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American Journal of Clinical Nutrition, Vol. 78, No. 5, 1046-1047, November 2003
© 2003 American Society for Clinical Nutrition

LETTER TO THE EDITOR

Reply to D Fuchs et al

Angel F Remacha

Department of Hematology
Hospital de Sant Pau
Avenida Padre Claret 167
Barcelona 08025
Spain
E-mail:aremacha{at}hsp.santpau.es

Josep Cadafalch

Department of Internal Medicine
Hospital de Sant Pau
Avenida Padre Claret 167
Barcelona 08025
Spain

Dear Sir:

We thank Fuchs et al for their kind letter. Unfortunately, their recent work (1) was not available to us and thus could not be included in the article of ours to which they refer (2). Essentially, both works coincided in many respects, given the previous data in this field (3). The improvement in vitamin B-12 concentrations in HIV-infected patients after highly active antiretroviral therapy (HAART) was expected because of the relation of vitamin B-12 concentrations with neutrophil counts and cobalophilin (R-binder). Neutrophil, CD4+, CD8+, and hemoglobin concentrations also increased as part of a general improvement in health after HAART. This general improvement also included increases in immune system activation markers. Nevertheless, the suggestion of "an amelioration of hyperhomocysteinemia" needs further comment. In our work, this amelioration could not be shown because homocysteine concentrations were not investigated in the group of patients before HAART treatment. Moreover, some studies in the pre-HAART era did not find a difference in homocysteine concentrations between HIV-infected patients and healthy subjects, regardless of vitamin B-12 concentrations.

Fuchs et al suggest an important role for antioxidants, S-adenosylmethionine, and homocysteine in the pathogenesis of vitamin B-12-related abnormalities (4, 5). Moreover, there is someevidence of antioxidant disturbances in HIV infection (6). Although the involvement of oxidative stress in neurologic disturbances due to vitamin B-12 deficiency arouses considerable interest, such involvement has yet to be shown. In this regard, other hypotheses have been proposed for the pathogenesis of cobalamin neuropathy, such as a decline in formate synthesis, disturbances in methylmalonic acid metabolism, and the action of inactive cobalamin analogues (7).

REFERENCES

  1. Sarcletti M, Quirchmair G, Weiss G, Fuchs D, Zangerle R. Increase of haemoglobin levels by anti-retroviral therapy is associated with a decrease in immune activation. Eur J Haematol 2003;70:17-25.[Medline]
  2. Remacha AF, Cadafalch J, Sardà P, Barceló M, Fuster M. Vitamin B-12 metabolism in HIV-infected patients in the age of highly active antiretroviral therapy: role of homocysteine in assessing vitamin B-12 status. Am J Clin Nutr 2003;77:420-4.[Abstract/Free Full Text]
  3. Remacha AF, Cadafalch J. Cobalamin deficiency in patients infected with the human immunodeficiency virus. Semin Hematol 1999;36:75-87.[Medline]
  4. McCaddon A, Regland B, Hudson P, Davies G. Functional vitamin B(12) deficiency and Alzheimer disease. Neurology 2002;58:1395-9.[Abstract/Free Full Text]
  5. Metz J. Pathogenesis of cobalamin neuropathy: deficiency of nervous system S-adenosylmethionine. Nutr Rev 1993;51:12-5.[Medline]
  6. Muller F, Svardal AM, Aukrust P, Berge RK, Ueland PM, Froland SS. Elevated plasma concentration of reduced homocysteine in patients with immunodeficiency virus infection. Am J Clin Nutr 1996;63:242-8.[Abstract/Free Full Text]
  7. Shevell MI, Rosenblatt DS. The neurology of cobalamin. Can J Neurol Sci 1992;19:472-86.[Medline]




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