[Pesticide poisoning referred to the Poison Center of Milan in 1995-1998]. / Intossicazioni da prodotti antiparassitari rilevate dal Centro Antiveleni di Milano nel periodo 1995-1998.

From 1995 through 1998 the Poison Control Centre of Milan identified 7594 cases of suspected or confirmed cases of acute pesticide poisoning. Domestic use products accounted for 4483 (59%) of the cases. Of these, 84% occurred at home and 48% in children under five. The most frequently reported domestic use products were pyrethrins/pyrethroids (26%), fertilizers (19%) and camphor/naphthalene (12%). Of 3111 cases (41%) due to agricultural products, 10% were children under five and 69% were males. Half of the poisonings from agricultural products occurred at home, the remainder at workplace. The products most frequently reported were organophosphates (26%), pyrethrins/pyrethroids (9%), and carbamates (9%). These preliminary data indicate the importance of implementing prevention programs to reduce pesticide poisonings with particular reference to young children.

No association between genetic hemochromatosis and alpha1-antitrypsin deficiency.

Genetic hemochromatosis and alpha1-antitrypsin (AAT) deficiency are frequent in white populations. Conflicting data on the association of the two conditions and on the severity of the disease in those in whom these disorders coexist have emerged from analyses of small numbers of patients. To determine if the frequency of AAT deficiency is increased in genetic hemochromatosis, we characterized this protein by isoelectric focusing and DNA analysis in 115 Italian patients with the disease and 290 controls. The frequency of AAT deficiency in patients with genetic hemochromatosis was similar to that in controls (10% and 9%, respectively). The prevalence of cirrhosis in patients with genetic hemochromatosis with MM phenotype was 53%, compared with 58% in those with non-MM phenotype; that of hepatocellular carcinoma, occurring only in cirrhotic patients, was 22% and 28%, respectively. In conclusion, the frequency of AAT deficiency was not increased in our large series of Italian patients with genetic hemochromatosis. Patients in whom the two defects coexisted did not appear to have a more severe disease, but the limited number of subjects with non-MM phenotype does not allow a conclusive evaluation of clinical differences between them and patients with genetic hemochromatosis with MM phenotype.