-
1.
Amiodarone induced myxedema coma: Two case reports and literature review.
Hawatmeh, A, Thawabi, M, Abuarqoub, A, Shamoon, F
Heart & lung : the journal of critical care. 2018;(4):429-431
Abstract
Amiodarone is a benzofuran derivative that contains 37% iodine by weight and is structurally similar to the thyroid hormones. Amiodarone has a complex effect on the thyroid gland, ranging from abnormalities of thyroid function tests to overt thyroid dysfunction, with either thyrotoxicosis or hypothyroidism. Myxedema coma secondary to amiodarone use has been rarely reported in the literature. Our two case reports are an add on to the literature, and illustrate that amiodarone is an important cause of thyroid dysfunction including hypothyroidism and myxedema coma. Hence, healthcare providers should have a high index of suspicion for these conditions while treating patients who are taking amiodarone therapy as early recognition and management are essential to optimize outcomes.
-
2.
Amiodarone-Induced Thyroid Dysfunction: A Clinical Update.
Elnaggar, MN, Jbeili, K, Nik-Hussin, N, Kozhippally, M, Pappachan, JM
Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association. 2018;(6):333-341
Abstract
Amiodarone is one of the most commonly prescribed antiarrhythmic agents in clinical practice owing to its efficacy, even with high toxicity profile. The high iodine content and the prolonged biological half-life of the drug can result in thyroid dysfunction in a high proportion of patients treated with amiodarone even after cessation of amiodarone. Both hypothyroidism and hyperthyroidism are common side effects that mandate regular monitoring of patients with thyroid function tests. Amiodarone-induced hypothyroidism (AIH) is diagnosed and managed in the same way as a usual case of hypothyroidism. However, differential diagnosis and clinical management of amiodarone-induced thyrotoxicosis (AIT) subtypes can be challenging. With the aid of a case snippet, we update the current evidence for the diagnostic work up and management of patients with amiodarone-induced thyroid dysfunction in this article.
-
3.
Flecainide Toxicity: A Case Report and Systematic Review of its Electrocardiographic Patterns and Management.
Valentino, MA, Panakos, A, Ragupathi, L, Williams, J, Pavri, BB
Cardiovascular toxicology. 2017;(3):260-266
Abstract
In the setting of flecainide toxicity, supraventricular tachycardia can manifest as a bizarre right or left bundle branch block, sometimes with a northwest axis, and can easily be mistaken for ventricular tachycardia leading to inappropriate therapy. We conducted a comprehensive literature review for cases of flecainide toxicity. We found 21 articles of flecainide toxicity in adult patients in which 22 ECG tracings were published. In patients with flecainide toxicity and QRS duration ≤ 200 ms, the ECGs were more likely to show RBBB, visible P waves (p = 0.03), and shorter QT (p = 0.02) and QTc intervals (p = 0.004). With QRS duration > 200 ms, the ECGs were more likely to show LBBB, loss of P waves, a northwest axis (p = 0.01), and longer QT and QTc intervals. Deaths were reported only in patients with QRS duration >200 ms, and the outcome of death or requirement for mechanical circulatory support was more prevalent in patients with a QRS duration > 200 ms [2/13 (15.4 %) vs. 6/10 (60 %), p = 0.04]. In patients with access to the medication, flecainide toxicity should be suspected with: (1) broad QRS, (2) RBBB morphology with QRS ≤ 200 ms; RBBB or LBBB morphology with QRS ≥ 200 ms (3) HR out of proportion to the degree of hemodynamic instability. The duration of the QRS interval is prognostic, with mortality and the requirement for mechanical circulatory support being more common in patients with a QRS > 200 ms.
-
4.
Amiodarone-induced thyroid dysfunction.
Danzi, S, Klein, I
Journal of intensive care medicine. 2015;(4):179-85
Abstract
Amiodarone is an effective medication for the treatment of cardiac arrhythmias. Originally developed for the treatment of angina, it is now the most frequently prescribed antiarrhythmia drug despite the fact that its use is limited because of potential serious side effects including adverse effects on the thyroid gland and thyroid hormones. Although the mechanisms of action of amiodarone on the thyroid gland and thyroid hormone metabolism are poorly understood, the structural similarity of amiodarone to thyroid hormones, including the presence of iodine moieties on the inner benzene ring, may play a role in causing thyroid dysfunction. Amiodarone-induced thyroid dysfunction includes amiodarone-induced thyrotoxicosis (AIT) and amiodarone-induced hypothyroidism (AIH). The AIT develops more commonly in iodine-deficient areas and AIH in iodine-sufficient areas. The AIT type 1 usually occurs in patients with known or previously undiagnosed thyroid dysfunction or goiter. The AIT type 2 usually occurs in normal thyroid glands and results in destruction of thyroid tissue caused by thyroiditis. This is the result of an intrinsic drug effect from the amiodarone itself. Mixed types are not uncommon. Patients with cardiac disease receiving amiodarone treatment should be monitored for signs of thyroid dysfunction, which often manifest as a reappearance of the underlying cardiac disease state. When monitoring patients, initial tests should include the full battery of thyroid function tests, thyroid-stimulating hormone, thyroxine, triiodothyronine, and antithyroid antibodies. Mixed types of AIT can be challenging both to diagnose and treat and therapy differs depending on the type of AIT. Treatment can include thionamides and/or glucocorticoids. The AIH responds favorably to thyroid hormone replacement therapy. Amiodarone is lipophilic and has a long half-life in the body. Therefore, stopping the amiodarone therapy usually has little short-term benefit.
-
5.
Spectrum of digoxin-induced ocular toxicity: a case report and literature review.
Renard, D, Rubli, E, Voide, N, Borruat, FX, Rothuizen, LE
BMC research notes. 2015;:368
Abstract
BACKGROUND Digoxin intoxication results in predominantly digestive, cardiac and neurological symptoms. This case is outstanding in that the intoxication occurred in a nonagenarian and induced severe, extensively documented visual symptoms as well as dysphagia and proprioceptive illusions. Moreover, it went undiagnosed for a whole month despite close medical follow-up, illustrating the difficulty in recognizing drug-induced effects in a polymorbid patient. CASE PRESENTATION Digoxin 0.25 mg qd for atrial fibrillation was prescribed to a 91-year-old woman with an estimated creatinine clearance of 18 ml/min. Over the following 2-3 weeks she developed nausea, vomiting and dysphagia, snowy and blurry vision, photopsia, dyschromatopsia, aggravated pre-existing formed visual hallucinations and proprioceptive illusions. She saw her family doctor twice and visited the eye clinic once until, 1 month after starting digoxin, she was admitted to the emergency room. Intoxication was confirmed by a serum digoxin level of 5.7 ng/ml (reference range 0.8-2 ng/ml). After stopping digoxin, general symptoms resolved in a few days, but visual complaints persisted. Examination by the ophthalmologist revealed decreased visual acuity in both eyes, 4/10 in the right eye (OD) and 5/10 in the left eye (OS), decreased color vision as demonstrated by a score of 1/13 in both eyes (OU) on Ishihara pseudoisochromatic plates, OS cataract, and dry age-related macular degeneration (ARMD). Computerized static perimetry showed non-specific diffuse alterations suggestive of either bilateral retinopathy or optic neuropathy. Full-field electroretinography (ERG) disclosed moderate diffuse rod and cone dysfunction and multifocal ERG revealed central loss of function OU. Visual symptoms progressively improved over the next 2 months, but multifocal ERG did not. The patient was finally discharged home after a 5 week hospital stay. CONCLUSION This case is a reminder of a complication of digoxin treatment to be considered by any treating physician. If digoxin is prescribed in a vulnerable patient, close monitoring is mandatory. In general, when facing a new health problem in a polymorbid patient, it is crucial to elicit a complete history, with all recent drug changes and detailed complaints, and to include a drug adverse reaction in the differential diagnosis.
-
6.
Effects of amiodarone, thyroid hormones and CYP2C9 and VKORC1 polymorphisms on warfarin metabolism: a review of the literature.
Tomisti, L, Del Re, M, Bartalena, L, Tanda, ML, Pucci, A, Pambianco, F, Danesi, R, Braverman, LE, Martino, E, Bogazzi, F
Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists. 2013;(6):1043-9
Abstract
OBJECTIVE To review the literature regarding the interaction among amiodarone therapy, thyroid hormone levels, and warfarin metabolism. METHODS A 73-year-old male with type 2 after describing an unusual case of amiodarone-induced thyrotoxicosis (AIT) who experienced a severe rise in international normalized ratio (INR) values after initiating warfarin therapy due to an unusual combination of excessive thyroid hormones, amiodarone therapy, and a genetic abnormality affecting warfarin metabolism. RESULTS Genetic analysis revealed that the patient was CYP2C9*2 wild-type, CYP2C9*3/*3 homozygous mutant, and VKORC1*3/*3 homozygous mutant. A review of the literature revealed that both mutations can independently affect warfarin metabolism. In addition, amiodarone therapy and the presence of thyrotoxicosis per se can affect warfarin metabolism and reduce the dose needed to maintain INR in the therapeutic range. The association of the 2 genetic polymorphisms in a patient with AIT is extremely rare and strongly impairs warfarin metabolism, exposing the patient to a high risk of overtreatment. CONCLUSIONS In patients with AIT, warfarin therapy should be gradually introduced, starting with a very low dose, because of the significant risk of warfarin overtreatment. Whether the genetic analysis of CYP2C9 and VKORC1 polymorphisms should be routinely performed in AIT patients remains conjectural.
-
7.
Successful treatment of catecholaminergic polymorphic ventricular tachycardia with flecainide: a case report and review of the current literature.
Pott, C, Dechering, DG, Reinke, F, Muszynski, A, Zellerhoff, S, Bittner, A, Köbe, J, Wasmer, K, Schulze-Bahr, E, Mönnig, G, et al
Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology. 2011;(6):897-901
Abstract
Catecholaminergic polymorphic ventricular tachycardia (CPVT) is an inherited arrhythmogenic disease that can cause sudden cardiac death due to ventricular fibrillation (VF). While pharmacological therapy with beta-blockers and/or Ca(2)(+) antagonists is often unreliable, a recent study has demonstrated that flecainide can effectively suppress arrhythmia in a murine model of CPVT as well as clinically in two human subjects suffering from CPVT. We here present the case of an 11-year-old boy suffering from CPVT-1 as well as a review of the current relevant literature. After resuscitation due to VF at age 9, an automated implantable cardioverter-defibrillator (ICD) was implanted in 2007. Under beta-blocker therapy, repeated shocks were delivered due to either fast ventricular tachycardia (VT) or VF. This persisted under additional therapy with verapamil. Implantable cardioverter-defibrillator routine interrogations showed frequent non-sustained VT with an average of 8.8 per day. Additionally, the patient suffered from impaired physical performance due to decreased chronotropic competence. In July 2009, flecainide was added to the beta-blocker/verapamil regimen, resulting in a plasma level of 0.20 mg/L. No ICD shock or sustained VT occurred until December 2010. Genetic testing revealed an RyR2 receptor mutation. The case demonstrates the challenge of diagnosis and management of CPVT. It furthermore supports recent experimental evidence that the class 1 antiarrhythmic drug flecainide can suppress CPVT. The presented case supports a novel strategy in treating CPVT with the class I antiarrhythmic agent flecainide.
-
8.
Syndrome of inappropriate antidiuretic hormone in association with amiodarone therapy: a case report and review of literature.
Afshinnia, F, Sheth, N, Perlman, R
Renal failure. 2011;(4):456-8
Abstract
BACKGROUND Amiodarone is a class III antiarrhythmic agent that is widely used in the treatment of a variety of arrhythmias. Several different systemic side effects are reported after use of this medication. In this article, we report a case that had developed syndrome of inappropriate antidiuretic hormone (SIADH) after starting treatment with this agent. CASE REPORT The patient is a 66-year-old male with past medical history of hypertension, hyperlipidemia, coronary artery disease, and class III New York Heart Association congestive heart failure who presented with monomorphic nonsustained ventricular tachycardia. A loading dose of amiodarone followed by maintenance dose was started. Baseline serum sodium of 138 mmol/L on admission decreased to 119 mmol/L by day 7, and a diagnosis of SIADH was made. The patient was not taking any other medication known to cause SIADH, nor had any such comorbidity to explain it. Serum sodium increased to 133 and 138 mmol/L, respectively, after 16 and 33 days from discontinuation of amiodarone. CONCLUSION SIADH is a rare but serious side effect of amiodarone and practicing physicians should be aware of this complication, particularly after loading dose of the medication.
-
9.
Nicorandil-induced oral ulceration: report of 3 cases and review of the Japanese literature.
Yamamoto, K, Matsusue, Y, Horita, S, Minamiguchi, M, Komatsu, Y, Kirita, T
Oral surgery, oral medicine, oral pathology, oral radiology, and endodontics. 2011;(6):754-9
Abstract
Nicorandil-induced oral ulceration in 3 Japanese patients is reported. The patients were men aged 86, 81, and 91 years. Ulcers of 15, 10, and 12 mm in diameter, respectively, were observed at the border of all of the patients' tongues. These were painful and persistent but not indurated. Irritation by the teeth or dentures was not evident. They had been administered nicorandil at a dose of 15 mg for 22, 54, and 90 months, respectively; therefore, ulceration induced by nicorandil was suspected. In consultation with the doctor, nicorandil was withdrawn. The ulcers disappeared 5, 8, and 9 weeks, respectively, after the cessation of nicorandil. No relapse of the ulcer was noted. The findings suggest that these were the examples of nicorandil-induced oral ulceration.
-
10.
[Skin adverse effects of amiodarone].
Zgazarová, S, Jedlicková, H, Vasků, V
Vnitrni lekarstvi. 2009;(10):976-80
Abstract
BACKGROUND Amiodarone has belonged to frequently used antiarrhythmic in the treatment of supraventricular and ventricular tachyarrhytmias since the sixties of the twentieth century. Amiodarone is a chemically iodinated benzofuran derivative with mono-N-desethylamiodarone as its major metabolite. OBJECTIVE This review is focused on numerous adverse reactions. The incidence of amiodarone induced side-effects ranges from 16-98% of patients receiving amiodarone and it appears to be dose related. CASE REPORTS We describe three cases of hyperpigmentation after using amiodarone in elder men. CONCLUSION Skin side effects are common, they usually occur as photosensitivity, more rarely as a slate-grey discoloration of the skin. Amiodarone induced slate-grey pigmentation is commonly observed in unprotected light exposed skin. Its incidence ranges from 2-57%. Hyperpigmentation is due to accumulation of amiodarone and its metabolites in the skin.