Abstract

Background: Pica is known to be common in children with sickle cell disease but there is no information about this disorder in adults with SCD. The cause of pica in SCD is not known; a small minority of cases are due to iron deficiency.

Aims: The purposes of this study are to characterize pica in adults with sickle cell disease, to compare it with pica as it occurs in children with the disorder, and to determine the prevalence of pica in the non-SCD siblings of individuals with SCD. The underlying hypothesis is that there is an unidentified nutritional deficiency which stimulates pica in individuals with SCD. The current report presents the data from adult SCD subjects.

Subjects and Methods: A structured interview was designed and administered to a convenience sample from Sickle Cell Clinic at UNC. Laboratory and radiologic data were collected from the subjects’ medical records. The data used were from steady state on the date closest to the interview date. No data that were more than 5 years from the interview date were used.

Results: There were 86 participants, 73 with SS or Sβ0thal, 13 with SC or Sβ+thal. The mean age was 37 years, with a range of 19 to 63. Fifty-five percent were female. Any pica. Seventy-six percent of the participants had had pica at some time during their lives; a similar proportion was found in both the SS/Sβ0thal as in the SC/Sβ+thal group. Pica was more prevalent in females, with 60% of females reporting ever having had pica vs 40 % of males. The majority of these reported having had pica as a child, with a mean age of onset of 7 years and a mean duration of 6 years. This group was significantly more likely to have a sibling with pica than those who had never had pica(52 vs 5%, p <.0001). Current pica. Sixteen percent (13 individuals) reported having pica currently, 10 females and 3 males; eleven were SS or Sβ0thal, and 2 were SC or Sβ+thal. All reported having begun pica during childhood at a mean age of 6 years. They were significantly more likely to report having been diagnosed with a nutritional deficiency than those without recent pica(39 v 14%, p=.04). Males with current pica had significantly lower bmi than those without pica (20 vs 23kg/m2, p=.0002). Although none with recent pica had ferritin within the iron deficient range, those with recent pica had significantly lower mean ferritin than those without recent pica (374 vs 1256ng/mL. p<.0069). No other hematologic or biochemical difference was seen between those with and without recent pica. There was also no difference in rate of osteopenia in the hip or spine, by xray, between the two groups. Seventy-five percent with current pica had a sibling with pica vs 34% without current pica(p=.007). Eighty-three percent reported having seen other family members eat non-food vs 50% of those without current pica. One third with current pica reported having been influenced by a family member to engage in pica, vs 9% of those without current pica.

Conclusions: Pica is common in SCD, but in a majority of cases it is a childhood phenomenon. Persistent pica in adults with SCD is associated with a low-normal bmi in males, significantly different than the unaffected males. Ferritin levels are high overall in this population but are significantly lower in those with recent pica than those without recent pica. The familial environment appears to affect the occurrence of pica; it cannot be determined from these data whether this influence is genetic or environmental.

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