Regulation of gastric function by gastrin releasing peptide.

LETTERS Hypomagnesaemia due to malabsorption is not always responsive to oral magnesium oxide supplementation alone We read with interest the Gut File report by Dr Ross and colleagues of hypomagnesaemia due to malabsorption, eventually responding to oral magnesium oxide supplementation (Gut 2001;48:857–8). Our experience however has been different. For the past seven years we have managed a 65 year old woman with short bowel syndrome (right hemicolectomy for Duke's C colorectal carcinoma and thereafter a terminal ileal resection for abscess formation). High ileostomy output was initially difficult to manage (after excluding infection, secreting gut hormone tumours by normal hormone levels, and despite dietary and pharmacological modifications). Clinical signs of hypomagnesaemia and hypocalcaemia ensued. An initial trial with magnesium glycero-phosphate (September 1992 to December 1993) was insufficient to sustain her serum magnesium levels requiring frequent " top ups " of intravenous magnesium. 1 In Decem-ber 1993, she was switched to magnesium oxide supplementation but despite this the frequency of intravenous magnesium " top ups " were not reduced. Compliance was not deemed to be an issue with our patient. Since then we have managed this woman while still taking magnesium oxide supplements with almost 3–6 monthly (fig 1) intravenous magnesium replacement through a peripheral line and have avoided insertion of a Hickman line and all its associated complications. 2 While we agree that a trial of magnesium oxide is prudent and until the pharmacokinetics are better understood, this preparation may not be sufficient, especially in patients with extensive resection of the small bowel, as demonstrated in our patient. al. Infectious complications among patients receiving home intravenous therapy with peripheral, central or peripherally placed central venous catheters. Hildebrand et al reported data suggesting that gastrin releasing peptide (GRP) may be a physiological regulator of pre-and postpran-dial gastric acid secretion (Gut 2001;49:23–8). Interestingly, these effects were independent of gastrin and the authors appropriately questioned the physiological role of gastrin in regulating gastric secretion. Several aspects of the authors' conclusions deserve further clarification and discussion. The authors concluded that alteration of somatostatin secretion is unlikely to explain the acid inhibitory action of BIM26226 because the GRP antagonist did not alter somatostatin mRNA levels. They also argued that the lack of change of gastrin mRNA supported the physiological data showing no alteration in gastrin secretion with BIM26226. In short term experiments such as these, it is incorrect to assume mRNA levels reflect peptide secretion rates. …