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PURPOSE: To evaluate the routine clinical value of attenuation-corrected whole-body fluorodeoxyglucose positron emission tomography in colorectal cancer, a total of 59 patients who were referred for evaluation of suspected or proven colorectal cancers were studied. METHODS: Positron emission tomography scans were recorded using a Siemens ECAT Exact 921/47. RESULTS: Median follow-up after the positron emission tomography study was 11 (mean, 12.3; range, 1-21) months. According to computed tomography, coloscopy, and ultrasound, we recorded eight apparently false-positive results. During later follow-up, however, three of those cases, which were negative with computed tomography, magnetic resonance imaging, sonography, or laparoscopy, turned out to be true-positive instead. In 3 patients, a primary colorectal cancer was suspected; in 26 patients, a recurrence of colorectal cancer was suspected. Eight patients were studied for follow-up after the history of colorectal cancer with no suspicion of recurrence. In 12 patients, the rise of serum tumor marker concentrations was the reason for the positron emission tomography study; 12 patients with known metastatic disease were also included ("restaging"). With regard to the entire patient population, we found an overall sensitivity of 100 percent, a specificity of 67 percent, and positive and negative predictive values of 92 and 100 percent, respectively. Being merely confirmative with respect to tumor recurrence or distant metastases in the majority of patients, positron emission tomography revealed a primary tumor in one patient and confirmed metastatic foci in several patients that had not been delineated by other imaging modalities. CONCLUSION: A whole-body positron emission tomography scan provides optimum conditions to locate metastatic lesions that might not be seen otherwise. There is a trend showing that positron emission tomography diagnostics as a consequence of early increased tumor markers is a highly sensitive combination, because computed tomography and magnetic resonance imaging were not as sensitive in early recurrences. Positron emission tomography, as performed in daily clinical practice, proved to be a powerful diagnostic tool in our subset of colorectal cancer patients.

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Spontaneous splenic rupture as a complication of infectious mononucleosis was diagnosed in a 19-year-old woman. Sonographic and MRI investigations revealed subcapsular hematoma of the spleen without overt rupture. The patient was managed conservatively. Somatostatin treatment was initiated in order to reduce splanchnic blood flow. Further clinical course of the patient was favourable. Seven days after the diagnosis of splenic rupture the patient was discharged from hospital. Non-operative management should be considered in patients with subcapsular splenic rupture to avoid complications of splenectomy (e.g. post-splenectomy sepsis).

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In the present study the effect of metastatic liver disease on hepatic drug metabolism has been examined by studying the pharmacokinetics of antipyrine and the urinary excretion of antipyrine and its three major metabolites (4-hydroxyantipyrine, norantipyrine, and 3-hydroxymethylantipyrine) in 12 patients with extensive metastatic liver disease, and in 12 matched healthy controls. In the patients total liver volume, the volume of the liver parenchyma, and the volume of the liver metastases were determined by computed tomography. The volume of liver metastases always exceeded 35% of the total liver volume. There were no significant differences between the patients and controls in plasma half-life, plasma clearance, or apparent volume of distribution of antipyrine. The cumulative urinary excretion of antipyrine and its three major metabolites was significantly lower in patients [44 (18) %] than in controls [71 (8) %]. The excretion of antipyrine itself was unchanged and the decrease in cumulative excretion was due to reduced excretion of the three metabolites. The results show that the activity of the hepatic mixed function oxidases was not impaired even in patients with extensive metastatic liver disease. This may be because liver metastases do not cause a corresponding reduction in the volume of normal hepatic parenchyma. The decreased urinary excretion of the three major metabolites of antipyrine, which are mainly glucuronidated, may have been due to an alteration in the process of conjugation.

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The binding capacity of human serum albumin (HSA) for small acidic molecules is known to be reduced in chronic renal failure (CRF). The contribution of competitive inhibition by accumulated endogenous ligands and of structural changes in HSA has now been evaluated. In a fluorimetric in vitro assay using HSA and two dansylated amino acids the inhibitory properties of various endogenous ligands were determined in concentration-effect studies. The effect of carbamylation of HSA on binding was also examined. The mode of inhibition, including binding parameters n and Ka, was determined. Finally, HSA binding in sera from controls and dialysis patients was compared in a modified assay. Thirty three substances were tested and were placed in 3 groups: strong inhibitors (IC50 < 3*10(-5) mol.l-1, e.g. indolyl acids, furanoic acids), medium inhibitors (IC50 > 3*10(-5), eg. vanillic acid), and no inhibition (e.g. urea, creatinine, guanidino compounds). Complete (> 80%) carbamylation of HSA reduced binding by 67% in a non-competitive mode. There was a significant reduction in the binding capacity of HSA from the dialysis patients (approximately 24%), irrespective of medication. It is concluded that the uraemic binding defect of HSA is caused by competitive inhibition by the many physiological ligands accumulated in CRF and structural modifications of HSA. The assay presented proved useful for the rapid analysis of possible HSA binding inhibitors and for testing large groups of patients, e.g. comparison of dialysis treatments, and pharmacological binding studies.

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A 19-year-old patient intending to commit suicide gave himself an intravenous injection of about 14 g methyliodide. The patient was admitted to our hospital in a state of somnolence and agitation followed by a cerebral convulsion and severe hypotension. The serum concentration of methyl iodide was measured by mass spectroscopy. In addition to an antidote therapy with acetylcysteine, haemoperfusion was performed followed by a remarkable decrease of the methyliodide concentration. The patient survived this severe intoxication and was discharged from the hospital after a week.

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A 64-year-old man with high malignant B-cell lymphoma in both adrenal glands was investigated. Adrenal insufficiency was his predominant symptom at presentation. Despite surgical resection of the malignancy and cytostatic chemotherapy leptomeningeal involvement occurred and the patient died nine month after the diagnosis. Nine so far reported cases with primary adrenal lymphoma were reviewed. One of these also developed lymphomatous leptomeningitis. Suggestions of a pathogenetic contribution of adrenal lymphoma to leptomeningeal involvement and arising therapeutic consequences in the treatment of primary adrenal lymphoma are discussed.

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