Causas más frecuentes de anemia en una población adulta de la ciudad de La Rioja.

La anemia constituye un problema importante de la salud pública que afecta tanto a niños como adultos. Existen múltiples causas que pueden desarrollarla, por lo que su estudio constituye una tarea ardua y a veces de difícil diagnóstico. El presente trabajo se enfoca en conocer las causas más frecuentes de anemia en la población adulta riojana (18–80 años) que acude a la interconsulta hematológica ambulatoria, en un servicio hematológico privado. A través de la revisión de historias clínicas (362), del periodo de Julio del 2008 a Julio del 2011, se estableció que la prevalecía de anemia fue mayor en mujeres (69%) que en hombres (19%). Los resultados obtenidos sugieren que la anemia de la enfermedad crónica y la deficiencia de hierro son las causas más comunes y frecuentes en la población adulta. Estadísticamente se estableció una significancia clínica, p-valor 0.001 (á= 0.05), entre las enfermedades subyacentes de un paciente y la edad del mismo, como factores que contribuyen al desarrollo de un síndrome anémico.Most common causes of anemia in an adult population City of La Rioja.AbstractAnaemia is a major problem of public health that affects both children and adults. There are many causes that can develop, so their study is an arduous and sometimes difficult to diagnose. This paper focuses on knowing the most common causes of anemia in adults Rioja (18-80 years) who comes to the outpatient hematology interconsultation in private hematology service. Through medical record review (362), the period of July 2008 to July 2011, it was established that the prevalence of anemia was higher in women (69%) than men (19%). The results suggest that anemia of chronic disease and iron deficiency are the most common and frequent in the adult population. Statistically established clinical significance, p-value 0.001 (á = 0.05), between a patient's underlying disease and age of the same, as factors contributing to the development of an anemic syndrome.Key words: Anemia; Adult; Causes; Multifactorieda

Treatment change as a predictor of outcome among patients with classic chronic graft-versus-host disease

We analyzed outcomes for 668 patients who had systemic treatment for chronic graft-versus-host disease (GVHD) to assess the utility of early treatment change for exacerbation of chronic GVHD as a surrogate for survival endpoints in clinical trials. Fifty-six percent of patients had treatment change within 2 years after diagnosis of chronic GVHD. The median onset of treatment change was 4.4 months (range, 0.3 – 50 months). The cumulative incidence of non-relapse mortality (NRM) at 2 years was 16%, and overall survival at 2 years was 74%. In time-dependent Cox models, treatment change was associated with an increase in risk of NRM (hazard ratio, 2.53; 95% CI, 1.7-3.7; p < .0001). The hazard ratio was attenuated by 6% per month of delay in treatment change. Our results confirm that exacerbation of chronic GVHD is associated with an increased risk of NRM and with decreased survival, but the strength of this association is not large enough to allow the use of early exacerbation as a surrogate for survival endpoints in clinical trials. Other measures of clinical benefit, such as response, will need to be developed as endpoints in phase II trials for patients with chronic GVHD

The inflammatory microenvironment in colorectal neoplasia

Peer reviewedPublisher PD

The nucleotide composition of microsatellites impacts both replication fidelity and mismatch repair in human colorectal cells

Microsatellite instability is a key mechanism of colon carcinogenesis. We have previously studied mutations within a (CA)13 microsatellite using an enhanced green fluorescent protein (EGFP)-based reporter assay that allows the distinction of replication errors and mismatch repair (MMR) activity. Here we utilize this assay to compare mutations of mono- and dinucleotide repeats in human colorectal cells. HCT116 and HCT116+chr3 cells were stably transfected with EGFP-based plasmids harboring A10, G10, G16, (CA)13 and (CA)26 repeats. EGFP-positive mutant fractions were quantitated by flow cytometry, mutation rates were calculated and the mutant spectrum was analyzed by cycle sequencing. EGFP fluorescence pattern changed with the microsatellite's nucleotide sequence and cell type and clonal variations were observed in mononucleotide repeats. Replication errors (as calculated in HCT116) at A10 repeats were 5–10-fold higher than in G10, G16 were 30-fold higher than G10 and (CA)26 were 10-fold higher than (CA)13. The mutation rates in hMLH1-proficient HCT116+chr3 were 30–230-fold lower than in HCT116. MMR was more efficient in G16 than in A10 clones leading to a higher stability of poly-G tracts. Mutation spectra revealed predominantly 1-unit deletions in A10, (CA)13 and G10 and 2-unit deletions or 1-unit insertion in (CA)26. These findings indicate that both replication fidelity and MMR are affected by the microsatellite's nucleotide composition

Multi-center real-world comparison of the fully automated Idylla (TM) microsatellite instability assay with routine molecular methods and immunohistochemistry on formalin-fixed paraffin-embedded tissue of colorectal cancer

Microsatellite instability (MSI) is present in 15-20% of primary colorectal cancers. MSI status is assessed to detect Lynch syndrome, guide adjuvant chemotherapy, determine prognosis, and use as a companion test for checkpoint blockade inhibitors. Traditionally, MSI status is determined by immunohistochemistry or molecular methods. The Idylla (TM) MSI Assay is a fully automated molecular method (including automated result interpretation), using seven novel MSI biomarkers (ACVR2A, BTBD7, DIDO1, MRE11, RYR3, SEC31A, SULF2) and not requiring matched normal tissue. In this real-world global study, 44 clinical centers performed Idylla (TM) testing on a total of 1301 archived colorectal cancer formalin-fixed, paraffin-embedded (FFPE) tissue sections and compared Idylla (TM) results against available results from routine diagnostic testing in those sites. MSI mutations detected with the Idylla (TM) MSI Assay were equally distributed over the seven biomarkers, and 84.48% of the MSI-high samples had >= 5 mutated biomarkers, while 98.25% of the microsatellite-stable samples had zero mutated biomarkers. The concordance level between the Idylla (TM) MSI Assay and immunohistochemistry was 96.39% (988/1025); 17/37 discordant samples were found to be concordant when a third method was used. Compared with routine molecular methods, the concordance level was 98.01% (789/805); third-method analysis found concordance for 8/16 discordant samples. The failure rate of the Idylla (TM) MSI Assay (0.23%; 3/1301) was lower than that of referenced immunohistochemistry (4.37%; 47/1075) or molecular assays (0.86%; 7/812). In conclusion, lower failure rates and high concordance levels were found between the Idylla (TM) MSI Assay and routine tests.Peer reviewe

ILC3 function as a double-edged sword in inflammatory bowel diseases

Inflammatory bowel diseases (IBD), composed mainly of Crohn’s disease (CD) and ulcerative colitis (UC), are strongly implicated in the development of intestinal inflammation lesions. Its exact etiology and pathogenesis are still undetermined. Recently accumulating evidence supports that group 3 innate lymphoid cells (ILC3) are responsible for gastrointestinal mucosal homeostasis through moderate generation of IL-22, IL-17, and GM-CSF in the physiological state. ILC3 contribute to the progression and aggravation of IBD while both IL-22 and IL-17, along with IFN-γ, are overexpressed by the dysregulation of NCR− ILC3 or NCR+ ILC3 function and the bias of NCR+ ILC3 towards ILC1 as well as regulatory ILC dysfunction in the pathological state. Herein, we feature the group 3 innate lymphoid cells’ development, biological function, maintenance of gut homeostasis, mediation of IBD occurrence, and potential application to IBD therapy