The mycotoxin zearalenone exhibits estrogenic and anabolic properties in several animal species, humans included. Food contamination by zearalenone is caused either by direct contamination of grains, fruits and their based-products or by "carry-over" of mycotoxins in animal tissues, milk and eggs after intake of contaminated feedstuff. Now, a survey on zearalenone contamination in breast milk of healthy primiparous women living in the Naples countryside was conducted. From 47 healthy primiparous women, breast milk samples were collected within the first six weeks after delivery as well as clinical data of mother-newborn pairs. Breast milk analyses were performed with both competitive indirect enzyme-linked immunosorbent assay and high-performance liquid chromatography with fluorescence detection. At 36.9 ± 2.6 days after vaginal delivery, the mean zearalenone contents of the breast milk samples was 1.13 ± 0.34 µg/L . The zearalenone levels correlated with both mother weights before pregnancy (r = -0.506; P < 0.001) and at delivery (r = -0.351; P < 0.05). The present results indicate that breast milk may be contaminated with zearalenone.

Background: Homozygous mutations in acid-labile subunit (IGFALS) gene result in short stature, very low circulating levels of acid-labile subunit (ALS), insulin growth factor 1 (IGF1) and insulin growth factor binding protein 3 (IGFBP3) and a poor response to growth hormone (GH). The impact of IGFALS mutations heterozygosity on growth is unknown. Patient and Methods: We describe a 10-year-old girl with severe short stature (height -3.2 SDS), heterozygous for a new IGFALS mutation. Results: The girl showed low circulating IGF1, IGFBP3 and ALS levels and normal GH secretion. We found a novel heterozygous frameshift IGFALS mutation (c.1283delA, p.Gln428Argfs*14). Size-exclusion chromatography showed a reduction of the IGF1, IGFBP3 and ALS 150-kDa ternary complex (by about 55%) compared to a control. An IGF-1 generation test, with two different GH dosages, showed a good response in term of increase in IGF1 and in formation of the ternary complex at size-exclusion chromatography. Clinical response after 6 months of therapy with GH was satisfactory (height velocity increased from 3 to 8 cm/year). Conclusion: We suggest that (1) heterozygous IGFALS mutations can be responsible for a subset of patients with severe short stature (below -2.5 SDS), low IGF1 (below -2 SDS) and normal GH secretion, and (2) the identification by IGFALS molecular screening of this subset of patients could help in the administration of the appropriate therapy.