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Previous Volume 334:1100-1105 April 25, 1996 Number 17 Next

	Since this article has no abstract, we have provided an extract of the first 100 words of the full text and any section headings.

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Glycolysis is the most important source of energy in red cells and working muscles. Inherited defects of glycolysis can cause hemolytic anemia, neurologic abnormalities, and myopathy with exercise intolerance. The severity of each of these cardinal manifestations may vary depending on the particular step in the glycolytic pathway that is involved and on residual enzyme activity, the expression of tissue-specific isozymes, and physicochemical properties of the mutant enzyme.^1,2 Aldolase A is one of the three isozymes of aldolase (the other two are B and C) responsible for the conversion of fructose-1,6-bisphosphate into glyceraldehyde-3-phosphate and dihydroxyacetone phosphate in the glycolytic pathway.³ . . . [Full Text of this Article]

Case Report

Methods

Morphologic and Biochemical Studies

Molecular Studies

Results

Morphologic and Biochemical Studies

Molecular Studies

Discussion

Source Information

From the Department of Pediatrics (J.K., A.B., R.R., B.G., F.L.) and the Institutes of Neuropathology (W.S.) and Clinical Chemistry (K.S.), Justus-Liebig University, Giessen; the Department of Pediatrics, Georg-August University, Göttingen (A.P., U.G.); and the Department of Neurology, Julius-Maximilians University, Würzburg (H.R.) — all in Germany.

Address reprint requests to Dr. Lampert at Abteilung Allgemeine Pädiatrie, Hämatologie und Onkologie, Zentrum für Kinderheilkunde, Justus-Liebig-Universität, Feulgenstraße 12, D-35385 Giessen, Germany.

References

Related Letters:

Inherited Metabolic Myopathy and Hemolysis Due to a Mutation in Aldolase A
Kopp A., Bistrian B. R., Kreuder J., Repp R., Lampert F.
Extract | Full Text  
N Engl J Med 1996; 335:1242-1243, Oct 17, 1996. Correspondence

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