Associated factors to non-use of formal health services in the Peruvian population: Analysis of the national household survey (Enaho) 2015

El objetivo del estudio fue estimar la prevalencia de la no utilización de los servicios formales de prestación de salud (NUSFPS) y sus factores asociados en Perú. Se realizó un análisis secundario de datos de la Encuesta Nacional de Hogares (ENAHO) del año 2015. Se definió como NUSFPS a aquellos participantes que, pese a haber presentado algún síntoma, malestar, enfermedad, recaída de enfermedad crónica o accidente durante el último mes, no acudieron a los servicios de salud. Se analizaron 35 036 participantes; la prevalencia de NUSFPS fue de 53,9% (IC95%:52,9-54,8). La NUSFPS fue superior en la costa (razón de prevalencia ajustada [RPa] = 1,24;IC95%:1,17-1,31), sierra (RPa = 1,38;IC95%:1,31-1,46) y selva (RP = 1,25;IC95%:1,18-1,33) en comparación a Lima Metropolitana. Hubo mayor prevalencia de NUSFPS en los participantes sin seguro (RPa = 1,59;IC95%:1,52-1,66) y afiliados al seguro integral de salud (RPa = 1,16;IC95%:1,11-1,22) comparados con los afiliados a la Seguridad Social. En conclusión, más de la mitad de los participantes padecieron NUSFPS, lo cual se asoció con condiciones geográficas y de aseguramiento. Se sugieren políticas públicas informadas en la evidencia para mejorar esta situación.The aim of the study was to estimate the prevalence of non-use of health services (NUHS) and its associated factors using the National Household Survey (ENAHO 2015). The participants were defined as NUHS if they have presented any symptoms, discomfort, illness, relapse of chronic illness or accident during the last month and did not go to the health services. 35036 participants were analyzed; the prevalence of NUHS was 53,9%. NUHS was higher in the coastal region (adjusted Prevalence Ratio [aPR]=1.24;95%CI:1.17-1.31), highlands (aPR=1.38;95%CI:1.31-1.46) and jungle (aPR=1.25,95%CI:1.18-1.33) compared to Lima. Likewise, there were a higher prevalence of NUHS in participants without health insurance (aPR=1.59;95%CI:1.52-1.66) and those affiliated to Ministry of Health insurance (aPR=1.16;95%CI:1.11-1.22) compared to those affiliated to Social Security. More than half of the participants suffered from NUHS, which was associated with geographical and health system conditions. It is required evidenced-informed public policies to improve this situation.Revisión por pare

Antibodies to endothelial cells in Behçet's disease: cell-binding heterogeneity and association with clinical activity

OBJECTIVES--To investigate the prevalence and characteristics of antibodies to endothelial cells (aEC) from large vessel and from microvasculature in a group of patients with Behçet's disease (BD) to determine the relationship of these antibodies with clinical and laboratory features of the disease. METHODS--Thirty patients with BD were prospectively and consecutively studied. The aEC were determined by enzyme-linked immunosorbent assay (ELISA) using endothelial cells derived from human umbilical vein (large vessel) as well as from retroperitoneal adipose tissue (microvasculature). RESULTS--Fifteen patients (50%) had aEC, either directed to large vessel [8(26%) patients] or microvascular [13(43%) patients] endothelial cells. The percentage of active patients was significantly higher in the aEC-positive group [12(80%) patients] compared with the aEC-negative group [5(33%) patients] (p < 0.05). CONCLUSIONS--Patients with BD have a high prevalence of aEC when microvascular endothelial cells are used in the assay. These antibodies seem to be a marker of disease activity in this condition, previously considered as negative for autoantibodies

The 9-bp deletion in region V of mitochondrial DNA: evidence of mutation recurrence

A deletion of one of the two copies of a 9-bp direct repeat sequence (CCCCCTCTA) in region V of mitochondrial DNA has previously been used as a polymorphic anthropological marker for people of east Asian origin, and to a lesser extent, in Oceanian and African populations. We report the presence of the 9-bp deletion in homoplasmy in skeletal muscle fibers and lymphocytes of a Spanish Caucasian individual. Other mitochondrial DNA polymorphisms associated with the 9-bp deletion characteristic of other populations were not present. Our results suggest that the 9-bp deletion probably originated independently in the maternal lineage of the propositus, and that it can thus be described as a recurrent mutation

Polymyositis/Dermatomyositis: the current position

Polymyositis/dermatomyositis are a heterogeneous group of diseases characterised by skeletal muscle inflammation and necrosis.' 2 Since an excellent clinical description in 1903 by Steiner of dermatomyositis, which is essentially still valid,3 much progress has been made towards our understanding of this group of diseases. The most widely used clinical classification of idiopathic inflammatory myopathies is the one proposed by Bohan and Peter in 1975.4 That was a landmark, providing guidelines in clinical practice to accurate diagnosis of inflammatory myopathies and standardisation of studies. Nonetheless, the classification was based on clinical data. In view of recent histological and immunological studies the classification proposed by Karpati et al in 1987 seems better to fit our current view of such diseases5 (table 1). In this review we focus on recent developments in polymyositis/dermatomyositis, analysing separately the currently considered third major form of inflammatory myopathy-inclusion body myositis

Progressive external ophthalmoplegia and the Kearns-Sayre syndrome: a clinical and molecular study of 6 cases

The Kearns-Sayre syndrome (KSS) associates progressive external ophthalmoplegia initiating prior to the age of 20 years and pigmentary retinitis with a series of other heterogeneous clinical manifestations. The incomplete syndrome is usually denominated progressive external ophthalmoplegia (PEO)-plus which is a sporadically appearing mitochondrial cytopathy associated with large deletions of a variable proportion of mitochondrial DNA (mtDNA) molecules. Six patients with PEO-plus/KSS in whom muscle biopsy was performed following a complete clinical study are described. The muscle was processed by conventional histochemical techniques, electron microscopy, and genetic study (Southern transference, polymerase chain reaction, restriction cartography and both manual and automatic sequencing). The percentage of mutated mtDNA molecules for each patient was obtained by densitometry. The 6 patients presented multiorganic clinical manifestations characteristics of most mitochondrial diseases. The presence of destructured red fibers were observed in all the biopsies. All the patients presented a deletion in the mtDNA of a size between 4,861 to 7,437 base pairs (bp). All the deletions appeared flanked by direct repetitions from 4 to 13 bp and one also presented inverse repetitions from 5 to 6 bp in the zone next to the rupture point. In the 6 cases heteroplasmia was observed with a variable percentage of deleted molecules from 23 to 56%. The molecular basis of progressive external ophthalmoplegia-plus/Kearns-Sayre syndrome appears to be the existence of sole, large deletions in the mitochondrial DNA with the varying in location and percentage conditioning the appearance of different phenotypes similar among themselves. The 7,437 base pair deletion was the most frequently observed in the patients analyzed

Simple and eco-friendly thermal regeneration of granular activated carbon from the odour control system of a full-scale WWTP: Study of the process in oxidizing atmosphere

Embargado hasta 15/01/2023Adsorption by granular activated carbon (GAC) is an efficient, reliable, and well-established technique for treating malodours in wastewater treatment plants (WWTPs). However, when the lifespan of GAC is over, it becomes a hazardous industrial waste, which is mostly discarded in landfills. In the framework of a sustainable economy, this work proposes an oxidative thermal regeneration of GAC from the odour control system of an urban WWTP for reuse, mainly as an odour adsorbent in WWTPs, avoiding the use of high-cost inert atmosphere and complex additional post-treatments. In this sense, GAC, from two deodorization points of the abovementioned facility, the pretreatment header (P1 sample) and sludge dewatering (P2 sample), has been characterized in depth, both before and after its regeneration. Previous characterization has shown that GAC regeneration conditions depend on the nature of adsorbed odorants after the same operating time, while post-regeneration characterization has proven the recovery of the GAC’s original properties. Thus, specific surface area (SBET) values above 550 m2/g have been reached for both P1 and P2, considerably exceeding the pristine sample (P0) value of 406 m2/g. Furthermore, the microporous structure was also recovered in both samples, highlighting the case of the almost non-porous P1 sample, whose micropore volume exceeded 1.27 times the value of the P0 sample (0.180 cm3/g) after regeneration. On the basis of the above, and taking into account the good regeneration efficiencies reached (72–98%), the oxidative thermal regeneration at temperatures no higher than 350 °C can be a simple and sustainable alternative to revalue GAC used in WWTPs

A nuclear defect in the 4p16 region predisposes to multiple mitochondrial DNA deletions in families with Wolfram syndrome.

Wolfram syndrome is a progressive neurodegenerative disorder transmitted in an autosomal recessive mode. We report two Wolfram syndrome families harboring multiple deletions of mitochondrial DNA. The deletions reached percentages as high as 85-90% in affected tissues such as the central nervous system of one patient, while in other tissues from the same patient and from other members of the family, the percentages of deleted mitochondrial DNA genomes were only 1-10%. Recently, a Wolfram syndrome gene has been linked to markers on 4p16. In both families linkage between the disease locus and 4p16 markers gave a maximum multipoint lod score of 3.79 at theta = 0 (Pi<0.03) with respect to D4S431. In these families, the syndrome was caused by mutations in this nucleus-encoded gene which deleteriously interacts with the mitochondrial genome. This is the first evidence of the implication of both genomes in a recessive disease

Circulating soluble adhesion molecules in patients with giant cell arteritis. Correlation between soluble intercellular adhesion molecule-1 (sICAM-1) concentrations and disease activity

Objective—To evaluate whether changes in concentrations of circulating adhesion molecules are related to disease activity in patients with giant cell arteritis (GCA). Methods—A sandwich ELISA was used to measure soluble intercellular adhesion molecule-1 (sICAM-1), sICAM-3, vascular cell adhesion molecule-1 (sVCAM-1), E-selectin (sE-selectin), and L-selectin (sL-selectin) in serum and plasma samples from patients with GCA. A cross sectional study was performed on 64 GCA patients at diVerent activity stages and on 35 age and sex matched healthy donors. Thirteen of these patients were evaluated at the time of diagnosis and serially during follow up. Results—At the time of diagnosis, sICAM-1 concentrations were significantly higher in active GCA patients than in controls (mean (SD) 360.55 (129.78) ng/ml versus 243.25 (47.43) ng/ml, p<0.001). In contrast, sICAM-3, sVCAM-1, sE-selectin, and sL-selectin values did not diVer from those obtained in normal donors. With corticosteroid administration, a decrease in sICAM-1 concentrations was observed, reaching normal values when clinical remission was achieved (263.18 (92.7) ng/ml globally, 293.59 (108.39) ng/ml in the group of patients in recent remission, and 236.83 (70.02) ng/ml in those in long term remission). In the 13 patients followed up longitudinally, sICAM-1 values also normalised with clinical remission (225.87 (64.25) ng/ml in patients in recent remission, and 256.29 (75.15) ng/ml in those in long term remission). Conclusions—Circulating sICAM-1 concentrations clearly correlate with clinically apparent disease activity in GCA patients. DiVerences with results previously found in patients with other vasculitides may indicate that diVerent pathogenic mechanisms contribute to vascular inflammation in diVerent disorder