Human herpesvirus-8 (HHV-8) causes Kaposi's sarcoma (KS) and lymphoproliferative disorders in both HIV-infected and uninfected patients. HHV-8 has a worldwide occurrence but infection rates vary according to a combination of geographic and behavioral risks. The main transmission route seems to be sexual, nevertheless, nasal secretions, saliva, blood, and organ graft have been proposed. HHV-8 was postulated as a new infectious agent for screening in blood donors. The aim of this study was to evaluate the prevalence of antibodies against HHV-8 antigens in blood donors of South America. Serum samples from 2,470 blood donors from Argentina, Brazil, and Chile corresponding to five geographic regions were studied by indirect immunofluorescence assay (IFA). Seroprevalence rate was 3.7% (92/2,470; 95% CI 2.9-4.5) in the entire blood donor population distributed as follows: Argentina, 4.0% (Buenos Aires city, 4.3%; Bahia Blanca, 2.4%; and Córdoba, 4.0%), Campinas (Brazil), 2.8%; and Santiago de Chile, 3.0%. There was no difference (P>0.05) between men and women or age related, except in Brazil where positive cases were 30-49-year-old males. The present study, which includes different geographical areas of multiple countries from South America, has not been done before. The results show similar prevalence rates among the studied zones corresponding to low-prevalence regions. South America is a large sub-continent with a wide spectrum of population and geographical characteristics, thus, more HHV-8 prevalence studies should be necessary to establish possible regional differences.

Mild chronic neutrofilia is a frequent reason for hematologic consultation and in 70% of the cases there is no identifiable cause. Objective: to determine if smoking habit could be the etiology for leucocytosis with neutrophilia in smokers with no other pulmonary associated disease. Materials and Methods: We questioned 300 consecutive blood donors from our institution, elaborating a complete record of smoking habit. Immediately before blood donation an automated complete blood count was performed. Leucocytosis was defined as a white cell count above 11 x 109/L, and neutrophilia as a neutrophil count over 7.7 x 109/L. All data is stated as mean value ± 1 SD. Results: we studied 195 (65%) men and 105 (35%) women (n=300). Mean age was 36.5 y.o. (18–69). Fifty-five percent (165/300) smoke or were previous smokers; 8.4% (14/165) of these, did not smoke at the time of this investigation, and only two have quit smoking a year prior to questioning. Mean time of duration of smoking habit was 16.4 years ± 10.6 and the average amount of cigarettes smoked through life (estimated from data referred along different phases of each subject’s history) was 1.26 x 105 ± 1.21 x 105. In the following table results from smokers (previous or actual) vs. non-smokers are compared. Leucocytosis was present in 37/165 (22.4%) of smokers and in 3/135 (2.2%) of non-smokers (p<0.001) and neutrophilia was noted in 19/165 (11.5%) of smokers and in 2/135 (1.5%) of non-smokers (p<0.001). None of the volunteers had a WBC count over 20 x 109/L. A direct association was established for the number of cigarettes smoked and the WBC count and neutrophil count. Discussion: smoking habit affects ciliar movement, inhibits alveolar macrophage function and produces hyperplasia on mucous glands within bronquial walls. These alterations result in entrapment of mucous secretions that will ultimately lead to bacterial colonization. The neutrophilia observed in smokers would be the result of a normal physiologic response to a potential infectious focus. In conclusion, is our understanding that the smoking habit should be considered as a common etiology for mild leucocytosis and neutrophilia. Smokers (n:165) Non-smokers (n:135) p (t-test) WBC x 109/L 9.6 ± 2.1 6.8 ± 1.3 < 0.001 Neutrophils x 109/L 5.7 ± 1.6 3.9 ± 1.0 < 0.001 Hct % 45.9 ± 3.7 45.2 ± 3.6 NS Platelets 207 ± 48.7 206.4 ± 45.8 NS

Introduction: The treatment of chronic myeloid leukemia (CML) suffered a dramatic change with the introduction of Imatinib mesylate. This drug has become the choice for first line treatment of CML. However, it has been shown that the effectiveness of the treatment requires a high compliance with the prescribed dose for a long period of time, and sub-dosing has been associated with a delay in achieving cytogenetic response and development of resistance. We conducted a prospective case-control study, in order to analyze how a better compliance affects the cytogenetic response to Imatinib. Materials and Methods: Between January and June 2006, 24 patients with newly diagnosed Phi (+) chronic phase CML were recruited and followed for the next 12 months. Patients were put on 400mg of Imatinib and were asked to note down all taken doses, and reasons for non-compliance. During each of the monthly visits, the dosing schedules were revised, non-adherence reasons were discussed and the medication was counted. All adverse events were noted and graded according to the NCI CTCAE (VERSION 3.0) code. Reductions or interruptions in the schedule were only allowed for related adverse events with a CTC score ≥3. All other events were treated accordingly, without modifications in the Imatinib dosing. As a control group, we matched each case with a chronic phase Phi (+) CML patient from our data base (controls were matched for sex, age, and hematological response). Only patients who received treatment with Imatinib and with complete information about dosing and adverse events were acceptable as controls. Compliance was measured as: mg taken /mg prescribed x 100 during the study period. Cytogenetic response was reported as the percentage of t(9;22) negative metaphases. Results: Twenty-four patients, 14 males with median age 55 yo (range: 23–82) were included in the study; three were lost to follow up, leaving only twenty-one for analysis of compliance. At the end of the year of follow up, all patients have achieved a complete hematological response. Compliance during the 12 months was 96.1 ± 9% 1SD for the cases group, which is clearly superior to the 80% reported in the setting of clinical trials. As for one year cytogenetic response, 60 ± 25% of the control group achieved a mayor response (Phi < 35%), while 89.9 ± 20% of the cases achieved that same response. This difference is statistically significant with a p=0.027. The incidence of adverse events was similar for both groups, being nausea, vomiting, peripheral edema and skin rash the most common ones. As for hematological toxicity, CTC grade 1–2 leucopenia (11%) and thrombocytopenia (17%) were the more frequent. However, although moderate, these were the main reasons for interruption or reduction of Imatinib dosage in the control group. Conclusions: This study shows that improving compliance is associated with a better cytogenetic response. As this response is the ultimate goal in the treatment of CML patients, physicians should make an effort to assure the best adherence to the treatment and avoid sub-dosing. Doing this will help patients obtain a better cytogenetic response which has already proved to be essential for long term survival in CML.

A woman on daclizumab developed thrombotic microangiopathy secondary to cyclosporine after a living-unrelated kidney transplant. Despite cyclosporine discontinuation, hemolysis persisted. The second dose of daclizumab was postponed 24 h, and after a maximum of two sessions of plasmapheresis (to avoid further modifications in daclizumab schedule) with plasma exchange, daclizumab was administered. Plasma infusions were prescribed until D-dimer and fibrinogen-degradation products normalized; thereafter, FK-506 was started without recurrence of the hemolytic picture and renal function restored. This observation suggests that in patients on daclizumab who develop thrombotic microangiopathy secondary to immunosuppressants, if discontinuation of the offending drug is unsuccessful, plasmapheresis with plasma exchange can be performed when the lowest levels of daclizumab exist, followed by daclizumab infusion. Plasma prescription must be continued thereafter until D-dimer and figrinogen-degradation products normalize. However, if hemolysis persists when daclizumab levels are high, plasma infusions are useful and plasmapheresis avoided. FK-506 administration did not result in recurrence of hemolysis during daclizumab induction.

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