IgE is a marker for visceral larva migrans.

Abstract

Dear Sir, Arora et al.[1] in their article titled “ophthalmic complications, including retinal detachment in hyperimmunoglobulinemia E (Job’s) syndrome: Case report and review of literature “have described a pediatric case. In a pediatric case report, source of history or “informer” should be mentioned. The informer (parents, grandparents, relatives, and stranger) decides reliability of history. A child can neither tell his age correctly nor can describe his problem accurately. In this case report nothing is mentioned about nutritional status of the child. Skinfold thickness is an age independent index[2] to diagnose under nutrition in situations where the child's age is not known. In scabies primary lesion is a burrow, a grey thread like serpentine line with a minute papule at the end, papules and papulovesicles may also be seen. Secondary streptococcal infection may result in acute glomerulonephritis. Scabies is an indicator of poor personal hygiene, overcrowding, lack of availability of basic amenities and poverty. A magnifying glass may be required to identify primary lesions. Vitamin D deficiency causes bone and joint abnormality. Probably pediatrician, radiologist, and orthopedician may be able to identify features of healed or active Vitamin D deficiency. Intestinal parasitic infections are an important determinant[3] of serum IgE level in children living in endemic areas of parasitic infection. Periodic anthelminthic treatments over 12 months are associated with reductions in IgE. The failure of anthelminthic treatment to reduce IgE levels to that considered “normal” in industrialized countries may be attributed to continued exposure of children to intestinal parasites or to the effects of infections in early life in programming a long lasting biased immunity. In industrialized countries total serum IgE level are affected by age and genetic factors. In intestinal parasitic infection serum IgE level may reach 22,608 IU/ml. Nail changes may be due to biting (habitual or stress) induced infection or poor hygiene. Ocular toxacariasis[4] cause peripheral granulomas, retinal folds, chronic endophthalmitis, and retinal detachment. Toxocariasis[5] is a wide spread native parasitosis caused by toxocara-type nematode larva. It is commonly seen in children less than 12 years of age in rural areas. They constitute neurological, ophthalmological, pulmonary, cutaneous, and sometimes rheumatological varieties. Periorbital edema, and strabismus has been described in children with visceral larva migrans. Usually differential diagnosis of allergy, eosinophilia-myalgia syndrome, neoplasia or other parasitic infections are made. Cerebral toxocariasis may present as encephalitis or mass lesion. Patient's characteristics and history, clinical symptoms and signs, positive serology, eosinophilia, increased levels of IgE are helpful markers in defining toxocariasis. Children may be anemic and stool culture may rule out other parasitic infection. Enzyme linked immunosorbent assay and Western blot are immunological test available to diagnose toxocariasis. Hypergamaglobulinemia may be present in some patient. Bilateral lagophthalmous indicates central nervous system involvement. Static and kinetic perimetry can be documented in patients greater than eight to ten years of age. In conclusion, the differential diagnosis of pediatric ophthalmology case is visceral larva migrans.