A 34-year-old man was found to have granulocytopenia with a white blood count of 2.3 x 10(9) l-1, consisting of 10% segmented neutrophils, 50% monocytes and 40% lymphocytes. A bone marrow aspirate showed 20% promyelocytes and 10% blasts with monoblastic features, and a smouldering myelomonocytic leukaemia was considered to be a possible diagnosis. In cold weather the patient experienced cold intolerance with acrocyanosis and small ulcerations on the ears. The test for heparin-precipitable protein ('cryofibrinogen') was strongly positive. During the following year, these signs and symptoms persisted, and the patient also developed constant moderate pain in the epigastric region. Gastroscopy revealed a large lymphoma of the stomach, which was a high-grade malignant centroblastic type of non-Hodgkin's lymphoma. After successful removal of the tumour, and six courses of potent cytostatic combinations, the patient recovered completely, and the granulocytopenia and cold intolerance disappeared.

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The stomachs of 8 healthy volunteers were intubated with a Levine tube under radiological control. In addition, a thin polyethylene tube was placed in the proximal duodenum. After a 1-hour period with no perfusion, the duodenum was perfused for two hours with 15% liver extract (LE) (pH 4.5--5.5; 1027 mosm/kg water) at a rate of 100 ml/hour either alone or in combination with intravenous infusion of different doses of exogenous pentagastrin. All subjects were also tested with the tubes in place for 3 hours, but with no perfusion or pentagastrin. Reflux to the stomach was monitored by addition of radioactive B12 to the perfusates. Plasma gastrin, gastric acid, and pepsin were measured in 15-minute periods. During perfusion of the proximal duodenum, where reflux of the perfusates was less than 4%, only a slight and inconstant change in plasma gastrin was seen. Gastric acid and pepsin outputs were increased to approx. 18% and 25% of the maximal pentagastrin stimulation respectively. Whereas 15% LE was shown to release gastrin by antral perfusion however, such release was not found by duodenal perfusion, except where reflux to the antrum was seen. The results suggest that intestinal stimulation of gastric secretion exists, but has not been found to be gastrin dependent in the present investigation.

The effect of beta-adrenergic blockade on the insulin hypoglycemia-induced gastric secretion was studied. Insulin-stimulated (0.15 IU/kg) gastric acid and pepsin output and serum gastrin were measured before and after beta-adrenergic blockade with propranolol (20 microgram/kg/min intravenous infusion) in gastric fistula and Heidenhain pouch dogs. Insulin injection caused acid and pepsin secretion from the gastric fistula, and both acid and pepsin secretion was significantly increased during beta-adrenergic blockade. Significant gastrin release was observed after insulin stimulation. However, the insulin-induced gastrin release was unaltered by intravenous infusion of propranolol. The Heidenhain pouch did not show any secretion in these experiments. It is concluded that beta-adrenergic blockade augments the hypoglycemia-induced gastric secretion in dogs. Furthermore, it seems that this effect is not dependent on vagally released gastrin.

Administration of 6-hydroxydopamine (6-OHDA) causes selective acute degeneration of the adrenergic nerve terminals--that is, a reversible chemical sympathectomy. The effect of this drug was studied on the insulin-stimulated gastric secretion. Insulin-stimulated (0.15-0.4 IU/kg) gastric acid and pepsin output and serum gastrin were measured before and after 6-OHDA treatment (40 mg/kg) in gastric fistula dogs. Chemical sympathectomy resulted in a highly significant increase in acid and pepsin secretion. However, the hypoglycemic gastrin release was unaltered except the peak response, which showed a significant reduction. These data confirm earlier observations that the sympathetic innervation of the stomach has an inhibitory effect on gastric secretion in the dog. Furthermore it seems that the adrenergic fibers in the vagus nerve might have some modulating effect on the insulin-induced gastrin release.