RESUMEN
Anti-tumor necrosis factor alpha (anti-TNF-α) comprises a group of drugs that inhibit the action of cytokine TNF-α, and are used to treat diseases mainly caused by this cytokine. An increase in cutaneous adverse events has been observed with similar anti-TNF biologic treatments frequently used in clinical practice.
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Adalimumab , Esclerodermia Localizada , Factor de Necrosis Tumoral alfa , Humanos , Adalimumab/efectos adversos , Adalimumab/uso terapéutico , Factor de Necrosis Tumoral alfa/antagonistas & inhibidores , Esclerodermia Localizada/inducido químicamente , Fibrosis/inducido químicamente , Antiinflamatorios/efectos adversos , Antiinflamatorios/uso terapéuticoAsunto(s)
Adalimumab , Proteínas Proto-Oncogénicas B-raf , Síndrome Uveomeningoencefálico , Humanos , Adalimumab/uso terapéutico , Adalimumab/efectos adversos , Síndrome Uveomeningoencefálico/tratamiento farmacológico , Proteínas Proto-Oncogénicas B-raf/antagonistas & inhibidores , Proteínas Proto-Oncogénicas B-raf/genética , Resistencia a Medicamentos , Femenino , Inhibidores de Proteínas Quinasas/efectos adversos , Inhibidores de Proteínas Quinasas/uso terapéutico , Masculino , Antiinflamatorios/uso terapéutico , Antiinflamatorios/efectos adversos , Persona de Mediana Edad , Sulfonamidas/uso terapéutico , Sulfonamidas/efectos adversosRESUMEN
Adalimumab is a human monoclonal antibody that selectively targets tumour necrosis factor-alpha (TNF- α), a cytokine involved in the pathogenesis of various inflammatory and autoimmune disorders. Adalimumab has been approved worldwide for the treatment of several chronic immune-mediated diseases, including rheumatoid arthritis, psoriasis, psoriatic arthritis, ankylosing spondylitis, Crohn's disease, ulcerative colitis, and juvenile idiopathic arthritis. One of the adverse reactions caused by Adalimumab is psoriasis. This study reports the case of a 37-year-old male with palmoplantar psoriasis triggered by adalimumab for treatment of Crohn's disease. This eruption resisted complete clearance with various potent corticosteroids. The patient was referred back to the treating rheumatologist to possibly change adalimumab to another type of therapy.
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Adalimumab , Antiinflamatorios , Enfermedad de Crohn , Psoriasis , Humanos , Adalimumab/efectos adversos , Adalimumab/uso terapéutico , Enfermedad de Crohn/tratamiento farmacológico , Masculino , Adulto , Psoriasis/inducido químicamente , Psoriasis/tratamiento farmacológico , Antiinflamatorios/efectos adversos , Antiinflamatorios/uso terapéuticoRESUMEN
Tirzepatide is a new drug targeting glucagon-like peptide 1(GLP1) and gastric inhibitory polypeptide (GIP) receptors. This drug has demonstrated great potential in improving the clinical outcomes of patients with type 2 diabetes. It can lead to weight loss, better glycemic control, and reduced cardiometabolic risk factors. GLP1 receptor agonists have been proven effective antidiabetic medications with possible cardiovascular benefits. Even though they have been proven to reduce the risk of major adverse cardiovascular events, their effectiveness in treating heart failure is unknown. Unlike traditional GLP1 receptor agonists, tirzepatide is more selective for the GIP receptor, resulting in a more balanced activation of these receptors. This review article discusses the possible mechanisms tirzepatide may use to improve cardiovascular health. That includes the anti-inflammatory effect, the ability to reduce cell death and promote autophagy, and also its indirect effects through blood pressure, obesity, and glucose/lipid metabolism. Additionally, tirzepatide may benefit atherosclerosis and lower the risk of major adverse cardiac events. Currently, clinical trials are underway to evaluate the safety and efficacy of tirzepatide in patients with heart failure. Overall, tirzepatide's dual agonism of GLP1 and GIP receptors appears to provide encouraging cardiovascular benefits beyond glycemic control, offering a potential new therapeutic option for treating cardiovascular diseases and heart failure.
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Enfermedades Cardiovasculares , Diabetes Mellitus Tipo 2 , Receptor del Péptido 1 Similar al Glucagón , Hipoglucemiantes , Incretinas , Humanos , Receptor del Péptido 1 Similar al Glucagón/agonistas , Receptor del Péptido 1 Similar al Glucagón/metabolismo , Enfermedades Cardiovasculares/tratamiento farmacológico , Enfermedades Cardiovasculares/prevención & control , Diabetes Mellitus Tipo 2/tratamiento farmacológico , Diabetes Mellitus Tipo 2/sangre , Hipoglucemiantes/uso terapéutico , Hipoglucemiantes/efectos adversos , Hipoglucemiantes/farmacología , Animales , Resultado del Tratamiento , Incretinas/uso terapéutico , Incretinas/efectos adversos , Receptores de la Hormona Gastrointestinal/agonistas , Receptores de la Hormona Gastrointestinal/metabolismo , Transducción de Señal/efectos de los fármacos , Glucemia/efectos de los fármacos , Glucemia/metabolismo , Sistema Cardiovascular/efectos de los fármacos , Sistema Cardiovascular/metabolismo , Sistema Cardiovascular/fisiopatología , Antiinflamatorios/uso terapéutico , Antiinflamatorios/efectos adversos , Biomarcadores/sangre , Medición de Riesgo , Receptor del Péptido 2 Similar al Glucagón , Polipéptido Inhibidor GástricoRESUMEN
This report describes a case of facial hyperpigmentation in a patient with Crohn's disease receiving adalimumab, a tumor necrosis factor (TNF)-alpha inhibitor. The onset of hyperpigmentation coincided with adalimumab administration, and its discontinuation resulted in significant improvement. Histopathological findings suggest a postinflammatory process at the dermo-epidermal junction. However, the precise mechanism remains unclear.
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Adalimumab , Enfermedad de Crohn , Hiperpigmentación , Humanos , Adalimumab/efectos adversos , Hiperpigmentación/inducido químicamente , Hiperpigmentación/patología , Enfermedad de Crohn/tratamiento farmacológico , Antiinflamatorios/efectos adversos , Antiinflamatorios/uso terapéutico , Femenino , Adulto , Factor de Necrosis Tumoral alfa/antagonistas & inhibidores , Cara/patología , MasculinoRESUMEN
Acute pancreatitis (AP) is a sudden inflammation of the pancreas which often manifests as a mild disease but can be associated with high morbidity and mortality. Drug-induced AP is rare and most likely underdiagnosed. Vedolizumab is a human monoclonal antibody with gut-selective integrin antagonist effect, and it is used for treatment of inflammatory bowel disease (IBD). Budesonid is a glucocorticoid which is released in the colon and it is also used in IBD treatment. This is a case report where vedolizumab or budesonide caused acute pancreatitis in a young man with ulcerative colitis.
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Anticuerpos Monoclonales Humanizados , Budesonida , Colitis Ulcerosa , Fármacos Gastrointestinales , Pancreatitis , Humanos , Colitis Ulcerosa/tratamiento farmacológico , Anticuerpos Monoclonales Humanizados/efectos adversos , Anticuerpos Monoclonales Humanizados/uso terapéutico , Masculino , Pancreatitis/inducido químicamente , Budesonida/efectos adversos , Budesonida/uso terapéutico , Fármacos Gastrointestinales/efectos adversos , Fármacos Gastrointestinales/uso terapéutico , Adulto , Enfermedad Aguda , Antiinflamatorios/efectos adversos , Antiinflamatorios/uso terapéutico , Glucocorticoides/uso terapéutico , Glucocorticoides/efectos adversosAsunto(s)
Angioplastia Coronaria con Balón , Antiinflamatorios , Reestenosis Coronaria , Paclitaxel , Stents , Humanos , Angioplastia Coronaria con Balón/instrumentación , Antiinflamatorios/administración & dosificación , Antiinflamatorios/efectos adversos , Antiinflamatorios/uso terapéutico , Ensayos Clínicos como Asunto , Materiales Biocompatibles Revestidos/efectos adversos , Reestenosis Coronaria/etiología , Stents Liberadores de Fármacos , Paclitaxel/administración & dosificación , Paclitaxel/efectos adversos , Paclitaxel/uso terapéutico , Stents/efectos adversosRESUMEN
BACKGROUND: A significant proportion of the global population has been infected with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) at some point since the onset of the pandemic. Although most individuals who develop coronavirus disease 2019 (COVID-19) recover without complications, about 6% have persistent symptoms, referred to as post-COVID-19 condition (PCC). Intervention studies investigating treatments that potentially alleviate PCC-related symptoms and thus aim to mitigate the global public health burden and healthcare costs linked to PCC are desperately needed. The PYCNOVID trial investigates the effects of Pycnogenol®, a French maritime pine bark extract with anti-inflammatory and antioxidative properties, versus placebo on patient-reported health status in people with PCC. METHODS: This is a single-center, placebo-controlled, quadruple blind, randomized trial. We aim to randomly assign 150 individuals with PCC (1:1 ratio) to receive either 200 mg Pycnogenol® or placebo daily for 12 weeks. Randomization is stratified for duration of PCC symptoms (≤ 6 months versus > 6 months) and presence of symptomatic chronic disease(s). The primary endpoint is perceived health status at 12 weeks (EuroQol-Visual Analogue Scale) adjusted for baseline values and stratification factors. Secondary endpoints include change in self-reported PCC symptoms, health-related quality of life, symptoms of depression and anxiety, cognitive function, functional exercise capacity, physical activity measured with accelerometry, and blood biomarkers for endothelial health, inflammation, coagulation, platelet function, and oxidative stress. Investigators, study participants, outcome assessors, and data analysts are blinded regarding the intervention assignment. Individuals with PCC were involved in the design of this study. DISCUSSION: This is the first trial to investigate the effects of Pycnogenol® versus placebo on patient-reported health status in people with PCC. Should the trial proof clinical effectiveness, Pycnogenol® may serve as a therapeutic approach to mitigate symptoms associated with PCC. TRIAL REGISTRATION: The study is registered at ClinicalTrials.gov. :NCT05890534, June 6, 2023.
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Flavonoides , Extractos Vegetales , Humanos , Extractos Vegetales/uso terapéutico , Extractos Vegetales/efectos adversos , Flavonoides/uso terapéutico , Ensayos Clínicos Controlados Aleatorios como Asunto , Calidad de Vida , COVID-19 , Resultado del Tratamiento , SARS-CoV-2/efectos de los fármacos , Estado de Salud , Tratamiento Farmacológico de COVID-19 , Síndrome Post Agudo de COVID-19 , Adulto , Femenino , Masculino , Antioxidantes/uso terapéutico , Antioxidantes/efectos adversos , Antiinflamatorios/uso terapéutico , Antiinflamatorios/efectos adversosRESUMEN
BACKGROUND: There is no known effective pharmacological therapy for long COVID, which is characterized by wide-ranging, multisystemic, fluctuating, or relapsing symptoms in a large proportion of survivors of acute COVID. This randomized controlled trial aims to assess the safety and efficacy of an anti-inflammatory agent colchicine, to reduce symptoms among those at high risk of developing long COVID. METHODS: This multi-centre, parallel arm, 1:1 individual randomized, placebo-controlled, double-blind superiority trial will enrol 350 individuals with persistent post-COVID symptoms. Participants will be randomized to either colchicine 0.5 mg once daily (< 70 kg) or twice daily (≥ 70 kg) or matched placebo for 26 weeks and will be followed up until 52 weeks after randomization. The primary trial objective is to demonstrate the superiority of colchicine over a placebo in improving distance walked in 6 min at 52 weeks from baseline. The secondary objectives are to assess the efficacy of colchicine compared to placebo with respect to lung function, inflammatory markers, constitutional symptoms, and mental health state. In a sub-sample of 100 participants, cardiac biomarkers of myocardial injury and myocardial oedema using MRI will be compared. DISCUSSION: Persistent inflammatory response following SARS-CoV-19 is one of the postulated pathophysiological mechanisms of long COVID. Colchicine, a low-cost anti-inflammatory agent, acts via multiple inflammatory pathways and has an established safety profile. This trial will generate evidence for an important health priority that can rapidly translate into practice. TRIAL REGISTRATION: This clinical trial has been registered prospectively on www. CLINICALTRIALS: gov with registration CTRI/2021/11/038234 dated November 24, 2021.
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Tratamiento Farmacológico de COVID-19 , COVID-19 , Colchicina , Humanos , Colchicina/uso terapéutico , Colchicina/efectos adversos , Método Doble Ciego , COVID-19/complicaciones , SARS-CoV-2 , Síndrome Post Agudo de COVID-19 , Antiinflamatorios/uso terapéutico , Antiinflamatorios/efectos adversos , Inflamación/tratamiento farmacológico , Enfermedades Cardiovasculares/prevención & control , Estudios Multicéntricos como Asunto , Ensayos Clínicos Controlados Aleatorios como Asunto , Resultado del Tratamiento , AdultoRESUMEN
BACKGROUND AND OBJECTIVE: The influence of concomitant prednisolone on clinical outcomes and safety in infliximab-treated ulcerative colitis (UC) patients is unknown. DESIGN, SETTING, PARTICIPANTS AND OUTCOME MEASURES: A retrospective cohort study was performed, including 147 UC patients treated with infliximab at a tertiary inflammatory bowel disease (IBD) centre. Primary outcome was corticosteroid-free clinical remission (CFCR) at week 14 and week 52. Patients were grouped according to prednisolone tapering regimens: standard (≤5 mg/week), fast (>5 mg/week), direct discontinuation or no prednisolone. Patients intolerant to corticosteroids and patients stopping corticosteroids in preparation for surgery including colectomy during their initial admission were excluded. RESULTS: There was no overall association between prednisolone exposure or no exposure and CFCR at weeks 14 or 52 of infliximab. The proportion of patients with C reactive protein ≤5 mg/L was higher in the standard tapering at week 14 as compared with faster regimens or no prednisolone. In subgroup analyses, the standard tapering was associated with a higher rate of CFCR at week 14 compared with the fast-tapering regimen in patients receiving ≥40 mg prednisolone at initiation of infliximab (64.3% vs 26.3%, p=0.04) and among patients admitted with acute severe UC (66.6% vs 23.5%, p<0.05). Similar data were seen at week 52. Prednisolone did not affect infliximab trough levels but increased infection rates (10/77 vs 2/70, p=0.03), in particular C. difficile infection. CONCLUSION: In UC patients with limited disease burden, prednisolone did not affect effectiveness of infliximab. However, patients with increased disease burden seem to benefit from corticosteroid combination therapy.
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Colitis Ulcerosa , Fármacos Gastrointestinales , Infliximab , Prednisolona , Inducción de Remisión , Humanos , Colitis Ulcerosa/tratamiento farmacológico , Infliximab/administración & dosificación , Infliximab/uso terapéutico , Estudios Retrospectivos , Prednisolona/administración & dosificación , Prednisolona/uso terapéutico , Masculino , Femenino , Adulto , Persona de Mediana Edad , Resultado del Tratamiento , Inducción de Remisión/métodos , Fármacos Gastrointestinales/administración & dosificación , Fármacos Gastrointestinales/uso terapéutico , Reducción Gradual de Medicamentos/métodos , Antiinflamatorios/administración & dosificación , Antiinflamatorios/uso terapéutico , Antiinflamatorios/efectos adversos , Proteína C-Reactiva/análisis , Proteína C-Reactiva/metabolismo , Glucocorticoides/administración & dosificación , Glucocorticoides/uso terapéutico , Glucocorticoides/efectos adversos , Quimioterapia CombinadaRESUMEN
This post hoc analysis of PIONEER I and II randomized clinical trials assesses whether receiving adalimumab is associated with decreased hematologic abnormalities and increased clinical improvement in patients with hidradenitis suppurativa.
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Adalimumab , Hidradenitis Supurativa , Humanos , Hidradenitis Supurativa/tratamiento farmacológico , Adalimumab/efectos adversos , Adalimumab/uso terapéutico , Adalimumab/administración & dosificación , Femenino , Masculino , Adulto , Persona de Mediana Edad , Enfermedades Hematológicas , Antiinflamatorios/uso terapéutico , Antiinflamatorios/administración & dosificación , Antiinflamatorios/efectos adversosRESUMEN
INTRODUCTION: Cannabidiol (CBD) is the primary non-psychoactive chemical derived from Cannabis Sativa, and its growing popularity is due to its potential therapeutic properties while avoiding the psychotropic effects of other phytocannabinoids, such as tetrahydrocannabinol (THC). Numerous pre-clinical studies in cellular and animal models and human clinical trials have demonstrated a positive impact of CBD on physiological and pathological processes. Recently, the FDA approved its use for the treatment of seizures, and clinical trials to test the efficacy of CBD in myocarditis and pericarditis are ongoing. AREAS COVERED: We herein reviewed the current literature on the reported effects of CBD in the cardiovascular system, highlighting the physiological effects and the outcomes of using CBD as a therapeutic tool in pathological conditions to address this significant global health concern. EXPERT OPINION: The comprehensive examination of the literature emphasizes the potential of CBD as a therapeutic option for treating cardiovascular diseases through its anti-inflammatory, vasodilatory, anti-fibrotic, and antioxidant properties in different conditions such as diabetic cardiomyopathy, myocarditis, doxorubicin-induced cardiotoxicity, and ischemia-reperfusion injury.
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Cannabidiol , Enfermedades Cardiovasculares , Cannabidiol/farmacología , Cannabidiol/uso terapéutico , Humanos , Enfermedades Cardiovasculares/tratamiento farmacológico , Animales , Antiinflamatorios/farmacología , Antiinflamatorios/efectos adversos , Antioxidantes/farmacologíaRESUMEN
Psoriasis, a prevalent chronic inflammatory skin disorder affecting 2-3% of the global population, has transcended its dermatological confines, revealing a profound association with cardiovascular diseases (CVD). This comprehensive review explores the intricate interplay between psoriasis and cardiovascular system, delving into genetic links, immune pathways, and adipose tissue dysfunction beyond conventional CVD risk factors. The pathophysiological connections unveil unique signatures, distinct from other inflammatory skin conditions, in particular psoriasis-specific genetic polymorphisms in IL-23 and TNF-α have consistently been linked to CVD. The review navigates the complex landscape of psoriasis treatments, addressing challenges and future directions in particular relevance to CVDs in psoriasis. Therapeutic interventions, including TNF inhibitors (TNFi), present promise in reducing cardiovascular risks, and methotrexate could constitute a favourable choice. Conversely, the relationship between IL-12/23 inhibitors and cardiovascular risk remains uncertain, while recent evidence indicates that Janus kinase inhibitors may not carry CVD risks. Emerging evidence supports the safety and efficacy of IL-17 and IL-23 inhibitors in patients with CVDs, hinting at evolving therapeutic paradigms. Lifestyle modifications, statins, and emerging therapies offer preventive strategies. Dedicated screening guidelines for CVD risk assessment in psoriasis are however lacking. Further, the impact of different disease phenotypes and treatment hierarchies in cardiovascular outcomes remains elusive, demanding ongoing research at the intersection of dermatology, rheumatology, and cardiology. In conclusion, unraveling the intricate connections between psoriasis and CVD provides a foundation for a holistic approach to patient care. Collaboration between specialties, advancements in screening methodologies, and a nuanced understanding of treatment impacts are essential for comprehensive cardiovascular risk management in individuals with psoriasis.
Psoriasis is a skin condition that not only affects the skin but is also linked to issues in the body's fat tissue, which can lead to inflammation and heart problems. The fat tissue in people with psoriasis contains various immune cells, contributing to obesity and insulin resistance. Research has found a strong connection between inflammation in fat tissues and cardiovascular problems in people with psoriasis. Specific substances released by fat tissue, like leptin, resistin, and adiponectin, can impact inflammation and cardiovascular health. Psoriasis patients often show increased levels of these substances. Treatment for psoriasis may influence cardiovascular health. Some studies suggest that certain medications, like methotrexate or TNF inhibitors, may lower the risk of heart events. However, there are also concerns about potential adverse effects, and further research is needed to fully understand how psoriasis treatments affect cardiovascular outcomes. To manage the cardiovascular risks associated with psoriasis, regular screening for heart-related issues is recommended. Lifestyle changes, such as a healthy diet, stress management, and smoking cessation, are also essential. Additionally, specific medications, like statins and metformin, may be beneficial in controlling cardiovascular risk factors in people with psoriasis. Despite advancements in understanding the relationship between psoriasis and cardiovascular health, there are still challenges. Research is ongoing to develop better screening guidelines and treatment strategies. Collaboration between dermatologists, rheumatologists, and cardiologists is crucial to address the complex nature of this condition and its impact on the heart.
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Enfermedades Cardiovasculares , Fármacos Dermatológicos , Factores de Riesgo de Enfermedad Cardiaca , Psoriasis , Humanos , Psoriasis/tratamiento farmacológico , Psoriasis/diagnóstico , Psoriasis/terapia , Psoriasis/genética , Psoriasis/fisiopatología , Enfermedades Cardiovasculares/epidemiología , Enfermedades Cardiovasculares/diagnóstico , Enfermedades Cardiovasculares/prevención & control , Enfermedades Cardiovasculares/fisiopatología , Fármacos Dermatológicos/uso terapéutico , Fármacos Dermatológicos/efectos adversos , Medición de Riesgo , Resultado del Tratamiento , Antiinflamatorios/uso terapéutico , Antiinflamatorios/efectos adversos , Predisposición Genética a la Enfermedad , Factores de Riesgo , Conducta de Reducción del RiesgoRESUMEN
BACKGROUND: Paclitaxel (PTX) is touted as an essential medicine due to its extensive use as a chemotherapeutic agent for various cancers and an antiproliferative agent for endovascular applications. Emerging studies in cardio-oncology implicate various vascular complications of chemotherapeutic agents. METHODS: We evaluated the inflammatory response induced by the systemic administration of PTX. The investigation included RNAseq analysis of primary human endothelial cells (ECs) treated with PTX to identify transcriptional changes in pro-inflammatory mediators. Additionally, we used dexamethasone (DEX), a well-known antiinflammatory compound, to assess its effectiveness in counteracting these PTX-induced changes. Further, we studied the effects of PTX on monocyte chemoattractant protein-1 (MCP-1) levels in the media of ECs. The study also extended to in vivo analysis, where a group of mice was injected with PTX and subsequently harvested at different times to assess the immediate and delayed effects of PTX on inflammatory mediators in blood and aortic ECs. RESULTS: Our RNAseq analysis revealed that PTX treatment led to significant transcriptional perturbations in pro-inflammatory mediators such as MCP-1 and CD137 within primary human ECs. These changes were effectively abrogated when DEX was administered. In vitro experiments showed a marked increase in MCP-1 levels in EC media following PTX treatment, which returned to baseline upon treatment with DEX. In vivo, we observed a threefold increase in MCP-1 levels in blood and aortic ECs 12 h post-PTX administration. Similar trends were noted for CD137 and other downstream mediators like tissue factor, vascular cell adhesion molecule 1, and E-selectin in aortic ECs. CONCLUSION: Our findings illustrate that PTX exposure induces an upregulation of atherothrombotic mediators, which can be alleviated with concurrent administration of DEX. Considering these observations, further long-term investigations should focus on understanding the systemic implications associated with PTX-based therapies and explore the clinical relevance of DEX in mitigating such risks.
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Antiinflamatorios , Quimiocina CCL2 , Dexametasona , Células Endoteliales , Mediadores de Inflamación , Ratones Endogámicos C57BL , Paclitaxel , Paclitaxel/efectos adversos , Paclitaxel/administración & dosificación , Humanos , Animales , Antiinflamatorios/farmacología , Antiinflamatorios/efectos adversos , Quimiocina CCL2/metabolismo , Quimiocina CCL2/genética , Dexametasona/efectos adversos , Mediadores de Inflamación/metabolismo , Células Cultivadas , Células Endoteliales/efectos de los fármacos , Células Endoteliales/metabolismo , Masculino , Enfermedad Iatrogénica , Células Endoteliales de la Vena Umbilical Humana/metabolismo , Células Endoteliales de la Vena Umbilical Humana/efectos de los fármacos , RNA-Seq , Factores de Tiempo , Regulación de la Expresión Génica/efectos de los fármacos , Transducción de Señal , RatonesRESUMEN
BACKGROUND AND AIMS: The terminal ileum is the most frequent site of Crohn's Disease (CD) that necessitates surgery. Of the postoperative complications (POCs) associated with ileocaecal resection for CD, intra-abdominal septic complications (IASCs) include anastomotic leak, abscesses, and entero-cutaneous fistula. We aimed to identify predictors of IASCs and severe POCs (Clavien-Dindo ≥3) after primary ileocaecal resection for CD. METHODS: This is a retrospective single-centre cohort study including all consecutive primary ileocaecal resection for CD in a tertiary IBD centre between 2004 and 2021. RESULTS: A total of 853 patients underwent primary ileocaecal resection for CD. 307 (36.6 %) patients were receiving antibiotics, 253 (29.8 %), systemic steroids, and 178 (21.0 %) oral budesonide at surgery. At 90 days, 260 (30.8 %) patients developed POCs, 62 (7.3 %) severe POCs, and 56 (6.6 %) IASCs. At multivariate analysis, severe POCs were associated with lower preoperative albumin levels (OR1.58, 95 %CI 1.02-2.50, p = 0.040) and a history of cardiovascular diseases (OR2.36, 95 %CI 1.08-7.84, p = 0.030). IASCs were associated with lower preoperative albumin levels (OR1.81, 95 %CI 1.15-2.94, p = 0.011) and oral budesonide (OR2.07, 95 %CI 1.12-3.83, p = 0.021) with a dose-dependent effect. CONCLUSIONS: The independent association, dose-dependent effect, and biological plausibility of budesonide and IASCs suggest a robust causal effect. Oral budesonide should be carefully assessed before primary ileocaecal resection for CD.
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Budesonida , Enfermedad de Crohn , Íleon , Complicaciones Posoperatorias , Humanos , Estudios Retrospectivos , Masculino , Femenino , Enfermedad de Crohn/cirugía , Enfermedad de Crohn/tratamiento farmacológico , Adulto , Budesonida/administración & dosificación , Budesonida/efectos adversos , Complicaciones Posoperatorias/etiología , Complicaciones Posoperatorias/epidemiología , Persona de Mediana Edad , Íleon/cirugía , Albúmina Sérica/análisis , Factores de Riesgo , Administración Oral , Ciego/cirugía , Fuga Anastomótica/etiología , Análisis Multivariante , Adulto Joven , Sepsis/etiología , Sepsis/sangre , Antiinflamatorios/administración & dosificación , Antiinflamatorios/efectos adversosRESUMEN
In the last century, there has been more than enough research that proved the association of high lipid and glucose levels with cardiovascular disease, thus establishing the current well-known traditional cardiovascular risk factors such as dyslipidemia, diabetes, and metabolic syndrome. Hence, these cardiovascular risk factors are target therapy for glucose and lipid-lowering agents to prevent adverse cardiovascular events. However, despite controlling the lipid and glucose levels, some studies demonstrated the subclinical atherosclerosis suggesting that these cardiovascular risk factors alone cannot account for the entire atherosclerosis burden. In the last years, large-scale clinical trials demonstrated the operation of the inflammatory pathway in atherosclerotic cardiovascular disease (ASCVD) by the immune system, both the innate (neutrophils, macrophages) and adaptive (T cell and other lymphocytes) limbs, contribute to atherosclerosis and atherothrombosis. In this regard, some studies that use antiinflammatory therapy targeting the immune system by modulating or blocking interleukins, also known as anti-cytokine therapy, have been shown to reduce the risk of adverse cardiovascular events in patients with previous coronary artery disease. In this regard, the U.S. Food and Drug Administration (FDA) approved the use of colchicine 0.5 mg once daily for reducing cardiovascular events in patients who have established ASCVD and high residual systemic inflammation. Therefore, measuring the systemic inflammation can improve the cardiovascular risk assessment and identify the subsets of patients that will benefit from anti-cytokine therapy after diagnosis of ASCVD or after myocardial revascularization.
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Antiinflamatorios , Biomarcadores , Glucemia , Citocinas , Factores de Riesgo de Enfermedad Cardiaca , Mediadores de Inflamación , Inflamación , Triglicéridos , Humanos , Antiinflamatorios/uso terapéutico , Antiinflamatorios/efectos adversos , Aterosclerosis/inmunología , Aterosclerosis/tratamiento farmacológico , Aterosclerosis/sangre , Biomarcadores/sangre , Glucemia/efectos de los fármacos , Glucemia/metabolismo , Enfermedades Cardiovasculares/prevención & control , Enfermedades Cardiovasculares/inmunología , Colchicina/uso terapéutico , Colchicina/efectos adversos , Citocinas/sangre , Citocinas/metabolismo , Inflamación/inmunología , Inflamación/tratamiento farmacológico , Inflamación/sangre , Mediadores de Inflamación/sangre , Mediadores de Inflamación/metabolismo , Medición de Riesgo , Factores de Riesgo , Resultado del Tratamiento , Triglicéridos/sangreAsunto(s)
Dexametasona , Implantes de Medicamentos , Enfermedad Iatrogénica , Hemorragia Retiniana , Humanos , Masculino , Antiinflamatorios/administración & dosificación , Antiinflamatorios/efectos adversos , Dexametasona/administración & dosificación , Dexametasona/efectos adversos , Implantes de Medicamentos/efectos adversos , Inyecciones Intravítreas/efectos adversos , Hemorragia Retiniana/inducido químicamente , Hemorragia Retiniana/etiología , Hemorragia Retiniana/diagnóstico , Anciano de 80 o más AñosRESUMEN
BACKGROUND: Bronchopulmonary dysplasia (BPD) remains an important complication of prematurity. Pulmonary inflammation plays a central role in the pathogenesis of BPD, explaining the rationale for investigating postnatal corticosteroids. Multiple systematic reviews (SRs) have summarised the evidence from numerous randomised controlled trials (RCTs) investigating different aspects of administrating postnatal corticosteroids. Besides beneficial effects on the outcome of death or BPD, potential short- and long-term harms have been reported. OBJECTIVES: The primary objective of this overview was to summarise and appraise the evidence from SRs regarding the efficacy and safety of postnatal corticosteroids in preterm infants at risk of developing BPD. METHODS: We searched the Cochrane Database of Systematic Reviews, MEDLINE, Embase, CINAHL, and Epistemonikos for SRs in April 2023. We included all SRs assessing any form of postnatal corticosteroid administration in preterm populations with the objective of ameliorating pulmonary disease. All regimens and comparisons were included. Two review authors independently checked the eligibility of the SRs comparing corticosteroids with placebo, and corticosteroids with different routes of administration and regimens. The included outcomes, considered key drivers in the decision to administer postnatal corticosteroids, were the composite outcome of death or BPD at 36 weeks' postmenstrual age (PMA), its individual components, long-term neurodevelopmental sequelae, sepsis, and gastrointestinal tract perforation. We independently assessed the methodological quality of the included SRs by using AMSTAR 2 (A Measurement Tool to Assess Systematic Reviews) and ROBIS (Risk Of Bias In Systematic reviews) tools. We assessed the certainty of the evidence using GRADE. We provided a narrative description of the characteristics, methodological quality, and results of the included SRs. MAIN RESULTS: We included nine SRs (seven Cochrane, two non-Cochrane) containing 87 RCTs, 1 follow-up study, and 9419 preterm infants, investigating the effects of postnatal corticosteroids to prevent or treat BPD. The quality of the included SRs according to AMSTAR 2 varied from high to critically low. Risk of bias according to ROBIS was low. The certainty of the evidence according to GRADE ranged from very low to moderate. Early initiated systemic dexamethasone (< seven days after birth) likely has a beneficial effect on death or BPD at 36 weeks' PMA (risk ratio (RR) 0.88, 95% confidence interval (CI) 0.81 to 0.95; number needed to treat for an additional beneficial outcome (NNTB) 16, 95% CI 10 to 41; I2 = 39%; 17 studies; 2791 infants; moderate-certainty evidence) and on BPD at 36 weeks' PMA (RR 0.72, 95% CI 0.63 to 0.82; NNTB 13, 95% CI 9 to 21; I2 = 39%; 17 studies; 2791 infants; moderate-certainty evidence). Early initiated systemic hydrocortisone may also have a beneficial effect on death or BPD at 36 weeks' PMA (RR 0.90, 95% CI 0.82 to 0.99; NNTB 18, 95% CI 9 to 594; I2 = 43%; 9 studies; 1376 infants; low-certainty evidence). However, these benefits are likely accompanied by harmful effects like cerebral palsy or neurosensory disability (dexamethasone) or gastrointestinal perforation (both dexamethasone and hydrocortisone). Late initiated systemic dexamethasone (≥ seven days after birth) may have a beneficial effect on death or BPD at 36 weeks' PMA (RR 0.75, 95% CI 0.67 to 0.84; NNTB 5, 95% CI 4 to 9; I2 = 61%; 12 studies; 553 infants; low-certainty evidence), mostly contributed to by a beneficial effect on BPD at 36 weeks' PMA (RR 0.76, 95% CI 0.66 to 0.87; NNTB 6, 95% CI 4 to 13; I2 = 14%; 12 studies; 553 infants; low-certainty evidence). No harmful side effects were shown in the outcomes chosen as key drivers to the decision to start or withhold late systemic dexamethasone. No effects, either beneficial or harmful, were found in the subgroup meta-analyses of late hydrocortisone studies. Early initiated inhaled corticosteroids probably have a beneficial effect on death and BPD at 36 weeks' PMA (RR 0.86, 95% CI 0.75 to 0.99; NNTB 19, 95% CI not applicable; I2 = 0%; 6 studies; 1285 infants; moderate-certainty evidence), with no apparent adverse effects shown in the SRs. In contrast, late initiated inhaled corticosteroids do not appear to have any benefits or harms. Endotracheal instillation of corticosteroids (budesonide) with surfactant as a carrier likely has a beneficial effect on death or BPD at 36 weeks' PMA (RR 0.60, 95% CI 0.49 to 0.74; NNTB 4, 95% CI 3 to 6; I2 = 0%; 2 studies; 381 infants; moderate-certainty evidence) and on BPD at 36 weeks' PMA. No evidence of harmful effects was found. There was little evidence for effects of different starting doses or timing of systemic corticosteroids on death or BPD at 36 weeks' PMA, but potential adverse effects were observed for some comparisons. Lowering the dose might result in a more unfavourable balance of benefits and harms. Moderately early initiated systemic corticosteroids, compared with early systemic corticosteroids, may result in a higher incidence of BPD at 36 weeks' PMA. Pulse dosing instead of continuous dosing may have a negative effect on death and BPD at 36 weeks' PMA. We found no differences for the comparisons of inhaled versus systemic corticosteroids. AUTHORS' CONCLUSIONS: This overview summarises the evidence of nine SRs investigating the effect of postnatal corticosteroids in preterm infants at risk for BPD. Late initiated (≥ seven days after birth) systemic administration of dexamethasone is considered an effective intervention to reduce the risk of BPD in infants with a high risk profile for BPD, based on a favourable balance between benefits and harms. Endotracheal instillation of corticosteroids (budesonide) with surfactant as a carrier is a promising intervention, based on the beneficial effect on desirable outcomes without (so far) negative side effects. Pending results of ongoing large, multicentre RCTs investigating both short- and long-term effects, endotracheal instillation of corticosteroids (budesonide) with surfactant as a carrier is not appropriate for clinical practice at present. Early initiated (< seven days after birth) systemic dexamethasone and hydrocortisone and late initiated (≥ seven days after birth) hydrocortisone are considered ineffective interventions, because of an unfavourable balance between benefits and harms. No conclusions are possible regarding early and late inhaled corticosteroids, as more research is needed.
Asunto(s)
Displasia Broncopulmonar , Glucocorticoides , Recién Nacido , Lactante , Humanos , Displasia Broncopulmonar/tratamiento farmacológico , Displasia Broncopulmonar/prevención & control , Antiinflamatorios/efectos adversos , Hidrocortisona/uso terapéutico , Dexametasona , Revisiones Sistemáticas como Asunto , Budesonida , TensoactivosAsunto(s)
Adalimumab , Esclerosis Múltiple , Espondilitis Anquilosante , Humanos , Espondilitis Anquilosante/tratamiento farmacológico , Adalimumab/efectos adversos , Esclerosis Múltiple/tratamiento farmacológico , Masculino , Adulto , Antiinflamatorios/efectos adversos , Antiinflamatorios/uso terapéutico , Antirreumáticos/efectos adversos , Persona de Mediana Edad , FemeninoRESUMEN
In recent years, adalimumab has been increasingly used in the chronic treatment of non-infectious uveitis. This case report aimed to describe a drug-induced adverse event in a 34-year-old man who presented with blurred vision and floaters in the right eye and was being treated for intermediate uveitis. The patient had started topical treatment with a diagnosis of uveitis at another center. Best corrected visual acuity at presentation was 0.8 (decimal) in the right eye and 1.0 in the left eye. On examination, the anterior chamber in the right eye was clear, with anterior vitreous cells and mild haze, and snow banking and vitreous opacities in the inferior periphery. Fluorescein angiography (FA) showed hyperfluorescence in the right disc and leakage in the inferior periphery. As the inflammation did not resolve with local treatment, systemic cyclosporine was administered, after which the patient exhibited vomiting and weakness. Cyclosporine was discontinued and adalimumab treatment was started. On examination 5 months later, bilateral vitreous cells and mild vitreous opacity were noted, and FA showed mild leakage in the inferior periphery bilaterally. In addition, a depigmented patchy vitiligo lesion was observed on the chin. Due to the persistence of intraocular inflammation and on the recommendation of the dermatology clinic, adalimumab treatment was continued and topical tacrolimus was started for the lesion. On examination 3 months later, the inflammatory findings had resolved and there was no progression of the vitiligo lesion. The patient's treatment was continued. Taken together with the previous literature findings, no pathology was found in the patient's systemic examination, suggesting that this lesion was a side effect of the treatment. Ophthalmologists should be alert for this side effect in patients receiving adalimumab.