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Peritoneal dialysis in mercurial diuretic intoxication
Volume 88 Number 1
Brief clinical and laboratory observations
Similar concerns have been noted previously for a different disease and distinct enzyme deficiency. In 1973 Vidgoff and associates 1~reported a family which included a woman with a marked deficiency of hexosominidase A in all tissues studied. She actually represents the carrier state for Tay-Sachs disease, though her hexosominidase A level taken alone would have suggested that she was an affected homozygote. There are thus at least two heritable disorders for which there is overlap between the carrier and the affected person in terms o f enzyme activity. Based on these findings, and considering the greater availability and less strict indications for prenatal diagnostic amniocentesis, it is suggested that great care be exercised in the diagnosis of these diseases, particularly in the interpretation of data for intrauterine diagnosis. The data and conclusions discussed here were presented in preliminary form to the Society for Pediatric Research, Denver, April 18, 1975.11 The typing skills of Cheryl Jirschele and the excellent technical assistance of Martha Sattler and Cameron Clark are gratefully acknowledged. We also thank Dr. Jules Leroy for the samples from Family 2 and their controls. REFERENCES 1. Wilson J, Lake BD, and Dunn HG: Krabbe's leukodystrophy, some clinical, genetic and pathogenic considerations, J Neurol Sci. 10:563, 1970.
2. Suzuki K, and Suzuki Y: Globoid cell leukodystrophy (Krabbe's disease): Deficiency of galactocerebroside betagalactosidase, Proc Natl Acad Sci USA 66:302, 1970. 3. Eto Y, Suzuki K, and Suzuki K: Globoid cell leukodystrophy (Krabbe's disease): isolation of myelin with normal glycolipid composition, J Lipid Res 11:473, 1970. 4. Miyatake T, and Suzuki K: Globoid cell leukodystrophy: Additional deficiency of psychosine galactosidase, Biochem Biophys Res Commun 48:538, 1972. 5. Wenger DA, Sattler M, and Markey SP: Deficiency of monogalactosyl diglyceride beta-galactosidase activity in Krabbe's disease, Biochem Biophys Res Commun 53:680, 1973. 6. Wenger DA, Sattler M, and Hiatt W: Globoid cell leukodystrophy: deficiency of lactosyl ceramide beta-galactosidase, Proc Nail Acad Sci USA 71:854, 1974. 7. Wenger DA, Sattler M, Clark C, and McKelvey H: An improved method for the identification of patients and carriers of Krabbe's disease, Clin Chim Acta 56:199, 1974. 8. Suzuki Y, and Suzuki K: Krabbe's globoid cell leukodystrophy: deficiency of galactocerebrosidase in serum, leukocytes and fibroblasts, Science 171:73, 1971. 9. Atkins L, and Milunsky A: Prenatal diagnosis of genetic disorders, in Milunsky A, editor, The prevention of genetic disease and mental retardation, Philadelphia, 1975, WB Saunders Company, p 250. 10. VidgoffJ, Buist NRM, and O'Brien JS: Absence of beta-Nacetyl-D-hexosaminidase A activity in a healthy woman, Am J Hum Genet 25:372, 1973. 11. Wenger DA, and Riccardi VM: The possible false diagnosis of Krabbe disease, Pediatr Res 9:319, 1975 (abstr).
tioned? More recently N-acetyl-D, L-penicillamine has been shown to be an effective agent in mercury poisoningr All these chelating agents, however, are ultimately dependent upon renal excretion of the mercury chelate complex to reduce the mercury blood level. Therefore peritoneal dialysis is indicated to remove this complex when the patient is anuric. ~
Peritoneal dialysis in mercurial diuretic intoxication Jean E. Robillard, M.D.,* Linda K. Rames, M.D., Robert L. Jensen, A.B., and Robert J. Roberts, M.D., Ph.D., Iowa City, Iowa ALTHOUGH
THE A P P R O P R I A T E
TREATMENT
Abbreviation used BAL: dimercaprol pro-
c e d u r e s for mercury intoxication are still debated, dimer-
caprol has been employed successfully in cases of acute poisoning by mercury salts? Calcium ethylene diamine tretra-acetate has also been used for treatment of acute mercury intoxication'-", however, its efficacy was ques-
From the Department of Pediatrics, University Hospitals. *Reprint address: Department of Pediatrics, Division of Nephrology, Ste-dustine Hospital, 3175 Chemin SainteCatherine, Montrkal, P.Q., Canada H3T 1C5.
79
This case report involves a child with congenital heart disease who was admitted in acute renal failure following intoxication with a mercurial diuretic (mercaptomerin). Blood levels and peritoneal clearance of mercury together with tissue levels of mercury from autopsy material are reported. CASE REPORT Patient T. M., a 3-month-old white female who had, during the neonatal period, a Rashkind procedure for transposition of the
80
Brief clinical and laboratory observations
The Journal of Pediatrics January 1976
Table I. Peritoneal clearance of mercury
l
Day I Day 2 Day 3
Volume (ml)
Dialysate[ Hg Serum Hg (l~g/dl) (#g/dl)
260 230 250 260 250
12.0 8.3 5.3 8.2 1.1
262 155 164 109 137
Time Clearance (rain) (ml/min) 22 36 35 29 27
0.54 0.34 0.23 0.68 0.07
Table II. Tissue levels of mercury
Normal value"
Present study Weight (gin) Heart Lung Liver Kidney Brain Muscle Fat
80 50 113 50 420 ---
Hg total t Hg content 1Hg content content (llg/lO0 gm (l~g/lO0 gm (l~g) of tissue) of tissue) 76 245 1,357 1,162 12.2 ---
95 489 1,201 2,324 29 227 240
15 10 30 275 10 15
great arteries, presented to the local physician in cardiac failure. The patient was hospitalized and treated with oxygen, digoxin, and mercaptomerin. Cardiac failure failed to improve despite repeated doses of mercaptomerin over a seven-day period (total of 62 mg of mercaptomerin was given). Subsequent development of oliguria merited referral to University Hospitals. On admission the patient presented with generalized cyanosis and respiratory distress. The blood pressure was 95/50 mm Hg, pulse rate 150/ minute, respirations 88/minute, and weight 3,620 gm. The hematocrit value was 43%. Urine analysis showed 4+ protein, 4+ glucose, and the presence of granular casts, red blood cells, white blood cells, and tubular epithelial cells. Other serum values were as follows: creatininc 5.1 mg/dl; blood urea nitrogen 114 mg/dl; sodium 136 mEq/1; potassium 7.1 mEq/l; chloride 90 mEq/l; carbon dioxide 17 mEq/1. The blood gases in Fxo~ of 40% showed a pH of 7.41, Paco 2of 34 mm Hg and Pao2 of 48 mm Hg. Blood and urine mercury levels determined before peritoneal dialysis were 456/zg/dl and 1,932/~g/dl, respectively. Subsequently peritoneal dialysis and intramuscular injections of BAL were begun. Peritoneal lavages were performed from the day of admission for seven days without interruption. During the second, third, and fourth day of dialysis, blood samples and dialysate aliquots were obtained at regular intervals for determination of mercury in both serum and dialysate. BAL was given intramuscularly, 12 mg every six hours, during the first seven days of hospitalization. During this period blood mercury level decreased from 456/Lg/dl to 79/~g/dl. The patient, who became
anuric after beginning peritoneal dialysis, produced 285 ml of urine on the eighth day of therapy. Thereafter BAL was decreased to 12 mg every 8 hours, on the thirteenth day of hospitalization the blood mercury level was 15 /~g/dl. She died on the fourteenth day subsequent to deterioration of the respiratory status and multiple cardiac arrests. Peritoneal clearance of mercury.* The calculated clearance of mercury determined on five different occasions over a three-day period ranged from 0.07 ml/minute to 0.68 ml/minute, with an average of 0.37 ml/minute (Table I). Tissue levels of mercury. Mercury levels in different tissues are presented in Table II along with normal adult values. Blood values in our patient decreased from an initial value of 456/~g/dl to 15/~g/dl. This last value was still elevated when compared to the normal value o f l /~g/dl.'~ Renal lesions. Calcified casts within the tubular lumen and some microscopic evidence of renal tubular regeneration were found. The glomeruli were normal. These findings are consistent with mercury intoxication. 7 DISCUSSION Toxic reactions with mercurial diuretics are rare when viewed against the frequency o f their use. However, toxic reactions, especially nephrotoxicity, have been well documented after prolonged administration with high dosage or an acute excessive dose of a mercurial diuretic. 7 In the present case two factors could explain the development of mercurial retention and subsequent toxic reactions. (1) Decreases in renal blood flow and in the glomerular filtration rate, usually related to congestive heart failure, ~ could have explained the patient's resistance to the mercurial diuretic therapy and the retention of organic mercurial substance. (2) This child was chronically hypoxic with a Pao~ of 40 to 50 m m Hg. It has been suggested that hypoxia 7 coupled with mitrochondrial dysfunction secondary to administered mercury 9 and impaired glomerular filtration rate 7 m a y be significant factors in the pathogenesis of mercurial nephrotoxicity. The value of dialysis in addition to chelating agents to remove mercury has been suggested? N o data are actually available, to our knowledge, to demonstrate the efficacy o f this therapy in infants and children. In our patient, the peritoneal clearance of mercury (0.37 m l / m i n u t e ) was below the dialysance values of mercury-BAL complex by hemodialysis (5 ml/minute) TM or by peritoneal dialysis in adults (1.5 m l / m i n u t e ) ? This low rate of peritoneal clearance found in our patient could be partially explained by smaller surface area of peritoneal m e m b r a n e and by possible impairment of perfusion of peritoneal vessels secondary to the patient's heart disease. Furthermore the efficacy of this therapy can also be questioned, because of the very high tissue levels of *Mercury levels were determined in blood and tissues using a modification of the method of Magos.'-"
Volume 88 Number 1
mercury that persisted (Table II) even after the blood mercury level decreased from 456/~g/dl to 15/~g/dl. The persistently high tissue levels of mercury obviously could have contributed to the deterioration and death of this patient despite the important fall in the concentration o f blood mercury. The underlying congenital heart disease and possible, but unlikely, BAL intoxication" should also be considered as factors that may have been involved in the death of this child. In conclusion, the therapeutic value of peritoneal dialysis for removing mercury from blood and tissues in young infants, even if associated with a chelating agent, is questionable and remains to be demonstrated. Peritoneal dialysis, however, remains the treatment of choice in uremia resulting from mercury intoxication in young infants, since this condition is potentially reversibleY The investigation of other chelating agents such as N-acetylpenicillamine should be encouraged particularly in light of the extremely high tissue levels that persisted in our patient treated with BAL.
B r i e f clinical and laboratory observations
3.
4.
5.
6.
7.
8.
9.
I0.
REFERENCES 1. Longcope WT, and Luetscher JA Jr: The uses of BAL (British anti-lewisite) in the treatment of the injurious effects of arsenic, mercury and other metallic poisons, Ann Intern Med 31:545, 1949. 2. Bell RF, Gilliland JC, and Dunn WS: Urinary mercury and
Mucocutaneous lymph node syndrome in the continental United States James S. Brown, M.D.,* Gerard J. Billmeier, Jr., M.D., Frederick Cox, M.D., Mazen Ibrahim, M.D., William P. Stepp, Jr., M.D.,
11. 12.
81
lead excretion in a case of mercuriatism: Differential excretion after administration of edathamit calcium and dimercaprol, Arch Ind Health 11:231, 1955. McCoy JE, Carre IJ, and Freem M: A controlled trial of edathamil calcium disodium in acrodynia, Pediatrics 25:304, 1960. Kark RAP, Poskanzer DC, Bullock JD, and Boylen G: Mercury poisoning and its treatment with N-acetyl-d, L-penicillamine, N Engl J Med 285:10, 1971. Lowenthal DT, Chardo F, and Reidenberg MM: Removal of mercury by peritoneal dialysis, Arch Intern Med 134:139, 1974. Joselow MM, Louria DB, and Browder AA: Mercurialism: Environmental and occupational aspects, Ann Intern Med 76:119, 1972. Freeman RB, Maher JF, Schreiner GE, and Mostofi FK: Renal tubular necrosis due to nephrotoxicity of organic mercurial diuretics, Ann Intern Med 57:34, 1962. Merrill AJ: Edema and decreased renal blood flow in patients with chronic congestive heart failure, J Clin Invest 25:389, 1946. Southard J~ Nitisewojo P, and Green DE: Mercurial toxicity and the perturbation of the mitochondrial control system, Fed Proc 33:2147, 1974. Maher J, and Schreiner GE: The dialysis of mercury and mercury-BAL complex, Clin Res 7:298, 1959. Randall RV, and Seeler AO: BAL, N Engi J Med 239:1004, 1948. Magos L: Atomic absorption determinaton of total inorganic, and organic mercury in blood, J Assoc Off Anal Chem 55:966, 1972.
MUCOCUTANEOUS LYMPH NODE SYNDROME or Kawasaki disease has been recently well described as a discrete clinical entity. It was first reported by Kawasaki 1 in Japan in t967 and has subsequently been extensively studied by the Japanese M L N S Research Committee, established in 1970. Since then nearly 7,000 cases have been reported in the Japanese literature? There have been eight case reports from Korea, a 12 from H a w a i i ? and eight from Greece? Abbreviation used MLNS: mucocutaneous lymph node syndrome
and Richard Gibson, M.D., Memphis, Tenn. From the Department of Pediatrics, The University o f Tennessee Center for the Health Sciences, and The General Pediatric and Infectious Diseases Services; St. Jude Children's Research Hospital. Supported by Childhood Cancer Research Center Grant CA-O8480 from the National Cancer Institute, General Research Support Grant RR-O5584 from the Division of Research Resources, National Institute o f Health, and by ALSAC. *Reprint address: Universityof Tennessee Child Development Center, 711 Jefferson Ave., Memphis, Tenn. 38105.
Typical cases of M L N S , as originally described, have not been reported in the continental United States but a recent review suggested the possibility that the disease does exist here. ~ We describe herein three cases which occurred in Memphis, Tennessee: one in N o v e m b e r , 1974, one in May, 1975, and one in June, 1975. One patient was an inner city urban resident and the other two were from suburban middle-class neighborhoods. In all three patients the following well-described clinical features of M L N S were manifest: fever, cervical adenitis, congested
Brief clinical and laboratory observations
Similar concerns have been noted previously for a different disease and distinct enzyme deficiency. In 1973 Vidgoff and associates 1~reported a family which included a woman with a marked deficiency of hexosominidase A in all tissues studied. She actually represents the carrier state for Tay-Sachs disease, though her hexosominidase A level taken alone would have suggested that she was an affected homozygote. There are thus at least two heritable disorders for which there is overlap between the carrier and the affected person in terms o f enzyme activity. Based on these findings, and considering the greater availability and less strict indications for prenatal diagnostic amniocentesis, it is suggested that great care be exercised in the diagnosis of these diseases, particularly in the interpretation of data for intrauterine diagnosis. The data and conclusions discussed here were presented in preliminary form to the Society for Pediatric Research, Denver, April 18, 1975.11 The typing skills of Cheryl Jirschele and the excellent technical assistance of Martha Sattler and Cameron Clark are gratefully acknowledged. We also thank Dr. Jules Leroy for the samples from Family 2 and their controls. REFERENCES 1. Wilson J, Lake BD, and Dunn HG: Krabbe's leukodystrophy, some clinical, genetic and pathogenic considerations, J Neurol Sci. 10:563, 1970.
2. Suzuki K, and Suzuki Y: Globoid cell leukodystrophy (Krabbe's disease): Deficiency of galactocerebroside betagalactosidase, Proc Natl Acad Sci USA 66:302, 1970. 3. Eto Y, Suzuki K, and Suzuki K: Globoid cell leukodystrophy (Krabbe's disease): isolation of myelin with normal glycolipid composition, J Lipid Res 11:473, 1970. 4. Miyatake T, and Suzuki K: Globoid cell leukodystrophy: Additional deficiency of psychosine galactosidase, Biochem Biophys Res Commun 48:538, 1972. 5. Wenger DA, Sattler M, and Markey SP: Deficiency of monogalactosyl diglyceride beta-galactosidase activity in Krabbe's disease, Biochem Biophys Res Commun 53:680, 1973. 6. Wenger DA, Sattler M, and Hiatt W: Globoid cell leukodystrophy: deficiency of lactosyl ceramide beta-galactosidase, Proc Nail Acad Sci USA 71:854, 1974. 7. Wenger DA, Sattler M, Clark C, and McKelvey H: An improved method for the identification of patients and carriers of Krabbe's disease, Clin Chim Acta 56:199, 1974. 8. Suzuki Y, and Suzuki K: Krabbe's globoid cell leukodystrophy: deficiency of galactocerebrosidase in serum, leukocytes and fibroblasts, Science 171:73, 1971. 9. Atkins L, and Milunsky A: Prenatal diagnosis of genetic disorders, in Milunsky A, editor, The prevention of genetic disease and mental retardation, Philadelphia, 1975, WB Saunders Company, p 250. 10. VidgoffJ, Buist NRM, and O'Brien JS: Absence of beta-Nacetyl-D-hexosaminidase A activity in a healthy woman, Am J Hum Genet 25:372, 1973. 11. Wenger DA, and Riccardi VM: The possible false diagnosis of Krabbe disease, Pediatr Res 9:319, 1975 (abstr).
tioned? More recently N-acetyl-D, L-penicillamine has been shown to be an effective agent in mercury poisoningr All these chelating agents, however, are ultimately dependent upon renal excretion of the mercury chelate complex to reduce the mercury blood level. Therefore peritoneal dialysis is indicated to remove this complex when the patient is anuric. ~
Peritoneal dialysis in mercurial diuretic intoxication Jean E. Robillard, M.D.,* Linda K. Rames, M.D., Robert L. Jensen, A.B., and Robert J. Roberts, M.D., Ph.D., Iowa City, Iowa ALTHOUGH
THE A P P R O P R I A T E
TREATMENT
Abbreviation used BAL: dimercaprol pro-
c e d u r e s for mercury intoxication are still debated, dimer-
caprol has been employed successfully in cases of acute poisoning by mercury salts? Calcium ethylene diamine tretra-acetate has also been used for treatment of acute mercury intoxication'-", however, its efficacy was ques-
From the Department of Pediatrics, University Hospitals. *Reprint address: Department of Pediatrics, Division of Nephrology, Ste-dustine Hospital, 3175 Chemin SainteCatherine, Montrkal, P.Q., Canada H3T 1C5.
79
This case report involves a child with congenital heart disease who was admitted in acute renal failure following intoxication with a mercurial diuretic (mercaptomerin). Blood levels and peritoneal clearance of mercury together with tissue levels of mercury from autopsy material are reported. CASE REPORT Patient T. M., a 3-month-old white female who had, during the neonatal period, a Rashkind procedure for transposition of the
80
Brief clinical and laboratory observations
The Journal of Pediatrics January 1976
Table I. Peritoneal clearance of mercury
l
Day I Day 2 Day 3
Volume (ml)
Dialysate[ Hg Serum Hg (l~g/dl) (#g/dl)
260 230 250 260 250
12.0 8.3 5.3 8.2 1.1
262 155 164 109 137
Time Clearance (rain) (ml/min) 22 36 35 29 27
0.54 0.34 0.23 0.68 0.07
Table II. Tissue levels of mercury
Normal value"
Present study Weight (gin) Heart Lung Liver Kidney Brain Muscle Fat
80 50 113 50 420 ---
Hg total t Hg content 1Hg content content (llg/lO0 gm (l~g/lO0 gm (l~g) of tissue) of tissue) 76 245 1,357 1,162 12.2 ---
95 489 1,201 2,324 29 227 240
15 10 30 275 10 15
great arteries, presented to the local physician in cardiac failure. The patient was hospitalized and treated with oxygen, digoxin, and mercaptomerin. Cardiac failure failed to improve despite repeated doses of mercaptomerin over a seven-day period (total of 62 mg of mercaptomerin was given). Subsequent development of oliguria merited referral to University Hospitals. On admission the patient presented with generalized cyanosis and respiratory distress. The blood pressure was 95/50 mm Hg, pulse rate 150/ minute, respirations 88/minute, and weight 3,620 gm. The hematocrit value was 43%. Urine analysis showed 4+ protein, 4+ glucose, and the presence of granular casts, red blood cells, white blood cells, and tubular epithelial cells. Other serum values were as follows: creatininc 5.1 mg/dl; blood urea nitrogen 114 mg/dl; sodium 136 mEq/1; potassium 7.1 mEq/l; chloride 90 mEq/l; carbon dioxide 17 mEq/1. The blood gases in Fxo~ of 40% showed a pH of 7.41, Paco 2of 34 mm Hg and Pao2 of 48 mm Hg. Blood and urine mercury levels determined before peritoneal dialysis were 456/zg/dl and 1,932/~g/dl, respectively. Subsequently peritoneal dialysis and intramuscular injections of BAL were begun. Peritoneal lavages were performed from the day of admission for seven days without interruption. During the second, third, and fourth day of dialysis, blood samples and dialysate aliquots were obtained at regular intervals for determination of mercury in both serum and dialysate. BAL was given intramuscularly, 12 mg every six hours, during the first seven days of hospitalization. During this period blood mercury level decreased from 456/Lg/dl to 79/~g/dl. The patient, who became
anuric after beginning peritoneal dialysis, produced 285 ml of urine on the eighth day of therapy. Thereafter BAL was decreased to 12 mg every 8 hours, on the thirteenth day of hospitalization the blood mercury level was 15 /~g/dl. She died on the fourteenth day subsequent to deterioration of the respiratory status and multiple cardiac arrests. Peritoneal clearance of mercury.* The calculated clearance of mercury determined on five different occasions over a three-day period ranged from 0.07 ml/minute to 0.68 ml/minute, with an average of 0.37 ml/minute (Table I). Tissue levels of mercury. Mercury levels in different tissues are presented in Table II along with normal adult values. Blood values in our patient decreased from an initial value of 456/~g/dl to 15/~g/dl. This last value was still elevated when compared to the normal value o f l /~g/dl.'~ Renal lesions. Calcified casts within the tubular lumen and some microscopic evidence of renal tubular regeneration were found. The glomeruli were normal. These findings are consistent with mercury intoxication. 7 DISCUSSION Toxic reactions with mercurial diuretics are rare when viewed against the frequency o f their use. However, toxic reactions, especially nephrotoxicity, have been well documented after prolonged administration with high dosage or an acute excessive dose of a mercurial diuretic. 7 In the present case two factors could explain the development of mercurial retention and subsequent toxic reactions. (1) Decreases in renal blood flow and in the glomerular filtration rate, usually related to congestive heart failure, ~ could have explained the patient's resistance to the mercurial diuretic therapy and the retention of organic mercurial substance. (2) This child was chronically hypoxic with a Pao~ of 40 to 50 m m Hg. It has been suggested that hypoxia 7 coupled with mitrochondrial dysfunction secondary to administered mercury 9 and impaired glomerular filtration rate 7 m a y be significant factors in the pathogenesis of mercurial nephrotoxicity. The value of dialysis in addition to chelating agents to remove mercury has been suggested? N o data are actually available, to our knowledge, to demonstrate the efficacy o f this therapy in infants and children. In our patient, the peritoneal clearance of mercury (0.37 m l / m i n u t e ) was below the dialysance values of mercury-BAL complex by hemodialysis (5 ml/minute) TM or by peritoneal dialysis in adults (1.5 m l / m i n u t e ) ? This low rate of peritoneal clearance found in our patient could be partially explained by smaller surface area of peritoneal m e m b r a n e and by possible impairment of perfusion of peritoneal vessels secondary to the patient's heart disease. Furthermore the efficacy of this therapy can also be questioned, because of the very high tissue levels of *Mercury levels were determined in blood and tissues using a modification of the method of Magos.'-"
Volume 88 Number 1
mercury that persisted (Table II) even after the blood mercury level decreased from 456/~g/dl to 15/~g/dl. The persistently high tissue levels of mercury obviously could have contributed to the deterioration and death of this patient despite the important fall in the concentration o f blood mercury. The underlying congenital heart disease and possible, but unlikely, BAL intoxication" should also be considered as factors that may have been involved in the death of this child. In conclusion, the therapeutic value of peritoneal dialysis for removing mercury from blood and tissues in young infants, even if associated with a chelating agent, is questionable and remains to be demonstrated. Peritoneal dialysis, however, remains the treatment of choice in uremia resulting from mercury intoxication in young infants, since this condition is potentially reversibleY The investigation of other chelating agents such as N-acetylpenicillamine should be encouraged particularly in light of the extremely high tissue levels that persisted in our patient treated with BAL.
B r i e f clinical and laboratory observations
3.
4.
5.
6.
7.
8.
9.
I0.
REFERENCES 1. Longcope WT, and Luetscher JA Jr: The uses of BAL (British anti-lewisite) in the treatment of the injurious effects of arsenic, mercury and other metallic poisons, Ann Intern Med 31:545, 1949. 2. Bell RF, Gilliland JC, and Dunn WS: Urinary mercury and
Mucocutaneous lymph node syndrome in the continental United States James S. Brown, M.D.,* Gerard J. Billmeier, Jr., M.D., Frederick Cox, M.D., Mazen Ibrahim, M.D., William P. Stepp, Jr., M.D.,
11. 12.
81
lead excretion in a case of mercuriatism: Differential excretion after administration of edathamit calcium and dimercaprol, Arch Ind Health 11:231, 1955. McCoy JE, Carre IJ, and Freem M: A controlled trial of edathamil calcium disodium in acrodynia, Pediatrics 25:304, 1960. Kark RAP, Poskanzer DC, Bullock JD, and Boylen G: Mercury poisoning and its treatment with N-acetyl-d, L-penicillamine, N Engl J Med 285:10, 1971. Lowenthal DT, Chardo F, and Reidenberg MM: Removal of mercury by peritoneal dialysis, Arch Intern Med 134:139, 1974. Joselow MM, Louria DB, and Browder AA: Mercurialism: Environmental and occupational aspects, Ann Intern Med 76:119, 1972. Freeman RB, Maher JF, Schreiner GE, and Mostofi FK: Renal tubular necrosis due to nephrotoxicity of organic mercurial diuretics, Ann Intern Med 57:34, 1962. Merrill AJ: Edema and decreased renal blood flow in patients with chronic congestive heart failure, J Clin Invest 25:389, 1946. Southard J~ Nitisewojo P, and Green DE: Mercurial toxicity and the perturbation of the mitochondrial control system, Fed Proc 33:2147, 1974. Maher J, and Schreiner GE: The dialysis of mercury and mercury-BAL complex, Clin Res 7:298, 1959. Randall RV, and Seeler AO: BAL, N Engi J Med 239:1004, 1948. Magos L: Atomic absorption determinaton of total inorganic, and organic mercury in blood, J Assoc Off Anal Chem 55:966, 1972.
MUCOCUTANEOUS LYMPH NODE SYNDROME or Kawasaki disease has been recently well described as a discrete clinical entity. It was first reported by Kawasaki 1 in Japan in t967 and has subsequently been extensively studied by the Japanese M L N S Research Committee, established in 1970. Since then nearly 7,000 cases have been reported in the Japanese literature? There have been eight case reports from Korea, a 12 from H a w a i i ? and eight from Greece? Abbreviation used MLNS: mucocutaneous lymph node syndrome
and Richard Gibson, M.D., Memphis, Tenn. From the Department of Pediatrics, The University o f Tennessee Center for the Health Sciences, and The General Pediatric and Infectious Diseases Services; St. Jude Children's Research Hospital. Supported by Childhood Cancer Research Center Grant CA-O8480 from the National Cancer Institute, General Research Support Grant RR-O5584 from the Division of Research Resources, National Institute o f Health, and by ALSAC. *Reprint address: Universityof Tennessee Child Development Center, 711 Jefferson Ave., Memphis, Tenn. 38105.
Typical cases of M L N S , as originally described, have not been reported in the continental United States but a recent review suggested the possibility that the disease does exist here. ~ We describe herein three cases which occurred in Memphis, Tennessee: one in N o v e m b e r , 1974, one in May, 1975, and one in June, 1975. One patient was an inner city urban resident and the other two were from suburban middle-class neighborhoods. In all three patients the following well-described clinical features of M L N S were manifest: fever, cervical adenitis, congested