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A 2-day closed workshop was held in Liverpool, United Kingdom, to discuss the results of research concerning symptom-based disorders (SBDs) caused by autoantibodies, share technical knowledge, and consider future plans. Twenty-two speakers and 14 additional participants attended. This workshop set out to consolidate knowledge about the contribution of autoantibodies to SBDs. Persuasive evidence for a causative role of autoantibodies in disease often derives from experimental "passive transfer" approaches, as first established in neurological research. Here, serum immunoglobulin (IgM or IgG) is purified from donated blood and transferred to rodents, either systemically or intrathecally. Rodents are then assessed for the expression of phenotypes resembling the human condition; successful phenotype transfer is considered supportive of or proof for autoimmune pathology. Workshop participants discussed passive transfer models and wider evidence for autoantibody contribution to a range of SBDs. Clinical trials testing autoantibody reduction were presented. Cornerstones of both experimental approaches and clinical trial parameters in this field were distilled and presented in this article. Mounting evidence suggests that immunoglobulin transfer from patient donors often induces the respective SBD phenotype in rodents. Understanding antibody binding epitopes and downstream mechanisms will require substantial research efforts, but treatments to reduce antibody titres can already now be evaluated.
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Dysautonomia, or dysfunction of the autonomic nervous system (ANS), may occur following an infectious insult and can result in a variety of debilitating, widespread, and often poorly recognized symptoms. Dysautonomia is now widely accepted as a complication of COVID-19 and is an important component of Post-Acute Sequelae of COVID-19 (PASC or long COVID). PASC shares many overlapping clinical features with other infection-associated chronic illnesses including Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) and Post-Treatment Lyme Disease Syndrome (PTLDS), suggesting that they may share common underlying mechanisms including autonomic dysfunction. Despite the recognition of this complication of Lyme disease in the care of patients with PTLD, there has been a scarcity of research in this field and dysautonomia has not yet been established as a complication of Lyme disease in the medical literature. In this review, we discuss the evidence implicating Borrelia burgdorferi as a cause of dysautonomia and the related symptoms, propose potential pathogenic mechanisms given our knowledge of Lyme disease and mechanisms of PASC and ME/CFS, and discuss the diagnostic evaluation and treatments of dysautonomia. We also outline gaps in the literature and priorities for future research.
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OBJECTIVE: The gastrointestinal (GI) tract is commonly affected in systemic sclerosis (SSc). A positive association between antivinculin antibody levels and GI symptom severity is reported in SSc. We sought to examine whether antivinculin antibodies associate with measures of GI dysmotility and extraintestinal clinical phenotype in SSc. METHODS: A total of 88 well-characterized patients with SSc and GI disease were assayed for antivinculin antibodies by enzyme-linked immunosorbent assay. Whole-gut scintigraphy, GI symptom scores, and clinical features of SSc were compared between patients with and without antibodies. RESULTS: Twenty of 88 (23%) patients had antivinculin antibodies, which were more prevalent in patients with slow gastric transit (35% versus 22%). In the univariate analyses, patients who were positive for antivinculin antibodies were more likely to have limited cutaneous disease (odds ratio [OR] 9.60 [95% confidence interval (95% CI) 1.19, 77.23]) and thyroid disease (OR 4.09 [95% CI 1.27, 13.21]). Such patients were also less likely to have lung involvement based on a Medsger Severity Score of ≥2 (OR 0.25 [95% CI 0.07, 0.92]). Higher levels of antivinculin autoantibodies were associated with less gastric emptying (ß coefficient -3.41 [95% CI -6.72, -0.09]). The association between antivinculin antibodies and each of these clinical features remained significant in the multivariable model. In particular, the presence of antivinculin antibodies (ß coefficient -6.20 [95% CI -12.33, -0.063]) and higher levels of antivinculin antibodies (ß coefficient -3.64 [95% CI -7.05, -0.23]) were each significantly associated with slower gastric transit. CONCLUSION: Antivinculin antibodies associate with slower gastric transit in SSc and may provide insight into GI complications of SSc.
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Enfermedades Gastrointestinales , Esclerodermia Sistémica , Humanos , Esclerodermia Sistémica/complicaciones , Autoanticuerpos , Enfermedades Gastrointestinales/diagnóstico , Enfermedades Gastrointestinales/etiología , Ensayo de Inmunoadsorción Enzimática , FenotipoRESUMEN
BACKGROUND: People with autoimmune or inflammatory conditions taking immunomodulatory/suppressive medications may have higher risk of novel coronavirus disease 2019 (COVID-19). Chronic disease care has also changed for many patients, with uncertain downstream consequences. METHODS: We included participants with autoimmune or inflammatory conditions followed by specialists at Johns Hopkins. Participants completed periodic surveys querying comorbidities, disease-modifying medications, exposures, COVID-19 testing and outcomes, social behaviors, and disruptions to healthcare. We assessed whether COVID-19 risk is higher among those on immunomodulating or suppressive agents and characterized pandemic-associated changes to care and mental health. RESULTS: In total, 265 (5.6%) developed COVID-19 over 9 months of follow-up (April-December 2020). Patient characteristics (age, race, comorbidity, medications) were associated with differences in social distancing behaviors during the pandemic. Glucocorticoid exposure was associated with higher odds of COVID-19 in models incorporating behavior and other potential confounders (odds ratio [OR]: 1.43; 95% confidence interval [CI]: 1.08, 1.89). Other medication classes were not associated with COVID-19 risk. Diabetes (OR: 1.72; 95% CI: 1.08, 2.73), cardiovascular disease (OR: 1.68; 95% CI: 1.24, 2.28), and kidney disease (OR: 1.76; 95% CI: 1.04, 2.97) were associated with higher odds of COVID-19. Of the 2156 reporting pre-pandemic utilization of infusion, mental health or rehabilitative services, 975 (45.2%) reported disruptions therein, which disproportionately affected individuals experiencing changes to employment or income. CONCLUSIONS: Glucocorticoid exposure may increase risk of COVID-19 in people with autoimmune or inflammatory conditions. Disruption to healthcare and related services was common. Those with pandemic-related reduced income may be most vulnerable to care disruptions.
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Enfermedades Autoinmunes , COVID-19 , Enfermedades Autoinmunes/epidemiología , Prueba de COVID-19 , Humanos , Pandemias , Factores de Riesgo , SARS-CoV-2RESUMEN
Background: People with autoimmune or inflammatory conditions who take immunomodulatory/suppressive medications may have a higher risk of novel coronavirus disease 2019 (COVID-19). Chronic disease care has also changed for many patients, with uncertain downstream consequences. Objective: Assess whether COVID-19 risk is higher among those on immunomodulating or suppressive agents and characterize pandemic-associated changes to care. Design: Longitudinal registry study. Participants: 4666 individuals with autoimmune or inflammatory conditions followed by specialists in neurology, rheumatology, cardiology, pulmonology or gastroenterology at Johns Hopkins. Measurements: Periodic surveys querying comorbidities, disease-modifying medications, exposures, COVID-19 testing and outcomes, social behaviors, and disruptions to healthcare. Results: A total of 265 (5.6%) developed COVID-19 over 9 months of follow-up (April-December 2020). Patient characteristics (age, race, comorbidity, medication exposure) were associated with differences in social distancing behaviors during the pandemic. Glucocorticoid exposure was associated with higher odds of COVID-19 in multivariable models incorporating behavior and other potential confounders (OR: 1.43; 95%CI: 1.08, 1.89). Other medication classes were not associated with COVID-19 risk. Diabetes (OR: 1.72; 95%CI: 1.08, 2.73), cardiovascular disease (OR: 1.68; 95%CI: 1.24, 2.28), and chronic kidney disease (OR: 1.76; 95%CI: 1.04, 2.97) were each associated with higher odds of COVID-19. Pandemic-related disruption to care was common. Of the 2156 reporting pre-pandemic utilization of infusion, mental health or rehabilitative services, 975 (45.2%) reported disruptions. Individuals experiencing changes to employment or income were at highest odds of care disruption. Limitations: Results may not be generalizable to all patients with autoimmune or inflammatory conditions. Information was self-reported. Conclusions: Exposure to glucocorticoids may increase risk of COVID-19 in people with autoimmune or inflammatory conditions. Disruption to healthcare and related services was common. Those with pandemic-related reduced income may be most vulnerable to care disruptions.
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OBJECTIVES: Systemic sclerosis (SSc) is an autoimmune fibrotic disease affecting multiple tissues including the lung. A subset of patients with SSc with lung disease exhibit short telomeres in circulating lymphocytes, but the mechanisms underlying this observation are unclear. METHODS: Sera from the Johns Hopkins and University of California, San Francisco (UCSF) Scleroderma Centers were screened for autoantibodies targeting telomerase and the shelterin proteins using immunoprecipitation and ELISA. We determined the relationship between autoantibodies targeting the shelterin protein TERF1 and telomere length in peripheral leucocytes measured by qPCR and flow cytometry and fluorescent in situ hybridisation (Flow-FISH). We also explored clinical associations of these autoantibodies. RESULTS: In a subset of patients with SSc, we identified autoantibodies targeting telomerase and the shelterin proteins that were rarely present in rheumatoid arthritis, myositis and healthy controls. TERF1 autoantibodies were present in 40/442 (9.0%) patients with SSc and were associated with severe lung disease (OR 2.4, p=0.04, Fisher's exact test) and short lymphocyte telomere length. 6/6 (100%) patients with TERF1 autoantibodies in the Hopkins cohort and 14/18 (78%) patients in the UCSF cohort had a shorter telomere length in lymphocytes or leukocytes, respectively, relative to the expected age-adjusted telomere length. TERF1 autoantibodies were present in 11/152 (7.2%) patients with idiopathic pulmonary fibrosis (IPF), a fibrotic lung disease believed to be mediated by telomere dysfunction. CONCLUSIONS: Autoantibodies targeting telomere-associated proteins in a subset of patients with SSc are associated with short lymphocyte telomere length and lung disease. The specificity of these autoantibodies for SSc and IPF suggests that telomere dysfunction may have a distinct role in the pathogenesis of SSc and pulmonary fibrosis.
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Autoanticuerpos/inmunología , Esclerodermia Sistémica/inmunología , Proteínas de Unión a Telómeros/inmunología , Adulto , Anciano , Autoanticuerpos/sangre , Autoantígenos/inmunología , Femenino , Humanos , Fibrosis Pulmonar Idiopática/sangre , Fibrosis Pulmonar Idiopática/inmunología , Masculino , Persona de Mediana Edad , Esclerodermia Sistémica/sangre , Complejo Shelterina , Telómero/patologíaRESUMEN
OBJECTIVE: The aim of this study is to describe 4 of the most common autoantibodies against components of the Th/To complex: human POP1 (hPOP1), RPP25, RPP30, and RPP40. We report their prevalence and clinical characteristics in a systemic sclerosis (SSc) population, and determine whether these specificities are associated with cancer. METHODS: A case-control study was performed using data from the Johns Hopkins Scleroderma Center Cohort. A total of 804 adult patients with SSc were included; 401 SSc patients with no history of cancer after at least 5 years of disease were compared to 403 SSc patients who ever had a history of cancer. Antibodies against hPOP1, RPP25, RPP30, and RPP40 were assayed by immunoprecipitation of 35 S-methionine-labeled proteins generated by in vitro transcription/translation. Demographic and clinical characteristics were compared between groups. RESULTS: Of 804 patients, 67 (8.3%) had antibodies against any component of the Th/To complex. Patients with antibodies to any component were significantly more likely to have limited cutaneous disease, less likely to have tendon friction rubs, and more likely to have findings consistent with interstitial lung disease or pulmonary hypertension. Patients with antibodies against hPOP1, RPP25, RPP30, and/or RPP40 were significantly less likely to develop cancer within 2 years of SSc onset (0% versus 11% of antibody-negative patients; P = 0.009). CONCLUSION: SSc patients who produce autoantibodies to components of the Th/To complex have a clinical phenotype characterized by limited cutaneous disease and pulmonary involvement. Our findings show that the presence of any Th/To autoantibody may have a protective effect against contemporaneous cancer.
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Autoanticuerpos/inmunología , Neoplasias/epidemiología , Ribonucleasa P/inmunología , Esclerodermia Difusa/inmunología , Esclerodermia Limitada/inmunología , Adulto , Proteínas Reguladoras de la Apoptosis/inmunología , Autoantígenos/inmunología , Femenino , Humanos , Enfermedades Pulmonares/inmunología , Enfermedades Pulmonares/fisiopatología , Masculino , Persona de Mediana Edad , Factores Protectores , Ribonucleoproteínas/inmunología , Esclerodermia Difusa/epidemiología , Esclerodermia Difusa/fisiopatología , Esclerodermia Limitada/epidemiología , Esclerodermia Limitada/fisiopatología , Esclerodermia Sistémica/epidemiología , Esclerodermia Sistémica/inmunología , Esclerodermia Sistémica/fisiopatologíaRESUMEN
INTRODUCTION: Intestinal pseudo-obstruction (IPO) is a rare and life-threatening complication of lupus. PATIENT CONCERNS: A patient with long-standing lupus developed recurrent abdominal pain and distension as well as nausea and emesis. DIAGNOSIS: Imaging showed dilated small bowel loops with air-fluid levels and bowel wall thickening. She also had bilateral hydronephrosis. INTERVENTIONS: She was given high-doses of intravenous steroids and cyclophosphamide. OUTCOMES: Her symptoms resolved within a week of starting immunosuppression. She was eventually transitioned to mycophenolate mofetil. She remained in remission and immunosuppression was successfully stopped after 1 year. CONCLUSIONS: Intestinal pseudo-obstruction is a rare complication of lupus that is often seen in association with ureterohydronephrosis and interstitial cystitis. This clinical syndrome is thought to be because of smooth muscle dysmotility of the gastrointestinal and genitourinary tracts, although the exact mechanism of dysmotility remains unknown. This condition is often responsive to immunosuppression if recognized and treated promptly.
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Hidronefrosis/etiología , Seudoobstrucción Intestinal/etiología , Lupus Eritematoso Sistémico/complicaciones , Adulto , Diagnóstico Diferencial , Femenino , Humanos , Hidronefrosis/diagnóstico por imagen , Hidronefrosis/terapia , Terapia de Inmunosupresión , Seudoobstrucción Intestinal/diagnóstico por imagen , Seudoobstrucción Intestinal/terapia , Lupus Eritematoso Sistémico/diagnóstico por imagen , Lupus Eritematoso Sistémico/terapiaRESUMEN
OBJECTIVE: Autonomic dysfunction is a known complication of systemic sclerosis (SSc) that can affect vascular tone, gastrointestinal (GI) motility, heart rate, and blood pressure control. We sought to quantify autonomic symptom burden in SSc, and to define the characteristics of patients with SSc and autonomic dysfunction. METHODS: Patients with SSc were consecutively recruited during routine clinical visits at the Johns Hopkins Scleroderma Center and asked to complete the Composite Autonomic Symptom Score (COMPASS)-31 questionnaire, a validated tool to assess symptoms of autonomic dysfunction. We determined the relationship between various clinical and serological features of SSc and the total COMPASS-31 scores and domain-specific scores using the Student t test or Wilcoxon rank-sum test for dichotomous variables and linear regression analysis for continuous variables. RESULTS: The study included 104 patients with SSc who completed the COMPASS-31 questionnaire. The mean COMPASS-31 score in this cohort was 24.9 ± 15.5, higher than COMPASS-31 scores from previously published healthy controls (8.9 ± 8.7). Compared to patients with mild or absent GI disease, patients with significant GI disease had higher scores across several subdomains of the COMPASS-31, including orthostatic intolerance (median 10.0 vs 0, p = 0.006) and secretomotor dysfunction (median 6.4 vs 4.3, p = 0.03). There was also a dose-response relationship between GI disease severity and autonomic symptom burden. CONCLUSION: Symptoms of autonomic dysfunction are common in SSc. Patients with more severe GI disease in SSc report more symptoms of dysautonomia across many facets of the autonomic nervous system.
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Enfermedades del Sistema Nervioso Autónomo/diagnóstico , Sistema Nervioso Autónomo/fisiopatología , Esclerodermia Sistémica/fisiopatología , Adulto , Anciano , Enfermedades del Sistema Nervioso Autónomo/fisiopatología , Femenino , Humanos , Masculino , Persona de Mediana Edad , Índice de Severidad de la Enfermedad , Encuestas y Cuestionarios , Evaluación de SíntomasRESUMEN
The inflammatory myopathies, which include dermatomyositis, polymyositis, and the immune-mediated necrotizing myopathies, are a heterogeneous group of autoimmune diseases that manifest with muscle, skin, or lung damage. Collectively, these autoimmune diseases result from loss of tolerance to a select group of self-antigens, although the precise mechanism through which this occurs is not known. Infection, malignancy, and certain medications including statins and the immune checkpoint inhibitors used in cancer therapy have been identified as potential immunologic triggers of the inflammatory myopathies. Some of these triggers are classically associated with specific myositis-specific autoantibodies (MSAs). The strong association between certain triggers and MSAs provides insights into how an immunologic event can lead to loss of tolerance to specific self-antigens, resulting in autoimmune disease. In this review, we discuss the proposed triggers of the inflammatory myopathies and their associations with MSAs, and provide insights into how these triggers may result in the inflammatory myopathies.
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Antineoplásicos/efectos adversos , Enfermedades Autoinmunes , Dermatomiositis , Inhibidores de Hidroximetilglutaril-CoA Reductasas/efectos adversos , Polimiositis , Animales , Antineoplásicos/uso terapéutico , Autoanticuerpos/inmunología , Autoantígenos/inmunología , Enfermedades Autoinmunes/inducido químicamente , Enfermedades Autoinmunes/inmunología , Enfermedades Autoinmunes/patología , Dermatomiositis/inducido químicamente , Dermatomiositis/inmunología , Dermatomiositis/patología , Humanos , Inhibidores de Hidroximetilglutaril-CoA Reductasas/uso terapéutico , Pulmón/inmunología , Pulmón/patología , Músculos/inmunología , Músculos/patología , Polimiositis/inducido químicamente , Polimiositis/inmunología , Polimiositis/patología , Piel/inmunología , Piel/patologíaRESUMEN
Amylin is a metabolic peptide hormone that is co-secreted with insulin from beta cells in the pancreas and activates many of the downstream targets of insulin. To investigate the relationship between this hormone and Alzheimer's disease (AD), we measured plasma human amylin levels in 206 subjects with AD, 64 subjects with mild cognitive impairment, and 111 subjects with no cognitive impairment and found significantly lower amylin levels among subjects with AD and mild cognitive impairment compared with the cognitively intact subjects. To investigate mechanisms underlying amylin's effects in the brain, we administered chronic infusions of the amylin analog pramlintide in the senescence-accelerated prone mouse, a mouse model of sporadic AD. Pramlintide administration improved performance in the novel object recognition task, a validated test of memory and cognition. The pramlintide-treated mice had increased expression of the synaptic marker synapsin I and the kinase cyclin-dependent kinase-5 in the hippocampus, as well as decreased oxidative stress and inflammatory markers in the hippocampus. A dose-dependent increase in cyclin-dependent kinase-5 and activation of extracellular-signal-regulated-kinases 1/2 by pramlintide treatment in vitro was also present indicating functionality of the amylin receptor in neurons. Together these results suggest that amylin analogs have neuroprotective properties and might be of therapeutic benefit in AD.
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Enfermedad de Alzheimer/tratamiento farmacológico , Enfermedad de Alzheimer/psicología , Cognición/efectos de los fármacos , Hipoglucemiantes/farmacología , Hipoglucemiantes/uso terapéutico , Polipéptido Amiloide de los Islotes Pancreáticos/farmacología , Polipéptido Amiloide de los Islotes Pancreáticos/uso terapéutico , Fármacos Neuroprotectores , Anciano , Anciano de 80 o más Años , Enfermedad de Alzheimer/metabolismo , Animales , Células Cultivadas , Quinasa 5 Dependiente de la Ciclina/metabolismo , Modelos Animales de Enfermedad , Femenino , Hipocampo/metabolismo , Humanos , Polipéptido Amiloide de los Islotes Pancreáticos/metabolismo , Masculino , Memoria/efectos de los fármacos , Ratones , Persona de Mediana Edad , Proteína Quinasa 1 Activada por Mitógenos/metabolismo , Proteína Quinasa 3 Activada por Mitógenos/metabolismo , Neuronas/metabolismo , Estrés Oxidativo , Receptores de Polipéptido Amiloide de Islotes Pancreáticos/metabolismo , Sinapsinas/metabolismoRESUMEN
OBJECTIVE: Dopaminergic neuronal death in Parkinson's disease (PD) is accompanied by oxidative stress and preceded by glutathione depletion. The development of disease-modifying therapies for PD has been hindered by a paucity of animal models that mimic these features and demonstrate an age-related progression. The EAAC1(-/-) mouse may be useful in this regard, because EAAC1(-/-) mouse neurons have impaired neuronal cysteine uptake, resulting in reduced neuronal glutathione content and chronic oxidative stress. Here we aimed to (1) characterize the age-related changes in nigral dopaminergic neurons in the EAAC1(-/-) mouse, and (2) use the EAAC1(-/-) mouse to evaluate N-acetylcysteine, a membrane-permeable cysteine pro-drug, as a potential disease-modifying intervention for PD. METHODS: Wild-type mice, EAAC1(-/-) mice, and EAAC1(-/-) mice chronically treated with N-acetylcysteine were evaluated at serial time points for evidence of oxidative stress, dopaminergic cell death, and motor abnormalities. RESULTS: EAAC1(-/-) mice showed age-dependent loss of dopaminergic neurons in the substantia nigra pars compacta, with more than 40% of these neurons lost by age 12 months. This neuronal loss was accompanied by increased nitrotyrosine formation, nitrosylated α-synuclein, and microglial activation. These changes were substantially reduced in mice that received N-acetylcysteine. INTERPRETATION: These findings suggest that the EAAC1(-/-) mouse may be a useful model of the chronic neuronal oxidative stress that occurs in PD. The salutary effects of N-acetylcysteine in this mouse model provide an impetus for clinical evaluation of glutathione repletion in PD.
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Acetilcisteína/farmacología , Dopamina/metabolismo , Transportador 3 de Aminoácidos Excitadores/metabolismo , Neuronas/efectos de los fármacos , Enfermedad de Parkinson/metabolismo , Sustancia Negra/efectos de los fármacos , Factores de Edad , Anciano , Análisis de Varianza , Animales , Western Blotting , Recuento de Células , Muerte Celular/efectos de los fármacos , Modelos Animales de Enfermedad , Transportador 3 de Aminoácidos Excitadores/genética , Humanos , Inmunohistoquímica , Ratones , Ratones Noqueados , Microglía/efectos de los fármacos , Microglía/metabolismo , Microglía/patología , Actividad Motora/efectos de los fármacos , Neuronas/metabolismo , Neuronas/patología , Estrés Oxidativo/efectos de los fármacos , Enfermedad de Parkinson/patología , Sustancia Negra/metabolismo , Sustancia Negra/patología , Tirosina 3-Monooxigenasa/metabolismoRESUMEN
OBJECTIVES: To evaluate whether the trend in patient selection or perioperative parameters were associated with treatment outcomes after percutaneous cryoablation (PCA) of renal masses. METHODS: We retrospectively analyzed our urological oncology database and identified 52 patients treated for a total of 54 renal masses. Univariate analysis was performed to evaluate whether the variables of age, gender, tumor size, number of probes used, total freezing time, preoperative creatinine, American Society of Anesthesia class, body mass index, or age-adjusted Charlson comorbidity index (CCI) score had an impact on the outcomes of treatment failure or the complication rate. RESULTS: During a mean follow-up of 21 months, recurrence-free, overall, and disease-specific (based on radiographic follow-up and biopsy) survival were 96.2%, 98.1% and 100%, respectively. The mean age-adjusted CCI score for patients with postoperative complications was 6.5, compared with a mean score of 3.0 in patients without postoperative complications (P = .02). The complication rate was also significantly higher when a greater number of cryoprobes were used during PCA (P < .005). None of the variables analyzed were predictive of treatment failure. CONCLUSIONS: Of the pre- and intraoperative variables studied, age-adjusted CCI score and number of cryoprobes used were the only variables with predictive value for outcomes in regard to treatment failure or complications. As investigators continue using cryoablation to treat renal masses, it is important to be able to completely and honestly counsel patients regarding the likelihood of complications and need for subsequent therapy in the setting of treatment failure.
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Criocirugía , Neoplasias Renales/cirugía , Anciano , Anciano de 80 o más Años , Carcinoma de Células Renales/diagnóstico , Carcinoma de Células Renales/cirugía , Criocirugía/efectos adversos , Criocirugía/métodos , Femenino , Humanos , Neoplasias Renales/diagnóstico , Masculino , Persona de Mediana Edad , Selección de Paciente , Radiografía Intervencional , Resultado del TratamientoRESUMEN
OBJECTIVE: To identify the factors that encourage or discourage internal medicine and pediatric residents regarding specializing in endocrinology with a focus on diabetes. METHODS: We conducted an electronic survey of internal medicine and pediatric residents using a $10 participation incentive. A total of 653 residents responded to the survey (estimated response rate of 9.2%)-626 from residency programs that were contacted for our survey and 27 from referrals. RESULTS: Among internal medicine and pediatric residents surveyed, 39 respondents (6.0%) planned to specialize in endocrinology, and 27 of these (4.1% of total respondents) planned to focus on diabetes. "Intellectual satisfaction," "emotional satisfaction," and "work-life balance" were identified by respondents as the most important factors in their choice of a specialty, with ratings of 5.5, 5.4, and 5.3 on a 6-point Likert scale. Among these factors identified as most important to a medical career, endocrinology with a focus on diabetes scored poorly with regard to intellectual and emotional satisfaction but received high ranking with regard to lifestyle. With regard to other factors, endocrinology was rated negatively on "compensation," "number of procedures," and "patient adherence to prescribed treatment." Exposure to diabetes during training had no major influence on the decision to enter endocrinology. CONCLUSION: Endocrinology with a focus on diabetes care is not an attractive specialty for most internal medicine and pediatric residents. Therefore, new strategies to attract residents to the field of diabetes care are needed.