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Temporal arteritis without an elevated erythrocyte sedimentation rate
LETTERS
1.
2. 3. 4.
Submitted
MANAGEMENT
July 24, 1986,
and accepted
OF MYELODYSPLASTIC
September
16, 1986
3, 1986, and accepted
September
22, 1986, and accepted
HARVEY
Clinical
1.
Sztern B, De Saint-Georges A, Telerman A, Lustman F: Sideroblastose majeure corrjgee par simple administration de folates. Presse Med 1984; 13: 1789.
Associate
OF THE MEDICAL
September
24, 1986
ELEVATED
J. BLUMENTHAL,
Submitted
September
M.D.
Professor of Neurology University of Oklahoma Tulsa Medical College Tulsa, Oklahoma 74104
Blumenthal HJ: Temporal arteritis, medical sas Med Sot 1978; 75: 201-205. 19, 1986, and accepted
emergency.
J Arkan-
September
24, 1986
18, 1986
GROUP G STREPTOCOCCAL BACTEREMIA JOYS
M.D.
To the Editor: The important contribution by Wong and Korn (Am J Med 1986; 80: 959-964) on temporal arteritis without an elevated erythrocyte sedimentation rate focuses on several important points. First, they correctly call attention to the fact that this phenomenon is probably greatly underestimated; they found only 36 reported cases of biopsy-proved temporal arteritis with low sedimentation rate; Case 6 in my report on temporal arteritis [l] should be added to this list. The diagnosis should not be dismissed when the sedimentation rate is low, and in these cases temporal artery biopsy becomes essential. There have been recommendations not to perform biopsy for fear of sacrificing a temporal artery that might be utilized in external-internal anastomosis for cerebral vascular disease; this procedure has recently been shown to have no benefit, and the benign procedure of temporal artery biopsy, when giving positive results will justify long-term treatment with steroids in those patients who are at high risk of complications from this medication.
M.D.
Hopital de Saint-Gilles Rue Marconi 142 1180 Brussels, Belgium
September
September
TEMPORAL ARTERITIS WITHOUT AN ERYT’HROCYTE SEDIMENTATION RATE
SYNDROMES
B. SZTERN, M.D. A. De SAINT-GEORGES, A. TELERMAN, M.D. F. LUSTMAN, M.D.
Submitted
W. KING,
Associate Professor of Medicine Louisiana State University Medical Center Department of Medicine Section of Infectious Diseases P.O. Box 33932 Shreveport, Louisiana 71130-3932 Submitted
To the Editor: We read Buzaid et al’s article regarding the management of myelodysplastic syndromes (Am J Med 1986; 80: 1149-l 157) with great interest. This publication concluded that no truly efficient treatment exists for these pathologic conditions, but that in certain isolated cases, interesting results are obtained. The drugs mentioned are pyridoxine for refractory anemia with “ringed sideroblasts,” androgens, 13-cis-retinoic acid, low doses of cytosine arabinoside and, in selected patients, polychemotherapy. We should like to point out that in a certain number of cases of sideroblastic anemia, the addition of folic acid proved to be useful. Indeed, in several nonalcoholic patients with sideroblastic anemia (more than 20 percent ringed sideroblasts) and low blood folate levels, we showed that the administration of folic acid could provoke the resolution of the myelodysplastic syndrome [I]. This result seemed even more interesting to us in view of the fact that, apart from his ringed sideroblasts, one of our patients presented at the beginning of the observation period with 10 percent myelobiasts in his bone marrow, which also disappeared with folic acid treatment.
1.
JOHN
Wynne J, Braunwald E: Sarcoidosis. In: Braunwald E, ed. Heart disease: a text book of cardiovascular medicine. Philadelphia: WB Saunders, 1980; 1464. Karlish AJ, MacGregor GA: Sarcoidosis, thyroiditis, and Addison’s disease. Lancet 1970; II: 330-333. Mayock RL, Bertrand P, Morisson CE, Scott JH: Manifestations of sarcoidosis. Am J Med 1963; 35: 67-89. Stone DJ, Schwarts A: A long term study of sarcoid and its modification by steroid therapy. Am J Med 1966; 41: 528-540.
TO THE EDITOR
LITERATURE
To the Editor: Thank you for the delightfully entitled article “Familial Male Pseudohermaphroditism due to 5Alpha-Reductase Deficiency in a Turkish Village” (Am J Med 1986; 81: 267-274). Gosh! and I didn’t even know villages had enzymes, much less enzyme deficiencies. I thank you and your reviewers for putting the fun back into reading the medical literature. Keep up the good work.
January
ENDOCARDITIS
AND
To the Editor: The recent article by Venezio et al (Am J Med 1986; 8 1: 2934) raises for discussion a number of important issues regarding group G streptococcal endocarditis and bacteremia. The authors reported a relatively high incidence (47 percent) of infective endocarditis in their patients with group G streptococcal bacteremia and stressed that this is at variance with other reports in the literature. On the contrary, at least two recent reports have shown a high incidence of infective endocarditis in such patients. We
1987
The American
Journal
of Medicine
Volume
82
187
1.
2. 3. 4.
Submitted
MANAGEMENT
July 24, 1986,
and accepted
OF MYELODYSPLASTIC
September
16, 1986
3, 1986, and accepted
September
22, 1986, and accepted
HARVEY
Clinical
1.
Sztern B, De Saint-Georges A, Telerman A, Lustman F: Sideroblastose majeure corrjgee par simple administration de folates. Presse Med 1984; 13: 1789.
Associate
OF THE MEDICAL
September
24, 1986
ELEVATED
J. BLUMENTHAL,
Submitted
September
M.D.
Professor of Neurology University of Oklahoma Tulsa Medical College Tulsa, Oklahoma 74104
Blumenthal HJ: Temporal arteritis, medical sas Med Sot 1978; 75: 201-205. 19, 1986, and accepted
emergency.
J Arkan-
September
24, 1986
18, 1986
GROUP G STREPTOCOCCAL BACTEREMIA JOYS
M.D.
To the Editor: The important contribution by Wong and Korn (Am J Med 1986; 80: 959-964) on temporal arteritis without an elevated erythrocyte sedimentation rate focuses on several important points. First, they correctly call attention to the fact that this phenomenon is probably greatly underestimated; they found only 36 reported cases of biopsy-proved temporal arteritis with low sedimentation rate; Case 6 in my report on temporal arteritis [l] should be added to this list. The diagnosis should not be dismissed when the sedimentation rate is low, and in these cases temporal artery biopsy becomes essential. There have been recommendations not to perform biopsy for fear of sacrificing a temporal artery that might be utilized in external-internal anastomosis for cerebral vascular disease; this procedure has recently been shown to have no benefit, and the benign procedure of temporal artery biopsy, when giving positive results will justify long-term treatment with steroids in those patients who are at high risk of complications from this medication.
M.D.
Hopital de Saint-Gilles Rue Marconi 142 1180 Brussels, Belgium
September
September
TEMPORAL ARTERITIS WITHOUT AN ERYT’HROCYTE SEDIMENTATION RATE
SYNDROMES
B. SZTERN, M.D. A. De SAINT-GEORGES, A. TELERMAN, M.D. F. LUSTMAN, M.D.
Submitted
W. KING,
Associate Professor of Medicine Louisiana State University Medical Center Department of Medicine Section of Infectious Diseases P.O. Box 33932 Shreveport, Louisiana 71130-3932 Submitted
To the Editor: We read Buzaid et al’s article regarding the management of myelodysplastic syndromes (Am J Med 1986; 80: 1149-l 157) with great interest. This publication concluded that no truly efficient treatment exists for these pathologic conditions, but that in certain isolated cases, interesting results are obtained. The drugs mentioned are pyridoxine for refractory anemia with “ringed sideroblasts,” androgens, 13-cis-retinoic acid, low doses of cytosine arabinoside and, in selected patients, polychemotherapy. We should like to point out that in a certain number of cases of sideroblastic anemia, the addition of folic acid proved to be useful. Indeed, in several nonalcoholic patients with sideroblastic anemia (more than 20 percent ringed sideroblasts) and low blood folate levels, we showed that the administration of folic acid could provoke the resolution of the myelodysplastic syndrome [I]. This result seemed even more interesting to us in view of the fact that, apart from his ringed sideroblasts, one of our patients presented at the beginning of the observation period with 10 percent myelobiasts in his bone marrow, which also disappeared with folic acid treatment.
1.
JOHN
Wynne J, Braunwald E: Sarcoidosis. In: Braunwald E, ed. Heart disease: a text book of cardiovascular medicine. Philadelphia: WB Saunders, 1980; 1464. Karlish AJ, MacGregor GA: Sarcoidosis, thyroiditis, and Addison’s disease. Lancet 1970; II: 330-333. Mayock RL, Bertrand P, Morisson CE, Scott JH: Manifestations of sarcoidosis. Am J Med 1963; 35: 67-89. Stone DJ, Schwarts A: A long term study of sarcoid and its modification by steroid therapy. Am J Med 1966; 41: 528-540.
TO THE EDITOR
LITERATURE
To the Editor: Thank you for the delightfully entitled article “Familial Male Pseudohermaphroditism due to 5Alpha-Reductase Deficiency in a Turkish Village” (Am J Med 1986; 81: 267-274). Gosh! and I didn’t even know villages had enzymes, much less enzyme deficiencies. I thank you and your reviewers for putting the fun back into reading the medical literature. Keep up the good work.
January
ENDOCARDITIS
AND
To the Editor: The recent article by Venezio et al (Am J Med 1986; 8 1: 2934) raises for discussion a number of important issues regarding group G streptococcal endocarditis and bacteremia. The authors reported a relatively high incidence (47 percent) of infective endocarditis in their patients with group G streptococcal bacteremia and stressed that this is at variance with other reports in the literature. On the contrary, at least two recent reports have shown a high incidence of infective endocarditis in such patients. We
1987
The American
Journal
of Medicine
Volume
82
187