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Romanian Academy
The Publishing House of the Romanian Academy
ACTA ENDOCRINOLOGICA (BUC)
The International Journal of Romanian Society of Endocrinology / Registered in 1938in Web of Science Master Journal List
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General Endocrinology
Bensalem A, Zribi N., Mnif E., Sellami A., Chakroun N.F., Ayadi F., Keskes L., Rebai T
Serum Inhibin B And Anti-Mullerian Hormone Assessment in Infertile Men with and Without Non-Obstructive AzoospermiaActa Endo (Buc) 2013 9(2): 181-188 doi: 10.4183/aeb.2013.181
AbstractContext. Inhibin B could be a good marker in predicting spermatogenetic activities and in discriminating men with spermatogenesis impairment, especially azoospermia and it would be considered as a current clinical tool in the future. Objective. This study aimed to investigate the clinical value of serum Inhibin B and AMH levels in subfertile men particularly in those with non-obstructive azoospermia (NOA). We conducted a prospective study to assess the role of inhibin B in the evaluation of male factor infertility. Patients and Methods. Thirty fertile men and three groups of infertile patients (n=91): normozoospermia (n = 40), oligozoospermia (n = 19) and NOA (n = 32), from Faculty of Medicine (Sfax, Tunisia) were investigated. Serum levels were measured by ELISA and by ELFA (FSH). Results. Inhibin B and AMH levels were significantly lower in NOA patients than in normozoospermic ones (72.6±76.8 pg/mL vs. 242.4± 124.7 pg/mL; p<0.001 and 3.7±2.9 ng/mL vs. 5.3±2.3 ng/mL; p<0.001). Only Inhibin B levels were significantly lower in NOA than in oligozoospermic (72.6±76.8 pg/mL vs. 141.3± 81.9 pg/mL;p<0.001) and were negatively correlated with FSH concentrations (r = -0.56, p = 0.001). But both Inhibin B and AMH were positively correlated with sperm count (r = 0.44, p < 0.0001and r = 0.26, p = 0.03 respectively). Conclusions. We conclude that our results support the literature data showing that serum Inhibin B level is strongly correlated with sperm count and suggesting that it could be a good marker in discriminating men with spermatogenesis impairment, especially NOA. -
Endocrine Care
Mircescu G, Capusa C, Andreiana I
The management of secondary hyperparathyroidism in chronic kidney diseaseActa Endo (Buc) 2005 1(2): 181-200 doi: 10.4183/aeb.2005.181
Abstract ReferencesSecondary hyperparathyroidism, i.e. increased synthesis and secretion of parathyroid hormone and gland hyperplasia, is commonly found in chronic kidney disease. Although it is, at first, an adaptive response to the loss of renal functions in order to maintain the calcium/phosphate homeostasis and normal bone turnover, it is also an important cause of increased morbidity in this clinical setting by leading to renal osteodystrophy and cardiovascular complications. Recent advances in the knowledge on the pathogenesis of parathyroid-related complications in renal failure allowed for new therapeutic approaches. However, many problems remain to be solved in the future. This paper briefly presents the current understanding of pathogenic mechanisms of hyperparathyroidism, bone disease and vascular calcification during chronic kidney disease. In addition, it summarizes the main therapeutic methods available today for controlling secondary hyperparathyroidism and the challenges of practitioners concerning this issue. Finally, the current status of secondary hyperparathyroidism management is analyzed, with emphasis on the Romanian experience.1. K/DOQI Clinical Practice Guidelines for Bone Metabolism and Disease in Chronic Kidney Disease. Am J Kidney Dis, 42(4, suppl 3):S1-S201, 2003. [CrossRef]2. Hsu C-Y, Chertow GM. Chronic renal confusion: Insufficiency, failure, dysfunction, or disease. Am J Kidney Dis, 36(2):415-418, 2000. [CrossRef]3. National Kidney Foundation. K/DOQI Clinical Practice Guidelines for Chronic Kidney Disease: Evaluation, Classification, and Stratification, Am J Kidney Dis, 39(suppl 1):S1-S92, 2002.4. Mircescu G, Capusa C. Chronic kidney disease: A useful concept for integrated approach of chronic renal failure (Part I). Medicina Interna, 1(4):17-28, 2004.5. Fournier A, Oprisiu R, Hottelart C et al. Renal osteodystrophy in dialysis patients: Diagnosis and treatment. Artif Org, 22(7):530-557, 1998. [CrossRef]6. Elder J. Pathogenesis and management of hyperparathyroidism in end-stage renal disease and after renal transplantation. Nephrology, 6:155-160, 2001. [CrossRef]7. Cozzolino M, Brancaccio D, Gallieni M, Galasi A, Slatopolsky E, Dusso A. Pathogenesis of parathyroid hyperplasia in renal failure. J Nephrol, 18(1):5-8, 2005.8. Dusso AS, Thadhani R, Slatopolsky E. Vitamin D receptor and analogs. Sem Nephrol, 24(1):10-16, 2004. [CrossRef]9. Dusso AS. Vitamin D receptor: Mechanisms for vitamin D resistance in renal failure. Kidney Int, 63(suppl 85):S6-S9, 2003. [CrossRef]10. Urena P, Frazao JM. Calcimimetic agents: Review and perspectives. Kidney Int, 63(suppl 85): S91- S96, 2003. [CrossRef]11. Slatopolsky E, Dusso A, Brown AJ. Control of uremic bone disease: Role of vitamin D analogs. Kidney Int, 61(suppl 80):S143-S148, 2002. [CrossRef]12. Fatica RA, Dennis VW. Cardiovascular mortality in chronic renal failure: hyperphosphatemia, coronary calcification, and the role of phosphate binders. Cleve Clinic J Med, 69(suppl 3):S21-S27, 2002. [CrossRef]13. Hruska KA, Saab G, Chaudhary LR, Quinn CO, Lund RJ, Surendran K. Kidney-bone, bone-kidney, and cell-cell communications in renal osteodystrophy. Semin Nephrol, 24(1):25-38, 2004. [CrossRef]14. Hercz G. Regulation of bone remodeling: Impact of novel therapies. Semin Dialysis, 14(1):55-60, 2001. [CrossRef]15. Malluche HH, Langub MC, Monier-Faugere M-C. The role of bone biopsy in clinical practice and research. Kidney Int, 56(suppl 73): S20-S25, 1999. [CrossRef]16. Couttenye MM, D?Haese PC, Verschoren WJ, Behets GJ, Schrooten I, De Broe ME. Low bone turnover in patients with renal failure. Kidney Int, 56(suppl 73): S70-S76, 1999. [CrossRef]17. Ganesh SK, Stack AG, Levin NW, Hulbert-Shearon TE, Port FK. Association of elevated serum PO4, Ca ? PO4 product and parathyroid hormone with cardiac mortality risk in chronic hemodialysis patients. J Am Soc Nephrol, 12(10):2131-2138, 2001.18. Giachelli CM, Jono S, Shioi A, Nishizawa Y, Mori K, Morii H. Vascular calcification and inorganic phosphate. Am J Kidney Dis, 38(suppl 1):S34-S37, 2001. [CrossRef]19. Wilmer WA, Magro CM. Calciphylaxis: Emerging concepts in prevention, diagnosis, and treatment. Semin Dialysis, 15(3):172-186, 2002. [CrossRef]20. Shanahan C. Bone turnover and extraosseous calcifications: Is there a relationship? Presentation at the ASN Renal Week, San Diego, Nov 2003, www.hdcn.com/symp/03asn/07/sha/sha.htm.21. Block G, Port FH. Calcium phosphate metabolism and cardiovascular disease in patients with chronic kidney disease. Semin Dialysis, 16(2):140-147, 2003. [CrossRef]22. Elder GJ. Targets for phosphate control in chronic kidney disease. Nephrology, 9:2-6, 2004. [CrossRef]23. Block GA, Martin KJ, de Francisco AM et al. Cinacalcet for secondary hyperparathyroidism in patients receiving hemodialysis. N Engl J Med, 350:1516-1525, 2004. [CrossRef]24. De Francisco AM, Ellis HA, Owen JP et al. Parathyroidectomy in chronic renal failure. Q J Med, 55(218):289-315, 1985.25. Malberti F, Marcelli D, Conte F, Limido A, Spotti D, Locatelli F. Parathyroidectomy in patients on renal replacement therapy: An epidemiologic study. J Am Soc Nephrol, 12:1242-1248, 2001.26. TominagaY, Uchida K, Haba T et al. More than 1000 cases of total parathyroidectomy with forearm autograft for renal hyperparathyroidism. Am J Kidney Dis, 38(4, suppl 1):S168-S171, 2001. [CrossRef]27. Mircescu G, C?pu?? C. Guidelines for surgical management of secondary hyperparathyroidism in dialysis patients. Nefrologia, 9(23-24):51-56, 2004.28. De Francisco AM, Fresnedo GF, Rodrigo E, Pinera C, Amado JA, Arias M. Parathyroidectomy in dialysis patients. Kidney Int, 61(suppl 80): S161-S166, 2002. [CrossRef]29. The CARI Guidelines (Caring for Australians with Renal Impairment) for bone disease, calcium, phosphate and parathyroid hormone. /www.kidney.org.au/cari/drafts/bone_management. Australian Kidney Foundation and Australia New Zealand Society of Nephrology30. Mircescu G et al, on behalf of the Romanian Society of Nephrology. Guidelines for best medical practice: Secondary hyperparathyroidism in chronic kidney disease, Ed. InfoMedica, Bucharest, 2005.31. Kim J, Pisoni RL, Danese MD et al. Achievement of proposed NKF-K/DOQI bone metabolism and disease guidelines : Results from the Dialysis Outcomes and Practice Patterns Study (DOPPS). Abstract for ASN Annual Meeting - San Diego, J Am Soc Nephrol (Nov), 1 -
Endocrine Care
Kacso IM, Lenghel A, Rusu CC, Rahaian R, Nita C, Craciun M, Luculescu N, Negru D, Hancu N, Bondor CI, Gherman Caprioara M
Determinants of plasma adiponectin levels in patients with type 2 diabetes mellitus and microalbuminuria or low grade proteinuriaActa Endo (Buc) 2010 6(2): 181-189 doi: 10.4183/aeb.2010.181
AbstractBackground. Recent experimental data show that increased plasma adiponectin in chronic kidney disease could be a response to inflammation.\r\nObjective. To identify factors influencing adiponectinemia in patients with type 2 diabetes (T2DM) and microalbuminuria or low grade proteinuria.\r\nDesign. 32 patients with urinary albumin excretion rate (UAER)> 30 mg/g creatinine but without significant proteinuria (< trace COMBUR) were included and compared to 59 normalbuminuric T2DM controls. History, anthropometric measurements, laboratory analysis, total plasma adiponectin were obtained.\r\nResults. In our patients with UAER of 273.51?57.26 mg/g creatinine and estimated glomerular filtration rate (eGFR) 64.92?4.56 mL/min, in simple regression, adiponectinemia\r\ncorrelates inversely to eGFR (p=0.02, r= -0.38), triglyceridemia (p=0.03, r=-0.37) and hemoglobin\r\n(Hb -p= 0.01, r=-0.45) and positively to HDL cholesterol (p=0.001, r=0.54) and UAER (p<0.0001, r=0.71); the two latter parameters remain significant in multiple regression. In controls, adiponectinemia correlates inversely to age (p=0.04, r=-0.26) and BMI (p=0.04, r=-0.24); these and UAER predict adiponectinemia in multiple regression. 11 patients have UAE superior to 300 mg/g creatinine and 21 are strictly microalbuminuric (mean UAER 653.16?97.02 and 83.68?10.28mg albumin/g creatinine respectively). In microalbuminuric patients serum C reactive protein (CRP) correlates positively (p=0.0008, r=0.68) and Hb negatively (p=0.04, r=-0.41) to adiponectinemia; in multiple regression adiponectinemia only depends on CRP. In proteinuric patients CRP and\r\nglycated Hb correlate to adiponectinemia in stepwise multiple regression.\r\nConclusion. Adiponectinemia is mainly predicted by UAER in our cohort whereas it depends on age and BMI in normalbuminuric T2DM controls; in strictly microalbuminuric\r\npatients CRP is a major predictor of adiponectinemia. -
Endocrine Care
Donbaloglu Z, Bedel A, Barsal Cetiner E, Singin B, Aydin Behram B, Tuhan H, Parlak M
Effects of the Gonadotropin-Releasing Hormone Agonist Therapy on Growth and Body Mass Index in Girls with Idiopathic Central Precocious PubertyActa Endo (Buc) 2022 18(2): 181-186 doi: 10.4183/aeb.2022.181
AbstractObjective. We aimed to examine the auxological findings of girls diagnosed with idiopathic central precocious puberty (CPP) at the end of the GnRHa treatment and to investigate the effect of related factors on the height gain of those patients. Design. Single-center, descriptive, cross-sectional retrospective study. Method. A total of 43 patients who were diagnosed with idiopathic CPP and treated with GnRHa between 2012 - 2021 were included in to the study. Results. A decline in height standard deviation score (SDS) from 1.20 ± 0.14 to 1.02 ± 0.06 during the therapy was observed (P<0.001). The bone age/chronological age ratio was decreased and predictive adult height was increased at the end of the therapy (P<0.001; P=0.001). Both the rates of being overweight and obesity were increased (38.6% to 50% and 9% to 15.9%) when the treatment onset compared to the end of therapy. At the end of the treatment, the mean body mass index (BMI) SDS of the overweight patients was still higher compared to the normal-weight group (P<0.001). Conclusion. We observed a positive effect of GnRHa therapy on height potential. An increase in BMI during the therapy has been also demonstrated especially in subjects who were overweight before treatment. -
General Endocrinology
Urkan M, Peker YS, Ozturk E
Minimally Invasive Parathyroidectomy for Primary HyperparathyroidismActa Endo (Buc) 2019 15(2): 182-186 doi: 10.4183/aeb.2019.182
AbstractContext. Primary hyperparathyroidism (PHPT), characterized by the inappropriate secretion of parathyroid hormone (PTH) with respect to the extracellular calcium concentration. Curative treatment of PHPT is surgery and bilateral neck exploration has been replaced by minimally invasive parathyroidectomy (MIP), with the advanced imaging technologies combined with radio-guided occult lesion localization (ROLL). Objectives. The present study analyzes the MIP data from 45 patients who underwent surgery for parathyroid adenoma and debates if MIP is a feasible technique for the treatment of PHPT. Design. The study presents the MIP excision data of 45 hyperparathyroidism patients with a 58-month follow up period. Results. Forty-five operations were performed for 48 parathyroid adenomas. The mean duration of operation was 22.7 (12-55) minutes. Mean follow-up was 14.2 (6- 26) months. All patients had normal postoperative calcium levels and PTH levels were normal in the follow-up period, except for one persistent hyperparathyroidism. Conclusions. ROLL-guided MIP is a feasible technique for parathyroid surgery and reduces surgeon based failure. It also provides the widespread application of parathyroid surgery by decreasing the need for specific experience. -
General Endocrinology
Sarac F, Tutuncuoglu P, Tavmergen E, Saygili F, Ozgen AG, Tuzun M
Glucose tolerance tests in the singleton and twin pregnancyActa Endo (Buc) 2009 5(2): 183-189 doi: 10.4183/aeb.2009.183
AbstractObjective. Gestational diabetes mellitus (GDM) is defined as glucose intolerance that\r\nis detected for the first time during pregnancy. Normal pregnancy induces insulin resistance\r\nthrough the diabetogenic effects of placental hormones. Glucose tolerance test results in\r\ntwin and singleton pregnancies were compared in this study.\r\nSubjects and Methods. A total of 360 pregnant women were studied. 200 women\r\n(mean age 31.60?2.10 yr) had singleton pregnancies (Group I) and 160 women (mean age\r\n28.20?2.70 yr) had twin pregnancies (Group II). 50- g, 1- hour glucose tolerance test was\r\nconducted on the first prenatal visit. An abnormal glucose screen defined as glucose > 140\r\nmg/dL was followed by a 100g, 3-hour glucose tolerance test. Gestational diabetes was\r\ndefined as the presence of two or more abnormal values during the 3-hour test.\r\nResults. Gestational diabetes was found in 4 of the 200 (2%) singleton pregnant\r\nwomen and 8 of the 160 (5%) twin pregnant women. Group I (Singleton) was further\r\ndivided into two subgroups according to whether the 1-hr plasma glucose level was < 140\r\nmg/dl (Group Ia) or >140 mg/dL (Group Ib). Likewise, Group II pregnancies was also\r\ndivided into two subgoups on the same basis. Mean screening test glucose levels were found\r\nto be 127.8?14.94 mg/dL in Group Ia and 150.8 ? 18.1 mg/dL in Group Ib women. Mean\r\nscreening test glucose levels of Group IIa subjects was 92.80 ? 18.30 mg/dL while that of\r\nGroup IIb subjects was 154.8 ? 27.0 mg/dL. Mean 1st h glucose levels of 100-g glucose\r\ntolerance test was found to be 131.4 ? 32.58 mg/dL in Group I, and 112.5 ? 39.6 mg/dL in\r\nGroup II. Mean 2nd h glucose tolerance test values were 133.2 ? 28.8 mg/dL in Group I and\r\n100.6?28.8 mg/dL in Group II. Mean 3rd h glucose tolerance test values were 107.6 ? 23.58\r\nmg/dl in Group I and 72?16.9 mg/dL in Group II.\r\nConclusion: Glucose screening results and 100-g, 3- hour glucose tolerance test\r\nvalues have been found to be lower in twin pregnancies than in singleton pregnancies.\r\nTherefore, we suggest that these findings be taken into account in developing diagnostic\r\ncriteria for gestational diabetes in twin or more pregnancies. -
Endocrine Care
Fringu FI, Sitar-Taut AV, Caloian B, Zdrenghea D, Comsa D, Gusetu G, Pop D
The Role of NT PRO-BNP in the Evaluation of Diabetic Patients with Heart FailureActa Endo (Buc) 2020 16(2): 183-191 doi: 10.4183/aeb.2020.183
AbstractContext. The prevalence of patients with concomitant heart failure (HF) and diabetes mellitus (DM) is high. Objective. To analyze the role of NT-pro-BNP levels in the evaluation of diabetic patients with heart failure. Design. Retrospective comparative cohort study. Subjects and Methods. A total of 174 patients admitted to our Cardiology Department, previously diagnosed with HF, were enrolled. Among these patients, 47.7% had DM. HF was defined according to the 2016 ESC criteria. The NT-pro BNP levels above 126 pg/mL indicate a high probability of heart failure. Results. In diabetic patients there were significant correlations between NT-pro-BNP values and the following parameters: hemoglobin (rho=-0.28, p=0.01), hematocrit (rho= -0.27, p=0.014), total cholesterol (rho= -0.21, p=0.048), triglycerides (rho= -0.283, p=0.01), ejection fraction (rho= -0.465, p<0.0001), end-diastolic volume (rho= 0.253, p= 0.026), end-systolic volume (rho= 0.29 p=0.01). Only the following 3 parameters: ejection fraction (p= 0.0009), hemoglobin (p= 0.0092) and triglycerides (p= 0.0380) were independent predictive factors for elevated NT-pro-BNP values. Conclusion. In diabetic heart failure patients, the value of NT-pro-BNP holds a pivotal role in the evaluation of their overall status, facilitating the establishment of correct management and follow-up. -
General Endocrinology
Saleh N, Elayan HE, Zihlif M
The Effect of Salbutamol on Pgc-1 a and Glut4 Mrna Expression in the Liver and Muscle of Elderly Diabetic MiceActa Endo (Buc) 2018 14(2): 184-191 doi: 10.4183/aeb.2018.184
AbstractPeroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) plays an important role in the regulation of cellular energy metabolism, and it is involved in obesity and type 2 diabetes mellitus (T2DM). Its expression is elevated in the liver of T2DM mouse models. Literature reports show that chronic β2 stimulation improved insulin sensitivity in T2DM. Objectives. We aimed to test the hypotheses that chronic β2 stimulation-induced improvement in insulin sensitivity involves changes in the expression of PGC-1α and glucose transporter 4 (GLUT4). Animals and Methods. We fed a locally inbred, 8 months old mice, a high fat diet (HFD) to induce diabetes. These mice gained weight and became insulin resistant. The β2 agonist salbutamol had a beneficial effect on both glucose tolerance and insulin sensitivity after 4 weeks. Results. Salbutamol beneficial effect persisted after 4 weeks of its discontinuation. HFD caused an up regulation of the hepatic PGC-1 α expression by 5.23 folds (P< 0.041) and salbutamol reversed this effect and caused a down regulation by 30.3 folds (P< 0.0001). PGC-1 α and GLUT4 expression in the muscle was not affected by salbutamol (P> 0.05). Conclusion. Down regulation of the liver’s PGC- 1 α contributes to the beneficial effect of the chronic β2 stimulation on glucose tolerance and insulin sensitivity in T2DM mice. -
General Endocrinology
Tekir O, Cevik C, Ozsezer Kaymak G, , Kaya A
The Effect of Diabetes Symptoms on Quality of Life in Individuals with Type 2 DiabetesActa Endo (Buc) 2021 17(2): 186-193 doi: 10.4183/aeb.2021.186
AbstractObjective. This study aimed to investigate the effect of symptoms of diabetes on the quality of life of individuals with Type 2 diabetes. Method. The study used a cross-sectional design. No sampling procedure was employed in the study; instead, 410 individuals presenting to the Balikesir Atatürk City Hospital Endocrinology and Internal Medicine Polyclinics between December 2016 and July 2017, diagnosed with Type 2 diabetes, and meeting the inclusion criteria were enrolled in the study sample. The study data were collected with a “Socio-demographic Characteristics Questionnaire”, the “Diabetes Symptom Checklist”, and the “SF-36 Quality of Life Questionnaire”. Results. The participants obtained the highest mean scores from the hyperglycemia subscale of the Diabetes Symptoms Checklist (3.35±0.60) and the mental health subscale of the SF-36 Quality of Life Questionnaire (50.65±8.10). The hypoglycemia, cardiology, psychology, and neurology variables included in the model were statistically significant and predicted 35% of the mental subscale score of the SF 36 questionnaire. SF 36 physical subscale score increased as the hypoglycemia, cardiology, psychology, and neurology scores decreased (p<0.05). Conclusion. The participants obtained high scores from the hyperglycemia subscale of the diabetes symptom checklist and mental health subscale of the quality of life questionnaire. Diabetes symptoms were found to affect the quality of life of individuals with diabetes. -
Endocrine Care
Trifanescu RA, Fica S, Ursu H, Dimulescu D, Coman I, Ceck C, Barbu C, Coculescu M
Tri-iodothyronine as a risk factor for atrial fibrillation in amiodarone-induced hyperthyroidismActa Endo (Buc) 2006 2(2): 187-202 doi: 10.4183/aeb.2006.187
AbstractAims: To assess if amiodarone maintains its antiarrhythmic efficacy in the presence of amiodarone-induced hyperthyroidism (AIT) and to identify the tri-iodothyronine (T3) threshold for atrial fibrillation in patients with AIT versus common hyperthyroidism.\r\nPatients and methods. Study group A consists in 49 patients (25 M/24 F) with AIT (220.83 ? 71.33 mg/day along 2.36 ? 2.25 years) and severe cardiopathies (9 valvulopathies, 40 ischaemic, dilatative and hypertensive cardiomyopathies), aged 57.87?12.63 years. Control group B consists in 51 hypothyroid (B1) or euthyroid patients (B2) treated with amiodarone (222.55 ? 68.78 mg/day along 2.67 ? 1.84 years) and also in 100 patients (23M/77F) with overt hyperthyroidism (B3), without major heart diseases, aged 52.74?12.85 years; TSH, total T3, total T4, free T4 were measured by radioimmunoassay. All were clinically, ECG and echocardiography evaluated.\r\nResults. Prevalence of arrhythmias recurrence was 59.2% (29/49 patients) in group A, significantly higher than in each control subgroups B: B1- 28% (7/25), B2- 15.45% (4/26) and B3- 20% (20/100), P< 0.001. Patients from study group A with AIT and T3 levels >250 ng/dL developed significantly more frequent atrial fibrillation (p= 0.04). However, in control group B3 with common hyperthyroidism, no T3 threshold for arrhythmias could be identified. Overall, there were no significant differences in total T3 levels with respect to the presence of atrial fibrillation in both study group A and subgroup B3 with common hyperthyroidism (p=ns).\r\nConclusion. Amiodarone antiarrhythmic efficacy is surpassed in AIT by the increased arrhythmic susceptibility of damaged myocardial tissue to minimally increased thyroid hormones levels. A tri-iodothyronine level > 250 ng/dL superimposed on preexistent proarrhythmic substrate in amiodarone-induced hyperthyroidism should be avoided.