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OBJECTIVES: To determine the prevalence of iron depletion and deficiency, and iron-deficiency anaemia, along with risk factors for iron depletion, in Australian-born children aged 12-36 months of Arabic-speaking background. DESIGN: Community-based survey. SETTING: Central Sydney Area Health Service (CSAHS), NSW, April to August, 1997. PARTICIPANTS: All children born at five Sydney hospitals between 1 May 1994 and 30 April 1996, whose mothers gave an Arabic-speaking country of birth and resided in the area served by the CSAHS. MAIN OUTCOME MEASURES: Full blood count (haemoglobin, mean corpuscular haemoglobin, mean corpuscular volume), plasma ferritin concentration, haemoglobin electrophoresis, potential risk factors for iron depletion. RESULTS: Families of 641 of the 1,161 eligible children were able to be contacted, and 403 agreed to testing (response rate, 62.9% among those contacted). Overall, 6% of children had iron-deficiency anaemia, another 9% were iron deficient without anaemia, and 23% were iron depleted. Multiple logistic regression analysis showed three significant independent risk factors for iron depletion: <37 weeks' gestation (odds ratio [OR], 5.88, P=0.001); mother resident in Australia for less than the median time of 8.5 years (OR, 1.96, P=0.016); and daily intake of >600 mL cows' milk (OR, 3.89, P=<0.001). CONCLUSION: Impaired iron status is common among children of Arabic background, and targeted screening is recommended for this group.

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Haemoglobinopathies are now common in Australia following the migration of people from areas of high prevalence. This article gives practical advice on the management of patients incidentally found to be heterozygotes for the more common forms and also outlines complications of major haemoglobinopathies that are seen in family practice.

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A 2 year old girl presented with fever, malaise, a maculopapular rash and lymphadenopathy followed by the onset of haemolytic anaemia and massive splenomegaly. Serology was consistent with acquired toxoplasmosis. A 6 week course of pyrimethamine resulted in a rise in the haemoglobin and reduction of the splenomegaly. During the subsequent 10 years, pyrimethamine treatment of three similar acute episodes resulted in similar clinical responses. There was no spontaneous improvement in the haemolytic anaemia or splenomegaly when pyrimethamine was initially withheld for 6, 1, and 1.5 months respectively during three of these episodes. Investigations did not reveal an immunodeficiency state. This case suggests the possibility of a previously unreported causal association between acquired toxoplasmosis and haemolytic anaemia in a child.

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In the past decade, we have studied four unrelated children with what we believe is a previously unreported disorder affecting the bone marrow and exocrine pancreas. During infancy these patients had the onset of severe, transfusion-dependent, macrocytic anemia plus a variable degree of neutropenia and thrombocytopenia. Their bone marrows had normal cellularity but were characterized by remarkable vacuolization of erythroid and myeloid precursors, hemosiderosis, and ringed sideroblasts. The vacuoles probably represented manifestations of cellular degeneration and death. In two patients, in vitro bone marrow cultures showed abnormal erythroid and myeloid progenitor cell growth and, in one child, abnormal vacuolated erythroid colonies. Family histories were unrevealing, parents were hematologically normal, and both sexes were involved. There was no evidence of specific nutritional deficiencies or exposure to agents associated with marrow vacuolization. A number of therapeutic interventions produced no effect. One child had clinical malabsorption. This child and one other had extensive pancreatic fibrosis at autopsy. The other two patients had findings indicating exocrine pancreatic dysfunction. Two children had splenic atrophy. This new syndrome, with associated bone marrow and exocrine pancreatic dysfunctions, differs in several respects from the syndrome of pancreatic liposis and neutropenia described by Shwachman et all and Bodian et al, and from other conditions with vacuolization of the marrow or sideroblastosis.

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Iron nutrition in infants was studied in a double-blind trial with artificial milk formula. Statistically significant differences were observed with the iron-fortified formula. Not all haematological indices showed significant differences. The fragiligraph technique result was the only parameter showing differences not influenced by other variables examined.

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Compensatory mechanisms in children with iron-deficiency anemia were evaluated by measuring erythrocytic organic phosphates and, in some cases, shifts in the P50 of the oxygen dissociation curve. In 19 children with nutritional anemia (hemoglobin values of 3.2 to 8.2 gm/dl) there was a calculated improved oxygen delivery to tissues equivalent to a hemoglobin level of at least 7.5 gm/dl. Transient decompensation was observed during acidosis. In five children with iron-deficiency anemia due to blood loss and in one child with rheumatoid arthritis no such compensatory changes were observed.

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