Baby Food Pouches, Baby-Led Weaning, and Iron Status in New Zealand Infants: An Observational Study.

Iron deficiency in infants can impact development, and there are concerns that the use of baby food pouches and baby-led weaning may impair iron status. First Foods New Zealand (FFNZ) was an observational study of 625 New Zealand infants aged 6.9 to 10.1 months. Feeding methods were defined based on parental reports of infant feeding at "around 6 months of age": "frequent" baby food pouch use (five+ times per week) and "full baby-led weaning" (the infant primarily self-feeds). Iron status was assessed using a venepuncture blood sample. The estimated prevalence of suboptimal iron status was 23%, but neither feeding method significantly predicted body iron concentrations nor the odds of iron sufficiency after controlling for potential confounding factors including infant formula intake. Adjusted ORs for iron sufficiency were 1.50 (95% CI: 0.67-3.39) for frequent pouch users compared to non-pouch users and 0.91 (95% CI: 0.45-1.87) for baby-led weaning compared to traditional spoon-feeding. Contrary to concerns, there was no evidence that baby food pouch use or baby-led weaning, as currently practiced in New Zealand, were associated with poorer iron status in this age group. However, notable levels of suboptimal iron status, regardless of the feeding method, emphasise the ongoing need for paying attention to infant iron nutrition.

PET-adapted therapy after three cycles of ABVD for all stages of Hodgkin lymphoma: results of the GATLA LH-05 trial.

The role of Ann Arbor staging in determining treatment intensity after achieving a negative positron emission tomography (PET) has not been established in classical Hodgkin lymphoma (cHL). Patients with stage I-IV cHL, received three cycles of ABVD (doxorubicin, bleomycin, vinblastine, dacarbazine) and an interim PET scan (PET3). PET3-negative patients received no further therapy. PET3-positive patients received three additional cycles of ABVD plus involved-field radiation therapy or salvage chemotherapy, if refractory to ABVD, and were re-evaluated by PET scan (PET6). Study endpoints were 3-year progression-free survival (PFS) and overall survival (OS) rates. Two hundred and thirty-nine patients with early-stage and 138 with advanced-stage were evaluable. Overall, 260 patients (70%) were PET3-negative and had higher 3-year PFS (90% vs. 65%; P < 0·0001) and OS (98% vs. 92%; P = 0·007) rates than PET3-positive patients. All PET3-negative patients, regardless of disease stage at diagnosis, achieved similarly good PFS (90-91%; P = 0·76) and OS (97-99%). The only independent prognostic factor for PFS was PET3-negativity (Hazard ratio 3·8; 95% confidence interval 2·4-6·3; P < 0·0001). This study suggests that cHL patients who achieve a negative PET3 following ABVD have an excellent outcome, regardless of stage at diagnosis. An appropriately powered, phase III trial will be necessary to confirm these findings.

Maternal and fetal outcomes in pregnant women with acute promyelocytic leukemia.

The management of pregnant women with acute promyelocytic leukemia (APL) is a challenge with limited evidence-based information available. We are reporting a series of 14 consecutive pregnant women with APL who were registered in the PETHEMA Data Centre between 1996 and 2012. APL was diagnosed during early pregnancy in five women, late pregnancy in seven, and two additional patients after delivery in an extremely poor clinical condition (pulmonary and cerebral hemorrhage). Eleven of the 12 patients eligible for induction therapy with all-trans retinoic acid and idarubicin achieved complete remission (CR 92 %) and are still in the first CR. All early pregnancies ended in abortion (four induced and one spontaneous), with four of them achieving CR. Eight of nine women in late pregnancy delivered a healthy infant (six cesarean section and two vaginal delivery). All eight babies developed normally. Our results confirm a high cure rate for pregnant women with APL who received all-trans retinoic acid and idarubicin for induction therapy, and an excellent outcome for babies when the disease is diagnosed during late pregnancy.

Valoración de índices plaquetarios en las trombocitopenias / Valuation of platelet índices in thrombocytopenia / Avaliagáo de índices plaquetários nas trombocitopenias

El objetivo de este trabajo fue determinar la utilidad clínica de los índices plaquetarios en la caracterización etiológica de las trombocitopenias. Se trata de un estudio descriptivo, retrospectivo y transversal. En pacientes controles se establecieron valores de referencia para número de plaquetas e índices plaquetarios, y éstos se evaluaron en pacientes donde coexistía trombocitopenia con algún desorden oncohematológico (linfoma no Hodgkin, linfoma Hodgkin, leucemia aguda, leucemia crónica, síndrome mielodisplásico, púrpura trombocitopénica inmune). La evaluación de laboratorio fue realizada al momento del diagnóstico, aún libre de tratamiento. En los casos de Púrpura Inmune (disminución de Volumen Plaquetario - Plaquetocrito, y aumento de Amplitud Plaquetaria); Leucemia Mieloide Crónica (aumento de la Amplitud Plaquetaria) y Linfoma no Hodgkin o Síndrome Mielodisplásico (disminución del Plaquetocrito), los índices plaquetarios podrían ser usados como herramienta diagnóstica orientadora. En cambio, no podrían contribuir al momento de diferenciar entre leucemias agudas, dado que no presentan diferencias significativas. Frente a un diagnóstico presuntivo de síndrome mielodiasplásico o leucemia mieloide aguda, el valor de Volumen Plaquetario Medio (VPM) podría contribuir como herramienta orientadora al diagnóstico, ya que sería más bajo en la leucemia aguda. El análisis de los resultados sugiere que en la práctica clínica los índices plaquetarios podrían contribuir de un modo significativo a la confirmación del diagnóstico.

The aim of this study was to determine the clinical utility of platelet indices in the etiological characterization of thrombocytopenia. It was a descriptive, retrospective and cross-sectional study. In control patients, reference values (platelet count and platelet indices) were established and they were used to assess platelet indices in patients where thrombocytopenia coexisted with some oncohematologic disorders (non-Hodgkin Lymphoma, Hodgkin Lymphoma, acute leukemia, chronic leukemia, myelodysplastic syndrome, immune thrombocytopenic purpura). Laboratory evaluation was performed at still treatment-free diagnosis. In the cases of Immune Purpura, (decreased platelet volume- plateletcrit, and increased platelet distribution width) Chronic Myeloid Leukemia (increased platelet distribution width) and non-Hodgkin lymphoma or myelodysplastic syndrome (decreased plateletcrit), platelet indices could be used as a "guiding diagnostic tool". However, they could not contribute to the differenciation between acute leukemias since they do not present any significant differences. In view of a presumptive diagnosis of mielodysplastic syndrome or acute myeloid leukemia, mean platelet value (MPV) could contribute to the diagnosis, since it would be lower in acute leukemia. The analysis of the results suggests that in clinical practice, platelet indices may contribute significantly to the confirmation of the diagnosis.

O objetivo deste trabalho foi determinar a utilidade clínica dos índices plaquetários na caracterizagáo etiológica das trombocitopenias. Trata-se de um estudo descritivo, retrospectivo e transversal. Em pacientes controle foram estabelecidos valores de referencia para número de plaquetas e índices plaquetários, e eles foram avaliados em pacientes onde coexistia trombocitopenia com alguma desordem onco-hematológica (linfoma náo Hodgkin, linfoma Hodgkin, leucemia aguda, leucemia crónica, síndrome mielodisplásica, púrpura trombocitopenia imune). A avaliagáo de laboratório foi realizada no momento do diagnóstico, ainda livre de tratamento. Nos casos de Púrpura Imune (diminuigáo de Volume Plaquetario - Plaquetócrito, e aumento de Amplitude Plaquetária); Leucemia Mieloide Crónica (aumento da Amplitude Plaquetária) e Linfoma náo Hodgkin ou Síndrome Mielodisplásica (diminuigáo do Plaquetócrito), os índices plaquetários poderiam ser usados como ferramenta diagnóstica orientadora. Entretanto, náo poderiam contribuir no momento de diferenciar entre leucemias agudas, visto que náo apresentam diferengas significativas. Diante de um diagnóstico presuntivo de síndrome mielodiasplásica ou leucemia mieloide aguda, o valor de Volume Plaquetário Médio (VPM) poderia contribuir como ferramenta orientadora para o diagnóstico, devido a que seria mais baixo na leucemia aguda. A análise dos resultados sugere que na prática clínica os índices plaquetários poderiam contribuir de um modo significativo para a confirmagáo do diagnóstico.

National survey outcomes on commercial probiotic food supplements in Italy.

To assess whether the probiotic food supplements, produced and distributed on the Italian market during 2005-2006, complied with the Italian Guidelines on Prebiotics and Probiotics, 72 samples from 29 processing plants were analyzed. The survey included 41 samples from processing plants and 31 samples of the same brand from retailers collected at timed intervals (3, 8 and 13 months). A polyphasic approach based on a suitable analytical collection method (genotypic identification of total bacteria - differential presumptive enumeration - genotypic identification of viable bacteria) was adopted to identify and quantify the microorganisms labelled and recovered from the probiotic supplements examined. Most supplements analyzed (87%) did not conform to the Italian guidelines and the differences were both quantitative and qualitative (number determination, purity, types and viability of microorganisms). Even though most labelled supplements (25 samples) indicated the presence of Bifidobacterium bifidum, this organism was only detected sporadically and always as dead cells. Unexpected results were obtained during our survey due to the absence of viability of Bacillus coagulans spores in some labelled supplements. Besides this, some of these supplements also contained other spore-forming species, identified as B. cereus that are toxin producing. We have also documented a widespread use of misclassified microbial species or species with fictitious names. The main factors involved in the absence of compliance were examined and the poor quality control applied by manufacturers was emphasized.

3-Nitropropionic acid increases frataxin expression in human lymphoblasts and in transgenic rat PC12 cells.

Friedreich ataxia (FRDA) is the most common recessive ataxia caused by reduced expression of frataxin, a nuclear encoded mitochondrial protein. In this study we examined the effects of 3-nitropropionic acid (3-NP) on frataxin expression in FRDA patient and control lymphoblasts and in rat pheochromocytoma cell line (PC12) overexpressing human frataxin. Our studies showed an up-regulation of frataxin expression in both FRDA and control lymphoblasts following exposure to 3-NP. In addition, in transgenic frataxin overexpressing cells 3-NP caused an increase of frataxin protein.

Up-regulation of c-Jun N-terminal kinase pathway in Friedreich's ataxia cells.

The severe reduction in mRNA and protein levels of the mitochondrial protein frataxin, encoded by the X25 gene, causes Friedreich ataxia (FRDA), the most common form of recessive hereditary ataxia. Increasing evidence underlines the pathogenetic role of oxidative stress in this disease. We generated an in vitro cellular model of regulated human frataxin overexpression. We identified, by differential display technique, the mitogen activated protein kinase kinase 4 mRNA down regulation in frataxin overexpressing cells. We studied the stress kinases pathway in this cellular model and in fibroblasts from FRDA patients. Frataxin overexpression reduced c-Jun N-terminal kinase phosphorylation. Furthermore, exposure of FRDA fibroblasts to several forms of environmental stress caused an up regulation of phospho-JNK and phospho-c-Jun. To understand if this susceptibility results in cell death, we have investigated the involvement of caspases. A significantly higher activation of caspase-9 was observed in FRDA versus control fibroblasts after serum-withdrawal. Our findings suggest the presence, in FRDA patient cells, of a 'hyperactive' stress signaling pathway. The role of frataxin in FRDA pathogenesis could be explained, at least in part, by this hyperactivity.