scholarly journals SAT-LB85 Use of Weekly Levothyroxine Regimen for Rapid Normalization of Thyroid Hormone Levels: A Case Report

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Jose Renato Martinez Escudero ◽  
Johnathan Kirupakaran ◽  
Alice Yau ◽  
Giovanna Rodriguez ◽  
Gul Bahtiyar

Abstract Background: Hypothyroidism affects around 4.6% of the U.S. population1. Non-adherence with thyroid hormone replacement is one of the biggest challenges in treating hypothyroidism1. The half-life of T4 and T3 in hypothyroidism is about 7.5 and 1.4 days respectively2. A large dose once-weekly administration of levothyroxine (Lt4) is possible3, 4. Recent publications suggest that once-weekly Lt4 does not increase the risk of cardiovascular events and is well tolerated by most of patients4. Once weekly Lt4 produces similar results as daily Lt4 as evidenced by thyroid function tests3,4, and potentially improves patient compliance and satisfaction with the treatment4. Clinical Course: A 29-year-old female with a history of Hashimoto’s hypothyroidism, polycystic ovarian syndrome, depression, presented with irregular menses. Her symptoms included depression, fatigue, increased appetite. Her TSH was grossly elevated at 217 uIU/mL (0.27-4.20 uIU/mL). However upon re-visit, after increasing Lt4 to 100 mcg daily her TSH increased to 280 uIU/mL. She admitted to non-adherence with her daily Lt4 prescription. Physical exam was notable for sinus bradycardia and slow mentation, otherwise unremarkable. Blood count, basic metabolic panel and hemoglobin A1C were within normal limits. Liver function tests showed mild transaminitis, ALT 46 U/L (10-45 U/L). Lt4 was started at 875 mcg per week. At five weeks, her TSH was 6.31 uIU/mL and at seven weeks, the patient was euthyroid with a TSH of 2.53 uIU/mL. Her periods have since normalized. Conclusion: The current discourse on weekly dosing mainly focuses on its use for non-adherent patients. This case provides a clear time course also demonstrating rapid normalization of TSH using weekly dosing. Weekly Lt4 dosing as first-line therapy in noncompliant depressed patients with severe hypothyroidism should be considered. 1.Hepp, Z., Wyne, K., Manthena, S., Wang, S. and Gossain, V. (2018). Adherence to thyroid hormone replacement therapy: a retrospective, claims database analysis. Current Medical Research and Opinion, 34(9), pp.1673-1678.2.Colucci, P., Yue, C., Ducharme, M. and Benvenga, S. (2010). A Review of the Pharmacokinetics of Levothyroxine for the Treatment of Hypothyroidism. European Endocrinology, 9(1), p.40.3.Jayakumari, C., Nair, A., Puthiyaveettil Khadar, J., Das, D., Prasad, N., Jessy, S., Gopi, A. and Guruprasad, P. (2019). Efficacy and Safety of Once-Weekly Thyroxine for Thyroxine-Resistant Hypothyroidism. Journal of the Endocrine Society, 3(12), pp.2184-2193.4.Rajput, R. and Pathak, V. (2017). The Effect of Daily versus Weekly Levothyroxine Replacement on Thyroid Function Test in Hypothyroid Patients at a Tertiary Care Centre in Haryana. European Thyroid Journal, 6(5), pp.250-254.

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A831-A831
Author(s):  
Rachel Beeson ◽  
Antoinette B Coe ◽  
David Reyes-Gastelum ◽  
Megan R Haymart ◽  
Maria Papaleontiou

Abstract Background: Thyroid hormone prescriptions have steadily increased in the past few years with levothyroxine being one of the most frequently prescribed medications in the United States. Population-based studies have shown that older age is a significant predictor for thyroid hormone initiation, with use continuing long-term. Thyroid hormone management in older adults is complicated by the presence of comorbidities and polypharmacy, particularly due to medications that can interfere with thyroid function tests. However, the prevalence of concurrent use of thyroid hormone and interfering medications in older adults and patient characteristics associated with this practice remain unknown. Methods: We conducted a population-based, retrospective cohort study of 538,137 thyroid hormone users aged ≥65 years from the Corporate Data Warehouse of the Veterans Health Administration (2004-2017). First, we described the prevalence of concurrent use of thyroid hormone and medications that commonly interfere with thyroid function tests (i.e., prednisone, prednisolone, carbamazepine, phenytoin, phenobarbital, amiodarone, lithium, interferon-alpha, tamoxifen). Then, we performed a multivariable logistic regression analysis to determine patient characteristics associated with concurrent use of thyroid hormone and at least one interfering medication during the study period. Covariates included in the model were patient age, sex, race, ethnicity and number of comorbidities. Results: Overall, 170,261 (31.6%) of patients were on at least one interfering medication while on thyroid hormone during the study period (median follow up 56 months). Non-white race [odds ratio (OR) 1.18, 95% confidence interval (CI) 1.15-1.21], compared to white race), Hispanic ethnicity (OR 1.11, 95% CI 1.08-1.14, compared to non-Hispanic), female sex (OR 1.12, 95% CI 1.08-1.15, compared to male sex), and presence of comorbidities (e.g. Charlson-Deyo Comorbidity Score ≥2, OR 2.47, 95% CI 2.43-2.52, compared to zero) were more likely to be associated with concurrent use of thyroid hormone and interfering medications. Older age (e.g., ≥85 years, OR 0.47, 95% CI 0.46 - 0.48, compared to age 65-74 years) was less likely to be associated with concurrent use of thyroid hormone and interfering medications. Conclusions: Almost one-third of older adults on thyroid hormone were taking medications that have been known to interfere with thyroid function tests. Our study highlights the complexity of managing thyroid hormone replacement in older patients, many of whom are at risk for adverse effects in the context of polypharmacy and comorbidities.


1996 ◽  
Vol 32 (6) ◽  
pp. 481-487 ◽  
Author(s):  
LA Frank

Five normal dogs and 22 dogs with dermatological signs suggestive of hypothyroidism were evaluated using thyrotropin-releasing hormone (TRH) and thyrotropin (TSH) stimulation. Thyroxine (T4) concentration after TRH stimulation was significantly lower than that obtained by TSH stimulation. It was not possible to identify hypothyroid dogs with the TRH-stimulation test, because some euthyroid dogs had either decreases in T4 or only slight increases in T4 concentrations after TRH stimulation. In addition, dogs with pyoderma had decreased responses in serum T4 after TRH stimulation, which became normal following treatment with antibiotics. Six of the 22 dogs were diagnosed as hypothyroid based on TSH results and responses to thyroid hormone replacement. It was concluded that TRH stimulation is not a useful means of diagnosing hypothyroidism in dogs.


2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Nikita Limara Rabelo Pagan ◽  
Melanie Quintana Serrano ◽  
Mary J Rodriguez Malave ◽  
Meilyn Reyes

Abstract Myxedema coma is a severe form of hypothyroidism representing a endocrinologic emergency. It requires prompt identification and management, as mortality rates exceed 50%. Its rarity stems from early recognition and thyroid medication availability. Its presentation can be non-specific, making it a challenging diagnosis. This is a 67-year-old male inmate who was brought to the ED due to hypoactivity. He had a long-standing history of bipolar disorder, and hypothyroidism receiving oral levothyroxine. On evaluation, patient had slowed mentation, GCS 14/15, sluggish reactive pupils, macroglossia, diffuse non-pitting edema, and delayed relaxation of the deep tendon reflexes in the extremities. Vital signs were abnormal; T: 35.2 °C, RR: 10 rpm, SpO2: 84 %, BP: 137/89 mmHg and HR: 42 bpm without chronotropism. 12-lead ECG revealed a complete atrioventricular block (AV block), with non-conductive P waves and idioventricular rhythm. Patient became hemodynamically unstable, transcutaneous pacemaker was placed. Dopamine infusion was initiated for adequate mean arterial pressure. Subsequently, a femoral transvenous pacemaker was performed. However, neurological deterioration prompted mechanical ventilation. Exploring reversible AV block etiologies, laboratory results were markedly elevated for TSH at 184.775 ng/mL and decreased T4 at 1.5 ng/mL. Lithium levels were therapeutic. Myxedema coma was identified and timely treatment was provided with intravenous thyroid hormone replacement, intravenous hydrocortisone, and supportive care. Patient was transferred to an ICU where TSH was monitored. After 5 days of receiving IV thyroid hormone replacement therapy, TSH improved. However, patient remained dependent on transvenous pacemaker, for which permanent pacemaker had to be placed. With further therapy, patient’s neurological status improved leading to extubation, and subsequent discharge. Thyroid hormones play a vital role in the electrical current of the heart; hence, disturbances may potentiate cardiac arrhythmias. Sinus bradycardia and QT interval prolongation are commonly seen. As the severity of hypothyroidism progresses, high-grade AV block may be encountered, being third degree AV block the most challenging and severe. Patients with high-degree AV block in the setting of reversible etiologies, commonly, do not need a permanent pacemaker. On the contrary, our patient developed complete dependence of the pacemaker for adequate cardiac synchrony, despite adequate replacement therapy. With this case, we illustrate the importance of a thorough evaluation in patients with AV block of unknown origin, with special attention to reversible etiologies. Thyroid function abnormalities should be promptly identified and managed for better outcomes. Furthermore, it may decrease cardiac death risk and the need for invasive procedures, such as permanent pacemaker placement.


1980 ◽  
Vol 95 (4) ◽  
pp. 472-478 ◽  
Author(s):  
A. Eugene Pekary ◽  
Jerome M. Hershman ◽  
Clark T. Sawin

Abstract. Basal serum TSH and the peak TSH response to a 500 μg TRH bolus were measured in 57 euthyroid and in 29 hypothyroid subjects either receiving graded thyroid hormone replacement or acutely removed from full replacement therapy. Serum TSH, total T4 and T3 were determined by sensitive radioimmunoassay methods. The peak versus basal TSH data for hypothyroid patients were linear within individuals. The regression slope of the peak versus basal TSH data for all hypothyroid subjects did not differ significantly from the corresponding slope for all euthyroid subjects. Basal and peak TSH versus T3 and T4 data for hypothyroid patients were also linear within each individual. Moreover, the regression of the basal TSH values averaged over the non-replacement to full replacement state against the TSH versus T3 slope had a significant negative correlation. This trend leads to an array of regression lines which average to the familiar hyperbolic relationship between thyrotrophin and thyroid hormone levels in man.


Prescriber ◽  
2018 ◽  
Vol 29 (12) ◽  
pp. 30-33
Author(s):  
Anh Tran ◽  
Steve Hyer ◽  
Gabriella Bathgate ◽  
Onyebuchi Okosieme

2013 ◽  
Vol 3 (2) ◽  
Author(s):  
Starry H. Rampengan

Abstract: Amiodarone is a highly effective anti-arrhythmic agent used in certain arrhythmias from supraventricular tachycardia to life-threatening ventricular tachycardia. Its use is associated with numerous side-effects that could deteriorate a patient’s condition. Consequently, a clinician should consider the risks and benefits of amiodarone before initiating the treatment.The thyroid gland is one of the organs affected by amiodarone. Amiodarone and its metabolite desethyl amiodaron induce alterations in thyroid hormone metabolism in the thyroid gland, peripheral tissues, and probably also in the pituitary gland. These actions result in elevations of serum T4 and rT3 concentrations, transient increases in TSH concentrations, and decreases in T3 concentrations. Both hypothyroidism and hyperthyroidism are prone to occur in patients receiving amiodarone. Amiodarone-induced hypothyroidism (AIH) results from the inability of the thyroid to escape from the Wolff-Chaikoff effect and is readily managed by either discontinuation of amiodarone or thyroid hormone replacement. Amiodarone-induced thyrotoxicosis (AIT) may arise from either iodine-induced excessive thyroid hormone synthesis (type I, usually with underlying thyroid abnormality), or destructive thyroiditis with release of preformed hormones (type II, commonly with apparently normal thyroid glands). Therefore, monitoring of thyroid function should be performed in all amiodarone-treated patients to facilitate early diagnosis and treatment of amiodarone-induced thyroid dysfunction. Key words: Amiodarone, thyroid function, side effect, management, monitoring.     Abstrak: Amiodaron adalah obat antiaritmia yang cukup efektif dalam menangani beberapa keadaaan aritmia mulai dari supraventrikuler takikardia sampai takikardia ventrikuler yang mengancam kehidupan. Namun penggunaan obat ini ternyata menimbulkan efek samping pada organ lain yang dapat menimbulkan perburukan keadaan pasien. Sehingga, dalam penggunaan amiodaron, klinisi juga harus menimbang keuntungan dan kerugian yang ditimbulkan oleh obat ini. Salah satu organ yang dipengaruhi oleh amiodaron adalah kelenjar tiroid. Amiodaron dan metabolitnya desetil amiodaron memengaruhi hormon tiroid pada kelenjar tiroid, jaringan perifer, dan mungkin pada pituitari. Aksi amiodaron ini menyebabkan peningkatan T4, rT3 dan TSH, namun menurunkan kadar T3. Hipotiroidisme dan tirotoksikosis dapat terjadi pada pasien yang diberi amiodaron. Amiodarone-induced hypothyroidism (AIH) terjadi karena ketidakmampuan tiroid melepaskan diri dari efek Wolff Chaikof, dan dapat ditangani dengan pemberian  hormon substitusi T4 atau penghentian amiodaron. Amiodarone-induced thyrotoxicosis (AIT) terjadi karena sintesis hormon tiroid yang berlebihan yang diinduksi oleh iodium (tipe I, biasanya sudah mempunyai kelainan tiroid sebelumnya) atau karena tiroiditis destruktif yang disertai pelepasan hormon tiroid yang telah terbentuk (tipe II, biasanya dengan kelenjar yang normal). Pemantauan fungsi tiroid seharusnya dilakukan pada semua pasien yang diberi amiodaron untuk memfasilitasi diagnosis dan terapi yang dini terjadinya  disfungsi tiroid yang diinduksi amiodaron. Kata Kunci: Amiodaron, fungsi tiroid, efek samping, penanganan, pemantauan.


2018 ◽  
Vol 8 (1) ◽  
pp. 24-28
Author(s):  
Sukriti Kumar ◽  
Sumit Rungta ◽  
Manish Gutch ◽  
Annesh Bhattacharya ◽  
Syed Mohd Razi ◽  
...  

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