The SIPAP classification together with tumour size is an optimal method for the registration of pituitary adenomas.

This report describes a multiple sclerosis (MS)-like disorder in a male patient with Leber's hereditary optic neuropathy (LHON) harbouring the mitochondrial DNA 11778 base pair mutation. Given the population frequencies of MS and LHON, coincidental occurrence is unlikely. Hypothetically the mitochondrial mutation underlying LHON may contribute to presumably immunologically mediated involvement of other myelinated axons in the central nervous system in susceptible individuals, producing a disorder indistinguishable from MS. We recommend that investigation for oligoclonal bands in CSF, evoked potentials and MR brain scan in these patients be supplemented with mitochondrial DNA analysis.

The secretory capacity, in vivo, of clinically non-functioning pituitary adenomas may possibly predict tumour volume reduction during intensive medical therapy. Ten patients (mean (range) 53 years (26-73)) with clinically non-functioning macroadenomas, > or = 10 mm were studied. The secretory capacity of the adenomas was examined using basal, NaCl and TRH-stimulated LH, FSH and alpha-subunit levels. The effect on tumour volume of 6 months' therapy with the combination of a somatostatin analogue, octreotide 200 microg x 3/day and a dopamine-D2-agonist, cabergoline 0.5 mg x 1/day was studied. The basal LH, FSH and alpha-subunit levels were determined before and during 6 months' therapy with octreotide and cabergoline, and MR scans were used to evaluate tumour volume before and during this period of therapy. Octopus-perimetry was used to examine the visual fields. A reduction in tumour volume (mean +/- SEM (range); 30% +/- 4% (18-46%)) during 6 months of combination therapy with octreotide and cabergoline was recorded only in patients with in vivo secretory potential. Tumour volume was not reduced in four patients: in three of these patients it remained unchanged while in one patient it was observed to have increased (by 14%). Of the six patients with pretherapy secretory capacity, one displayed a very high basal level of alpha-subunit (74 microg/l) despite unmeasurable levels of LH and TSH, and an FSH-level of 1 IU/l. The other five patients presented paradoxical LH, FSH and/or alpha-subunit responses to TRH. A reduction in basal levels of LH, FSH and/or alpha-subunit was observed in all six patients, and the maximum reduction of at least one of the hormonal levels was 66% +/- 7% (50-98%). The basal levels of LH, FSH and alpha-subunit in the 10 patients were (mean +/- SEM (range)), 3.0 IU/l +/- 1.0 (0.0-7.4), 12.7 IU/l +/- 5.0 (0.0-39.0) and 9.0 IU/l +/- 7.0 (0.2-74.0). During six months of therapy with octreotide and cabergoline, the basal levels of LH, FSH and alpha-subunit were reduced by > or = 50% in seven patients - including the six patients with in vivo secretion prior to therapy. No new visual field defects were detected during therapy and no deterioration of existing visual field defects was recorded. The medical therapy was well tolerated. The in vivo basal and TRH-stimulated secretory capacity of LH, FSH and alpha-subunit predicted tumour reduction following intensive medical therapy in all of our patients with non-functioning pituitary adenomas.

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.

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