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1.
J Endocrinol Invest ; 46(11): 2343-2352, 2023 Nov.
Artículo en Inglés | MEDLINE | ID: mdl-37037973

RESUMEN

PURPOSE: To evaluate the prevalence, risk factors and evolution of diabetes mellitus (DM) after targeted treatment in patients with primary aldosteronism (PA). METHODS: A retrospective multicenter study of PA patients in follow-up at 27 Spanish tertiary hospitals (SPAIN-ALDO Register). RESULTS: Overall, 646 patients with PA were included. At diagnosis, 21.2% (n = 137) had DM and 67% of them had HbA1c levels < 7%. In multivariate analysis, family history of DM (OR 4.00 [1.68-9.53]), the coexistence of dyslipidemia (OR 3.57 [1.51-8.43]) and advanced age (OR 1.04 per year of increase [1.00-1.09]) were identified as independent predictive factors of DM. Diabetic patients were on beta blockers (46.7% (n = 64) vs. 27.5% (n = 140), P < 0.001) and diuretics (51.1% (n = 70) vs. 33.2% (n = 169), p < 0.001) more frequently than non-diabetics. After a median follow-up of 22 months [IQR 7.5-63.0], 6.9% of patients developed DM, with no difference between those undergoing adrenalectomy and those treated medically (HR 1.07 [0.49-2.36], p = 0.866). There was also no significant difference in the evolution of glycemic control between DM patients who underwent surgery and those medically treated (p > 0.05). CONCLUSION: DM affects about one quarter of patients with PA and the risk factors for its development are common to those of the general population. Medical and surgical treatment provides similar benefit in glycemic control in patients with PA and DM.


Asunto(s)
Diabetes Mellitus , Hiperaldosteronismo , Humanos , Prevalencia , España/epidemiología , Diabetes Mellitus/epidemiología , Diabetes Mellitus/etiología , Factores de Riesgo , Hiperaldosteronismo/complicaciones , Hiperaldosteronismo/epidemiología , Hiperaldosteronismo/terapia , Sistema de Registros
2.
J Endocrinol Invest ; 45(5): 1071-1077, 2022 May.
Artículo en Inglés | MEDLINE | ID: mdl-35015288

RESUMEN

AIM: To describe a case series of thyrotoxicosis likely triggered by SARS-CoV-2 vaccination and to warn physicians about this potential correlation. To report clinical, laboratory and imaging findings and provide further information that goes in line with the underlying mechanisms. METHODS: Single-center case series based on all the information collected in the hospital medical records, as well as the temporal sequence between the onset of symptoms and COVID-19 vaccination. RESULTS: We report 8 cases with thyrotoxicosis after SARS-CoV-2 vaccination. 4 cases of Graves' disease (GD), 2 cases of subacute painful thyroiditis (SAT), 1 case of concurrent GD and SAT and 1 case of atypical subacute thyroiditis. Five patients received BNT162b2 mRNA vaccine, 3 patients 1273 mRNA vaccine. The onset of symptoms following vaccination ranged from 10 to 14 days in six of eight patients and from 7 to 8 weeks in two patients. CONCLUSIONS: Several hypotheses have been proposed to explain the potential correlation between SARS-CoV-2 vaccination and thyrotoxicosis, including immune system hyper-stimulation, molecular mimicry and Autoimmune/Autoinflammatory Syndrome Induced by Adjuvants (ASIA). We should pay greater attention to thyroid disorders in patients receiving vaccine against SARS-CoV-2.


Asunto(s)
COVID-19 , Enfermedad de Graves , Tiroiditis Subaguda , Tirotoxicosis , Vacuna BNT162 , COVID-19/prevención & control , Vacunas contra la COVID-19/efectos adversos , Enfermedad de Graves/diagnóstico , Humanos , SARS-CoV-2 , Tiroiditis Subaguda/diagnóstico , Tiroiditis Subaguda/etiología , Tirotoxicosis/diagnóstico , Tirotoxicosis/etiología , Vacunación/efectos adversos , Vacunas Sintéticas , Vacunas de ARNm
3.
Endocrinol. nutr. (Ed. impr.) ; 55(supl.2): 73-77, ene. 2008. tab
Artículo en Español | IBECS | ID: ibc-61989

RESUMEN

Las hormonas incretinas son péptidos liberados en el tracto gastrointestinal en respuesta a la ingesta de nutrientes, que potencianl a liberación de insulina y ayudan en el mantenimiento homeostático de la glucemia. El concepto de esta acción incretina se basó en la observación de quela respuesta secretora de insulina a la administración oral de glucosa era superior a la respuesta a cantidades equivalentes de glucosa administrada intravenosa. El efecto incretina se estima que es responsable de hasta el 70% de la secreción de insulina en respuesta a la glucosa oral y es causado principalmente por 2 hormonas intestinales: glucagon-like peptide (GLP-1) y glucose-dependent insulinotropic peptide (GIP).En la diabetes tipo 2, además del efecto deficiente de las incretinas, también se ha encontrado una alteración en la secreción de GLP-1.La administración exógena de GLP-1 ayuda a la normalización de la glucemia tanto basal como posprandial; sin embargo, el GLP-1 es rápidamente degradado por la enzima dipeptidil peptidasa (DPP-IV).Esta circunstancia ha llevado al desarrollo de fármacos análogos deGLP-1, con mayor resistencia a la degradación enzimática o a fármacos inhibidores de DPP-IV. El mecanismo por el cual las incretinas causan su efecto regulador sobre la homeostasis energética es en parte todavía desconocido y es actualmente un área de intensa investigación (AU)


The incretin hormones are peptides released in the gastrointestinal tract in response to nutrient ingestion. These hormones enhance insulin release and help to maintainglycemic homeostasis. The concept of incretin action was based on the observation that the secretory response of insulin to oral glucose administration is greater than that to equivalent quantities of intravenous glucose. The incret in effect is estimated to be responsible for up to 70% of insulin secretion in response to oral glucose and is mainly caused by two gastrointestinal hormones: glucagon-like peptide (GLP-1) y glucose-dependent insulinotropic peptide(GIP). In type 2 diabetes, in addition to a deficiency in incretin-mediated insulinsecretion, alterations in GLP-1 secretion have also been found. Exogenous GLP-1secretion helps to restore normal levels of both basal and postprandial blood glucose. However, GLP-1 is rapidly degraded by the dipeptidyl peptidase enzyme (DPP-IV). This phenomenon has led to the development ofGLP-1 analogs, which are more resistant to enzyme degradation or DPP-IV inhibitors. The mechanism through which the incretin hormones exert their regulatory effect onenergy homeostasis remains unknown and is currently the subject of intense research (AU)


Asunto(s)
Humanos , Masculino , Femenino , Incretinas/uso terapéutico , Hipoglucemia/tratamiento farmacológico , Hipoglucemia/epidemiología , Polipéptido Inhibidor Gástrico/metabolismo , Polipéptido Inhibidor Gástrico/uso terapéutico , Péptidos Similares al Glucagón/metabolismo , Péptidos Similares al Glucagón/uso terapéutico , Inhibidores de la Dipeptidil-Peptidasa IV/uso terapéutico , Incretinas/farmacología , Incretinas/fisiología , Incretinas/farmacocinética , Inhibidores de la Dipeptidil-Peptidasa IV/metabolismo , Inhibidores de la Dipeptidil-Peptidasa IV/farmacología , Inhibidores de la Dipeptidil-Peptidasa IV/farmacocinética
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