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Treatment of hypertension in acrodynia
EDITORIAL CORRESPONDENCE
Prophylaxis for rheumatic fever using benzathine penicillin To the Editor." In a recent article (J PEDIATR 1992;121:569-72), Arguedas and Mohs dealt with a decline in the incidence of rheumatic fever in Costa Rica after suspected streptococcal infection was treated with benzathine penicillin. The health authorities should be congratulated for having accomplished such a nationwide program. I think an important omission is made in the reference list; the authors do not refer to the report by Feinstein et al.I who conducted a controlled follow-up study in a population of 391 patients who had had a previous attack of rheumatic fever. The drug regimens assigned were as follows: oral penicillin, sulfadiazine, and benzathine penicillin. The last proved to be the most effective. Furthermore, Feinstein et al. assessed compliance with the three therapies. This work, after the one published by Marshall et al. 2 to show the efficacy of streptomycin in the treatment of tuberculosis, is the oldest among controlled follow-up studies. I believe that we should take into account a report published 38 years ago, especially considering that its content and method were models for current research studies. Miguel Martell, MD Departamento de Neonatologia Hospital de Clinicas-Montevideo Centro Latinoamericano de Perinatologia Casilla de Correo 627 11000 Montevideo, Uruguay 9/35/48607
a complication and a consequence of dietary protein intolerance. Their conclusions are strongly supported by the clinical experience as published by our group, 2 as well as others. 35 All 37 patients with methemoglobinemia and diarrhea were acidotic (the majority had moderate to severe acidosis), and none was breast fed at the time of the event. Murray and Christie seem to provide a long-awaited explanation for the phenomenon, and a new incentive for the promotion of breast-feeding. Ron Dagan, MD Director, Pediatric Infectious Disease Unit Soroka Medical Center Beer-Sheva 84101, Israel 9/35/48602
REFERENCES
1. Murray KF, Christie DL. Dietary protein intolerance in infants with transient methemoglobinemia and diarrhea. J PED1ATR 1993;122:90-2. 2. Dagan R, Zaltstein E, Gorodischer R. Methemoglobinemia in young infants with diarrhea. Eur J Pediatr 1988;147:87-9. 3. Heyman I. Methemoglobinemia in infants. Harefuah 1954; 46:144-6. 4. Kohne E, Leupold D, Bienzle U, Meder R, Kleihauer E. "Enteritis" toxische Methemoglobinemie bei S/iuglingen mit schwerer Enteritis infolge Kuhmilchallergie. Klin Paediatr 1974; 186:500-2. 5. Yano SS, Danish EH, Edward H. Transient methemoglobinemia with acidosis in infants. J PEDIATR 1982;100:415-8.
REFERENCES
1. Feinstein AR, Wood HF, Epstein JA, et al. A controlled study of three methods of prophylaxis against streptococcal infection in a population of rheumatic children. II. Results of the first three years of the study including methods for evaluating the maintenance of oral prophylaxis. N Engl J Med 1959;260:697702. 2. Marshall G, Blacklock JWS, Cameron C, et al. Streptomycin treatment of pulmonary tuberculosis: a medical research council investigation. BMJ !948;2:769-82.
Transient methemoglobinemia, diarrhea, and dietary protein intolerance To the Editor." I read with interest the article by Murray and Christie. 1 The authors conclude that transient methemoglobinemia with diarrhea is
Treatment of hypertension in acrodynia To the Editor." 1 read with interest the case report by Henningsson et al. entitled "Acute Mercury Poisoning (Acrodynia) Mimicking Pheochromocytoma in an Adolescent" (1993;122:252-3). Although the authors mentioned that "there was no blood pressure response to therapy with nifedipine and phenoxybenzamine," later they recorded that "his blood pressure was 140/100 mm Hg while he was supine, 130/60 while sitting, and 90/50 while standing; he was still taking the antihypertensive medications." These blood pressure values were markedly lower than his initial level (160/120 mm Hg). In addition, it was noticed that he was not in "immediate distress" at that time. We have treated an 8-year-old girl with acrodynia with nifedipine (0.2 mg/kg four times a day initially).1 The pinkish color of the nose faded and the pain in the extremities decreased the next day, so the nifedipine dose was increased (0.2 mg/kg six times per
667
668
Editorial correspondence
The Journal of Pediatrics October 1993
day) because her blood pressure (170/130 mm Hg) was not affected. When her symptoms started to regress, mild proteinuria disappeared and her blood pressure came under control (130/90 mm Hg) in 9 days; nifedipine therapy was continued at the same dose and the patient discharged. Within 2 weeks her appetite improved, though some discoloration of her fingertips remained; this discoloration completely regressed within 1IA months, and her urinary mercury excretion became normal. A control study for treatment could not be carried out in such a rare disease. The authors' findings might also indicate that blood pressure could be controlled with this treatment. If the patient with acrodynia does not continue to be exposed to the source, as in the authors' case, he or she might respond better to nifedipine, as in our patient.
~inasi Ozsoylu, MD Professor of Pediatrics and Hematology Hacettepe University Faculty of Medicine Department of Pediatrics and Hacettepe Children's Hospital 06100 Ankara, Turkey 9/35/48747 REFERENCE 1. t~zsoylu S, Sarikayalar F, Aksoy A. Nifedipine in treatment of acrodynia. Turkish J Pediatr 1989;31:159-61.
Reply To the Editor: Vascular smooth muscle is one of the primary sites of action for calcium-channel blockers; one would expect that nifedipine would reduce hypertension and improve those signs of acrodynia that are secondary to vasospasm. In our brief clinical report we mentioned that the patient had previously been treated with nifedipine and phenoxybenzamine with no reported blood pressure response; our initial reading of 140/100 mm Hg during treatment with antihypertensive medication perhaps represented a marginal improvement over his physician's initial reading of 160/120 mm Hg, but he had in fact undergone symptomatic deterioration. In the hospital therapy with his antihypertensive medication was discontinued and he had no change in blood pressure. Perhaps we could have achieved more effective control of blood pressure and symptoms if we had persevered with larger doses of nifedipine or other drugs. However, the purpose of the report was to emphasize the importance of making a correct diagnosis of acrodynia to permit specific therapy aimed at removing all the toxic effects of elemental mercury exposure. We believe that only early diagnosis and initiation of chelation therapy will obviate long-term complications in this preventable disorder. Symptomatic therapy with nifedipine and other agents is useful but of secondary importance.
C. Henningsson, MD L. McGonigle, MD J.S.D. Winter, MD Department of Pediatrics University of Alberta Edmonton, Alberta T6G 2S2; Canada 9/35/48748
Physiopathologic mechanism of hypercalciuria in renal glucosuria To the Editor: Schneider et al./reported the association of renal glucosuria with hypercalciuria in five children. These patients maintained their hypercalciuria after fasting, and in one of them who was administered 300 mg of calcium per day the hypercalciuria persisted. In all cases, parathyroid hormone (PTH) levels were normal. On the basis of these results, the authors concluded that the hypercalciuria was caused by a decrease in renal tubular reabsorption of calcium. Various studies, especially those by Sutton and Walker, 2 Filipponi et al., 3 Pacifici et al., 4 and Bataille et al., 5 have helped to show the existence of fasting hypercalciuria produced by an increment in bone resorption caused by a mechanism independent of PTH, mediated by the action of prostaglandin E23 or by interleukin-l.4 In all these studies the diagnosis of hypercalciuria of resorptive origin was based on the excretion of increased amounts of calcium despite the exclusion of dairy products (dietary calcium-independent hypercalciuria), the presence of fasting hypercalciuria, normal PTH levels, and reduced vertebral mineral density. There is no reason to suppose that this type of hypercalciuria cannot occur in children. Although the cases reported by Schneider et al. suggest that the hypercalciuria was of renal tubular origin, we believe that, given the normal PTH values, the possibility of a non-renal origin should not be ruled out, as has been shown in other tubulopathies such as Bartter syndrome, 6 familial renal hypouricemia, 7 or even diabetes mellitus, s
Victor G. Nieto, MD Jesits Chahin, MD Margarita Monge, MD Pediatric Nephrology Unit Hospital Ntra. Sra. de la Candelaria Santa Cruz de Tenerife Canary Islands, Spain 9/35/49272 REFERENCES 1. Schneider D, Gauthier B, Trachtman H. Hypercalciuria in children with renal glycosuria: evidence of dual renal tubular reabsorptive defects. J PEDIATR 1992;121:715-9. 2. Sutton RAL, Walker VR. Bone resorption and hypercalciuria in calcium stoneformers. Metabolism 1986;35:485-8. 3. Filipponi P, Mannarelli C, Pacifici R, et al. Evidence for a prostaglandin-mediated bone resorptive mechanism in subjects with fasting hypercalciuria. Calcif Tissue Int 1988; 43:61-6. 4. Pacifici R, Rothstein M, Rifas L, et al. Increased monocyte interleukin-1 activity and decreased vertebral bone density in patients with fasting idiopathic hypercalciuria. J Clin Endocrinol Metab 1990;71:138-45. 5. Bataille P, Achard JM, Fournier A, et al. Diet, vitamin D and vertebral mineral density in hypercalciuric calcium stone formers. Kidney Int 199l;39:1193-205. 6. Restrepo de Rovetto C, Welch TR, Hug G, Clark K, Bergstrom W. Hypercalciuria with Bartter syndrome: evidence for an abnormality of vitamin D metabolism. J PEDIATR 1989; 115:397-404.
Prophylaxis for rheumatic fever using benzathine penicillin To the Editor." In a recent article (J PEDIATR 1992;121:569-72), Arguedas and Mohs dealt with a decline in the incidence of rheumatic fever in Costa Rica after suspected streptococcal infection was treated with benzathine penicillin. The health authorities should be congratulated for having accomplished such a nationwide program. I think an important omission is made in the reference list; the authors do not refer to the report by Feinstein et al.I who conducted a controlled follow-up study in a population of 391 patients who had had a previous attack of rheumatic fever. The drug regimens assigned were as follows: oral penicillin, sulfadiazine, and benzathine penicillin. The last proved to be the most effective. Furthermore, Feinstein et al. assessed compliance with the three therapies. This work, after the one published by Marshall et al. 2 to show the efficacy of streptomycin in the treatment of tuberculosis, is the oldest among controlled follow-up studies. I believe that we should take into account a report published 38 years ago, especially considering that its content and method were models for current research studies. Miguel Martell, MD Departamento de Neonatologia Hospital de Clinicas-Montevideo Centro Latinoamericano de Perinatologia Casilla de Correo 627 11000 Montevideo, Uruguay 9/35/48607
a complication and a consequence of dietary protein intolerance. Their conclusions are strongly supported by the clinical experience as published by our group, 2 as well as others. 35 All 37 patients with methemoglobinemia and diarrhea were acidotic (the majority had moderate to severe acidosis), and none was breast fed at the time of the event. Murray and Christie seem to provide a long-awaited explanation for the phenomenon, and a new incentive for the promotion of breast-feeding. Ron Dagan, MD Director, Pediatric Infectious Disease Unit Soroka Medical Center Beer-Sheva 84101, Israel 9/35/48602
REFERENCES
1. Murray KF, Christie DL. Dietary protein intolerance in infants with transient methemoglobinemia and diarrhea. J PED1ATR 1993;122:90-2. 2. Dagan R, Zaltstein E, Gorodischer R. Methemoglobinemia in young infants with diarrhea. Eur J Pediatr 1988;147:87-9. 3. Heyman I. Methemoglobinemia in infants. Harefuah 1954; 46:144-6. 4. Kohne E, Leupold D, Bienzle U, Meder R, Kleihauer E. "Enteritis" toxische Methemoglobinemie bei S/iuglingen mit schwerer Enteritis infolge Kuhmilchallergie. Klin Paediatr 1974; 186:500-2. 5. Yano SS, Danish EH, Edward H. Transient methemoglobinemia with acidosis in infants. J PEDIATR 1982;100:415-8.
REFERENCES
1. Feinstein AR, Wood HF, Epstein JA, et al. A controlled study of three methods of prophylaxis against streptococcal infection in a population of rheumatic children. II. Results of the first three years of the study including methods for evaluating the maintenance of oral prophylaxis. N Engl J Med 1959;260:697702. 2. Marshall G, Blacklock JWS, Cameron C, et al. Streptomycin treatment of pulmonary tuberculosis: a medical research council investigation. BMJ !948;2:769-82.
Transient methemoglobinemia, diarrhea, and dietary protein intolerance To the Editor." I read with interest the article by Murray and Christie. 1 The authors conclude that transient methemoglobinemia with diarrhea is
Treatment of hypertension in acrodynia To the Editor." 1 read with interest the case report by Henningsson et al. entitled "Acute Mercury Poisoning (Acrodynia) Mimicking Pheochromocytoma in an Adolescent" (1993;122:252-3). Although the authors mentioned that "there was no blood pressure response to therapy with nifedipine and phenoxybenzamine," later they recorded that "his blood pressure was 140/100 mm Hg while he was supine, 130/60 while sitting, and 90/50 while standing; he was still taking the antihypertensive medications." These blood pressure values were markedly lower than his initial level (160/120 mm Hg). In addition, it was noticed that he was not in "immediate distress" at that time. We have treated an 8-year-old girl with acrodynia with nifedipine (0.2 mg/kg four times a day initially).1 The pinkish color of the nose faded and the pain in the extremities decreased the next day, so the nifedipine dose was increased (0.2 mg/kg six times per
667
668
Editorial correspondence
The Journal of Pediatrics October 1993
day) because her blood pressure (170/130 mm Hg) was not affected. When her symptoms started to regress, mild proteinuria disappeared and her blood pressure came under control (130/90 mm Hg) in 9 days; nifedipine therapy was continued at the same dose and the patient discharged. Within 2 weeks her appetite improved, though some discoloration of her fingertips remained; this discoloration completely regressed within 1IA months, and her urinary mercury excretion became normal. A control study for treatment could not be carried out in such a rare disease. The authors' findings might also indicate that blood pressure could be controlled with this treatment. If the patient with acrodynia does not continue to be exposed to the source, as in the authors' case, he or she might respond better to nifedipine, as in our patient.
~inasi Ozsoylu, MD Professor of Pediatrics and Hematology Hacettepe University Faculty of Medicine Department of Pediatrics and Hacettepe Children's Hospital 06100 Ankara, Turkey 9/35/48747 REFERENCE 1. t~zsoylu S, Sarikayalar F, Aksoy A. Nifedipine in treatment of acrodynia. Turkish J Pediatr 1989;31:159-61.
Reply To the Editor: Vascular smooth muscle is one of the primary sites of action for calcium-channel blockers; one would expect that nifedipine would reduce hypertension and improve those signs of acrodynia that are secondary to vasospasm. In our brief clinical report we mentioned that the patient had previously been treated with nifedipine and phenoxybenzamine with no reported blood pressure response; our initial reading of 140/100 mm Hg during treatment with antihypertensive medication perhaps represented a marginal improvement over his physician's initial reading of 160/120 mm Hg, but he had in fact undergone symptomatic deterioration. In the hospital therapy with his antihypertensive medication was discontinued and he had no change in blood pressure. Perhaps we could have achieved more effective control of blood pressure and symptoms if we had persevered with larger doses of nifedipine or other drugs. However, the purpose of the report was to emphasize the importance of making a correct diagnosis of acrodynia to permit specific therapy aimed at removing all the toxic effects of elemental mercury exposure. We believe that only early diagnosis and initiation of chelation therapy will obviate long-term complications in this preventable disorder. Symptomatic therapy with nifedipine and other agents is useful but of secondary importance.
C. Henningsson, MD L. McGonigle, MD J.S.D. Winter, MD Department of Pediatrics University of Alberta Edmonton, Alberta T6G 2S2; Canada 9/35/48748
Physiopathologic mechanism of hypercalciuria in renal glucosuria To the Editor: Schneider et al./reported the association of renal glucosuria with hypercalciuria in five children. These patients maintained their hypercalciuria after fasting, and in one of them who was administered 300 mg of calcium per day the hypercalciuria persisted. In all cases, parathyroid hormone (PTH) levels were normal. On the basis of these results, the authors concluded that the hypercalciuria was caused by a decrease in renal tubular reabsorption of calcium. Various studies, especially those by Sutton and Walker, 2 Filipponi et al., 3 Pacifici et al., 4 and Bataille et al., 5 have helped to show the existence of fasting hypercalciuria produced by an increment in bone resorption caused by a mechanism independent of PTH, mediated by the action of prostaglandin E23 or by interleukin-l.4 In all these studies the diagnosis of hypercalciuria of resorptive origin was based on the excretion of increased amounts of calcium despite the exclusion of dairy products (dietary calcium-independent hypercalciuria), the presence of fasting hypercalciuria, normal PTH levels, and reduced vertebral mineral density. There is no reason to suppose that this type of hypercalciuria cannot occur in children. Although the cases reported by Schneider et al. suggest that the hypercalciuria was of renal tubular origin, we believe that, given the normal PTH values, the possibility of a non-renal origin should not be ruled out, as has been shown in other tubulopathies such as Bartter syndrome, 6 familial renal hypouricemia, 7 or even diabetes mellitus, s
Victor G. Nieto, MD Jesits Chahin, MD Margarita Monge, MD Pediatric Nephrology Unit Hospital Ntra. Sra. de la Candelaria Santa Cruz de Tenerife Canary Islands, Spain 9/35/49272 REFERENCES 1. Schneider D, Gauthier B, Trachtman H. Hypercalciuria in children with renal glycosuria: evidence of dual renal tubular reabsorptive defects. J PEDIATR 1992;121:715-9. 2. Sutton RAL, Walker VR. Bone resorption and hypercalciuria in calcium stoneformers. Metabolism 1986;35:485-8. 3. Filipponi P, Mannarelli C, Pacifici R, et al. Evidence for a prostaglandin-mediated bone resorptive mechanism in subjects with fasting hypercalciuria. Calcif Tissue Int 1988; 43:61-6. 4. Pacifici R, Rothstein M, Rifas L, et al. Increased monocyte interleukin-1 activity and decreased vertebral bone density in patients with fasting idiopathic hypercalciuria. J Clin Endocrinol Metab 1990;71:138-45. 5. Bataille P, Achard JM, Fournier A, et al. Diet, vitamin D and vertebral mineral density in hypercalciuric calcium stone formers. Kidney Int 199l;39:1193-205. 6. Restrepo de Rovetto C, Welch TR, Hug G, Clark K, Bergstrom W. Hypercalciuria with Bartter syndrome: evidence for an abnormality of vitamin D metabolism. J PEDIATR 1989; 115:397-404.