The hypotonic effect of intranasal and intravenous glucagon in gastrointestinal radiology

Pacchioni, M.; Orena, C; Panizza, Pietro; Cucchi, E; Maschio, Andrea; Pontiroli, Antonio E.

doi:10.1007/bf00199643

Cited by 13 publications

(6 citation statements)

References 22 publications

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“…As mentioned earlier, spike activity in the myoelectrical recording is an electrical counterpart of contractions; thus the reduced number of spike bursts was suggestive of reduced contractility. This agrees with previous studies showing that intestinal hypomotility or reduced intestinal contractility was associated with diabetes …”

Section: Discussionsupporting

confidence: 94%

Hyperglycemia‐induced small intestinal dysrhythmias attributed to sympathovagal imbalance in normal and diabetic rats

Ouyang

Foreman

et al. 2015

Neurogastroenterology Motil

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Section: Discussionsupporting

confidence: 94%

Hyperglycemia‐induced small intestinal dysrhythmias attributed to sympathovagal imbalance in normal and diabetic rats

Ouyang

Foreman

et al. 2015

Neurogastroenterology Motil

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“…When administered intravenously at the dose of 0.1±1 mg, it produces hypotony of lower esophageal sphincter, stomach and duodenum within 1 min, its effects lasting from 9 to 25 min [11]. As for the present, the effects of glucagon on pyloric sphincter are not well defined: Radiological evidence is in favor of a hypertonic effect, which could explain the delayed gastric emptying [11,12]. However, a role on delayed gastric emptying could also be played by the lack of push of the atonic stomach to empty barium suspension into the duodenum.…”

Section: Discussionmentioning

confidence: 89%

Compared effect of a genetically engineered glucagon and hyoscine N-butylbromide on double-contrast barium meal study

et al. 1998

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The aim of this study was to compare the effects of a genetically engineered glucagon (geG) and hyoscine N-butylbromide (HBB) on the quality of double-contrast barium meal (DCBM) study. Two hundred sixty-four patients scheduled for DCBM were randomized to receive intravenously geG 0.25 mg (geG-25), or geG 0.5 mg (geG-50), or HBB 20 mg as hypotonic agent. The evaluation concerned: duration of isolated visualization of the stomach (A); gastric mucosal coating (B); visualization of areae gastricae (C); quality of duodenal cap (D) and loop (E) study; delay, if any, of duodenal study (F). Global significant differences (P from 0.0183 to < 0.0001) were found for A, C, D, and F. GeG-50 allowed the longest isolated gastric visualization (P < 0.0001); geG-25 allowed more extensive visualization of areae gastricae than HBB (P = 0.0006); HBB allowed a better study of duodenal cap (P = 0.0052) and loop (P = 0.0190) than geG-25; geG-50 prolonged the examination time (P < 0.01). No adverse effect was observed with geG within 1 h after DCBM. In conclusion, geG can be safely used as a hypotonic agent in DCBM. When DCBM is focused on the stomach, 0.25 mg of geG is the optimal choice; if DCBM is focused on the duodenum, 0.5 mg of geG (with a prolonged examination time) or 20 mg of HBB (with a less effective study of the stomach) should be used.

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“…However, in the setting in which intranasal glucagon is given to an individual with severe cognitive impairment and often loss of consciousness, this will not be relevant. Nausea and vomiting, well-known consequences of glucagon administration owing to relaxation of gastrointestinal smooth muscle ( 23 ), occurred at similar frequencies with both glucagon preparations.…”

Section: Discussionmentioning

confidence: 96%

Intranasal Glucagon for Treatment of Insulin-Induced Hypoglycemia in Adults With Type 1 Diabetes: A Randomized Crossover Noninferiority Study

et al. 2015

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OBJECTIVETreatment of severe hypoglycemia with loss of consciousness or seizure outside of the hospital setting is presently limited to intramuscular glucagon requiring reconstitution immediately prior to injection, a process prone to error or omission. A needle-free intranasal glucagon preparation was compared with intramuscular glucagon for treatment of insulin-induced hypoglycemia.RESEARCH DESIGN AND METHODSAt eight clinical centers, a randomized crossover noninferiority trial was conducted involving 75 adults with type 1 diabetes (mean age, 33 ± 12 years; median diabetes duration, 18 years) to compare intranasal (3 mg) versus intramuscular (1 mg) glucagon for treatment of hypoglycemia induced by intravenous insulin. Success was defined as an increase in plasma glucose to ≥70 mg/dL or ≥20 mg/dL from the glucose nadir within 30 min after receiving glucagon.RESULTSMean plasma glucose at time of glucagon administration was 48 ± 8 and 49 ± 8 mg/dL at the intranasal and intramuscular visits, respectively. Success criteria were met at all but one intranasal visit and at all intramuscular visits (98.7% vs. 100%; difference 1.3%, upper end of 1-sided 97.5% CI 4.0%). Mean time to success was 16 min for intranasal and 13 min for intramuscular (P < 0.001). Head/facial discomfort was reported during 25% of intranasal and 9% of intramuscular dosing visits; nausea (with or without vomiting) occurred with 35% and 38% of visits, respectively.CONCLUSIONSIntranasal glucagon was highly effective in treating insulin-induced hypoglycemia in adults with type 1 diabetes. Although the trial was conducted in a controlled setting, the results are applicable to real-world management of severe hypoglycemia, which occurs owing to excessive therapeutic insulin relative to the impaired or absent endogenous glucagon response.

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The hypotonic effect of intranasal and intravenous glucagon in gastrointestinal radiology

Cited by 13 publications

References 22 publications

Hyperglycemia‐induced small intestinal dysrhythmias attributed to sympathovagal imbalance in normal and diabetic rats

Hyperglycemia‐induced small intestinal dysrhythmias attributed to sympathovagal imbalance in normal and diabetic rats

Compared effect of a genetically engineered glucagon and hyoscine N-butylbromide on double-contrast barium meal study

Intranasal Glucagon for Treatment of Insulin-Induced Hypoglycemia in Adults With Type 1 Diabetes: A Randomized Crossover Noninferiority Study

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