Elevated serum concentrations of beta 2-Microglobulin (beta 2-MG) has
been reported in a variety of chronic diseases and solid tumors. We de
termined serum beta 2-MG concentrations in 140 subjects divided into f
ive groups: group 1, 34 patients with proven chronic pancreatitis, 8 o
f whom were studied during a painful relapse; group 2, 40 patients wit
h pancreatic cancer staged according to the Cubilla-Fitzgerald classif
ication; group 3, 40 healthy subjects; group 4, 10 patients with diges
tive nonpancreatic carcinomas; group 5, 16 patients with benign digest
ive nonpancreatic diseases. Serum soluble interleukin-2 receptor (sIL-
2R) was also determined in all patients with pancreatic diseases as an
index of immune system activation. In addition, serum CA 19-9 was ass
ayed in patients of groups 2 and 4, and C-reactive protein (CRP) of gr
oups 1 and 5. Renal function, evaluated by serum creatinine determinat
ion, was normal in all subjects studied. Patients with pancreatic canc
er and those with chronic pancreatitis had serum concentrations of bet
a 2-MG significantly higher than those of healthy subjects (p < 0.001
and p < 0.005, respectively). Patients with stage I and stage III panc
reatic cancer had similar serum levels of beta 2-MG, and these concent
rations were significantly lower than those of patients with stage II
tumors (p < 0.002 and p < 0.05, respectively). In chronic pancreatitis
patients, those studied during painful relapse of the disease had ser
um concentrations of beta 2-MG similar to those studied during clinica
l remission. A good correlation was found between serum concentrations
of these two proteins (r = 0.73, p < 0.001). In patients with pancrea
tic cancer, serum beta 2-MG and serum CA 19-9 were abnormally high in
85 and 75%, respectively; in those with digestive nonpancreatic carcin
omas, beta 2-MG was abnormally high in all patients, whereas CA 19-9 w
as so in 70%. Elevated serum levels of beta 2-MG in patients with panc
reatic cancer may be the result of increased tumor cell turnover or to
activation of the immune response by malignancy; the concomitant seru
m elevation of beta 2-MG and sIL-2R in these patients supports the lat
ter hypothesis. The simultaneous increase in serum levels of sIL-2R, b
eta 2-MG, and CRP in patients with chronic pancreatitis probably refle
cts a persistent activation of the immune response during clinical rem
ission of the disease as well.