Continuous infusion of glucagon induces severe hyponatremia and thrombocytopenia in a premature neonate.

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.

Human endogenous retrovirus with a high genomic sequence homology with IDDMK(1,2)22 is not specific for Type I (insulin-dependent) diabetic patients but ubiquitous.

AIMS/HYPOTHESIS: It has been reported recently that a novel human endogenous retroviral gene, insulin-dependent diabetes mellitus (IDDM)K(1,2)22, was expressed in the plasma of Type I diabetic patients but not in that of nondiabetic control subjects. This investigation was initiated to determine the specificity of the selective expression of IDDMK(1,2)22 in diabetic patients. METHODS: We isolated the total RNA from the plasma and lymphocytes of 13 new onset Type I diabetic patients and 10 normal control subjects and amplified it by reverse transcriptase polymerase chain reaction. We then determined the presence of IDDMK(1,2)22 with a specific primer set, U3/R-poly(A), used in a recent report and the 5 'SAg/3 'SAg primer set recognizing the putative superantigen encoding the region of the IDDMK(1,2)22 envelope (env) gene. In addition, we carried out nested PCR of the U3/R-poly(A) polymerase chain reaction product using U3N/R primers. RESULTS: We found no difference in the presence of the polymerase chain reaction products between diabetic patients and all nondiabetic subjects tested. Sequencing of the U3/R-poly(A) polymerase chain reaction products showed that the exact sequence of IDDMK(1,2)22 was not present in any of the samples tested, neither in the plasma of diabetic patients nor in that of nondiabetic control subjects. Endogenous retroviral sequences with 90-93% sequence homology to IDDMK(1,2)22 were, however, equally present in both the diabetic and nondiabetic subjects. CONCLUSION/INTERPRETATION: We conclude that a human endogenous retroviral gene with high sequence homology with IDDMK(1,2)22 is not specific for diabetic patients but, rather, is ubiquitous.

Use of immunoglobulin A-antiendomysial antibody to screen for celiac disease in North American children with type 1 diabetes.

OBJECTIVE: Our objective was to determine if a serological marker, the immunoglobulin A antiendomysial antibody (IgA-EMA), can be used to screen for celiac disease in North American children with type 1 diabetes. RESEARCH DESIGN AND METHODS: Subjects included 236 diabetes clinic patients and 56 gastrointestinal clinic patients who underwent intestinal biopsy for suspected malabsorption. Total IgA and IgA-EMA assays were performed. Diabetic patients who were positive for IgA-EMA were asked to undergo biopsy. RESULTS: Of 236 diabetic patients tested, none were IgA deficient and 19 were positive for IgA-EMA (8%). Of 17 patients biopsied, 12 had celiac disease and 3 were symptomatic. The estimated prevalence of celiac disease was 5.1%, consistent with data from European diabetic clinics. Of the 56 gastrointestinal clinic patients, the 3 who were IgA-EMA positive had biopsies diagnostic of celiac disease. Three were found to be IgA deficient, one of whom had celiac disease. Of the 50 IgA-sufficient and IgA-EMA-negative patients, 1 had celiac disease and 49 did not. The IgA-EMA test had a sensitivity of 94% and a specificity of 91% for IgA-sufficient biopsied patients. CONCLUSIONS: IgA-EMA is an appropriate tool for demonstrating an increased prevalence of celiac disease in a North American pediatric diabetic population. Positive testing should be confirmed by intestinal biopsy, and false-positive results require serial follow-up. Symptomatic children require biopsy regardless of their IgA-EMA status.