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Pb encephalopathy mimicking Reye syndrome
Volume 95 Number 3
Editorial correspondence
Reply To the Editor: Preston's letter has properly called attention to the implications for infant nutrition raised by the recognition that Clostridium botulinum can produce its toxin in vivo in the infant gut, in some cases so rapidly that typical crib death results. M y colleagues and I have had under active investigation several factors that may govern such intestinal colonization and toxin production, including the possible differential availability of iron to C. botulinum from either formula, breast milk, or other dietary sources such as cereal. We are presently analyzing the data collected from our first 50 hospitized patients and their controls and plan to publish the results in the near future. Stephen S. Arnon, M.D. Infectious Disease Section California Department of Health Services Berkeley, CA 94704
495
of her anemia, and abatement of the chipping lead-ladened paint in her house. The abnormal liver enzymes were confusing initially, but the CSF protein concentration is usually normal in Reye syndrome and was elevated in this lead-burdened child. Peter D. Magnus, M.D., F.A.A.P., M.P.H. 17260 Kohfield Road Bend, OR 97701 Richard J. Powers, M.D. Albin Leong, M.D. CHLA 4560 Sunset Bird Los Angeles, CA 90054 REFERENCE
!.
Fox DW, Hart MC, Bergeson PS, Jarrett PB, Stillman AE, and Huxtable RJ: Pyrrolizidine (Senecio) intoxication mimicking Reye syndrome, J PEDIATR 93:980, 1978.
Reply Pb encephalopathy mimicking Reye syndrome To the Editor: We have an addition to make to the "discussion" of the article entitled "Pyrrolizidine (Senecio) intoxication mimicking Reye syndrome."' The authors state that "several diseases produce encephalopathy, elevation of serum transaminase values, and other signs of liver dysfunction." In addition to those cited, we would like to add lead encephalopathy. A recent example was a 21-month-old black girl admitted to Children's Hospital of Los Angeles with a four-day history of vomiting, anorexia, and lethargy. She was anemic (Hgb 7.8 gm/dl; MCV 62 /~3), and mildly dehydrated. CSF showed a normal pressure, 5 leukocytes/mm 3, and a protein concentration of 173 mg/dl (normal CSF and blood glucose concentration). Serum enzymes were SGOT 152 IU and SGPT 124 IU; serum ammonia level was 242 #g/dl. The initial impressions were iron deficiency anemia with Reye snydrome, toxic encephalopathy, 'acute gastroenteritis, gastrointestinal obstruction, or hepatitis. Approximately 12 hours after admission, after being "rehydrated," the patient had a grand mal seizure lasting 10 minutes, and eventually needed ventilatory assistance for several hours. Several hours after the medical management of her seizures and cerebral edema, however, "lead flecks" were noted on the admission flat plate, and long bone films revealed "lead lines." The patient was chelated immediately (dimercaprol and versenate) for seven days, and later for five days more; she has received two more out-patient series of chelations with CaNaEDTA alone. Her pre-chelation blood lead concentration was 231 /~g/dl, and her first erythrocyte protoporphyrin obtained 13 days after the first chelation (when her blood lead had diminished to 46 btg/dl), was still markedly elevated at 829/Lg/dl. Fortunately, this patient has made a successful recovery after chelation therapy, correction
To the Editor: The differentiation of Reye syndrome from lead poisoning encephalopathy has previously been commented upon? However, Drs. Magnus, Powers, and Leong are to be congratulated on their astute differentiation of this case. They once again emphasize the importance of a good history and physical, and also of knowing the disease entities prevalent in your community. Donald W. Fox, D.O. Perinatal Services Welborn Baptist Hospital 401 S.E. Sixth St Evansville, I N 47713 Paul S. Bergeson, M.D. Good Samaritan Hospital Phoenix, A Z 85072 REFERENCE
1. Schubert W, Bobo RC, Partin JC, et al: Reye's syndrome, Disease-A-Month December, 1975.
Cerebral blood flow re intracranial hemorrhage To the Editor: We read the recent paper by Lou et aP with great interest. Impaired autoregulation of cerebral blood flow (CBF) in asphyxiated infants is noteworthy and, as they postulate, may have an etiologic implication to neonatal intracranial hemorrhage (ICH). We wish to draw your attention to some of our recent observations in this regard. To evaluate various factors which may contribute to ICH, 40 variables were analyzed in 198 consecutive infants requiring
Editorial correspondence
Reply To the Editor: Preston's letter has properly called attention to the implications for infant nutrition raised by the recognition that Clostridium botulinum can produce its toxin in vivo in the infant gut, in some cases so rapidly that typical crib death results. M y colleagues and I have had under active investigation several factors that may govern such intestinal colonization and toxin production, including the possible differential availability of iron to C. botulinum from either formula, breast milk, or other dietary sources such as cereal. We are presently analyzing the data collected from our first 50 hospitized patients and their controls and plan to publish the results in the near future. Stephen S. Arnon, M.D. Infectious Disease Section California Department of Health Services Berkeley, CA 94704
495
of her anemia, and abatement of the chipping lead-ladened paint in her house. The abnormal liver enzymes were confusing initially, but the CSF protein concentration is usually normal in Reye syndrome and was elevated in this lead-burdened child. Peter D. Magnus, M.D., F.A.A.P., M.P.H. 17260 Kohfield Road Bend, OR 97701 Richard J. Powers, M.D. Albin Leong, M.D. CHLA 4560 Sunset Bird Los Angeles, CA 90054 REFERENCE
!.
Fox DW, Hart MC, Bergeson PS, Jarrett PB, Stillman AE, and Huxtable RJ: Pyrrolizidine (Senecio) intoxication mimicking Reye syndrome, J PEDIATR 93:980, 1978.
Reply Pb encephalopathy mimicking Reye syndrome To the Editor: We have an addition to make to the "discussion" of the article entitled "Pyrrolizidine (Senecio) intoxication mimicking Reye syndrome."' The authors state that "several diseases produce encephalopathy, elevation of serum transaminase values, and other signs of liver dysfunction." In addition to those cited, we would like to add lead encephalopathy. A recent example was a 21-month-old black girl admitted to Children's Hospital of Los Angeles with a four-day history of vomiting, anorexia, and lethargy. She was anemic (Hgb 7.8 gm/dl; MCV 62 /~3), and mildly dehydrated. CSF showed a normal pressure, 5 leukocytes/mm 3, and a protein concentration of 173 mg/dl (normal CSF and blood glucose concentration). Serum enzymes were SGOT 152 IU and SGPT 124 IU; serum ammonia level was 242 #g/dl. The initial impressions were iron deficiency anemia with Reye snydrome, toxic encephalopathy, 'acute gastroenteritis, gastrointestinal obstruction, or hepatitis. Approximately 12 hours after admission, after being "rehydrated," the patient had a grand mal seizure lasting 10 minutes, and eventually needed ventilatory assistance for several hours. Several hours after the medical management of her seizures and cerebral edema, however, "lead flecks" were noted on the admission flat plate, and long bone films revealed "lead lines." The patient was chelated immediately (dimercaprol and versenate) for seven days, and later for five days more; she has received two more out-patient series of chelations with CaNaEDTA alone. Her pre-chelation blood lead concentration was 231 /~g/dl, and her first erythrocyte protoporphyrin obtained 13 days after the first chelation (when her blood lead had diminished to 46 btg/dl), was still markedly elevated at 829/Lg/dl. Fortunately, this patient has made a successful recovery after chelation therapy, correction
To the Editor: The differentiation of Reye syndrome from lead poisoning encephalopathy has previously been commented upon? However, Drs. Magnus, Powers, and Leong are to be congratulated on their astute differentiation of this case. They once again emphasize the importance of a good history and physical, and also of knowing the disease entities prevalent in your community. Donald W. Fox, D.O. Perinatal Services Welborn Baptist Hospital 401 S.E. Sixth St Evansville, I N 47713 Paul S. Bergeson, M.D. Good Samaritan Hospital Phoenix, A Z 85072 REFERENCE
1. Schubert W, Bobo RC, Partin JC, et al: Reye's syndrome, Disease-A-Month December, 1975.
Cerebral blood flow re intracranial hemorrhage To the Editor: We read the recent paper by Lou et aP with great interest. Impaired autoregulation of cerebral blood flow (CBF) in asphyxiated infants is noteworthy and, as they postulate, may have an etiologic implication to neonatal intracranial hemorrhage (ICH). We wish to draw your attention to some of our recent observations in this regard. To evaluate various factors which may contribute to ICH, 40 variables were analyzed in 198 consecutive infants requiring