iodine
Fuentes regulatorias consultadas
Indicaciones aprobadas
- Antisepsia general de pequeñas heridas superficiales y desinfección de piel antes de punción venosa o cirugía.
Contraindicaciones
Absolutas
- Hipersensibilidad al yodo o excipientes; pacientes quemados; neonatos de 0–1 mes.
Advertencias clínicas
- Advertencia mayor · No ingerir. Evitar uso regular o prolongado, heridas grandes o abiertas, quemaduras extensas y uso con insuficiencia hepática o renal, trastorno tiroideo o litio; controlar función tiroidea si el uso es prolongado o extenso. — CIMA/AEMPS, ficha técnica 57232
- Advertencia mayor · No usar vendaje oclusivo por riesgo de quemadura. Es inflamable: proteger del calor y evitar ojos, oídos y mucosas. — CIMA/AEMPS, ficha técnica 57232
- La absorción de yodo puede interferir con las pruebas de función tiroidea y producir falsos positivos en pruebas de sangre oculta en heces u orina. — CIMA/AEMPS, ficha técnica 57232
Interacciones medicamentosas
- SeveraLitio
Mecanismo: El uso prolongado conjunto puede producir un efecto hipotiroideo aditivo.
Recomendación: Evitar el uso prolongado conjunto y vigilar función tiroidea si fuese necesario.
CIMA/AEMPS, ficha técnica 57232https://cima.aemps.es/cima/dochtml/ft/57232/FT_57232.html
Eventos adversos
Comunes (≥1%)
Raras: irritación local, prurito o quemazón
Raros pero graves
Hipersensibilidad de frecuencia no establecida, con posible angioedema, artralgias, hemorragia cutánea, eosinofilia, fiebre, linfadenopatía, púrpura o urticaria · Alteraciones de la función renal o tiroidea tras uso en heridas extensas, quemaduras o durante períodos prolongados; frecuencia no establecida
Embarazo y lactancia
La experiencia en humanos sugiere que el yodo puede causar malformaciones congénitas y que su exceso perjudica al feto. Evitar el uso continuado, excesivo o en áreas extensas durante el embarazo y la lactancia; atraviesa la placenta y pasa a la leche y puede causar hipotiroidismo fetal o disfunción tiroidea o bocio en el lactante.
Bibliografía reciente (PubMed)
Trace elements and vitamins, named together micronutrients (MNs), are essential for human metabolism. Recent research has shown the importance of MNs in common pathologies, with significant deficiencies impacting the outcome. This guideline aims to provide information for daily clinical nutrition practice regarding assessment of MN status, monitoring, and prescription. It proposes a consensus terminology, since many words are used imprecisely, resulting in confusion. This is particularly true for the words "deficiency", "repletion", "complement", and "supplement". The expert group attempted to apply the 2015 standard operating procedures (SOP) for ESPEN which focuses on disease. However, this approach could not be applied due to the multiple diseases requiring clinical nutrition resulting in one text for each MN, rather than for diseases. An extensive search of the literature was conducted in the databases Medline, PubMed, Cochrane, Google Scholar, and CINAHL. The search focused on physiological data, historical evidence (published before PubMed release in 1996), and observational and/or randomized trials. For each MN, the main functions, optimal analytical methods, impact of inflammation, potential toxicity, and provision during enteral or parenteral nutrition were addressed. The SOP wording was applied for strength of recommendations. There was a limited number of interventional trials, preventing meta-analysis and leading to a low level of evidence. The recommendations underwent a consensus process, which resulted in a percentage of agreement (%): strong consensus required of >90% of votes. Altogether the guideline proposes sets of recommendations for 26 MNs, resulting in 170 single recommendations. Critical MNs were identified with deficiencies being present in numerous acute and chronic diseases. Monitoring and management strategies are proposed. This guideline should enable addressing suboptimal and deficient status of a bundle of MNs in at-risk diseases. In p
Background: Hashimoto thyroiditis (HT) is the most common cause of hypothyroidism in iodine-sufficient areas. Selenium is an essential trace element required for thyroid hormone synthesis and exerts antioxidant effects. Therefore, it may be of relevance in the management of HT. Methods: We conducted a systematic review and meta-analysis of randomized controlled trials (RCTs) to evaluate the effect of selenium supplementation on thyroid function (thyrotropin [TSH], free and total thyroxine [fT4, T4], free and total triiodothyronine [fT3, T3]), thyroid antibodies (thyroid peroxidase antibodies [TPOAb], thyroglobulin antibodies [TGAb], thyrotropin receptor antibody [TRAb]), ultrasound findings (echogenicity, thyroid volume), immune markers, patient-reported outcomes, and adverse events in HT. The study protocol was registered on PROSPERO (CRD42022308377). We systematically searched MEDLINE, Embase, CINHAL, Web of Science, Google Scholar, and the Cochrane CENTRAL Register of Trials from inception to January 2023 and searched citations of eligible studies. Two independent authors reviewed and coded the identified literature. The primary outcome was TSH in patients without thyroid hormone replacement therapy (THRT); the others were considered secondary outcomes. We synthesized the results as standardized mean differences (SMD) or odds ratio (OR), assessed risk of bias using the Cochrane RoB 2 tool, and rated the evidence using the Grading of Recommendations Assessment, Development, and Evaluation (GRADE) approach. Results: We screened 687 records and included 35 unique studies. Our meta-analysis found that selenium supplementation decreased TSH in patients without THRT (SMD -0.21 [confidence interval, CI -0.43 to -0.02]; 7 cohorts, 869 participants; I2 = 0%). In addition, TPOAb (SMD -0.96 [CI -1.36 to -0.56]; 29 cohorts; 2358 participants; I2 = 90%) and malondialdehyde (MDA; SMD -1.16 [CI -2.29 to -0.02]; 3 cohorts; 248 participants; I2 = 85%) decreased in patients with a
Preoperative skin antisepsis is an established procedure to prevent surgical site infections (SSIs). The choice of antiseptic agent, povidone iodine or chlorhexidine gluconate, remains debated. To determine whether povidone iodine in alcohol is noninferior to chlorhexidine gluconate in alcohol to prevent SSIs after cardiac or abdominal surgery. Multicenter, cluster-randomized, investigator-masked, crossover, noninferiority trial; 4403 patients undergoing cardiac or abdominal surgery in 3 tertiary care hospitals in Switzerland between September 2018 and March 2020 were assessed and 3360 patients were enrolled (cardiac, n = 2187 [65%]; abdominal, n = 1173 [35%]). The last follow-up was on July 1, 2020. Over 18 consecutive months, study sites were randomly assigned each month to either use povidone iodine or chlorhexidine gluconate, each formulated in alcohol. Disinfectants and skin application processes were standardized and followed published protocols. Primary outcome was SSI within 30 days after abdominal surgery and within 1 year after cardiac surgery, using definitions from the US Centers for Disease Control and Prevention's National Healthcare Safety Network. A noninferiority margin of 2.5% was used. Secondary outcomes included SSIs stratified by depth of infection and type of surgery. A total of 1598 patients (26 cluster periods) were randomly assigned to receive povidone iodine vs 1762 patients (26 cluster periods) to chlorhexidine gluconate. Mean (SD) age of patients was 65.0 years (39.0-79.0) in the povidone iodine group and 65.0 years (41.0-78.0) in the chlorhexidine gluconate group. Patients were 32.7% and 33.9% female in the povidone iodine and chlorhexidine gluconate groups, respectively. SSIs were identified in 80 patients (5.1%) in the povidone iodine group vs 97 (5.5%) in the chlorhexidine gluconate group, a difference of 0.4% (95% CI, -1.1% to 2.0%) with the lower limit of the CI not exceeding the predefined noninferiority margin of -2.5%; results we
Thyroid disorders are prevalent in pregnant women. Furthermore, thyroid hormone has a critical role in fetal development and thyroid dysfunction can adversely affect obstetric outcomes. Thus, the appropriate management of hyperthyroidism, most commonly caused by Graves disease, and hypothyroidism, which in iodine sufficient regions is most commonly caused by Hashimoto thyroiditis, in pregnancy is important for the health of both pregnant women and their offspring. Gestational transient thyrotoxicosis can also occur during pregnancy and should be differentiated from Graves disease. Effects of thyroid autoimmunity and subclinical hypothyroidism in pregnancy remain controversial. Iodine deficiency is the leading cause of hypothyroidism worldwide. Despite global efforts to eradicate iodine deficiency disorders, pregnant women remain at risk of iodine deficiency due to increased iodine requirements during gestation. The incidence of thyroid cancer is increasing worldwide, including in young adults. As such, the diagnosis of thyroid nodules or thyroid cancer during pregnancy is becoming more frequent. The evaluation and management of thyroid nodules and thyroid cancer in pregnancy pose a particular challenge. Postpartum thyroiditis can occur up to 1 year after delivery and must be differentiated from other forms of thyroid dysfunction, as treatment differs. This Review provides current evidence and recommendations for the evaluation and management of thyroid disorders in pregnancy and in the postpartum period.