Background. There is evidence that activation of coagulation by influe
ncing tumour biology may have impact on clinical course of lung cancer
. Patients and methods. We measured the activation markers thrombin-an
tithrombin complex (TAT) and prothrombin fragment F1+2 in 99 lung canc
er patients immediately after diagnosis, before antineoplastic treatme
nt. Outcome was assessed at the end of appropriate standard primary th
erapy (four to six courses of chemotherapy, surgery or radiation). Res
ults and conclusions. The activation markers (means +/- SEM) were lowe
r in the 33 responders (RSP; complete or partial remission) than in th
e 66 non-responders (NRSP): TAT 3.96 +/- 0.48 vs. 9.69 +/- 1.57 mu g/l
(P < 0.001), and F1+2 1.09 +/- 0.09vs. 1.64 +/- 0.25 nmol/l (P < 0.05
). TAT levels were > 6 mu g/l in 30 of 66 (45%) NRSP, but only 4 of 33
(12%) RSP. 88% of patients with TAT less than or equal to 6 mu g/l ac
hieved remission, and 45% with TAT > 6 mu g/l (P = 0.0014). In the sub
group of 46 patients with advanced disease, the six RSP showed lower T
AT than the 40 NRSP: 4.65 +/- 0.94 vs. 11.92 +/- 2.49 mu g/l (P < 0.01
); one of six (17%) RSP, but 21 of 40 (53%) NRSP showed TAT > 6 mu g/l
. These data suggest that in lung cancer the activation of coagulation
is an independent prognostic factor, since TAT levels were different
between RSP and NRSP, also within the homogeneously unfavourable metas
tatic subgroup. It should be further studied, whether TAT can identify
patients, whose prognosis could be improved by anticoagulation as an
adjunct to standard antineoplastic therapy.