Glycogen Storage Diseases Types I-VII Medication

  • Author: Ljubomir Stojanov, MD, PhD; Chief Editor: Dirk M Elston, MD   more...
 
Updated: Jan 25, 2012
 

Medication Summary

No specific drug treatment is recommended for GSD type Ia. Appropriately treat concurrent infections with antibiotics. Allopurinol (Zyloprim), a xanthine oxidase inhibitor, therapy can reduce uric acid levels in the blood and prevent occurrence of gout and kidney stones in adult life.

Hyperlipidemia can be reduced by lipid-lowering drugs (eg, 3-hydroxy-3-methylglutaryl coenzyme A [HMG-CoA] reductase inhibitors, fibric acid derivatives). HMG-CoA reductase inhibitors of cholesterol biosynthesis in the liver are known as statins. Because of a high risk of myositis, the drugs may be recommended only after age 12 years. A new inhibitor of cholesterol absorption, ezetimibe, in a dose of 10 mg/d, can reduce low-density lipoprotein (LDL) cholesterol levels and has small triglyceride-lowering effects.

In patients with renal lesions, microalbuminuria can be reduced with angiotensin-converting enzyme (ACE) inhibitor therapy. In addition to their antihypertensive effects, ACE inhibitors are renoprotective and reduce albuminuria. Nephrocalcinosis and renal calculi can be prevented with citrate therapy.

Severe infection and chronic inflammatory bowel disease in patients with GSD type Ib should be treated with antibiotics and granulocyte-macrophage colony-stimulating factors (Neupogen).

Cardioglycosides and diuretics are prescribed for cardiovascular insufficiency in patients with GSD type II. Respiratory bacterial infections (aspiration pneumonia) in patients with GSD type II are treated with antibiotics. Enzyme replacement therapy has been approved as an orphan drug by the FDA.

No effective treatment is available for GSD types III, IV, V, and VII. Some patients with GSD type V may benefit from creatine supplement.

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Iron salts

Class Summary

These agents correct iron deficiency.

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Ferrous sulfate (Feosol, Feratab, Fer-Iron)

 

Used to control anemia in patients with GSD types Ia or Ib.

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Uricosuric agents

Class Summary

These agents reduce production of uric acid without disrupting the biosynthesis of vital purines.

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Allopurinol (Zyloprim)

 

Used to control elevated serum uric acid levels in patients with GSD types Ia or Ib.

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Growth factors

Class Summary

These agents activate and stimulate production, maturation, migration, and cytotoxicity of neutrophils.

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Filgrastim (Neupogen)

 

Granulocyte colony-stimulating factor used in patients with GSD type Ib with severe infections, in those with pseudocolitis, and in patients as a preventive measure.

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Glycogenolytic agents

Class Summary

These agents elevate blood glucose levels.

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Glucagon (GlucaGen)

 

Used to treat GSD types V and VII. Pancreatic alpha cells of the islets of Langerhans produce glucagon, a polypeptide hormone. Exerts opposite effects of insulin on blood glucose. Glucagon elevates blood glucose levels by inhibiting glycogen synthesis and by enhancing formation of glucose from noncarbohydrate sources such as proteins and fats (gluconeogenesis). Increases hydrolysis of glycogen to glucose (glycogenolysis) in liver in addition to accelerating hepatic glycogenolysis and lipolysis in adipose tissue. Glucagon also increases force of contraction in the heart and has a relaxant effect on the GI tract.

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Angiotensin-converting enzyme (ACE) inhibitors

Class Summary

Reduce microalbuminuria, have antihypertensive effects, and are renoprotective.

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Lisinopril (Prinivil, Zestril)

 

Prevents conversion of angiotensin I to angiotensin II and lowers aldosterone secretion; in some patients may cause cough and angioedema.

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Ramipril (Altace)

 

Prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in lower aldosterone secretion.

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Captopril (Capoten)

 

Prevents conversion of angiotensin I to angiotensin II, resulting in lower aldosterone secretion

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Enalapril (Vasotec)

 

Competitive inhibitor of ACE. Reduces angiotensin II levels, decreasing aldosterone secretion.

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Enzyme replacements

Class Summary

Recombinant human enzyme glucosidase alfa has recently been designated an orphan drug for GSD type II (Pompe disease).

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Alglucosidase alfa (Myozyme)

 

Recombinant human enzyme alpha-glucosidase (rhGAA) indicated as an orphan drug for treatment of Pompe disease. Replaces rhGAA, which is deficient or lacking in persons with Pompe disease. Alpha-glucosidase is essential for normal muscle development and function. Binds to mannose-6-phosphate receptors and then is transported into lysosomes; undergoes proteolytic cleavage that results in increased enzymatic activity and ability to cleave glycogen. Improves infant survival without requiring invasive ventilatory support compared with historical controls without treatment.

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Contributor Information and Disclosures
Author

Ljubomir Stojanov, MD, PhD  Lecturer in Metabolism and Clinical Genetics, University of Belgrade School of Medicine, Serbia

Disclosure: Nothing to disclose.

Coauthor(s)

Djordjije Karadaglic, MD, DSc  Professor, School of Medicine, University of Podgorica, Podgorica, Montenegro

Djordjije Karadaglic, MD, DSc is a member of the following medical societies: American Academy of Dermatology, European Academy of Dermatology and Venereology, and Serbian Association of DermatoVenereologists

Disclosure: Nothing to disclose.

Milos D Pavlovic, MD, PhD  Head of Immunodermatology, Professor, Department of Dermatology and Venereology, Military Medical Academy, Belgrade, Serbia

Milos D Pavlovic, MD, PhD is a member of the following medical societies: European Academy of Dermatology and Venereology

Disclosure: Nothing to disclose.

Specialty Editor Board

Jacek C Szepietowski, MD, PhD  Professor, Vice-Head, Department of Dermatology, Venereology and Allergology, Wroclaw Medical University; Director of the Institute of Immunology and Experimental Therapy, Polish Academy of Sciences, Poland

Disclosure: Stiefel GSK Company Salary Employment; Orfagen Consulting fee Consulting; Maruho Consulting fee Consulting; Astellas Consulting fee Consulting; Abbott Consulting fee Consulting; Leo Pharma Consulting fee Consulting

David F Butler, MD  Professor of Dermatology, Texas A&M University College of Medicine; Chair, Department of Dermatology, Director, Dermatology Residency Training Program, Scott and White Clinic, Northside Clinic

David F Butler, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, American Society for Dermatologic Surgery, American Society for MOHS Surgery, Association of Military Dermatologists, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Jeffrey Meffert, MD  Assistant Clinical Professor of Dermatology, University of Texas School of Medicine at San Antonio

Jeffrey Meffert, MD is a member of the following medical societies: American Academy of Dermatology, American Medical Association, Association of Military Dermatologists, and Texas Dermatological Society

Disclosure: Nothing to disclose.

Glen H Crawford, MD  Assistant Clinical Professor, Department of Dermatology, University of Pennsylvania School of Medicine; Chief, Division of Dermatology, The Pennsylvania Hospital

Glen H Crawford, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, Phi Beta Kappa, and Society of USAF Flight Surgeons

Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD  Director, Ackerman Academy of Dermatopathology, New York

Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Additional Contributors

The authors and editors of eMedicine gratefully acknowledge the contributions of previous Chief Editor, William D. James, MD, to the development and writing of this article.

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An infant with glycogen storage disease type Ia. Note the typical facial aspect resembling a doll's face.
Glycogen storage disease type I. Abdominal sonogram showing large nodules in the liver.
A child with glycogen storage disease type Ia.
Glycogen storage disease type II. Photomicrograph of the liver. Note the intensively stained vacuoles in the hepatocytes (periodic acid-Schiff, original magnification X 27).
Glycogen storage disease type II. Photomicrograph of the liver. Note the regular reticular net and hepatocytes vacuolization (Gordon-Sweet stain, original magnification X 25).
 
 
 
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