Encephalopathy childhood

R. O., Plasma amino acids in childhood epileptic encephalopathies, Epilepsy Res., 34, 221, 1999. 

Health effects that have been associated with lead exposures during infancy or childhood include, anemia (Schwartz et al. 1990) (and related disorders of heme synthesis), neurological impairment (e.g., encephalopathy), renal alterations, and colic (Chisolm 1962, 1965 Chisolm and Harrison 1956), and impaired metabolism of vitamin D (Mahaffey et al. 1982 Rosen and Chesney 1983). Death from encephalopathy may occur with PbB levels 125 pg/dL. In addition to the above effects, the following health effects have been associated with lead exposures either in utero, during infancy or during... 

Fatty liver, encephalopathy, and sudden unexpected death in early childhood due to medium-chain acyl-coenzyme A dehydrogenase deficiency. 

Reye, R.D.K., Morgan, G., Baral, J. Encephalopathy and fatty degeneration of the viscera. A disease entity in childhood. Lancet 1963/11 749 -751... 

Gleeson JG, duPlessis AJ, Barnes PD, Riviello JJ Jr. Cyclosporin A acute encephalopathy and seizure syndrome in childhood clinical features and risk of seizure recurrence. J Child Neurol 1998 13(7) 336 4. 

The 1994 report of the Institute of Medicine concluded that the evidence was inadequate to accept or reject a causal relation between MMR and encephalopathy, and it is known that the incidence of encephalitis after measles immunization of healthy children tends to be lower than the observed incidence of encephalitis of unknown cause. Two large studies have been negative. In a study analogous to the British Childhood Encephalopathy Study there were no increased risks of either encephalopathy or neurological sequelae after measles immunization (19). A retrospective case-control study through the CDC Vaccine Safety DataUnk assessing the risk for 300 000 doses of MMR found not a single case of encephalitis/ encephalopathy within 30 days of the administration of MMR (20). In contrast, the review mentioned above (18) reported an association between measles vaccine and encephalopathy. However, the conclusion of the report of the Institute of Medicine is still valid, namely that evidence is stiU inadequate to accept or reject a causal relation between measles vaccine and these diseases. 

In 1993, Miller and colleagues (28) and Madge and colleagues (29) presented the results of a 10-year follow-up study of the National Childhood Encephalopathy Study... 

Madge N, Diamond J, Miller D, Ross E, McManus C, Wadsworth J, Yule W, Frost B. The National Childhood Encephalopathy stndy a 10-year foUow-np. A report on the medical, social, behavionral and edncational ontcomes after serious, acute, neurological illness in early childhood. Dev Med Child Nenrol Snppl 1993 68 1-118. 

Schreeder MT, Favero MS, Hughes JR, et al Dialysis encephalopathy and aluminum exposure an epidemiologic analysis. Journal of Chronic Diseases 36 581-593, 1983 Sedman AB, Wilkening GN, Warady BA, et al Encephalopathy in childhood secondary to aluminum toxicity. J Pediatr 105 836-838, 1984 Terry RD, Pena C Experimental production of neurofibrillary degeneration. J Neuro-pathol Exp Neurol 24 200-210, 1965... 

Nevin R How lead exposure relates to temporal changes in IQ, violent crime, and unwed pregnancy. Environ Res 83 1-22, 2000 Niklowitz WJ, Mandybur TI Neurofibrillary changes following childhood lead encephalopathy. J Neuropathol Exp Neurol 34 445-455, 1975... 

To complicate matters further, in childhood diabetes, in recent years, type 2 diabetes, characterized by insulin-resistance instead of insulin absence, has become more prevalent among children. Just one decade ago, it would not have been included in the differential diagnosis of pediatric encephalopathy. Recognition of type 2 diabetes in children, and its potential lethality, is very recent. A report fi om Horida in 2004 described a cluster of seven obese African American youth who were initially thought to have died from DKA due to type 1 diabetes, despite meeting the criteria for the hyperglycemic hyperosmolar state characteristic of type 2 diabetes and not for DKA. All had previously unrecognized type 2 diabetes (Morales and Rosenbloom, 2004). 

It was earlier noted that human childhood lead encephalopathy is found with blood lead levels in the range 100-800/tg Pb/100 ml. It is a widely held view that animal models of human lead encephalopathy are of limited value (perhaps due to early experiments on adult animals, which, like man, show relatively little neurological disturbance even with prolonged and intensive dosage). However, this chapter shows that with lead exposure during development, blood levels of the same order of magnitude are associated both in man and rat with comparable encephalopathic lesions. 

Ohnishi, A., Schilling, K., Brimijoin, W. S., Lambert, E. H., Fairbanks, V. G. and Dyck, P. J. (1977). J. Neuropathol, Exp, Neurol, 36, 499 Okazaki, H., Aronson, S. M., DiMaio, D. J. and Olvera, J. E. (1963). Acute lead encephalopathy of childhood. Histological and chemical studies with particular reference to angiopathic aspects. Trans, Am, Neurol, Assoc, 88, 248 Oliver, T. (1891). Lead Poisoning, (Edinburgh Bentland)... 

American children with severe Pb poisoning, mainly due to Pb paint Acute and chronic pediatric Pb encephalopathy Early studies that established U.S. childhood Pb poisoning as a serious problem confirmed the Australian child Pb poisoning findings foretold the later epidemic of U.S. childhood Pb poisoning Blackfan (1917), Thomas and Blackfan (1914), McKhann and Vogt (1926)... 

Niklowitz, W.J., Mandybur, T.I., 1975. Nemofibrillary changes following childhood lead encephalopathy case report. J. Nerrropathol. Exp. Nerrrol. 34, 445—455. 

This chapter describes the acute and chronic nephrotoxic effects of lead in human populations. These effects have long been recognized in chronic adult occupational lead exposures and in nonoccupational adult exposures arising from dietary Pb intakes, producing disorders such as gouty nephropathy. In acute childhood Pb exposure, severe kidney effects in the form of Fanconi syndrome were identified in the early pediatric literature. The syndrome often co-occurred with acute encephalopathy. 

Rosenfeldt, V., Valerius, N.H., and Paerregaard, A. 2000. Regression of HIV-assoeiated progressive encephalopathy of childhood during HAART. Scand J Infect Dis 22(5), 571-574. 

Subcellular mechanisms in lead toxicity Significance in childhood encephalopathy, neurological sequelae, and late dementias. In Neurotoxicology, edited by L. Roizin, H. Shiraki, and N. Arcevic (ed.) p. 289. New York Raven Press (1977). 

One such issue is age, which is of concern from at least two perspectives. The first is the life cycle stage at which exposure occurs. The predominant focus of experimental studies has been prenatal and neonatal lead treatment. Such exposure regimens, however, have little correspondence with the environmental lead exposures encountered by humans. The National Academy of Sciences (NAS, 1975) reported, for example, that the peak incidence of childhood lead encephalopathy and elevated lead burden occurs between 1 and 3 years of age, a stage of maturation far more advanced than that represented by prenatal or neonatal rodents. Dobbing (1951) has suggested that the newborn rat is equivalent to an 15-week-old fetus. 

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