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Two patients are described with metastatic neuroendocrine tumours of the pancreas head and region of Vater. After surgery, administration of the long-acting somatostatin analogue octreotide was started. In the first patient we found an IgG-lambda paraproteinaemia and a parathyroid hormone-related protein (PTHrP) driven hypercalcaemia. By increasing the dose of octreotide the paraproteinaemia disappeared. In the second patient with a metastasized somatostatin producing neuroendocrine tumour, octreotide showed a long-term stabilizing effect on symptoms and progression of disease. The role of octreotide in the induction of changes in biological behaviour of malignant neuroendocrine cells is discussed.

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The fee-for-service system is a growing problem for insurers and governments. The main reason for this is the open-ended character of this system which makes cost-control a very difficult task. The pressures on the fee-for-service system are becoming more pronounced, especially in countries such as Canada, Germany and the Netherlands which use budget restrictions on national health care expenditure (macro caps). In these countries policy makers are searching for an alternative payment system and an appropriate definition of a corresponding status for doctors. The alternative, however, does not have to lead automatically to a salaried status of doctors in the hospital organization. The Dutch experience of the change of the payment system for medical specialists illustrates the transition to a new 'negotiated order'. The introduction of the 'lump sum' and the sub-contractor relationship with the insurance companies leaves the organizational autonomy of medical specialists intact. In exchange the medical specialists cooperate with the insurers in trying to control the costs of health care. In this process of strategic change, two factors are very significant, i.e. the new leadership of the local medical specialists and the governmental 'circumvention' of the powerful associations of doctors and insurers.

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BACKGROUND: The efficacy of mesalazine enemas depends on intraluminal concentration of the drug and is therefore limited by the enema distribution in the colon. Active ulcerative colitis changes colon motility and this leads to uncertainty about enema spread. AIM: To assess the influence of disease activity on enema distribution, we conducted a physician-blinded, longitudinal study of the retrograde spread of three mesalazine enemas. METHODS: Thirty-one patients with mild to moderate ulcerative colitis were subdivided into three groups, and treated with 2 g mesalazine in 30 mL (group I, n = 10), 4 g mesalazine in 60 mL (group II, n = 12) or 1 g mesalazine in 100 mL (group III, n = 9). All patients received oral mesalazine 500 mg t.d.s. Enemas were labelled by adding 10 MBq (99mTc)technetium-sulphur colloid. Anterior scintigraphic images were taken at the start of the study and after 12 weeks of therapy; retrograde spread was assessed by calculating the percentage of the enema in each colonic segment. RESULTS: The activity score of ulcerative colitis diminished significantly after 12 weeks of treatment, but five patients dropped out of the study. At the start of treatment enema activity in group I was mainly concentrated in the sigmoid (99%); in group II activity was found in the rectum (9%), the sigmoid (61%) and the descending colon (15%); in group III activity was distributed between the sigmoid (66%) and descending colon (25%). The colonic distribution of mesalazine enemas was not influenced by disease activity. CONCLUSION: Volume, but not disease activity, is the important determinant of retrograde colonic spread of mesalazine enemas in ulcerative colitis.

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Two patients with eosinophilic gastroenteritis are described. The predominant eosinophilic infiltration of the mucosal layer of the upper gastrointestinal tract resulted in severe protein-losing enteropathy and peripheral eosinophilia in one patient and a malabsorption syndrome due to saccharose and lactose intolerance in another patient. There was a wide range of abdominal symptoms, depending on the site and extent of the disease. The diagnosis was based upon typical biopsy findings. There was a marked lack of any biochemical abnormality. The course of the disease was chronic and relapsing. Symptoms were not controlled with corticosteroids alone; only after the addition of disodium chromoglycate per os was prolonged disease control achieved.

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Ferritin-like particles were observed in bile canaliculi of patients with iron overload. These particles have been further investigated by: a staining method enhancing the size and contrast of ferritin protein, and electron probe microanalysis detecting the presence of the elements iron and phosphorus. Morphological observation of coated vesicles in the cytoplasm adjacent to the bile canaliculi and coated pits in the canalicular membrane suggests a transport mechanism via membrane-bound organelles. Support is given to the theory that part of the iron, stored in the liver, leaves the hepatocyte by excretion of ferritin into the bile.

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Depot iron, ferritin iron, and ferritin protein were measured in 34 liver needle biopsy specimens obtained from patients with primary and secondary iron-loading diseases. The patients were classified as idiopathic hemochromatosis (14), porphyria cutanea tarda (4), and iron-loading anemias (16). With accumulation of depot iron, the amount of liver ferritin protein increased, however, the ratio of ferritin protein to depot iron fell at concentrations of depot iron in excess of 1,000 micrograms per gm of liver. The liver ferritin protein concentration was not influenced by the specific kind of the iron storage disorder. The mean iron content of ferritin molecules increased about 50% in profound iron overload. In low grade iron overload, the bulk of depot iron was present as ferritin; however, in subjects with heavy iron overload, depot iron consisted of approximately equal amounts of hemosiderin (nonferritin iron) and ferritin iron.

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