Biomedical subjects

A Immel

Publications and source records attributed to A Immel.

5 recordsLinked to original sources

PubMed1997

Prognostic impact of an activation of coagulation in lung cancer.

BACKGROUND: There is evidence that activation of coagulation by influencing tumour biology may have impact on clinical course of lung cancer. PATIENTS AND METHODS: We measured the activation markers thrombin-antithrombin complex (TAT) and prothrombin fragment F1 + 2 in 99 lung cancer patients immediately after diagnosis, before antineoplastic treatment. Outcome was assessed at the end of appropriate standard primary therapy (four to six courses of chemotherapy, surgery or radiation). RESULTS AND CONCLUSIONS: The activation markers (means +/- SEM) were lower in the 33 responders (RSP; complete or partial remission) than in the 66 non-responders (NRSP): TAT 3.96 +/- 0.48 vs. 9.69 +/- 1.57 micrograms/l (P < 0.001), and F1 + 2 1.09 +/- 0.09 vs. 1.64 +/- 0.25 nmol/l (P < 0.05). TAT levels were > 6 micrograms/l in 30 of 66 (45%) NRSP, but only 4 of 33 (12%) RSP. 88% of patients with TAT < or = 6 micrograms/l achieved remission, and 45% with TAT > 6 micrograms/l (P = 0.0014). In the subgroup of 46 patients with advanced disease, the six RSP showed lower TAT than the 40 NRSP: 4.65 +/- 0.94 vs. 11.92 +/- 2.49 micrograms/l (P < 0.01); one of six (17%) RSP, but 21 of 40 (53%) NRSP showed TAT > 6 micrograms/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 metastatic 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.

Antithrombin III↗

PubMed1995

D-dimer tests detect both plasmin and neutrophil elastase derived split products.

Both plasmin and elastase, a protease released from neutrophil granulocytes, are known to degrade fibrin(ogen). This raises the possibility that elevated plasma levels of split products such as D-dimer may in part result from elastase action. After incubation in vitro of fibrinogen and fibrin clots with elastase, a clearcut increase of D-dimer immunoreactivity was demonstrated by two commercial ELISA kits. In the plasma of 79 patients with inflammatory bowel disease, D-dimer values measured by one of the ELISA kits were correlated significantly not only with markers of thrombin and plasmin activation, but also with elastase-alpha 1-antitrypsin complexes (r = 0.3555; P = 0.014). Thus, the findings of this study suggest that indeed the D-dimer levels in patients with inflammatory disorders are influenced by neutrophil elastase. New tests discriminating effects of activated haemostasis from proteolysis by neutrophil enzymes might be helpful in differential diagnosis and monitoring of therapy.

Enzyme-Linked Immunosorbent Assay↗

PubMed1994

Ulcerative colitis and Crohn's disease: factor XIII, inflammation and haemostasis.

An important role has been ascribed to plasma factor XIII (FXIII) in inflammation and wound healing. FXIII is necessary for fibrin stabilization and interacts with connective tissue and adhesive proteins and cells. In a prospective study, FXIII activity and parameters of coagulation, fibrinolysis and inflammation, were determined in patients with ulcerative colitis (UC; 13 active, 22 moderate) and Crohn's disease (CD; 36 active, 45 moderate). FXIII levels were lower in active than in moderate UC and CD, and were < 70% of normal values in 7/13 patients with active UC, and in 7/36 patients with active CD, although the median values did not fall below the normal range. FXIII was somewhat higher in active UC patients responding to therapy. The FXIII levels were widely scattered, and low values appear to be due to greatly enhanced turnover. A correlation between FXIII and the systemic levels of markers of activation of haemostasis and inflammation was lacking, but there was a correlation with the extent of bowel involvement. FXIII levels were lower in the patients with involvement beyond the sigmoid colon in CU (p = 0.0045), and both small and large bowel segments in CD (p = 0.0223) patients. This points to local consumption and/or loss of FXIII within the inflamed tissue, and provides an argument for FXIII substitution in the treatment of acute episodes of inflammatory bowel diseases.

Adolescent↗

PubMed1993

Activators of coagulation in cultured human lung-tumor cells.

Tumor matrix generation and tumor cell growth are supported by coagulation processes within the tumor tissue. Activators of coagulation were searched for in suspensions of 9 permanent human squamous-cell lung-cancer (EPLC 32MI, U1752), large-cell lung-cancer (LCLC 97TMI, LCLC 103H, U1810), and small-cell lung-cancer (N-592, H-526, DMS79, 86MI) cell lines. Incubation with these cells shortened the recalcification time in normal plasma (also in the presence of antibodies against tissue factor) or coagulation-factor-VII-, VIII-, IX- or X-deficient plasmas. The activators of coagulation in the 2 most active cell lines (U1752 and LCLC 103H) were further characterized in purified systems: the cleavage of chromogenic substrates, and the generation of markers of pro-thrombin activation were assessed. Three activators of coagulation were found in intact or sonicated cell suspensions and culture supernatants: (i) a tissue factor (TF)-like activity; (ii) an activity activating factor X, which in contrast to "cancer pro-coagulant" was not inhibited by iodoacetamide; and (iii) an activity-activating pro-thrombin, which was inhibited by the serine protease inhibitor PMSF and appeared to require plasmatic co-factor(s). The heterogeneous expression of coagulation activators by lung-tumor cell lines might be of significance for tumor biology and response to therapy.

Blood Coagulation↗

PubMed1993

Activation of coagulation and fibrinolysis in patients with lung cancer: relation to tumour stage and prognosis.

Activation of coagulation and fibrinolysis within tumour tissues is thought to be associated with tumour growth, angiogenesis, and metastasis. The plasma levels of markers of thrombin and plasmin generation are sensitive tools for monitoring activation of coagulation and fibrinolysis. We studied 47 patients with histologically confirmed lung cancer, 15 with small cell (SCLC) and 32 with non-small cell lung cancer (NSCLC). The plasma levels of the following markers were assessed:thrombin-antithrombin III complex (TAT), prothrombin activation fragment F1 + 2, plasmin-alpha 2-antiplasmin complex (PAP) and the split product from cross-linked fibrin, D-dimer. The first sample was obtained before receiving any specific antineoplastic treatment. The patients were followed thereafter until treatment was terminated. There was no difference in activation markers between patients with SCLC and NSCLC. Comparing patients with limited disease to those with extensive disease, there were significant differences in TAT (median 3.0 (1.9-9.8) vs 5.3 (1.8-35.6) micrograms/l,P = 0.021) and D-dimer (569 (135-1948) vs 1288 (120-2221) micrograms/l, P = 0.014). According to the response to subsequent treatment, those who achieved complete or partial tumour remission had significantly lower baseline levels samples than non-responders (TAT 2.9 (1.9-4.0) vs 4.7 (1.8-35.6) micrograms/l,P = 0.0047;D-dimer 527 (135-1149) vs 1242 (120-2221) micrograms/l, P = 0.0013). Thus, the increase of TAT and D-dimer appears to be related to tumour spread. The results suggest that high levels of these markers might be a sign of unfavourable prognosis in patients with lung cancer.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenocarcinoma↗