RESUMO
Amiodarone is a class 3 antiarrhythmic drug which may be associated with thyroid dysfunction. Amiodarone-induced thyrotoxicosis (AIT) is classified as type 1 (AIT 1; which may develop in the presence of latent autoimmune hyperthyroid condition) or type 2 (AIT 2; which develops in an apparently normal thyroid resulting from destructive thyroiditis). AIT 1 routinely requires treatment with thionamides, whereas AIT 2 is treated with steroids. Resistance to the conventional treatment of hyperthyroidism is not commonly found in clinical practice. This report discusses a case of AIT 2 resistant to conventional treatment. Despite being on high doses of carbimazole and steroids (prednisolone), the patient remained thyrotoxic. Cholestyramine, a bile salt sequestrant, was used as an adjunctive therapy resulting in significant clinical and biochemical improvement. The patient subsequently became euthyroid and is being followed up in endocrine clinic.
Assuntos
Amiodarona , Tireotoxicose , Amiodarona/efeitos adversos , Antiarrítmicos/efeitos adversos , Resina de Colestiramina/uso terapêutico , Humanos , Tireotoxicose/induzido quimicamente , Tireotoxicose/tratamento farmacológicoRESUMO
A growing body of evidence demonstrates that the oncogenic miRNAs are critical components that are involved in breast cancer (BC) progression. Thus, they are attracting a great deal of consideration as they provide opportunities for the novel avenues for developing BC targeted therapy. In the current review, we try to discuss the key oncogenic miRNAs implicated in cell migration, invasion and metastasis (e.g., miR-9, miR-10b, miR-10b-5p, miR-17/9, miR-21, miR-103/107, miR-181b-1, miR-301, miR-301a, miR-373, miR- 489, miR-495 and miR-520c), apoptosis inhibition (e.g., miR-21, miR-155, miR-181, miR-182 and miR-221/222), cell proliferation (e.g., miR-221/222, miR-17/92, miR-21, miR-301a, miR-155, miR-181 b, miR-182, miR-214, miR-20b, miR-29a, miR-196, miR-199a-3p, miR- 210, miR-301a, miR-375, miR-378-3p and miR-489), and angiogenesis (e.g., miR-9, miR-17/92 cluster, miR-93 and miR-210). In particular, here, we considered miRNA-based therapeutic approaches to summarize the evidence for their potential therapeutic uses in clinical practice. Therefore, miRNA mimics (i.e., replacement and restoration of miRNAs) and inhibition therapy (e.g., anti-miRNA oligonucleotides (AMO), antagomiRs or antisense oligonucleotides (ASOs): cholesterol-conjugated anti-miRs and locked nucleic acid (LNA)), miRNA sponges, nanoparticles (NPs), multiple-target anti-mirna antisense oligonucleotide technology (MTg-AMOs), and artificial miRNAs (amiRNAs) have been indicated throughout the article as much as possible.