The Pig from North Jersey

Abstract

The telephone rang one morning and it was Peri Kamalakar, a physician who specialized in pediatric hematology. I met Peri in 1972, when I first came to New Jersey as a young attending pediatrician. I was the director of the pediatric clinic and Peri was the pediatric chief resident. He went on to study pediatric hematology and oncology and returned to the hospital years later as its pediatric hematologist. He had a patient that he wanted to discuss with me. The child was one of a set of twins that he was seeing for anemia (the child’s hemoglobin was 8.2 g/dL with a normal of over 11), referred by her pediatrician. The child in question had a low mean cell volume (MCV, a measurement of the size of a red blood cell with a normal of 70–100 fL) The child’s MCV was 50 fL, and she also had a low mean cell hemoglobin concentration (MCH, a measure of the concentration of hemoglobin, the oxygen carrying molecule, inside each red blood cell). This combination is commonly seen in iron deficiency, a common problem in small, rapidly growing children whose diets are frequently insufficient in iron. He had treated the child for iron deficiency thinking that the child had iron deficiency and thalassemia minor, a not uncommon inherited abnormality of hemoglobin formation seen in many individuals with ethnic origins in the greater Mediterranean basin (this child was ethnically an Italian American). Interestingly, he thought to draw a blood lead level and found that the lead level was elevated, 37 mcg/dL, which is in the moderately elevated range. (In 2012 the United States Centers for Disease Control and Prevention set a “reference level” for childhood blood lead levels at the top 2.5% of the population, or at that time 5 mcg/dL.) His call was to determine what I would suggest to do about the elevation in the lead level. I suggested that the treatment for iron deficiency continue and that he coordinate an investigation be initiated by the local health department in an effort to find the source of lead-exposure and to eliminate it. I further suggested that the lead level be watched to see if it might drop with the rise in the child’s iron and hemoglobin. Three months later, in August, his office called and told me that the child’s lead level was now 42 mcg/dL and I suggested hospitalization. Such an approach, I explained, would enable us to treat the child, lowering her lead level while separating her from any possible source of further lead exposure. During her hospitalization the public health officials could do their sleuthing, to determine the exposure source and eliminate it. The basic tenet of treatment of lead poisoning is to find the source or sources of exposure and to eliminate it/them. Medical therapy with medication is considered only as adjunctive therapy to the removal from the source.