Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report on a 35-week gestation infant who developed severe hyponatremia and thrombocytopenia after continuous infusion of glucagon for the treatment of intractable hypoglycemia. Given these serious side effects,glucagon infusion should be avoided in the treatment of premature infants.hypoglycemia, glucose, small for gestational age. Hypoglycemia is commonly seen in premature infants, and the provision of a standard glucose intake is often not sufficient to maintain euglycemia. For these infants, an increase in glucose infusion to provide 4 to 8 mg/kg/min is initially recommended.1 Should this approach fail, pharmacologic agents such as corticosteroids or diazoxide are indicated.1 When the serum glucose in premature or small for gestational age infants cannot be adequately maintained, a glucagon infusion is now suggested as the best treatment approach.2,3 We report the use of glucagon infusion for the treatment of severe hypoglycemia in a premature infant. A severe hyponatremia associated with transient convulsions and thrombocytopenia was observed in the neonate after treatment. Discontinuation of the glucagon infusion resulted in prompt resolution of these abnormalities.
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PMID:Continuous infusion of glucagon induces severe hyponatremia and thrombocytopenia in a premature neonate. 1250 83

The pituitary adenylate cyclase-activating polypeptide (PACAP) is a neuropeptide of the vasoactive intestinal peptide/secretin/glucagon superfamily. Studies in two related patients with a partial trisomy 18p revealed three copies of the PACAP gene and elevated PACAP concentrations in plasma. The patients suffer from severe mental retardation and have a bleeding tendency with mild thrombocytopenia, and their fibroblasts show increased PACAP mRNA levels. The PACAP receptor (vasoactive intestinal peptide/pituitary adenylate cyclase-activating peptide receptor 1 [VPAC1]) in platelets and fibroblasts is coupled to adenylyl cyclase activation. Accordingly, we found increased basal cAMP levels in patients' platelets and fibroblasts, providing a basis for the reduced platelet aggregation in these patients. Megakaryocyte-specific transgenic overexpression of PACAP in mice correspondingly increased PACAP release from platelets, reduced platelet activation, and prolonged the tail bleeding time. In contrast, the PACAP antagonist PACAP(6-38) or a monoclonal PACAP antibody enhanced the collagen-induced aggregation of normal human platelets, and in PACAP knockout mice, an increased platelet sensitivity toward collagen was found. Thus, we found that PACAP modulates platelet function and demonstrated what we believe to be the first hemostatic defect associated with PACAP overexpression; our study suggests the therapeutic potential to manage arterial thrombosis or bleeding by administration of PACAP mimetics or inhibitors, respectively.
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PMID:The pituitary adenylate cyclase-activating polypeptide is a physiological inhibitor of platelet activation. 1506 23