Background. Thirty previously untreated patients with metastatic colorectal carcinoma were randomized as part of two multicenter Phase III trials. Twenty‐two patients were randomized to receive either 5‐fluorouracil (5‐FU)/interferon alfa‐2A (IFN‐α) or 5‐FU/leucovorin (11 patients in each arm). Eight patients were randomized to receive 5‐FU/IFN‐α or 5‐FU alone (4 patients in each arm). Methods. Twenty‐three patients (13 patients treated with 5‐FU/IFN‐α and 10 patients treated with 5‐FU/leucovorin or 5‐FU alone) were evaluated regularly for response by computed tomography (CT) scans of the abdomen when treatment began and then every 6‐8 weeks. Results. Incidentally, four patients developed hepatic steatosis during treatment with IFN‐α and 5‐FU. The diagnosis was based on a decreased CT value of the liver parenchyma by repeated CT scans of the abdomen during treatment, and this diagnosis was verified histologically by liver biopsy. There was no relationship to cumulative IFN‐α or 5‐FU dose. Based on posttreatment CT scans, the liver parenchyma changes were reversible after therapy was stopped, and there were no significant clinical sequelae. No patients treated with 5‐FU/leucovorin or 5‐FU alone experienced a decreased CT value of the liver parenchyma. Conclusion. Hepatic steatosis was been observed in approximately 30% of patients treated with IFN‐α and 5‐FU. The hepatic changes were fully reversible after the treatment was stopped. Recognition of this condition is important to prevent a patient from being labeled as having progressive hepatic metastases.

SUMMARY Material from 100 consecutive operations on herniated discs has been investigated for amyloid. Various degrees of amyloid degeneration were found in disc tissue from 41 patients. Material from patients over 50 years old showed significantly more amyloid than that from younger patients; there was no sex difference. Eighteen patients had previously been operated on for herniated discs; seven of these (39%) had pyrophosphate deposits in their disc tissue, often in close topographical relation to amyloid. 26% of the patients had calcium phosphate deposits and 29% had slight inflammation-both without relation to amyloid. No pathogenetic correlation between amyloid degeneration and herniation of intervertebral disc tissue could be shown.Amyloid deposits in intervertebral discs were first described by Bywaters and Dorling in 1970' in a patient with myelomatosis and amyloid in several organs and joints. Amyloid in disc tissue has also been described in association with severe primary amyloidosis.2 More recently, amyloid has been described in tissue from surgically removed herniated intervertebral discs.3 4 One of us (CL) has just shown a very high incidence of amyloid degeneration of the vertebral column in a consecutive series of non-selected autopsies.The object of the present investigation has been to ascertain the occurrence of amyloid in tissue from 100 consecutive operations on herniated discs and to relate the findings to age, previous surgery on the vertebral column, and to other histopathological changes. Materials and methodsTissue from 100 consecutive operations on herniated discs performed at the neurosurgical department, Odense University Hospital were studied by light microscopy and electron microscopy.Immediately after operation all the removed tissue was fixed in 10% formalin for at least 24

The two-dimensional xenon-133 inhalation method was used to measure cortical blood flow in 16 patients with small subcortical ischemk infarcts and in 10 patients with larger cortical infarcts in the chronic phase of stroke. An abnormal hemispheric asymmetry of blood flow was seen, not only in patients with cortical infarcts, but also in those with subcortical infarcts. In the patients with subcortical infarcts, focal areas of reduced cortical blood flow were seen in the symptomatic hemisphere remote from the tissue destruction, usually including part of the noninfarcted frontoparietal cortex. The cortical dysfunction may have contributed to the clinical manifestations including aphasia, which was present in 14 of the 16 patients with subcortical lesions. (Stroke 1989;20:211-216)

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ABSTRACT. Højer‐Pedersen E, Petersen OF (Departments of Neurology and Radiology, Odense University Hospital, Odense, Denmark). Subcortical arteriosclerotic encephalopathy (Binswanger's disease). Presentation of two cases. Subcortical arteriosclerotic encephalopathy (SAE) (Binswanger's disease) was previously diagnosed almost exclusively at autopsy and considered to be very rare. Recent studies, however, indicate that an in vivo diagnosis might be made by means of computed tomography (CT) or nuclear magnetic resonance, resulting in a much more frequent recognition of this chronic encephalopathy of middle‐aged, hypertensive patients. Two cases are presented, in which the clinical and CT findings made a diagnosis of SAE very probable.