l‐Asparaginase treatment during induction therapy in acute lymphoblastic leukaemia (ALL) is known to be frequently complicated by thromboembolic events. It was recently suggested that l‐asparaginase derived from Erwinia chrysanthemi alters the coagulation system less severely than does Escherichia coli asparaginase. In a series of 11 adult patients with ALL, we investigated some parameters of the coagulation system during treatment with Erwinia asparaginase. The doses employed were rather high; all patients below the age of 60 years received 15000 U/m2 daily over 14 days. In accordance with what is known from treatment with E. coli asparaginase, we observed significant lowering of antithrombin as well as of fibrinogen. However, as to fibrinogen indeed a significant decrease had occurred prior to the institution of Erwinia asparaginase treatment. The most striking observation in the present study was that the levels of prothrombin complex, reflecting the function of K‐vitamin dependent coagulation factors II, VII and X, remained within normal ranges during treatment. This indicates that these coagulation factors were not affected by Erwinia asparaginase, an observation at variance with several reports where E. coli asparaginase was investigated. This latter observation was the only finding which could lend support to the view that Erwinia asparaginase affects the coagulation system less than E. coli asparaginase. Finally, one of our patients developed a sinus thrombosis, a severe thrombotic complication.

Background. Hairy cell leukemia (HCL) has been associated with several disease states. In this study, a possible association is reported between HCL and renal cell carcinoma (RCC) and colorectal carcinoma (CRC). Methods. A retrospective study of the case records of 50 patients with HCL in a study of α‐interferon (α‐IFN) treatment of HCL. Results. Three of 50 patients with HCL studied had RCC, and 2 of these also had CRC. In addition, two other patients had CRC. The other malignant lesions developed either before or after the diagnosis of HCL. In all patients, the HCL responded to α‐interferon (α‐IFN), but in four patients, the second lesion was diagnosed during IFN treatment. Conclusions. These findings could indicate that IFN does not correct a possible common basic etiologic defect and shows that even early CRC and RCC do not respond to the IFN doses administered. These findings should be considered in future trials of IFN treatment of these diseases. The authors also recommend a reevaluation of the frequency of second malignant lesions in HCL; this may be important particularly with the increased survival in patients with HCL who receive a‐IFN treatment.

Mucosal lesions were produced in feline small intestine by evoking a simulated intestinal shock (local hypotension at 30 mm Hg and stimulation of regional sympathetic vasoconstrictor nerves at 6 Hz for 2 h). The degree of mucosal damage was correlated to the level of intestinal blood flow. Microscopically characteristic lesions developed regularly in the small intestinal mucosa when intestinal blood flow was reduced below 12 ml/min × 100 g during the regional shock. The mucosal damage was graded histologically. No difference was found between untreated controls and cats in which the intestinal lumen was perfused with nitrogenated saline. Perfusion with oxygenated saline and i.v. injections of methylprednisolone on the other hand, prevented almost completely the development of the lesions. Albumin, activated charcoal and aprotinin instilled into the intestinal lumen reduced to some extent the mucosal damage. The obtained data support the view that hypoxia is the key factor in the pathogenesis of the mucosal lesions. However, epithelial and intraluminal enzymes are probably important contributing factors.

The relationship between the mucosal lesions in the gut, observed after a 2-hour period of regional hypotension, and the blood pressure fall seen after the hypotensive period was investigated in cats. Untreated controls were compared to animals treated with intraluminal perfusion with nitrogenated or oxygenated saline or treated with intraluminal instillation of albumin, activated charcoal or aprotinin or i.v. injections of methylprednisolone. Untreated controls and cats perfused with nitrogenated saline exhibited a pronounced reduction in arterial blood pressure during the first posthypotensive hour. In the animals treated with methylprednisolone or perfused intraluminally with oxygenated saline only a small fall of blood pressure was observed. In the remaining groups of animals a moderate blood pressure reduction was noted. These results suggest a causal relationship between the intestinal mucosal damage and the posthypotensive cardiovascular derangement possibly via the release of cardiotoxic material from the hypoxic intestinal villi.

Patients with relapsed aggressive lymphoma after high dose chemotherapy have a very poor prognosis and long-term survival is rare. Most patients are not eligible for allogeneic stem cell transplantation in this setting and treatment, therefore, becomes palliative. A few studies have shown that trofosfamide, an oral alkylating agent, may be effective as palliative treatment in non-Hodgkin's lymphoma. Trofosfamide therapy is considered rather non-toxic with an overall response rate from 50 to 80%. Most responses are, however, partial and their duration is short. We report a patient with a very aggressive ALK + anaplastic large cell lymphoma (ALCL), relapsing shortly after high dose chemotherapy. Unrelated allogeneic transplantation was hot possible. After several radio/chemotherapy regimens trofosfamide was started as palliative treatment. This therapy resulted in a complete remission, still ongoing, 27 months after termination of intravenous cytotoxic therapy and 16 months after withdrawal of trofosfamide. Thus, in this particular case, trofosfamide turned out to be an unexpectedly effective salvage therapy for an otherwise very aggressive relapsing ALCL.