FREE NEJM E-TOC    HOME   |   SUBSCRIBE   |   CURRENT ISSUE   |   PAST ISSUES   |   COLLECTIONS   |   Search Term  Advanced Search

Sign in | Get NEJM's E-Mail Table of Contents — Free | Subscribe

Previous Volume 337:712 September 4, 1997 Number 10 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.

	Full Text Purchase this article Add to Personal Archive Add to Citation Manager Notify a Friend E-mail When Cited PubMed Citation

To the Editor: Gaucher's disease is caused by deficiency of the lysosomal enzyme acid -glucocerebrosidase that leads to an accumulation of glucocerebroside in the cells of the reticuloendothelial system.¹ The disease is classified into three types according to the presence or absence of neurologic symptoms. Type 1 (non-neuronopathic) is the most common; the clinical signs include hepatosplenomegaly, pancytopenia, and bone involvement. The last of these is probably the most disabling feature and may result in irreversible skeletal damage, such as osteoporosis, osteonecrosis with collapse of major joints, and pathologic fractures with secondary deformity. Enzyme-replacement therapy with modified -glucocerebrosidase (alglucerase) is . . . [Full Text of this Article]

References

This article has been cited by other articles:

• Wenstrup, R. J., Bailey, L., Grabowski, G. A., Moskovitz, J., Oestreich, A. E., Wu, W., Sun, S. (2004). Gaucher disease: alendronate disodium improves bone mineral density in adults receiving enzyme therapy. Blood 104: 1253-1257 [Abstract] [Full Text]  
• Wenstrup, R J, Roca-Espiau, M, Weinreb, N J, Bembi, B (2002). Skeletal aspects of Gaucher disease: a review. Br. J. Radiol. 75: A2-12 [Abstract] [Full Text]