1 A prospective multicentre study of all acute poisonings among adults admitted to hospital (n = 1145) or dying outside hospital (n = 67) in Oslo was performed during 1980. 2 Of the 1212 episodes, 98.3% were self-poisonings, giving an annual incidence of 2.8 per 1000 inhabitants (%o), 3.1‰ in males and 2.6‰ in females. 3 The main toxic agents among the self-poisoned patients were ethanol (19.7%), benzodiazepines (17.8%), opiates (14.9%), neuroleptics (10.4%) and antidepressants (9.3%). In 58.9% of the episodes more than one toxic agent was taken. 4 Abuse among the self-poisoned patients was significantly ( p < 0.005) more common among males than females (64.2 v. 34.5%). 5 The rate of suicide attempts was significantly ( p < 0.005) higher among females than males (20.2 v. 12.9%), females showing increasing rate with age. However, when excluding abusers the rate of suicide attempts was similar in both sexes (27.6 v. 25.0%). 6 Compared to a reference population self-poisonings were most common in the lower middle and the lowest social classes. Patients in these social classes, however, showed a lower rate of suicide attempts than those in the two highest social classes. 7 Overall mortality was 6.0% ( n = 73), but 91.8% of all deaths occurred outside hospital indicating the importance of including these figures when self-poisonings are studied.

Free protein S, protein C, and C4b-binding protein (C4b-BP) were measured in randomly selected outpatients: 22 with Crohn's disease (CD) and 16 with ulcerative colitis (UC). Active disease was recorded in 10 patients with CD and 4 with UC. Fourteen patients (63.6%) with CD and 4 (25%) with UC had free protein S values below the normal range, with mean values of 62% and 78% of that found in healthy control subjects (p < 0.01). The C4b-BP level was 127% in patients with CD as compared with 89% in both healthy subjects and UC patients (p < 0.01). The protein C levels were similar in the three groups. The present results add to the factors already known favouring thromboembolic complications in inflammatory bowel disease and which might play a major role both for the pathogenesis and for the increased tendency to venous thromboembolism in these diseases.

Background. To elucidate the disturbed hemostatic balance in patients with pancreatic cancer, the levels of plasma coagulation inhibition and coagulation activation were determined. Methods. Twenty‐one patients with adenocarcinoma of the pancreas were followed from time of diagnosis until death, using plasma analyses of coagulation inhibitors and a molecular marker of coagulation activation (thrombin‐antithrombin complex, TAT). Results. TAT was increased significantly at the time of diagnosis of pancreatic cancer compared with age‐adjusted healthy control subjects (mean, 6.2 ± 4.6 μg/1 [standard deviation] versus 2.0 ± 0.7 μg/l). It increased with disease progression (mean in the terminal phase, 14.1 μg/l; P < 0.05). Plasma levels of tissue factor pathway inhibitor (TFPI) also were increased significantly at the time of diagnosis compared with the control group (mean, 176 ± 80% versus 127 ± 29%; P < 0.05). The TFPI decreased to normal levels (121 ± 40%) after surgical removal of the pancreatic tumor (n = 4) or relief of the cholestasis using a bypass procedure (n = 6). The TFPI levels increased significantly as the malignant disease progressed (from 1‐3 months postoperatively to the terminal phase of disease; mean, 114 ± 52% versus 154 ± 60%). There was a significant positive correlation between TFPI levels and bilirubin levels; the correlation coefficient at diagnosis was 0.70 (P < 0.001). The levels of the coagulation inhibitors antithrombin, heparin cofactor II, protein C, and free protein S decreased significantly with disease progression compared with the normal values found at diagnosis. Conclusions. The mechanism for TFPI increase in cancer is not known. It may be related to the preoperative cholestasis seen in this study, but the increased degree of coagulation activation also may contribute.

Multifocal intestinal infarctions, due to thrombosis in small vessels, might be a pathogenetic mechanism for Crohn's disease (CD). Deficiency of free protein S may contribute to the development of such thrombotic occlusions. In the present study free protein S was measured in 54 patients with CD. In 31 patients (57.4%) the plasma concentrations of free protein S were below the lower normal range. The mean value of free protein S in CD patients was 72.2%, as compared with 97.5% in healthy subjects (p < 0.01). The concentrations of C4b-binding protein and protein C were similar in the two groups. Free protein S levels were not correlated to disease activity, previous surgery or complications, extraintestinal manifestations, or current medical therapy. The impairment of the protein S/protein C/thrombomodulin system found in patients with CD favours coagulation and might be of importance for both the development of CD and its thromboembolic complications.

Abstract. Intravascular injection of purified 70‐kDa protease or GCAT‐LPS from Aeromonas salmonicida, or both, invariably led to consumptive coagulopathy within 2h in Atlantic salmon, Salmo salar L. By entering the coagulation cascade at two different levels, the two enzymes work in concert in thrombus formation, the significance being that circulatory failure is probably the major cause of death in acute furunculosis. Only intravascular injection of GCAT‐LPS led to consumptive coagulopathy in rainbow trout, Oncorhynchus mykiss (Walbaum), despite the fact that trout received only half the GCAT dose, and/or four times the protease activity administered to salmon. These results indicate that salmon is, by far, the most susceptible to protease and suggest that rainbow trout is the most susceptible to GCAT‐LPS. The substrate profile of the purified protease gave supporting evidence that it works as activated coagulation factor X. The protease is inhibited in vitro by antithrombin and by α2‐macroglobulin and both inhibitors are consumed in vivo in response to intravascular administration of the enzymes, thus showing a potential for AT and α2M to inhibit the protease also in vivo. Provided such plasma antiprotease activities are correlated with resistance to the disease, and the inhibitors show genetic variation they would be promising candidates for indirect selection and hence a means to prevent furunculosis independently of vaccines. Circulating inhibitors of GCAT‐LPS remain to be identified.