Neuropathy infants

There has been one report of the development, within 2 years, of sensory neuropathy in an infant with vitamin Be -dependent seizures treated with 2,000 mg per day, but over the following 16 years, the neuropathy did not progress (McLachlan and Brown, 1995). However, most reports of patients with vitamin Be dependency diseases (Section 9.4.3) do not mention sensory neuropathy. One study has reported electrophysiological and neurological examination of 17 homocystinuric patients who had been treated with 200 to 500 mg ofvitamin Be per day for 10 to 24 years there was no evidence ofneuro-pathy (Mpofu et al., 1991). 

There has been one report of the development, within 2 yeetrs, of sensory neuropathy in an infant with vitamin Be -dependent seizures treated with... 

Vincristine is an anticancer drug that causes peripheral neuropathy, and, in clinical trials, younger patients appeared to be more susceptible to this toxicity. Vincristine clearance based on BSA was lower in infants compared to older children and adolescents (Figure 23.14), thus a dose scaled to BSA would result in higher plasma concentrations in younger patients... 

The functions of vitamin E may be to take up (scavenge) the free radicals generated by normal metabolic process and by substances in the environment, e.g. hydrocarbons, and so to prevent them attacking polyunsaturated fats in cell membranes with resultant cellular injury. A deficiency s5mdrome is now recognised, including peripheral neuropathy with spinocerebellar degeneration and a haemolytic anaemia in premature infants. 

Willems JL, Nicaise M, DeBisschop HC Delayed neuropathy by the organophosphorus nerve agents soman and tabun. Arch Toxicol 55 76-77, 1984 Xintaras C, Burg JR, Tanaka S, et al NIOSH Health Survey of Velsicol Pesticide Workers Occupational Exposure to Leptophos and Other Chemicals. Cincinnati, OH, U.S. Department of Health, Education, and Welfare, 1978 Zwiener RJ, Ginsburg CM Organophosphate and carbamate poisoning in infants and children. Pediatrics 81 121-126, 1988... 

Nitrofurantoin (Macrodanrin, Furadanrin, Macrobid) [Urinary Anri-infective] WARNING Pulm Rxns possible Uses Prevendon Rx UTE Action Bacteriostatic iaterferes w/ carbohydrate metabolism. Dose Adults. Suppression 50-100 mg/d PO Rx 50-100 mg PO qid Peds. Suppression 1-2 mg/kg/d ia 1—2 + doses, max 100 mg/d Rx 5—7 mg/lcg/24 h ia 4 + doses (w/ food/milk/antacid) Caution [B, +] Avoid w/ CrCl <60 ml ymin, PRG at term Contra Renal failure, infants <1 mo Disp Cperipheral neuropathy Interactions T Effects W/ probenecid, sulfinpyrazone 4 effects w/ antacids, quinolones EMS May affect glucose (hypoglycemia) may discolor urine OD May cause N/V give IV fluids... 

Concomitant deficiencies of other B vitamins, notably thiamine and pyridoxine, probably participate in the pathogenesis of the dementia of pellagra. Pyridoxine deficiency is associated with a peripheral neuropathy in adults and seizures in infants. Victor and Adams (1956) found that pyridoxine-depleted monkeys develop diffuse cerebral pathology similar to, but not absolutely the same as, that found in human pellagra. 

Lead colic has long been recognized among clinicians as a symptomatic correlate of clinical-level lead exposures in infants, toddlers, and highly exposed lead workers. The earlier literature has been described in several expert consensus documents (NAS/NRC, 1972 U.S. CDC, 1978 U.S. EPA, 1977, 1986). Typically, the clinical G1 effects of Pb that are clustered under the label of lead colic include anorexia, abdominal pain, constipation, nausea, and vomiting. These may empt along with acute encephalopathy or be a persistent feature of chronic neuropathy in infants and toddlers, while Pb workers are typically plagued with chronic G1 disturbances. 

Vitamin E deficiency is seen rarely in humans. However, there may be a risk of vitamin E deficiency in premature infants because the placenta does not transfer a-tocopherol to the fetus in adequate amounts. When it occurs in older children and adults, it is usually a result of lipoprotein deficiencies or a lipid malabsorption syndrome. These include patients with abetalipoproteinemia or homozygous hypobeta-lipoproteinemia, those with cholestatic disease, and patients receiving total parenteral nutrition. There is also an extremely rare disorder in which primary vitamin E deficiency occurs in the absence of lipid malabsorption. This disorder is a rare autosomal recessive neurodegenerative disease caused by mutations in the gene for a-TTP. This disorder is known as ataxia with vitamin E deficiency (AVED). Patients with AVED have extraordinary low plasma vitamin E concentrations (<5pgml ) and have an onset between 4 and 18 years, with progressive development of peripheral neuropathy,... 

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