We have reviewed 30 reports of Merkel cell tumour and described a further five cases in order to establish a database and from this more clearly define the biology of this tumour, prognostic factors that govern outcome, and optimal management. After excision alone of the primary lesion, local recurrence occurred in 39 per cent of patients and regional failure occurred in 46 per cent. In contrast, in patients treated by excision plus prophylactic treatment (adjuvant node dissection and/or adjuvant radiation), local recurrence occurred in 26 per cent and regional failure in 22 per cent. Locoregional recurrence carried an ominous significance with 67 per cent of patients subsequently dying of the disease. For patients who either presented with regional disease or later developed regional disease, the best outcome (44 per cent survival with mean follow-up of 40 months) was obtained following treatment by therapeutic node dissection with or without radiation. In contrast, treatment of regional disease with radiation alone was associated with only a 20 per cent survival rate. Unfavourable prognostic factors included young age, lesions sited in the head and neck or trunk, male sex, and the presence of locoregional failure and/or systemic disease. We conclude that Merkel cell tumours behave in a similar manner to the aggressive variants of melanoma and that minimal treatment consists of wide surgical resection of the primary lesion (with a margin of 2.5-3 cm) coupled with resection and probably also radiation of regional disease if present. In addition, consideration should be given to prophylactic node dissection in node negative patients, especially in those patients with unfavourable prognostic factors.
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This experiment was performed to determine if plasma glucose homeostasis is maintained in normal human volunteers during light exercise (40% maximal oxygen consumption [VO2 Max]) when changes in insulin and glucagon are prevented. Hormonal control was achieved by the infusion of somatostatin, insulin, and glucagon. Glucose kinetics and oxidation rates were determined with stable isotopic tracers of glucose, and by indirect calorimetry. Two different rates of replacement of insulin and glucagon were used; in one group, insulin was clamped at 19.8±2.6 AU/ml (high-insulin group), and in the other group insulin was clamped at 9.2±1.3 jzU/ml (low-insulin group). Glucagon was maintained at 261±16.2 and 124±6.4 pg/ml, respectively, in the high-insulin and low-insulin groups.Without hormonal control, plasma glucose homeostasis was maintained during exercise because the increase in glucose uptake was balanced by a corresponding increase in glucose production. When changes in insulin and glucagon were prevented, plasma glucose concentration fell, particularly in the high-insulin group. Glucose uptake increased to a greater extent than when hormones were not controlled, and glucose production did not increase sufficiently to compensate. The increase in glucose uptake in the hormonal control groups was associated with an increased rate of glucose oxidation. When euglycemia was maintained by glucose infusion in the hormonal control subjects, the modest increase in glucose production that otherwise occurred was prevented.
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