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Introduction: The human parvovirus B19 (pvB19) is well known as a cause of chronic anemia and red cell aplasia, this due to the high tropism for the erythroid progenitor cells where it replicates. Some reports have suggested that the infection of this virus is related to an erythropoietin resistance in patients with chronic anemia and kidney failure. The most frequent causes of erythropoietin resistance are iron deficiency, chronic inflammation process, vitamin deficiency, hyperparathyroidism and malignancies among others. The aim of this study was to detect the viral DNA of PvB19 and its correlation with hemoglobin levels and human erythropoietin dosage in patients with kidney failure under hemodialysis treatment. Patients and Methods: All patients had chronic renal failure and were undergoing hemodialysis. The detection of the viral DNA was performed by qualitative polymerase chain reaction (PCR). The PCR reaction was carried out using one specifically designed primer set for PvB19 that encoded for a structural capsid protein (VP1). Erythropoietin resistance (ER) was diagnosed using the European Best practice Guidelines as stated by Hay N (Nephrology, 2002). Results: A total of 58 samples of peripheral blood were obtained from patients with chronic kidney failure. Mean age was 59.41 (23 to 85 years) and mean Hemoglobin levels were 10.1 g/dL (7–14). Iron was normal in all patients and no patient had active infections. Fifty two patients (89.65%) were receiving recombinant erythropoietin. Among all the samples, 3 cases met ER criteria but only in 1 of them did we find the viral DNA (1.72%). Three cases (5.17%) positive to the viral DNA were found in the non erythropoietin resistance group. Conclusion: Although ours is a small group and we are still gathering samples, up until now, no relation appears to exist between the presence of PvB19 genetic material and ER.

Introduction: Anemia is a common finding in most developing countries. Of all populations, children are the ones who suffer most from anemia due to the long-term effects it can have on their growth and development. Large scale public programs to prevent anemia should always be based on epidemiological studies from significant sample sizes. Patients and Methods: We included elementary school children from the state of Nuevo León, in northern Mexico (pop 4.2 million). We selected the children from eight public schools, six from Monterrey’s metropolitan area (pop 3.5 million) and two from the suburban area (pop. 0.5 million), mimicking the population distribution in our state. Three of these elementary schools give out school lunches consisting of milk and peanuts. Hemoglobin levels were obtained by using a Beckman-Coulter HMX® automated system (Miami, FL). We defined anemia as less than 12 g/dL of hemoglobin. Results: After obtaining informed consent from the parents, we studied 1,137 children (550 males, 587 females), all of them between 6 and 12 years of age. Mean hemoglobin was 13.18 g/dL for females and 13.27 g/dL for males. We found 53 cases of anemia: 21 males and 32 females. Among the 53 anemic patients, 50 had hemoglobin between 11–12 g/dL, 1 between 10–11g/dL and 2 between 9–10 g/dL. We found significant differences in mean leukocyte numbers (7,200 vs 6,500/uL P=0.018); Mean Corpuscular Volume (82.9 vs 82.10 fL P=0.39); Mean Corpuscular Hemoglobin (29 vs 28.6 ug P=0.001), between the non-anemic and the anemic patients. Comparing the number of anemic children between schools with (28.7%) and without (71.3%) school lunches, the proportion of anemic children was significantly increased (26 vs 27 P=0.001) in schools that do not provide this school lunch. Conclusions: Our results show a very accurate picture of the status of anemia in the urban and suburban areas of the state of Nuevo Leon in northeastern Mexico. Although one anemic child is one to many, our results show marked improvement when compared with our national means. Even though there are other factors that influence the absence of anemia in the different schools, the administration of the school lunch appears to have beneficial effects on anemia in our population.

INTRODUCTION: Acute Graft-versus-host disease (aGVHD) is a major complication of allogeneic stem cell transplantation (alloSCT). Risk factors include patient age, sex matching, CMV status and degree of match. Regulatory T cells are critical for immune tolerance processes such as aGVHD, and express the transcription factor FOXP3, a member of the forkhead/winged-helix family, identified as a key regulatory gene required for the development and activity of these cells. It has been suggested that genetic expression of FOXP3 is inversely correlated with the severity of the GVHD. We studied donor’s DNA looking for 5 polymorphisms on the promoter region of the FOXP3 gene, and we tried to correlate them with presence and degree of aGVHD. PATIENTS AND METHODS: We studied donors of stem cells for allogeneic stem cell transplants. We looked for the presence of the following polymorphisms by PCR: POL01 −5906 T/A rs2869211; POL03 −3279 A/C rs3761548 ; POL04 −2383 C/T rs3761549 ; POL05 −1383 C/T rs2232364 ; POL06 −924 A/G rs2232365. RESULTS: Our sample consisted of 31 donors, all siblings. In them we found only 2 of the 5 FOXP3 polymorphisms, either as homozygous or heterozygous. These polymorphisms were found in 15/31 donors, with 12 being homozygous (38.7%), and 3 heterozygous (9.7%). These genes polymorphisms were POL03 y POL06. The most observed polymorphism was POL-06 with 9 cases, while POL-03 was found in 6 donors. Only sex difference and CMV status had an elevated hazard ratio for developing GVHD (HR=1.18, CI95%: 0.18 to 7.64; p=0.85) and (HR=3.0, CI95%: 0.07 to 126; p=0.46) respectively. We found no statistically significant difference in the incidence of GVHD between patients who had received cells from donor with or without a FOXP3 polymorphism (p=0.87). When we analyzed the risk of presenting GVHD, results suggest that having one of the 2 positive polymorphisms of the FOXP3 gene could have a protective effect for the patient. For POL03 HR=0.87, CI95%:0.18 to 4.14; p=0.86, and for POL06, HR=1, CI95%: 0.37 to 2.64, p=0.67. CONCLUSIONS: Even though our sample is still small to make conclusive remarks, we believe that our results point toward some level of “protection” from acute GVHD in patients receiving cells from donors expressing POL03 and POL06. It is also worthwhile mentioning the relatively high frequency of these polymorphisms, as well as the absence of the other 3.

CNS infiltration of neoplastic B-cell lymphocytes both in acute leukemia as well as in lymphoma, carry very bad prognosis. There are no universal guidelines for the prophylaxis of such CNS relapse in these patients. Current prophylactic regimes have early and late side effects, sometimes with severe toxicities. Although rituximab has improved treatment results in lymphoproliferative diseases, it cannot reach the CNS when administered systemically (Feugier, Ann Oncol 2004, Rubenstein, Blood 2004). Schulz (Haematologica 2004) used this drug in the treatment of relapse of primary brain lymphomas with positive results using a dose of 10 to 40mg, and estimated 25mg to be a good standardized dose. After approval from our ethics committee and obtaining the informed consent signature, patients received 25 mg of intrathecal rituximab (IT-R) according to the standard intrathecal regimen, plus the standard systemic chemotherapy protocol in our department. Side effects were evaluated according to the NIC toxicity scale. Nine patients have been enrolled in the protocol so far: 8 were male and 1 female, median of age was 49 years (range 14–72). A total of 57 IT-R were administered to our patients (median: 6, range 3–15). They had the following diagnosis: Two with large diffuse B cell lymphoma (LDBCL); two with mantle cell lymphoma (one of them blastic type), three with acute lymphoblastic leukemia; one with Burkitt’s lymphoma (BL) and one with anaplastic lymphoma. Two patents had initial CNS infiltration; the blastic type Mantle Cell Lymphoma (patient 2) and the anaplastic Lymphoma (patient 9); these patients received IT-R three times per week, plus two extra doses after complete remission in CNS. Median follow-up was 9 months (range: 3–15 months). All patients had risk factors that warranted prophylaxis (see table). Toxicity included headache in 35% of administrations (Grade I/II), temporal paresthesias in 24.5% of administrations (lasting a median of 5 minutes, range 2–15), neuropathic pain and vomit in 12.3% of administrations (grade I/II), fever and chills in 7% of administrations (Grade I/II). All side effects were temporary and no patient has shown neurological or other late toxicities. The patient with mantle cell lymphoma infiltrated to CNS achieved complete remission after 5 doses of IT-R which continues after autologous stem cell transplantation. The use of rituximab as IT-R is safe and effective. We are starting a phase II study using IT rituximab as prophylaxis and treatment, in a larger group of patients.