Letters to Editor Selenium Deficiency and
Cardiomyopathy To the Editor: I read with interest the &dquo;Case Report&dquo; by Reeves et al,l concerning the reversible cardiomyopathy in the 22year-old woman with Crohn’s disease. The authors have attributed the cardiomyopathy to a selenium deficiency. As I am presently involved with a case of marginal selenium deficiency and a cardiomyopathy that also resolved within one month, I have certain questions concerning their report. There are many causes of a dilated cardiomyopathy. The best current reference is by Johnson and PalaciOS2 in their review of the subject in 1982. Among the acute causes of dilated cardiomyopathies are hypocalcemia and hypophosphatemia, two possible causes in this woman with Crohn’s disease with diarrhea, anorexia, cachexia, and apparent malnutrition.2 No mention was made of these possible abnormalities that would have also been corrected by proper nutrition. Another point is that in prior case reports, the patients had significant deficiencies of selenium. In one case report of a boy from China who developed Keshan disease, the plasma selenium was one-fourth to one-eighth of the normal values given.’ In another patient described by Fleming et al,4 the serum value was one-tenth the normal values given. In their report, the woman presented with a selenium level that was two-thirds of the normal value given. In addition, some researchers have noted that the effects of a selenium deficiency may be related to the effects of other enzymes and nutrients involved with antioxidant activity.’ For example, in certain animals myocardial disease will occur when selenium and vitamin E deficiency coexist.’ I presume that the patient was receiving a vial of multivitamins with her total parenteral nutrition each day which included vitamin E. It would have been interesting to measure the levels of vitamin E pre- and post-therapy, to see if this had any additional influence on the recovery of this
patient. I would have liked for the authors to have addressed these issues. .........
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T&dquo;&dquo;&dquo;II. - -
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--- .... T&dquo;&dquo;’rIo.
SCOTT MATTHEW
BOLHACK, M.D. Clinical Fellow in Nutrition/Metabolism Hospital of the University of Pennsylvania 3400 Spruce Street, 4 Silverstein Philadelphia, PA 19104-4283
2. Johnson
pathies
RA, Palacios I: Medical Progress—Dilated cardiomvoof the adult. N Engl J Med 307:1051-1057, 1119-1126,
1982 3. Clinical nutrition cases—Prevention of Keshan cardiomyopathy by sodium selenite. Nutr Rev 38:278-279, 1980 4. Fleming CR, Lie JT, McCall JT, et al: Selenium deficiency and fatal cardiomyopathy in a patient of home parenteral nutrition. Gastroenterology 83:689-693, 1982 5. Editorial: Selenium perspective. Lancet 1:685, 1983 6. Johnson RA, Baker SS, Fallon JT, et al: An Occidental case of cardiomyopathy and selenium deficiency. N Engl J Med 304:1210-
1212, 1981
Response
to Letter from
Dr. Bolhack To the Editor: Thank you for the opportunity to respond to the letter from Dr. Scott Matthew Bolhack. His points are well taken. (1) There was no evidence of either hypocalcemia or hypophosphatemia in our patient. (2) In our patient, a serum selenium was not drawn until 5 days after initiation of total parenteral nutrition (TPN), including 20 pg of selenium daily. The patient described by Fleming et all had a whole blood (not serum) value of one-tenth of the mean of the controls listed. In our case, we reported the serum level as 4, and when compared to the listed range of 6 to 16 with a mean of 11, our value of 4 was one-third (not two-thirds) of the normal mean. The fact that Fleming’s patientl died further reflects that he had a more profound selenium deficiency. (3) Our patient did receive 10 IU of vitamin E daily with the TPN. We did not measure the levels of vitamin E pre- and post-TPN therapy. WILLIAM C. REEVES, M.D. Professor & Section Head Section of Cardiology STEFAN P. MARCUARD, M.D., F.A.C.P. Assistant Professor of Medicine Gastroenterology Section East Carolina University School of Medicine Greenville, NC 27858
REFERENCES
REFERENCES 1. 1. Reeves
WC, Marcuard SP, Willis SE, et al: Reversible cardiomyopathy due to selenium deficiency. JPEN 13:663-665, 1989
Fleming CR. Lie JT, McCall JT, et al: Selenium deficiency and fatal cardiomyopathy in a patient of home parenteral nutrition. Gastroenterology 83:689-693, 1982
Downloaded from pen.sagepub.com433 at Purdue University on June 23, 2015
Cardiomyopathy To the Editor: I read with interest the &dquo;Case Report&dquo; by Reeves et al,l concerning the reversible cardiomyopathy in the 22year-old woman with Crohn’s disease. The authors have attributed the cardiomyopathy to a selenium deficiency. As I am presently involved with a case of marginal selenium deficiency and a cardiomyopathy that also resolved within one month, I have certain questions concerning their report. There are many causes of a dilated cardiomyopathy. The best current reference is by Johnson and PalaciOS2 in their review of the subject in 1982. Among the acute causes of dilated cardiomyopathies are hypocalcemia and hypophosphatemia, two possible causes in this woman with Crohn’s disease with diarrhea, anorexia, cachexia, and apparent malnutrition.2 No mention was made of these possible abnormalities that would have also been corrected by proper nutrition. Another point is that in prior case reports, the patients had significant deficiencies of selenium. In one case report of a boy from China who developed Keshan disease, the plasma selenium was one-fourth to one-eighth of the normal values given.’ In another patient described by Fleming et al,4 the serum value was one-tenth the normal values given. In their report, the woman presented with a selenium level that was two-thirds of the normal value given. In addition, some researchers have noted that the effects of a selenium deficiency may be related to the effects of other enzymes and nutrients involved with antioxidant activity.’ For example, in certain animals myocardial disease will occur when selenium and vitamin E deficiency coexist.’ I presume that the patient was receiving a vial of multivitamins with her total parenteral nutrition each day which included vitamin E. It would have been interesting to measure the levels of vitamin E pre- and post-therapy, to see if this had any additional influence on the recovery of this
patient. I would have liked for the authors to have addressed these issues. .........
--
-
-....---
----
T&dquo;&dquo;&dquo;II. - -
--
.
--- .... T&dquo;&dquo;’rIo.
SCOTT MATTHEW
BOLHACK, M.D. Clinical Fellow in Nutrition/Metabolism Hospital of the University of Pennsylvania 3400 Spruce Street, 4 Silverstein Philadelphia, PA 19104-4283
2. Johnson
pathies
RA, Palacios I: Medical Progress—Dilated cardiomvoof the adult. N Engl J Med 307:1051-1057, 1119-1126,
1982 3. Clinical nutrition cases—Prevention of Keshan cardiomyopathy by sodium selenite. Nutr Rev 38:278-279, 1980 4. Fleming CR, Lie JT, McCall JT, et al: Selenium deficiency and fatal cardiomyopathy in a patient of home parenteral nutrition. Gastroenterology 83:689-693, 1982 5. Editorial: Selenium perspective. Lancet 1:685, 1983 6. Johnson RA, Baker SS, Fallon JT, et al: An Occidental case of cardiomyopathy and selenium deficiency. N Engl J Med 304:1210-
1212, 1981
Response
to Letter from
Dr. Bolhack To the Editor: Thank you for the opportunity to respond to the letter from Dr. Scott Matthew Bolhack. His points are well taken. (1) There was no evidence of either hypocalcemia or hypophosphatemia in our patient. (2) In our patient, a serum selenium was not drawn until 5 days after initiation of total parenteral nutrition (TPN), including 20 pg of selenium daily. The patient described by Fleming et all had a whole blood (not serum) value of one-tenth of the mean of the controls listed. In our case, we reported the serum level as 4, and when compared to the listed range of 6 to 16 with a mean of 11, our value of 4 was one-third (not two-thirds) of the normal mean. The fact that Fleming’s patientl died further reflects that he had a more profound selenium deficiency. (3) Our patient did receive 10 IU of vitamin E daily with the TPN. We did not measure the levels of vitamin E pre- and post-TPN therapy. WILLIAM C. REEVES, M.D. Professor & Section Head Section of Cardiology STEFAN P. MARCUARD, M.D., F.A.C.P. Assistant Professor of Medicine Gastroenterology Section East Carolina University School of Medicine Greenville, NC 27858
REFERENCES
REFERENCES 1. 1. Reeves
WC, Marcuard SP, Willis SE, et al: Reversible cardiomyopathy due to selenium deficiency. JPEN 13:663-665, 1989
Fleming CR. Lie JT, McCall JT, et al: Selenium deficiency and fatal cardiomyopathy in a patient of home parenteral nutrition. Gastroenterology 83:689-693, 1982
Downloaded from pen.sagepub.com433 at Purdue University on June 23, 2015
