eMedicine Specialties > Dermatology > Pediatric Diseases

Glycogen Storage Diseases Types I-VII: Follow-up

Author: Ljubomir Stojanov, MD, PhD, Professor, University of Belgrade School of Medicine, Serbia
Coauthor(s): Djordjije Karadaglic, MD, DSc, Professor, School of Medicine, University of Podgorica, Podgorica, Montenegro; Milos D Pavlovic, MD, PhD, Head of Immunodermatology, Professor, Department of Dermatology and Venereology, Military Medical Academy, Belgrade, Serbia
Contributor Information and Disclosures

Updated: Mar 10, 2009

Follow-up

Further Inpatient Care

  • GSD type I: The primary goals are good control of hypoglycemia and other metabolic disturbances, such as hyperlactatemia, hyperuricemia, and hyperlipidemia.
  • GSD type II: Further inpatient care is necessary in instances of respiratory insufficiency.
  • GSD types V and VII: Hospital treatment is necessary during renal insufficiency due to rhabdomyolysis.

Further Outpatient Care

  • GSD type I
    • After the initial diagnostic hospitalization, conduct further follow-up on an outpatient basis.
    • In infants and young children, follow-up is usually planned bimonthly. Examine the patient regularly for other metabolic disturbances, such as hyperlactatemia, hyperuricemia, and hyperlipidemia, in addition to glycemia. Check arterial blood pressure and renal function regularly.
    • Importantly, monitor for infections in patients with GSD type Ib.
    • In older children, perform liver ultrasonography at least once a year to rule out hepatic adenomas. When hepatic adenomas are found, commonly around the end of the second decade of life, close follow-up is necessary for early detection of possible malignant change.
  • GSD type II
    • Counsel patients with juvenile and adult forms concerning possible complications and risks of respiratory disorders.
    • Provide genetic counseling for prenatal diagnosis in further pregnancies.
  • GSD type III
    • Follow-up examination of glycemia and transaminase levels is indicated.
    • Follow-up with a cardiologist is required.
  • GSD type IV
    • Regular checkup of liver function is indicated.
    • Genetic counseling concerning recurrent risks in future pregnancies is necessary.
  • GSD types V and VII: Instruct patients to avoid strenuous physical activities.

Complications

  • GSD type I
    • Bacterial infections and cerebral edema are caused by prolonged hypoglycemia and metabolic acidosis. Patients with GSD type Ib are susceptible to bacterial infections, including CNS infections.
    • Long-term complications encompass growth retardation, hepatic adenomas with a high rate of malignant change, xanthomas, gout, and glomerulosclerosis. Long-term complications result from metabolic disturbances, mostly hypoglycemia.
      • Chronic metabolic lactic acidosis and changes in the proximal renal tubule cells can lead to osteopenia and rickets with severe skeletal deformities or bone fractures, particularly of the distal extremities. Such skeletal problems seriously impair the patient's mobility.
      • Elevated uric acid excretion along with segmental glomerular sclerosis gradually causes a decrease in the glomerular function with proteinuria, hematuria, arterial hypertension, and chronic renal failure. Because of incomplete distal tubular acidosis, a number of patients develop hypercalciuria, nephrocalcinosis, and calculosis. In a 2002 report, Mundy and Lee20 presented the hypothesis that GSD type I and diabetes mellitus share the common mechanism for renal dysfunction. This mechanism may be due to a convergence of their metabolic sequelae in upregulation of flux through the pentose phosphate pathway that yields triose phosphate molecules, which are precursors of the lipid diacylglycerol. Diacylglycerol plays an important role in the intrarenal renin-angiotensin system via the protein kinase C pathway.
      • Long-standing disease may be accompanied by hepatic adenomas prone to malignant alteration.
    • Other uncommon complications include vaso-obstructive pulmonary disease and chronic pancreatitis caused by hyperlipidemia.
    • Acute hypoglycemia may be fatal, and long-term complications include irreversible damage to the CNS.
    • Early death usually caused by acute metabolic complications (eg, hypoglycemia, acidosis), bleeding in the course of various surgical procedures (in all patients with GSD type I), and infections (in patients with GSD type Ib) is now uncommon with improving care and treatment.
    • Late complications, such as renal failure, hypertension, or malignant alteration of hepatic adenomas, may be responsible for mortality in adolescent and adult patients.
  • GSD type II
    • Aspiration pneumonia may be a complication.
    • In the infantile form, progressive cardiorespiratory insufficiency usually causes death by the end of the first year of life.
    • In the juvenile form, death is usually due to respiratory insufficiency, although a few cases have been described that were caused by the rupture of an intracranial aneurysm formed from glycogen accumulation in the smooth muscle cells of the arterial wall.
    • In the adult form, death due to respiratory insufficiency (eg, sleep apnea) may occur many years after the first signs of the disease have appeared.
  • GSD type III: The cirrhosis found in some patients is of a mild degree and does not have a significant impact on the course of the disease. Patients with cardiac involvement (ie, patients with GSD type IIIa), regardless of their age, have a risk of cardiovascular disturbances resulting as a complication of their GSD.
  • GSD type IV
    • In the classic form, progressive liver cirrhosis rapidly leads to hepatic insufficiency so that a fatal outcome may be expected before the end of the second year of life. Rarely, children with GSD type IV may survive longer.
    • Fetal hydrops and intrauterine leg contractures may be found in more severe forms.
    • Liver cirrhosis is not always progressive.
    • Moderately severe variants exist, and affected children survive longer and with predominantly muscular lesions.
  • GSD type VI: Serious complications are unknown.
  • GSD types V and VII: Renal insufficiency caused by rhabdomyolysis may occur.

Prognosis

  • GSD type I: The prognosis is better than in the past provided that all the available dietary and medical measures are implemented.
  • GSD type II
    • The prognosis is poor in the infantile form.
    • The prognosis varies in the juvenile form.
    • The prognosis is relatively good in the adult form.
  • GSD type III
    • The prognosis of GSD type III is better than that of GSD type I.
    • Many patients with GSD type III survive to adulthood.
    • GSD type IIIb is a milder form of the disease, while in GSD type IIIa, the prognosis depends largely on the cardiac involvement.
    • In most patients, the prognosis is good.
    • Liver size and transaminases levels return to baseline.
    • Most patients attain normal height at puberty.
  • GSD type IV: The prognosis is poor. Most children with GSD type IV die by age 2-4 years because of hepatic insufficiency.
  • GSD types V and VII: The prognosis varies.
  • GSD type VI
    • The course is benign.
    • The size of the liver decreases with age and returns to baseline at or around puberty.
    • All the patients attain normal height.

Patient Education

  • GSD type I
    • First, instruct parents, and later adult patients, concerning the measures required to control hypoglycemia and other metabolic abnormalities; such measures include proper care and nutrition.
    • Explain the important role played by continuous overnight feeding by means of a nasogastric tube. Teach parents to place the tube by themselves and control the entire feeding process.

Miscellaneous

Medicolegal Pitfalls

  • GSD types I-V and VII: The failure to inform parents of a patient with GSD concerning the 25% risk in future pregnancies is a pitfall.
  • GSD type VI: The failure to inform parents concerning the 25% risk of recurrences in future pregnancies in hepatic phosphorylase deficiency and 50% risk in phosphorylase kinase deficiency is a pitfall.

Special Concerns

  • GSD type II
    • Amniocentesis is necessary for amniotic fluid or chorion biopsy with the aim of prenatal diagnosis.
    • Females with the adult form may have a healthy pregnancy and labor.
    • Early prenatal diagnosis is possible.
 
Acknowledgments

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.



More on Glycogen Storage Diseases Types I-VII

Overview: Glycogen Storage Diseases Types I-VII
Differential Diagnoses & Workup: Glycogen Storage Diseases Types I-VII
Treatment & Medication: Glycogen Storage Diseases Types I-VII
Follow-up: Glycogen Storage Diseases Types I-VII
Multimedia: Glycogen Storage Diseases Types I-VII
References
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Further Reading

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Keywords

GSD, GSD type I, GSD Ia, GSD Ib, GSD lc, GSD Id, GSD type II, GSD type III, GSD type IV, GSD type V, GSD type VI, GSD type VII, von Gierke disease, von Gierke's disease, hepatorenal glycogenosis, acid maltase deficiency, Pompe disease, Pompe's disease, Forbes-Cori disease, Forbes-Cori's disease, limit dextrinosis, Andersen disease, Andersen's disease, amylopectinosis, McArdle disease, McArdle's disease, Hers disease, Hers' disease, Tarui disease, Tarui's disease, glucose-6-phosphatase deficiency, prototypic lysosomal disease, muscle phosphorylase deficiency, hepatic phosphorylase deficiency, phosphofructokinase deficiency, PFK deficiency

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Contributor Information and Disclosures

Author

Ljubomir Stojanov, MD, PhD, Professor, 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.

Medical Editor

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 Salary Employment

Pharmacy Editor

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
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.

Managing Editor

Jeffrey Meffert, MD, Assistant Clinical Professor of Dermatology, University of Texas Health Science Center-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.

CME Editor

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, Department of Dermatology, Geisinger Medical Center
Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.

 
 
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