AL systemic amyloidosis is the most common and lethal form of amyloidosis. Macrophage inflammatory protein-1 alpha (MIP-1α) is a member of the CC chemokine family which is primarily associated with cell adhesion and migration. Adrenomedullin, and more the mid-regional fragment of proadrenomedullin (MR-proADM), comprising amino acids 45–92, have immune modulating, metabolic and vascular actions.
Aim of the study was to evaluate MIP-1α and MR-proADM serum levels in patients with systemic AL λ amyloidosis at presentation to find out potential differences useful to define a characteristic inflammatory pattern. Blood samples were collected from 7 patients with systemic AL amyloidosis (median age 68 yrs) and from 10 age-matched healthy control individuals referred to our Unit and analyzed for serum MIP-1 α and MR-proADM levels. For every patient 1 sample of peripheral blood have been obtained. The blood was separated into plasma at the time of blood draw and frozen to −80°C. Two-group comparisons were performed using the Mann-Whitney U test and paired t test. Correlation analyses were performed using Spearman rank correlation. All statistical tests were two tailed and p < 0. 05 was considered statistically significant.
Serum MIP-1α levels were significantly higher in AL amyloidosis patients (median 25. 04 pg/mL; IQR 12. 77) compared to the control group (median 2. 54 pg/mL; IQR 0. 34; p=0. 0007). Also serum MR-proADM levels were significantly increased in AL amyloidosis patients (median 1. 15 nmol/L, IQR 0. 6 vs median 0. 42 nmol/L, IQR 0. 18; p=0. 0008). In addition, a positive correlation between MIP-1α and MR-proADM has been observed in the group of patients with systemic amyloidosis (r2=0. 82, p=0. 034).
The increase of MIP-1α and MR-proADM serum levels in patients with systemic AL amyloidosis at presentation is indicative of active basal inflammation which can contribute to organ damage, in particular heart and kidneys, due to microvascular impairment. On the basis of our results, MIP-1α and MR-proADM could be used as new serum markers of inflammation in AL amyloidosis patients, with possible role in monitoring of organ damage.
No relevant conflicts of interest to declare.
Asterisk with author names denotes non-ASH members.