SummaryIn a prospective multicenter trial, 149 consecutive patients with phlebographically proven proximal and/or distal deep vein thrombosis of the leg were randomly allocated to receive subcutaneously for 10 days either low molecular weight heparin CY 216 (Fraxiparine) in a fixed dose or unfractionated heparin (UFH) in doses adjusted according to the activated partial thromboplastin time. Pre- and post-treatment phlebograms were assessed blindly using the Arnesen’s score system in 134 patients available for analysis of the treatment efficacy. The mean phlebographic score after 10 days of treatment was significantly decreased in both groups (p <0.001) in comparison with the baseline score but the difference in score changes between the two groups was not statistically significant. There was an improvement in 45/ 68 patients (66%) in the Fraxiparine group and in 32/66 patients (48%) in the UFH group, and an increase in the thrombus size in 10/68 (15%) and 12/66 (18%), respectively. One symptomatic non-fatal pulmonary embolism and one major bleeding episode were observed in the UFH group. During a follow-up period of 3 months, two rethromboses had occurred in the UFH group and none in the Fraxiparine group. It is concluded that subcutaneous fixed dose Fraxiparine is safe and at least as effective as subcutaneous adjusted UFH in the treatment of deep vein thrombosis.

Human chorionic gonadotropin (HCG)-like immunoreactivity has been found in many non-trophoblastic tumours, but the biological behaviour of HCG-producing cells has not been clarified yet. The aim of the study was to estimate the frequency of serum HCG beta subunit (s beta HCG) elevation in patients with small-cell lung cancer (SCLC) and to assess its possible prognostic role in this type of tumour. An attempt was also made to reclassify the histology in selected cases to see whether the elevated (s beta HCG) level is connected with any special subtype of small-cell lung cancer. A total of 156 SCLC patients entered the study: 93 men, 63 women, median age 58 years. s beta HCG activity was measured by immunoenzyme assay (Abbott EIA beta HCG 15-15) before treatment. s beta HCG elevation (above 5 mIU/ml) was found in 21 of 156 patients (14%). Response to treatment after chemotherapy (complete and partial response) was obtained in only 48% of those patients in whom elevated s beta HCG was found, in comparison to the 73% response rate observed in the remaining patients. Only 5% of patients with elevated s beta HCG survived 2 years, in comparison to 21% surviving for 2 years among the remaining patients. The prognostic significance of elevated s beta HCG and extent of disease were independent of each other (Cox's proportional-hazard model). Thus s beta HCG elevation in SCLC seems to be a marker of more resistant tumours and of poor prognosis. We have not found any connection between the subtype of small-cell lung cancer and elevated s beta HCG. Elevated s beta HCG was found in 2 out of 11 patients with oat-cell carcinoma, in 3 out of 10 patients with an intermediate cell type and in 5 out of 13 patients with small-cell lung cancer in which the assessment of the subtype was not possible.

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This study was designed to assess the value of tumor marker evaluation in pericardial fluid for the recognition of malignant pericarditis. Thirty-six patients with signs and symptoms of large pericardial effusion entered the study. Pericardiocentesis with pericardial fluid drainage was performed in all of them. CEA and NSE levels were evaluated in the pericardial fluid and compared to pericardial fluid cytology. The median CEA value in malignant effusions was 80 ng/ml (range 0-305 ng/ml) and in non-malignant ones 1.26 ng/ml (range 0.2-18.4 ng/ml), p < 0.01. The sensitivity of CEA elevation above 5 ng/ml for the recognition of malignant pericarditis was 73% and the specificity was 90%. Pericardial fluid cytology was positive in 22 of 26 patients with malignant pericarditis (85%). CEA exceeding 5 ng/ml or positive cytology were seen in 96% of the patients with malignant pericarditis. The median NSE value in malignant pericardial effusions was 41.8 micrograms/l (range 2-172 micrograms/l) and in non-malignant ones 5.85 micrograms/l (range 1-83.9 micrograms/l), p < 0.3. For the differential diagnosis of large pericardial effusions we would recommend simultaneous cytologic examination of pericardial fluid and CEA assessment. NSE measurement in hemorrhagic pericardial fluid is of limited value.

Neuron-specific enolase (NSE) is a glycolytic enzyme localized within neuronal and neuroendocrine tissues. Serum NSE is widely used as a marker of neuroendocrine tumors. Moderate serum NSE elevation has been reported in some patients with benign lung diseases. We decided to investigate whether the elevation of serum NSE in non-neoplastic lung diseases is connected with hypoxemia and to what extent the recovery of sufficient ventilation with a respirator may influence NSE concentrations. Serum NSE was estimated by means of radioimmunoassay in 83 patients with various non-neoplastic lung diseases. Serum NSE exceeding 12.5 micrograms/L was significantly more frequent in patients with marked hypoxemia (PaO2 < 6.67 kPa; p = 0.03) than in others. The median NSE value in the group of patients without respiratory failure (Ro) was 7.2 micrograms/L (10% > 12.5 micrograms/L), in the group of patients with respiratory failure not requiring mechanical ventilation (Rf) it was 8.5 micrograms/L (24% > 12.5 micrograms/L), and in the group of patients with respiratory failure requiring mechanical ventilation (Rfv) 13.1 micrograms/L (60% > 12.5 micrograms/L). The differences between the Rfv group and the other two groups (Rf and Ro) were significant (P = 0.049 and p = 0.0004, respectively). During successful mechanical ventilation elevated serum NSE decreased to values below the cutoff in 8/10 patients. We conclude that serum NSE elevation is a frequent event in patients with terminal hypoxemia in the course of benign lung diseases. Normalization of serum NSE is observed in the majority of patients during the first week of mechanical ventilation.