No abstract

Parenteral exposure to blood-borne infectious agents is a relevant risk among healthcare workers in our region, particularly in defined job categories and hospital areas (surgeons, nurses, surgical, and intensive care areas). Immunization and educational efforts should be made along with better designs of devices to reduce the risk of infection.

We describe a large outbreak associated with a crusted (Norwegian) scabies case in an immunocompromised patient following treatment with TNF-α inhibitor (adalimumab) for psoriasis arthritis. The increasing use of TNF-α inhibitors should induce clinicians to consider this serious parasitic infection when evaluating skin rashes in patients receiving biologic therapies.

In 1985-1986, 634 adult dialysis patients were tested prior to hepatitis B vaccination, representing 40% of the total patients in Latium, an Italian region. HBsAg and anti-HBs prevalences were 7.1 and 36.0%, respectively. Merck, Sharp & Dohme (MSD) and Pasteur plasma-derived vaccines were randomly allocated to the 44 dialysis units. An anti-HBs response greater than or equal to 10 IU/l was elicited in 58.5% of 236 subjects tested at 6 months, 63.4% MSD and 52.4% Pasteur (p n.s.). The relatively low response to the vaccine in this high-risk group stresses the need to improve the efficacy of the vaccination and to maintain policies of environmental control.

Troxacitabine is a cytotoxic deoxycytidine analogue with an unnatural L-configuration, which is activated by deoxycytidine kinase (dCK). The configuration is responsible for differences in the uptake and metabolism of troxacitabine compared to other deoxynucleoside analogues. To determine whether troxacitabine has an advantage over other nucleoside analogues several cell lines resistant to cladribine and gemcitabine were exposed to troxacitabine, while blast cells from pediatric leukemia patients were tested for cross-resistance with other deoxynucleoside analogues. The gemcitabine resistant AG6000 (IC50: >3000 nM), and the cladribine resistant CEM (IC50: 150 nM) and HL-60 (IC50: >3000 nM) cell lines, all with no or decreased dCK expression, were less sensitive to troxacitabine than their wild type counterparts (IC50; A2780: 410, CEM: 71 and HL-60: 158 nM). dCK protein expression in CEM was higher than in HL-60, which, in turn, was higher than in A2780. Catalytically inactive p53 seems to increase the sensitivity to troxacitabine. The patient samples showed a large range of sensitivity to troxacitabine, similar to other deoxynucleoside analogues. Cross-resistance with all other deoxynucleoside analogues was observed.