triamcinolone
Fuentes regulatorias consultadas
Indicaciones aprobadas
- Tratamiento sistémico IM cuando la vía oral no es posible y tratamiento intraarticular o intrasinovial de trastornos inflamatorios seleccionados que responden a corticoides.
Contraindicaciones
Absolutas
- Infección sistémica; la vía IM está contraindicada en púrpura trombocitopénica idiopática.
- Hipersensibilidad a triamcinolona acetónido o excipientes.
Advertencias clínicas
- Advertencia mayor · No administrar por vía epidural o intratecal: se han notificado acontecimientos neurológicos graves con corticoides por estas vías no autorizadas. — CIMA/AEMPS, ficha técnica 44901
- Advertencia mayor · Usa la dosis mínima eficaz y reduce gradualmente tras tratamientos prolongados; la retirada brusca puede precipitar insuficiencia suprarrenal. — CIMA/AEMPS, ficha técnica 44901
- Advertencia mayor · Puede aumentar la susceptibilidad a infecciones, reactivar infecciones latentes y enmascarar sus signos. Evita vacunas vivas con dosis inmunosupresoras. — CIMA/AEMPS, ficha técnica 44901
- Advertencia mayor · Vigila glucemia, presión arterial, electrolitos, salud ósea, síntomas psiquiátricos y complicaciones oculares y gastrointestinales durante el tratamiento sistémico. — CIMA/AEMPS, ficha técnica 44901
Interacciones medicamentosas
- ModeradaInhibidores o inductores de CYP3A4
Mecanismo: Pueden aumentar o reducir la exposición sistémica al glucocorticoide.
Recomendación: Vigila eficacia y toxicidad y ajusta solo bajo supervisión clínica.
CIMA/AEMPS, ficha técnica 44901
- SeveraVacunas vivas
Mecanismo: La inmunosupresión puede favorecer infección diseminada y reducir la respuesta vacunal.
Recomendación: Evita vacunas vivas durante tratamiento inmunosupresor; planifica la vacunación con el equipo tratante.
CIMA/AEMPS, ficha técnica 44901
- ModeradaAntidiabéticos, diuréticos y AINE
Mecanismo: Los glucocorticoides pueden antagonizar el control glucémico, agravar la pérdida de potasio y aumentar el riesgo gastrointestinal.
Recomendación: Controla glucemia y electrolitos y valora gastroprotección o alternativas según el riesgo.
CIMA/AEMPS, ficha técnica 44901
Eventos adversos
Raros pero graves
Anafilaxia, lesión articular o tendinosa, necrosis avascular y supresión suprarrenal
Embarazo y lactancia
Durante el embarazo, úsalo solo si el beneficio esperado supera el riesgo y vigila al recién nacido tras dosis altas o prolongadas. En lactancia, individualiza según dosis y duración.
Bibliografía reciente (PubMed)
Allergic rhinitis affects an estimated 15% of the US population (approximately 50 million individuals) and is associated with the presence of asthma, eczema, chronic or recurrent sinusitis, cough, and both tension and migraine headaches. Allergic rhinitis occurs when disruption of the epithelial barrier allows allergens to penetrate the mucosal epithelium of nasal passages, inducing a T-helper type 2 inflammatory response and production of allergen-specific IgE. Allergic rhinitis typically presents with symptoms of nasal congestion, rhinorrhea, postnasal drainage, sneezing, and itching of the eyes, nose, and throat. In an international study, the most common symptoms of allergic rhinitis were rhinorrhea (90.38%) and nasal congestion (94.23%). Patients with nonallergic rhinitis present primarily with nasal congestion and postnasal drainage frequently associated with sinus pressure, ear plugging, muffled sounds and pain, and eustachian tube dysfunction that is less responsive to nasal corticosteroids. Patients with seasonal allergic rhinitis typically have physical examination findings of edematous and pale turbinates. Patients with perennial allergic rhinitis typically have erythematous and inflamed turbinates with serous secretions that appear similar to other forms of chronic rhinitis at physical examination. Patients with nonallergic rhinitis have negative test results for specific IgE aeroallergens. Intermittent allergic rhinitis is defined as symptoms occurring less than 4 consecutive days/week or less than 4 consecutive weeks/year. Persistent allergic rhinitis is defined as symptoms occurring more often than 4 consecutive days/week and for more than 4 consecutive weeks/year. Patients with allergic rhinitis should avoid inciting allergens. In addition, first-line treatment for mild intermittent or mild persistent allergic rhinitis may include a second-generation H1 antihistamine (eg, cetirizine, fexofenadine, desloratadine, loratadine) or an intranasal antihista
Chronic pruritus, defined as itch experienced for 6 weeks or longer, affects approximately 22% of people in their lifetime. Approximately 1% of physician visits are for the chief concern of chronic pruritus. Chronic pruritus is associated with adverse outcomes, including impaired sleep and reduced quality of life. Chronic pruritus can be categorized by etiology into inflammatory, neuropathic, or a combination of inflammatory and neuropathic pruritus. Chronic pruritus is due to inflammation in approximately 60% of patients and may be caused by eczema, psoriasis, or seborrheic dermatitis. Chronic pruritus is due to a neuropathic or mixed etiology in approximately 25% of patients. Neuropathic causes of chronic pruritus include postherpetic neuralgia and notalgia paresthetica and are typically due to localized or generalized nerve dysregulation. Approximately 15% of people with chronic pruritus have other causes including systemic diseases with secondary itch, such as uremic pruritus and cholestatic pruritus, medication-induced pruritus such as pruritus due to immunotherapy, and infectious etiologies such as tinea corporis and scabies. When few primary changes are present, a thorough history, review of symptoms, and laboratory evaluation should be performed, particularly for people with chronic pruritus lasting less than 1 year. Clinicians should consider the following tests: complete blood cell count, complete metabolic panel, and thyroid function testing to evaluate for hematologic malignancy, liver disease, kidney disease, or thyroid disease. First-line treatment for inflammatory chronic pruritus includes topical anti-inflammatory therapies such as hydrocortisone (2.5%), triamcinolone (0.1%), or tacrolimus ointment. Approximately 10% of patients do not respond to topical therapies. In these patients, referral to dermatology and systemic oral or injectable treatments such as dupilumab or methotrexate may be considered. When no underlying systemic disease associated wi
A chalazion is one of the most common eye conditions presenting as a mass lesion of the eyelids. It is seen in all age groups. Chalazion is a non-inflammatory process and develops due to retained secretion of the meibomian or Zeis glands. Treatment of choice differs among clinicians and may include application of warm compress onto eyelids, lid hygiene, using local antibiotic ointment with or without steroids, injecting steroid solution (triamcinolone acetonide) into the lesion and surgical removal of the lesion by incision and curettage. In addition, there are some other experimented methods such as injection of botulinum toxin A, tarsal trephination, removal of chalazion by application of CO2 laser or cryogenic action. However, there is currently no commonly agreed treatment of choice. In this review, we aimed to summarize findings from clinical trials and hopefully, identify a treatment of choice in chalazion.
Osteoarthritis (OA) is the most prevalent arthritis-type and is a major contributor to chronic joint pain, impaired physical function, and limited mobility. By the end of 2020, a total of 595 million, equal to 7·6% of the global population, had OA; this figure is expected to rise exponentially by 2050. Even while the disorder's intricate pathophysiology is starting to appear intelligible, we are yet to have a cure for the disorder. OA is typically managed with traditional palliative measures, such as topical and systemic analgesics, including non-steroidal anti-inflammatory drugs, therapeutic exercise, and braces. Sometimes, intra-articular glucocorticoids, viscosupplementation, or regenerative interventions provide short-term pain relief and functional improvement; some may require arthroplasty. Researchers continue their efforts to unveil a new therapeutic target to be effective in OA that modifies symptoms and arrests disease progression as well. In the present literature review, insights into new therapeutic strategies in OA, for example, liposome-based dexamethasone, microspore-based triamcinolone, nerve growth factor antagonist, anti-ADAMTS-5 (A Disintegrin And Metalloproteinase Thrombospoidin Motifs - 5), pentosan polysulfate sodium, allogeneic stem cells, C-C chemokine receptor type-4 (CCR4) ligand 17 inhibitor, Wnt-signaling inhibitor, and anti-obesity medications are provided.
Recurrent aphthous stomatitis (RAS) is a common chronic disease in the oral mucosa that affects about 20% of the population. It is characterized by solitary or multiple, recurrent, small ulcers with erythematous haloes and yellow/gray floors. RAS can be managed through a wide variety of preventative measures and therapies, intending to reduce ulcer pain, stimulate ulcer healing, and/or prevent ulcer recurrence. First-line treatment options include topical medications in the form of corticosteroids (triamcinolone acetonide), anti-inflammatory drugs (amlexanox), antibiotics (doxycycline), and antiseptics (lidocaine). In more severe cases of RAS where local treatment is insufficient, systemic drugs in the form of corticosteroids (prednisone), immunomodulatory drugs (thalidomide), and antibiotics/antimicrobials (clofazimine) can prove effective. This review will summarize current treatment options for RAS with discussion of prevention, topical measures, natural treatments, systemic therapies, and new potential therapies. Furthermore, this review will provide recommendations on therapeutic options for RAS based on disease severity and patient circumstances.