Pediatric Guillain-Barre Syndrome Medication

  • Author: Marc P DiFazio, MD; Chief Editor: Amy Kao, MD   more...
 
Updated: Jan 26, 2012
 

Medication Summary

The goals of pharmacotherapy are to reduce morbidity and prevent complications. Intravenous immunoglobulin (IVIG) is the predominant choice in childhood Guillain-Barré syndrome (GBS). DVT prophylaxis should be initiated and stress gastritis prophylaxis with H2 blockers (eg, ranitidine) may be beneficial. A bowel routine should also be instituted, as gastroparesis secondary to autonomic dysfunction and/or extended bed rest is not uncommon.

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Blood products

Class Summary

IVIG is an effective treatment of autoimmune neuropathies in general. It can reduce duration of hospitalization as well as need or duration for mechanical ventilation.

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IVIG (Gammagard, Gamimune)

 

Features relevant to efficacy may include neutralization of circulating myelin antibodies through anti-idiotypic antibodies; down-regulation of proinflammatory cytokines, including interferon-gamma; blockade of Fc receptors on macrophages; suppression of inducer T and B cells and augmentation of suppressor T cells; blockade of complement cascade; promotion of remyelination; and a 10% increase in CSF IgG.

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Histamine2-Receptor Antagonists

Class Summary

H2-receptor antagonists are reversible competitive blockers of histamines at the H2 receptors, particularly those in the gastric parietal cells, where they inhibit acid secretion. The H2 antagonists are highly selective, do not affect the H1 receptors, and are not anticholinergic agents.

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Cimetidine (Tagamet)

 

Cimetidine inhibits histamine at H2 receptors of gastric parietal cells, which results in reduced gastric acid secretion, gastric volume, and hydrogen concentrations.

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Ranitidine (Zantac)

 

Ranitidine inhibits histamine stimulation of the H2 receptor in gastric parietal cells, which, in turn, reduces gastric acid secretion, gastric volume, and hydrogen ion concentrations.

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Famotidine (Pepcid)

 

Famotidine competitively inhibits histamine at H2 receptor of gastric parietal cells, resulting in reduced gastric acid secretion, gastric volume, and hydrogen ion concentrations.

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Nizatidine (Axid)

 

Nizatidine competitively inhibits histamine at the H2 receptor of the gastric parietal cells, resulting in reduced gastric acid secretion, gastric volume, and reduced hydrogen concentrations.

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Contributor Information and Disclosures
Author

Marc P DiFazio, MD  Associate Professor, Department of Neurology, Uniformed Services University of the Health Sciences; Director, Pediatric Subspecialty Services, Shady Grove Adventist Hospital for Children

Marc P DiFazio, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Cerebral Palsy and Developmental Medicine, American Academy of Neurology, Child Neurology Society, and Movement Disorders Society

Disclosure: Nothing to disclose.

Coauthor(s)

Nitin C Patel, MD, MPH  Professor of Clinical Neurology and Child Health, Department of Child Health, Chief for Developmental Pediatrics and Child Neurology, Specialist in Pediatrics/Neurology, University of Missouri Hospital and Clinics at Columbia

Nitin C Patel, MD, MPH is a member of the following medical societies: American Academy of Neurology, American Epilepsy Society, American Headache Society, and Child Neurology Society

Disclosure: Nothing to disclose.

Mita N Patel  University of Missouri-Columbia School of Medicine

Disclosure: Nothing to disclose.

Sameer Chhibber, MD, FRCPC  Neuromuscular Fellow, Department of Neurology, Brigham and Women's Hospital and Massachusetts General Hospital, Harvard Medical School

Disclosure: Nothing to disclose.

Brian S Tseng, MD, PhD  Assistant Professor, Department of Neurology, Division of Pediatric Neurology, Harvard Medical School, Massachusetts General Hospital

Brian S Tseng, MD, PhD is a member of the following medical societies: Child Neurology Society

Disclosure: Nothing to disclose.

Chief Editor

Amy Kao, MD  Attending Neurologist, Children's National Medical Center

Amy Kao, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Pediatrics, American Epilepsy Society, and Child Neurology Society

Disclosure: Nothing to disclose.

Additional Contributors

Neil A Busis, MD Chief, Division of Neurology, Department of Medicine, Head, Clinical Neurophysiology Laboratory, University of Pittsburgh Medical Center-Shadyside

Neil A Busis, MD is a member of the following medical societies: American Academy of Neurology and American Association of Neuromuscular and Electrodiagnostic Medicine

Disclosure: Nothing to disclose.

Jennifer A Markowitz, MD Attending Physician, Department of Neurology, Children's Hospital Boston

Jennifer A Markowitz, MD is a member of the following medical societies: Child Neurology Society

Disclosure: Nothing to disclose.

Robert Stanley Rust Jr, MD, MA Thomas E Worrell Jr Professor of Epileptology and Neurology, Co-Director of FE Dreifuss Child Neurology and Epilepsy Clinics, Director, Child Neurology, University of Virginia School of Medicine; Chair-Elect, Child Neurology Section, American Academy of Neurology

Robert Stanley Rust Jr, MD, MA is a member of the following medical societies: American Academy of Neurology, American Epilepsy Society, American Headache Society, American Neurological Association, Child Neurology Society, International Child Neurology Association, and Society for Pediatric Research

Disclosure: Nothing to disclose.

Sarah Sheikh, MBBCh, MSc, MRCP Neuromuscular Fellow, Department of Neurology, Brigham and Women's Hospital

Sarah Sheikh, MBBCh, MSc, MRCP is a member of the following medical societies: American Academy of Neurology, Massachusetts Medical Society, and Royal College of Physicians of the UK

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

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