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RATIONALE: End-expiratory lung volume (EELV) is reduced in mechanically ventilated patients, especially in pathologic conditions. The resulting heterogeneous distribution of ventilation increases the risk for ventilation induced lung injury. Clinical measurement of EELV however, remains difficult. OBJECTIVE: Validation of a novel continuous capnodynamic method based on expired carbon dioxide (CO2) kinetics for measuring EELV in mechanically ventilated critically-ill patients. METHODS: Prospective study of mechanically ventilated patients scheduled for a diagnostic computed tomography exploration. Comparisons were made between absolute and corrected EELVCO2 values, the latter accounting for the amount of CO2 dissolved in lung tissue, with the reference EELV measured by computed tomography (EELVCT). Uncorrected and corrected EELVCO2 was compared with total CT volume (density compartments between - 1000 and 0 Hounsfield units (HU) and functional CT volume, including density compartments of - 1000 to - 200HU eliminating regions of increased shunt. We used comparative statistics including correlations and measurement of accuracy and precision by the Bland Altman method. MEASUREMENTS AND MAIN RESULTS: Of the 46 patients included in the final analysis, 25 had a diagnosis of ARDS (24 of which COVID-19). Both EELVCT and EELVCO2 were significantly reduced (39 and 40% respectively) when compared with theoretical values of functional residual capacity (p < 0.0001). Uncorrected EELVCO2 tended to overestimate EELVCT with a correlation r2 0.58; Bias - 285 and limits of agreement (LoA) (+ 513 to - 1083; 95% CI) ml. Agreement improved for the corrected EELVCO2 to a Bias of - 23 and LoA of (+ 763 to - 716; 95% CI) ml. The best agreement of the method was obtained by comparison of corrected EELVCO2 with functional EELVCT with a r2 of 0.59; Bias - 2.75 (+ 755 to - 761; 95% CI) ml. We did not observe major differences in the performance of the method between ARDS (most of them COVID related) and non-ARDS patients. CONCLUSION: In this first validation in critically ill patients, the capnodynamic method provided good estimates of both total and functional EELV. Bias improved after correcting EELVCO2 for extra-alveolar CO2 content when compared with CT estimated volume. If confirmed in further validations EELVCO2 may become an attractive monitoring option for continuously monitor EELV in critically ill mechanically ventilated patients. TRIAL REGISTRATION: clinicaltrials.gov (NCT04045262).
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Capnografía , Enfermedad Crítica , Mediciones del Volumen Pulmonar , Humanos , Masculino , Femenino , Enfermedad Crítica/terapia , Estudios Prospectivos , Persona de Mediana Edad , Anciano , Mediciones del Volumen Pulmonar/métodos , Capnografía/métodos , Respiración Artificial/métodos , COVID-19 , Tomografía Computarizada por Rayos X/métodos , AdultoRESUMEN
We report for the first time the whole development of a biosensing system based on the Interferometric Optical Detection Method (IODM) enriched with gold nanoparticles (AuNPs), acting as interferometric enhancers for improving the performance of immunoassays. For this purpose, the Lactoferrin sandwich immunoassay model was employed. We describe in detail the entire value chain from the AuNPs production, its functionalization, and characterization with anti-Lactoferrin (anti-LF), the biosensing response of these conjugates as well as their corresponding calculation of the kinetic constants, performance comparison of the readout interferometric signals versus Scanning Electron Microscopy (SEM) and the percentage of the sensing surface covered. Finally, a Lactoferrin sandwich immunoassay was carried out and correlated with Enzyme-Linked ImmunoSorbent Assay (ELISA), and the Limit of Detection and sensitivity figures were obtained. As a result, we demonstrate how the AuNPs act as interferometric amplifiers of the IODM for improving the biosensing response, opening the possibility of being applied in multiple biological detection applications.
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The standard rapid approach for the diagnosis of coronavirus disease 2019 (COVID-19) is the detection of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) RNA. The detection of specific anti-SARS-CoV-2 immunoglobulins is crucial for screening people who have been exposed to the virus, whether or not they presented symptoms. Recent publications report different methods for the detection of specific IgGs, IgMs, and IgAs against SARS-CoV-2; these methods mainly detect immunoglobulins in the serum using conventional techniques such as rapid lateral flow tests or enzyme-linked immunosorbent assay (ELISA). In this article, we report the production of recombinant SARS-CoV-2 spike protein and the development of a rapid, reliable, cost-effective test, capable of detecting immunoglobulins in serum and saliva samples. This method is based on interferometric optical detection. The results obtained using this method and those obtained using ELISA were compared. Owing to its low cost and simplicity, this test can be used periodically for the early detection, surveillance, detection of immunity, and control of the spread of COVID-19.
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BACKGROUND: Medical curricula have historically been designed in a top-down approach, usually excluding students. While Delphi panels have been used as a tool for medical education curricula design, none have been conducted in Ecuador. In addition, no such approach has ever included students both as panelists and researchers. MATERIAL AND METHODS: Four Delphi panels were developed and conducted using a participatory approach that allowed medical students to take part both as expert panelists and researchers: specifically, students developed the questionnaire and conducted a qualitative synthesis. Questionnaire responses were anonymized and dispatched online to panelists. The information was organized and collected to develop the qualitative syntheses and prepare the final statements. RESULTS: Thirty-two medical students participated between February and May 2018. A total of 32 questions were developed, corresponding to five different categories. For some questions, consensus was reached; for other questions, general statements were obtained.Discussion and conclusion: Developing the questionnaire, responding to it and analyzing the answers allowed students to raise significant concerns regarding medical education topics proposing relevant policy and curricula change. Participatory Delphi panels can be an efficient tool to obtain organized feedback, improve student class involvement, and promote research skills.
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Educación de Pregrado en Medicina , Educación Médica , Estudiantes de Medicina , Curriculum , Técnica Delphi , Ecuador , HumanosAsunto(s)
Betacoronavirus/patogenicidad , Infecciones por Coronavirus/complicaciones , Livedo Reticularis/diagnóstico , Neumonía Viral/complicaciones , Trombosis/diagnóstico , Biopsia , COVID-19 , Infecciones por Coronavirus/inmunología , Infecciones por Coronavirus/virología , Pie , Humanos , Livedo Reticularis/etiología , Livedo Reticularis/patología , Masculino , Persona de Mediana Edad , Pandemias , Neumonía Viral/inmunología , Neumonía Viral/virología , SARS-CoV-2 , Piel/patología , Trombosis/etiología , Trombosis/patologíaRESUMEN
No disponible
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Humanos , Femenino , Anciano , Fluorodesoxiglucosa F18/análisis , Tomografía de Emisión de Positrones/instrumentación , Tomografía de Emisión de Positrones/métodos , Tomografía de Emisión de Positrones , Neoplasias de la Tiroides/cirugía , Neoplasias de la Tiroides , Nódulo Tiroideo/patología , Nódulo Tiroideo , Glándula Tiroides/patología , Glándula Tiroides/cirugía , Glándula Tiroides , Carcinoma/complicaciones , Carcinoma/cirugía , Carcinoma , Metástasis de la Neoplasia/patología , Metástasis de la NeoplasiaAsunto(s)
Fluorodesoxiglucosa F18 , Radiofármacos , Neoplasias de la Tiroides/diagnóstico por imagen , Fluorodesoxiglucosa F18/farmacocinética , Humanos , Tomografía Computarizada por Tomografía de Emisión de Positrones , Pronóstico , Radiofármacos/farmacocinética , Sensibilidad y Especificidad , Neoplasias de la Tiroides/metabolismo , Nódulo Tiroideo/diagnóstico por imagen , Nódulo Tiroideo/metabolismoRESUMEN
In this Letter, we demonstrate for the first time the experimental capability for the biochemical sensing of resonant nanopillars (RNPs) arrays. These arrays are fabricated over a glass substrate and are optically integrated from the backside of this substrate. The reflectivity profiles of the RNPs arrays are measured by infiltrating different ethanol fractions in water in order to evaluate the optical response for the different refractive indexes, which range from 1.330 to 1.342. A linear fit of the resonant modes shift is observed as a function of the bulk refractive index of the liquid infiltrated. For the type of transducer analyzed, a relative sensitivity of 10017 cm(-1)/Refractive Index Unit (RIU) is achieved, allowing us to reach a competitive Limit of Detection (LoD) in the order of 1×10(-5) RIU.
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Etanol/análisis , Nanotecnología/instrumentación , Fenómenos Ópticos , Límite de Detección , Microscopía , Agua/químicaRESUMEN
Environmental disturbances define the diversity and assemblage of species, affecting the functioning of ecosystems. Fire is a major disturbance of Mediterranean pine forests. Pines are highly dependent on the ectomycorrhizal (EM) fungal symbiosis, which is critical for tree recruitment under primary succession. To determine the effects of time since fire on the structure and recovery of EM fungal communities, we surveyed the young Pinus pinaster regenerate in three sites differing in the elapsed time after the last fire event. Pine roots were collected, and EM fungi characterized by sequencing the internal transcribed spacer (ITS) and the large subunit (LSU) regions of the nuclear ribosomal (nr)-DNA. The effects of the elapsed time after fire on the EM community structure (richness, presence/absence of fungi, phylogenetic diversity) and on soil properties were analysed.Fungal richness decreased with the elapsed time since the fire; although, the phylogenetic diversity of the EM community increased. Soil properties were different depending on the elapsed time after fire and particularly, the organic matter, carbon-to-nitrogen (C/N) ratio, nitrogen and iron significantly correlated with the assemblage of fungal species. Ascomycetes, particularly Tuberaceae and Pezizales, were significantly over-represented on saplings in the burned site. On seedlings, a significant over-representation of Rhizopogonaceae and Atheliaceae was observed in the most recently burned site, while other fungi (i.e. Cortinariaceae) were significantly under-represented. Our results are consistent with the hypothesis that fire can act as a selective agent by printing a phylogenetic signal on the EM fungal communities associated with naturally regenerated pines, pointing out to some groups as potential fire-adapted fungi.
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Biota , Incendios , Micorrizas/clasificación , Micorrizas/aislamiento & purificación , Pinus/microbiología , Raíces de Plantas/microbiología , Carbono/análisis , Análisis por Conglomerados , ADN de Hongos/química , ADN de Hongos/genética , ADN Ribosómico/química , ADN Ribosómico/genética , ADN Espaciador Ribosómico/química , ADN Espaciador Ribosómico/genética , Genes de ARNr , Hierro/análisis , Datos de Secuencia Molecular , Micorrizas/genética , Nitrógeno/análisis , Compuestos Orgánicos/análisis , Filogenia , ARN de Hongos/genética , ARN Ribosómico/genética , Análisis de Secuencia de ADN , Suelo/químicaRESUMEN
Podocytes are critically important for maintaining the integrity of the glomerular filtration barrier and preventing albuminuria. Recently, it has become clear that to achieve this, they need to be insulin sensitive and produce an optimal amount of VEGF-A. In other tissues, insulin has been shown to regulate VEGF-A release, but this has not been previously examined in the podocyte. Using in vitro and in vivo approaches, in the present study, we now show that insulin regulates VEGF-A in the podocyte in both mice and humans via the insulin receptor (IR). Insulin directly increased VEGF-A mRNA levels and protein production in conditionally immortalized wild-type human and murine podocytes. Furthermore, when podocytes were rendered insulin resistant in vitro (using stable short hairpin RNA knockdown of the IR) or in vivo (using transgenic podocyte-specific IR knockout mice), podocyte VEGF-A production was impaired. Importantly, in vivo, this occurs before the development of any podocyte damage due to podocyte insulin resistance. Modulation of VEGF-A by insulin in the podocyte may be another important factor in the development of glomerular disease associated with conditions in which insulin signaling to the podocyte is deranged.
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Insulina/metabolismo , Podocitos/metabolismo , Factor A de Crecimiento Endotelial Vascular/metabolismo , Animales , Humanos , Resistencia a la Insulina , Ratones , Ratones Noqueados , ARN Mensajero/metabolismoRESUMEN
Acute hepatic failure secondary to acetaminophen (APAP) poisoning is associated with high mortality. Protein tyrosine phosphatase 1B (PTP1B) is a negative regulator of tyrosine kinase growth factor signaling. In the liver, this pathway confers protection against injury. However, the involvement of PTP1B in the intracellular networks activated by APAP is unknown. We have assessed PTP1B expression in APAP-induced liver failure in humans and its role in the molecular mechanisms that regulate the balance between cell death and survival in human and mouse hepatocytes, as well as in a mouse model of APAP-induced hepatotoxicity. PTP1B expression was increased in human liver tissue removed during liver transplant from patients for APAP overdose. PTP1B was upregulated by APAP in primary human and mouse hepatocytes together with the activation of c-jun (NH2) terminal kinase (JNK) and p38 mitogen-activated protein kinase (p38 MAPK), resulting in cell death. Conversely, Akt phosphorylation and the antiapoptotic Bcl2 family members BclxL and Mcl1 were decreased. PTP1B deficiency in mouse protects hepatocytes against APAP-induced cell death, preventing glutathione depletion, reactive oxygen species (ROS) generation and activation of JNK and p38 MAPK. APAP-treated PTP1B(-/-) hepatocytes showed enhanced antioxidant defense through the glycogen synthase kinase 3 (GSK3)ß/Src kinase family (SKF) axis, delaying tyrosine phosphorylation of the transcription factor nuclear factor-erythroid 2-related factor (Nrf2) and its nuclear exclusion, ubiquitination and degradation. Insulin-like growth factor-I receptor-mediated signaling decreased in APAP-treated wild-type hepatocytes, but was maintained in PTP1B(-/-) cells or in wild-type hepatocytes with reduced PTP1B levels by RNA interference. Likewise, both signaling cascades were modulated in mice, resulting in less severe APAP hepatotoxicity in PTP1B(-/-) mice. Our results demonstrated that PTP1B is a central player of the mechanisms triggered by APAP in hepatotoxicity, suggesting a novel therapeutic target against APAP-induced liver failure.
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Acetaminofén/toxicidad , Glucógeno Sintasa Quinasa 3/metabolismo , Hepatocitos/efectos de los fármacos , Factor 2 Relacionado con NF-E2/metabolismo , Proteína Tirosina Fosfatasa no Receptora Tipo 1/metabolismo , Receptor IGF Tipo 1/metabolismo , Animales , Apoptosis , Células Cultivadas , Enfermedad Hepática Inducida por Sustancias y Drogas/metabolismo , Enfermedad Hepática Inducida por Sustancias y Drogas/patología , Glutatión/metabolismo , Glucógeno Sintasa Quinasa 3/antagonistas & inhibidores , Glucógeno Sintasa Quinasa 3/genética , Glucógeno Sintasa Quinasa 3 beta , Hepatocitos/citología , Hepatocitos/metabolismo , Humanos , Proteínas Quinasas JNK Activadas por Mitógenos/metabolismo , Ratones , Proteína 1 de la Secuencia de Leucemia de Células Mieloides , Estrés Oxidativo/efectos de los fármacos , Fosforilación , Proteína Tirosina Fosfatasa no Receptora Tipo 1/antagonistas & inhibidores , Proteína Tirosina Fosfatasa no Receptora Tipo 1/genética , Proteínas Proto-Oncogénicas c-akt/metabolismo , Proteínas Proto-Oncogénicas c-bcl-2/metabolismo , Interferencia de ARN , ARN Interferente Pequeño/metabolismo , Especies Reactivas de Oxígeno/metabolismo , Transducción de Señal , Proteínas Quinasas p38 Activadas por Mitógenos/metabolismoRESUMEN
Diabetic nephropathy is the most common cause of endstage renal disease. Approaches targeting angiotensin II significantly delay its progression. However, many patients still need renal replacement therapy. High throughput techniques such as unbiased gene expression profiling and proteomics may identify new therapeutic targets. Cell death is thought to contribute to progressive renal cell depletion in chronic nephropathies. A European collaborative effort recently applied renal biopsy transcriptomics to identify novel mediators of renal cell death in diabetic nephropathy. Twenty-five percent of cell death regulatory genes were upor downregulated in diabetic kidneys. TNF-related apoptosisinducing ligand (TRAIL) and osteoprotegerin had the highest level of expression. In diabetic nephropathy, tubular cells and podocytes express TRAIL. Inflammatory cytokines, including MIF via CD74, upregulate TRAIL. A high glucose environment sensitized renal cells to the lethal effect of TRAIL, while osteoprotegerin is protective. These results suggest that, in addition to glucose levels, inflammation and TRAIL are therapeutic targets in diabetic nephropathy.
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Nefropatías Diabéticas/genética , Ligando Inductor de Apoptosis Relacionado con TNF/genética , Nefropatías Diabéticas/complicaciones , Nefropatías Diabéticas/tratamiento farmacológico , Humanos , Hiperglucemia/complicaciones , Inflamación/complicaciones , Transcripción GenéticaRESUMEN
La nefropatía diabética es la causa más común de enfermedad renal crónica terminal. La modulación terapéutica de la angiotensina II retarda, pero no evita, su progresión. La muerte celular contribuye a la pérdida de masa renal en las nefropatías crónicas. Un consorcio europeo empleó la transcriptómica en biopsias renales para identificar nuevos mediadores implicados en la muerte de la célula renal durante la nefropatía diabética. Un 25% de los genes relacionados con la muerte celular estaban expresados diferencialmente en la nefropatía diabética. TRAIL y osteoprotegerina fueron los genes más sobre expresados, y también estaba aumentado CD74. Las células tubulares y podocitos expresan TRAIL bajo la regulación de citocinas proinflamatorias(MIF vía CD74, TNF). La hiperglucemia sensibiliza a las células renales a la apoptosis inducida por TRAIL, mientras que la osteoprotegerina protege. Estos resultados sugieren que, además de la glucemia, la inflamación y TRAIL pueden ser objetivos terapéuticos en la nefropatía diabética (AU)
Diabetic nephropathy is the most common cause of end stage renal disease. Approaches targeting angiotensin II significantly delay its progression. However, many patients still need renal replacement therapy. High throughput techniques such as unbiased gene expression profiling and proteomics may identify new therapeutic targets. Cell death is thought to contribute to progressive renal cell depletion in chronic nephropathies. A European collaborative effort recently applied renal biopsy transcriptomics to identify novel mediators of renal cell death in diabetic nephropathy. Twenty-five percent of cell death regulatory genes were up or down regulated in diabetic kidneys. TNF-related apoptosis inducing ligand (TRAIL) and osteoprotegerin had the highest-level of expression. In diabetic nephropathy, tubular cells and podocytes express TRAIL. Inflammatory cytokines, including MIF via CD74, up regulate TRAIL. A high glucose environment sensitized renal cells to the lethal effect of TRAIL, while osteoprotegerin is protective. These results suggest that, in addition to glucose levels, inflammation and TRAIL are therapeutic targets in diabetic nephropathy (AU)
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Humanos , Nefropatías Diabéticas/fisiopatología , Insuficiencia Renal Crónica/fisiopatología , Complicaciones de la Diabetes/fisiopatología , Osteoprotegerina , Apoptosis/fisiología , Receptores del Ligando Inductor de Apoptosis Relacionado con TNF/análisis , Progresión de la Enfermedad , Biomarcadores/análisis , Hiperglucemia/fisiopatologíaRESUMEN
No disponible
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Humanos , Insuficiencia Renal/fisiopatología , Lesión Renal Aguda/fisiopatología , Citocinas/análisis , Linfotoxina-alfa/análisis , Apoptosis , Receptores del Factor de Necrosis Tumoral/análisisRESUMEN
A high glucose concentration is shared by peritoneal dialysis (PD)and diabetes mellitus (DM). High glucose leads to tissue injury indiabetes. Peritoneal dialysis research has emphasized the role of glucose degradation products in tissue injury. Apoptosis induction is one of the mechanisms of tissue injury induced both by glucose and glucose degradation products. We now review the role of apoptosis and its regulation by glucose degradation products in antibacterial defense and loss of renal function in diabetes mellitus and peritoneal dialysis. The pathogenic role of the recently identified glucose degradation product 3,4-di-deoxyglucosone-3-ene (3,4-DGE) is detailed. Available therapeutic strategies include the use of peritoneal dialysis solutions containing alow concentration of glucose degradation products. Based on preclinical results, specific targeting of apoptosis regulatory factor should be explored in the clinical setting (AU)
En la diálisis peritoneal (DP) y la diabetes mellitus (DM)altas concentraciones de glucosa se asocian a daño tisular. La apoptosis es uno de los mecanismos de daño tisular. Los productos de degradación de la glucosa (PDGs) se producen a partir de la glucosa tanto in vivo, en diabéticos, como durante el procesamiento de las soluciones de DP e inducen apoptosis en distintos tipos celulares. La apoptosises un modo activo de muerte celular con control molecular, regulada por moléculas intracelulares y extracelulares que dan lugar a distintas vías pro y antiapoptóticas, susceptibles de manipulación terapéutica. Entre estas se encuentran las caspasas, una familia de protein cisteasas que se comportan como moléculas iniciadoras o efectoras de la apoptosis. Entre los PDGs conocidos, la 3,4 dideoxiglucosona(3,4 DGE) es el principal componente letal de las soluciones de DP. La 3,4 DGE induce apoptosis en leucocitos y células tubulares de riñón. La inhibición de la apoptosis de leucocitos mejora la defensa antibacteriana peritoneal. Proponemos que los PDGs pueden estar implicados en el empeoramiento de la defensa antibacteriana y en lapérdida progresiva de la función renal en pacientes diabéticos y en DP. Entre las posibles estrategias terapéuticas destacamos el empleo de soluciones de DP con baja concentración de PDGs, que podrían disminuir la incidencia y gravedad de las peritonitis así como conservar la función renal residual. Otra posible estrategia seria el empleo de fármacos inhibidores de la apoptosis patológica (AU)
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Humanos , Diálisis Peritoneal/métodos , Hiperglucemia/fisiopatología , Diabetes Mellitus/fisiopatología , Apoptosis/fisiología , Productos Finales de Glicación Avanzada/efectos adversos , Soluciones para Diálisis/efectos adversos , Caspasas/análisisRESUMEN
A high glucose concentration is shared by peritoneal dialysis (PD) and diabetes mellitus (DM). High glucose leads to tissue injury in diabetes. Peritoneal dialysis research has emphasized the role of glucose degradation products in tissue injury. Apoptosis induction is one of the mechanisms of tissue injury induced both by glucose and glucose degradation products. We now review the role of apoptosis and its regulation by glucose degradation products in antibacterial defense and loss of renal function in diabetes mellitus and peritoneal dialysis. The pathogenic role of the recently identified glucose degradation product 3,4-di-deoxyglucosone- 3-ene (3,4-DGE) is detailed. Available therapeutic strategies include the use of peritoneal dialysis solutions containing a low concentration of glucose degradation products. Based on preclinical results, specific targeting of apoptosis regulatory factor should be explored in the clinical setting.
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Apoptosis/fisiología , Diabetes Mellitus/tratamiento farmacológico , Diabetes Mellitus/inmunología , Diálisis Peritoneal , Apoptosis/efectos de los fármacos , Infecciones Bacterianas/inmunología , Diabetes Mellitus/microbiología , HumanosRESUMEN
Tubular cell loss is prominent both in acute and chronic renal failure. Apoptosis and its regulatory mechanisms contribute to cell number regulation in the kidney. The potential role of apoptosis ranges from induction and progression to repair of renal injury. However, therapeutic interest has focused in preventing the apoptotic loss of tubular cells that leads to acute and chronic renal failure. Death ligands and receptors, such as tumor necrosis factor and Fas ligand, proapoptotic and antiapoptotic Bcl2 family members and caspases have all been shown to participate in apoptosis regulation in the course of renal cell injury. Nevertheless, the precise role of these proteins is unclear, and the participation of most known apoptosis regulatory proteins has not been studied. We now review the role of apoptosis in renal injury, the potential molecular targets of therapeutic intervention, the therapeutic weapons to modulate the activity of these targets and the few examples of therapeutic intervention on apoptosis, with emphasis in acute renal failure.
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Túbulos Renales/citología , Lesión Renal Aguda/patología , Apoptosis/fisiología , Supervivencia Celular , Retículo Endoplásmico/fisiología , Humanos , Mitocondrias/fisiología , Receptores del Factor de Necrosis Tumoral/fisiología , Proteína bcl-X/fisiologíaRESUMEN
The objective of this study was to determine the prevalence of antibodies against alpha-fodrin (alpha-fodrin) of the immunoglobulin G (IgG) isotype in Sjögren's syndrome (SS), as defined by European Community Study Group (ESG) and ESG-modified criteria. We arrived at the prevalence and mean concentrations of IgG anti-alpha-fodrin antibodies using enzyme-linked immunosorbent assay (ELISA) in 507 patients with SS, primary SS (pSS), and secondary SS (sSS), classified according to either the ESG or the ESG-modified criteria. IgG anti-alpha-fodrin antibodies were detected in 6/507 (1.2%) and 4/228 (1.7%) of the SS group, according to the ESG or ESG-modified criteria, respectively. Similar prevalence was found for patients with pSS or sSS. Anti-Ro/SSA antibodies were present in 151/409 (36.9%) vs. 149/213 (70.0%) of the SS group, 85/195 (43.6%) vs. 83/101 (82.2%) of the pSS group, and 66/214 (30.8%) vs. 66/112 (58.9%) of the sSS group. Anti-La/SSB antibodies were detected in 77/403 (19.1%) vs. 73/212 (34.4%) of the SS group, 47/194 (24.2%) vs. 45/101 (44.5%) of the pSS group, and 30/209 (14.3%) vs. 28/111 (25.2%) of the sSS group. No clinical associations were found. Only two IgG anti-alpha-fodrin-positive sera were anti-Ro/SSA-negative. We conclude that IgG antibodies against alpha-fodrin are present in a small percentage of people with SS, pSS, and sSS. The lower prevalence in patients classified according to the ESG criteria reflects the lower specificity of these criteria. IgG anti-alpha-fodrin antibodies can be detected in some SS patients whose sera do not contain anti-Ro/SSA antibodies.