respectively). Finally, we studied the inflammation-based score in patients with hormonally inactive tumours; LMR and NLR were significantly different between inactive ACC (n=10) and inactive ACA (n=215) (P=0.040 and P=0.031, respectively).

Conclusion: Inflammation-based scores are related to steroid secretion both in ACC and ACA. ACCs present a higher grade of inflammation regardless of their secretion, likely as a feature of malignancy per se.