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Peter N Taylor - One of the best experts on this subject based on the ideXlab platform.
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falling threshold for treatment of borderline elevated thyrotropin levels balancing benefits and risks evidence from a large community based study
JAMA Internal Medicine, 2014Co-Authors: Peter N Taylor, Ahmed Iqbal, Caroline Minassian, Adrian Sayers, Mohd Shazli Draman, Rosemary Greenwood, William Hamilton, Onyebuchi E Okosieme, Vijay PanickerAbstract:DESIGN, SETTING, PARTICIPANTS, AND EXPOSURE Retrospective cohort study using data from the United Kingdom Clinical Practice Research Datalink. Among 52 298 individuals who received a prescription for Levothyroxine between January 1, 2001, and October 30, 2009, we extracted data about the thyrotropin level before Levothyroxine therapy initiation, clinical symptoms, and thyrotropin levels up to 5 years after Levothyroxine was initiated. We excluded persons who had a history of hyperthyroidism, pituitary disease, or thyroid surgery; those who were taking thyroid-altering medication or if the Levothyroxine prescription was related to pregnancy; and those who did not have a thyrotropin level measured within 3 months before the initiation of Levothyroxine.
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falling threshold for treatment of borderline elevated thyrotropin levels balancing benefits and risks evidence from a large community based study
JAMA Internal Medicine, 2014Co-Authors: Peter N Taylor, Ahmed Iqbal, Caroline Minassian, Adrian Sayers, Mohd Shazli Draman, Rosemary Greenwood, William Hamilton, Onyebuchi E Okosieme, Vijay PanickerAbstract:Importance Rates of thyroid hormone prescribing in the United States and the United Kingdom have increased substantially. If some of the increase is due to lowering the thyrotropin threshold for treatment, this may result in less benefit and greater harm. Objective To define trends in thyrotropin levels at the initiation of Levothyroxine sodium therapy and the risk of developing a suppressed thyrotropin level following treatment. Design, Setting, Participants, and Exposure Retrospective cohort study using data from the United Kingdom Clinical Practice Research Datalink. Among 52 298 individuals who received a prescription for Levothyroxine between January 1, 2001, and October 30, 2009, we extracted data about the thyrotropin level before Levothyroxine therapy initiation, clinical symptoms, and thyrotropin levels up to 5 years after Levothyroxine was initiated. We excluded persons who had a history of hyperthyroidism, pituitary disease, or thyroid surgery; those who were taking thyroid-altering medication or if the Levothyroxine prescription was related to pregnancy; and those who did not have a thyrotropin level measured within 3 months before the initiation of Levothyroxine. Main Outcomes and Measures The median thyrotropin level at the time of the index Levothyroxine prescription, the odds of initiation of Levothyroxine therapy at thyrotropin levels of 10.0 mIU/L or less, and the age-stratified odds of developing a low or suppressed thyrotropin level after Levothyroxine therapy. Results Between 2001 and 2009, the median thyrotropin level at the initiation of Levothyroxine therapy fell from 8.7 to 7.9 mIU/L. The odds ratio for prescribing Levothyroxine at thyrotropin levels of 10.0 mIU/L or less in 2009 compared with 2001 (adjusted for changes in population demographics) was 1.30 (95% CI, 1.19-1.42; P < .001). Older individuals and individuals with cardiac risk factors had higher odds of initiation of Levothyroxine therapy with a thyrotropin level 10.0 mIU/L or less. At 5 years after Levothyroxine initiation, 5.8% of individuals had a thyrotropin level of <0.1 mIU/L. Individuals with depression or tiredness at baseline had increased odds of developing a suppressed thyrotropin level, whereas individuals with cardiac risk factors (eg, atrial fibrillation, diabetes mellitus, hypertension, and raised lipid levels) did not. Conclusions and Relevance We observed a trend toward Levothyroxine treatment of more marginal degrees of hypothyroidism and a substantial risk of developing a suppressed thyrotropin level following therapy. Large-scale prospective studies are required to assess the risk-benefit ratio of current practice. Primary hypothyroidism is one of the most common chronic disorders in Western populations and is largely managed in primary care. Levothyroxine sodium prescriptions in the United States have increased substantially in recent years (from 49.8 million in 2006 to 70.5 million in 2010). A similar increase has been observed in England and Wales, with Levothyroxine prescriptions rising from 17.1 million (in 2006) to 23.4 million (in 2010), up from only 7 million prescriptions in 1998 data. Several factors have probably contributed to this rise. In England and Wales, a proportion may be attributed to a fall in the mean duration of prescriptions from 60 to 45 days. Thyroid function testing has also increased substantially, and in any year 18% to 25% of individuals have their thyroid function tested, likely resulting in increased case finding. However, an additional factor may be a lowering of the thyrotropin threshold at which Levothyroxine is initiated. This practice would be important to identify because it might be associated with more marginal benefits and with increased relative risk of patient harm. The results of studies published before 2001 suggested that between 15% and 20% of individuals taking Levothyroxine are overtreated and develop a low thyrotropin level, most likely because of inadequate monitoring. Overtreatment is associated with an increased risk of fractures and atrial fibrillation. American Thyroid Association guidelines recommend consideration of Levothyroxine therapy at thyrotropin levels of 10.0 mIU/L or less when there are clear symptoms of hypothyroidism, positive thyroid autoantibodies, or evidence of atherosclerotic cardiovascular disease or heart failure (evidence level B). Data from Scotland in 2001 indicated that most patients had Levothyroxine initiated at thyrotropin levels of 10.0 mIU/L or less, with 45% to 48% of patients having therapy commenced with a thyrotropin level less than 6.0 mIU/L. In this study, we used a large United Kingdom (UK) population-based database to examine trends in thyrotropin levels before and after Levothyroxine therapy initiation since 2001 and assessed the potential for adverse outcomes from current practice.
Vijay Panicker - One of the best experts on this subject based on the ideXlab platform.
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falling threshold for treatment of borderline elevated thyrotropin levels balancing benefits and risks evidence from a large community based study
JAMA Internal Medicine, 2014Co-Authors: Peter N Taylor, Ahmed Iqbal, Caroline Minassian, Adrian Sayers, Mohd Shazli Draman, Rosemary Greenwood, William Hamilton, Onyebuchi E Okosieme, Vijay PanickerAbstract:DESIGN, SETTING, PARTICIPANTS, AND EXPOSURE Retrospective cohort study using data from the United Kingdom Clinical Practice Research Datalink. Among 52 298 individuals who received a prescription for Levothyroxine between January 1, 2001, and October 30, 2009, we extracted data about the thyrotropin level before Levothyroxine therapy initiation, clinical symptoms, and thyrotropin levels up to 5 years after Levothyroxine was initiated. We excluded persons who had a history of hyperthyroidism, pituitary disease, or thyroid surgery; those who were taking thyroid-altering medication or if the Levothyroxine prescription was related to pregnancy; and those who did not have a thyrotropin level measured within 3 months before the initiation of Levothyroxine.
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falling threshold for treatment of borderline elevated thyrotropin levels balancing benefits and risks evidence from a large community based study
JAMA Internal Medicine, 2014Co-Authors: Peter N Taylor, Ahmed Iqbal, Caroline Minassian, Adrian Sayers, Mohd Shazli Draman, Rosemary Greenwood, William Hamilton, Onyebuchi E Okosieme, Vijay PanickerAbstract:Importance Rates of thyroid hormone prescribing in the United States and the United Kingdom have increased substantially. If some of the increase is due to lowering the thyrotropin threshold for treatment, this may result in less benefit and greater harm. Objective To define trends in thyrotropin levels at the initiation of Levothyroxine sodium therapy and the risk of developing a suppressed thyrotropin level following treatment. Design, Setting, Participants, and Exposure Retrospective cohort study using data from the United Kingdom Clinical Practice Research Datalink. Among 52 298 individuals who received a prescription for Levothyroxine between January 1, 2001, and October 30, 2009, we extracted data about the thyrotropin level before Levothyroxine therapy initiation, clinical symptoms, and thyrotropin levels up to 5 years after Levothyroxine was initiated. We excluded persons who had a history of hyperthyroidism, pituitary disease, or thyroid surgery; those who were taking thyroid-altering medication or if the Levothyroxine prescription was related to pregnancy; and those who did not have a thyrotropin level measured within 3 months before the initiation of Levothyroxine. Main Outcomes and Measures The median thyrotropin level at the time of the index Levothyroxine prescription, the odds of initiation of Levothyroxine therapy at thyrotropin levels of 10.0 mIU/L or less, and the age-stratified odds of developing a low or suppressed thyrotropin level after Levothyroxine therapy. Results Between 2001 and 2009, the median thyrotropin level at the initiation of Levothyroxine therapy fell from 8.7 to 7.9 mIU/L. The odds ratio for prescribing Levothyroxine at thyrotropin levels of 10.0 mIU/L or less in 2009 compared with 2001 (adjusted for changes in population demographics) was 1.30 (95% CI, 1.19-1.42; P < .001). Older individuals and individuals with cardiac risk factors had higher odds of initiation of Levothyroxine therapy with a thyrotropin level 10.0 mIU/L or less. At 5 years after Levothyroxine initiation, 5.8% of individuals had a thyrotropin level of <0.1 mIU/L. Individuals with depression or tiredness at baseline had increased odds of developing a suppressed thyrotropin level, whereas individuals with cardiac risk factors (eg, atrial fibrillation, diabetes mellitus, hypertension, and raised lipid levels) did not. Conclusions and Relevance We observed a trend toward Levothyroxine treatment of more marginal degrees of hypothyroidism and a substantial risk of developing a suppressed thyrotropin level following therapy. Large-scale prospective studies are required to assess the risk-benefit ratio of current practice. Primary hypothyroidism is one of the most common chronic disorders in Western populations and is largely managed in primary care. Levothyroxine sodium prescriptions in the United States have increased substantially in recent years (from 49.8 million in 2006 to 70.5 million in 2010). A similar increase has been observed in England and Wales, with Levothyroxine prescriptions rising from 17.1 million (in 2006) to 23.4 million (in 2010), up from only 7 million prescriptions in 1998 data. Several factors have probably contributed to this rise. In England and Wales, a proportion may be attributed to a fall in the mean duration of prescriptions from 60 to 45 days. Thyroid function testing has also increased substantially, and in any year 18% to 25% of individuals have their thyroid function tested, likely resulting in increased case finding. However, an additional factor may be a lowering of the thyrotropin threshold at which Levothyroxine is initiated. This practice would be important to identify because it might be associated with more marginal benefits and with increased relative risk of patient harm. The results of studies published before 2001 suggested that between 15% and 20% of individuals taking Levothyroxine are overtreated and develop a low thyrotropin level, most likely because of inadequate monitoring. Overtreatment is associated with an increased risk of fractures and atrial fibrillation. American Thyroid Association guidelines recommend consideration of Levothyroxine therapy at thyrotropin levels of 10.0 mIU/L or less when there are clear symptoms of hypothyroidism, positive thyroid autoantibodies, or evidence of atherosclerotic cardiovascular disease or heart failure (evidence level B). Data from Scotland in 2001 indicated that most patients had Levothyroxine initiated at thyrotropin levels of 10.0 mIU/L or less, with 45% to 48% of patients having therapy commenced with a thyrotropin level less than 6.0 mIU/L. In this study, we used a large United Kingdom (UK) population-based database to examine trends in thyrotropin levels before and after Levothyroxine therapy initiation since 2001 and assessed the potential for adverse outcomes from current practice.
Serdar Guler - One of the best experts on this subject based on the ideXlab platform.
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the impact of Levothyroxine sodium treatment on oxidative stress in hashimoto s thyroiditis
European Journal of Endocrinology, 2016Co-Authors: Ihsan Ates, Mustafa Altay, Fatma Meric Yilmaz, Canan Topcuoglu, Nisbet Yilmaz, Dilek Berker, Serdar GulerAbstract:OBJECTIVE: Although several studies reported increased oxidative stress in Hashimoto's thyroiditis (HT), the effect of Levothyroxine treatment on oxidative status is not studied extensively. Therefore, we conducted this study to investigate the effects of Levothyroxine replacement on oxidative stress in HT. DESIGN AND METHODS: Thirty-six patients recently diagnosed with HT-related hypothyroidism and 36 healthy controls were included in the study. Levothyroxine replacement was started to patients with hypothyroidism, and had been followed-up for 6 months. RESULTS: Mean basal serum total antioxidant status (TAS), total thiol, arylesterase, and paraoxonase 1 (PON1) levels were significantly lower, and serum total oxidant status (TOS) and oxidative stress index (OSI) were significantly higher in the patients with hypothyroid than the controls. In the hypothyroid group serum TAS, total thiol, arylesterase, and PON1 levels increased and serum TOS and OSI levels decreased significantly after Levothyroxine treatment. Pretreatment serum TAS, total thiol, PON1, and arylesterase levels were positively correlated with free Levothyroxine (fT4) and negatively correlated with thyroid-stimulating hormone (TSH), antithyroid peroxidase (anti-TPO), and antithyroglobulin (anti-TG) levels. Also, pretreatment serum TOS and OSI levels were negatively correlated with fT4 levels and positively correlated with TSH, anti-TPO, and anti-TG. We have also found that the fT4 and anti-TPO levels are independent predictors of the oxidative stress parameters in stepwise multivariable linear regression analysis. CONCLUSION: This study suggests that Levothyroxine replacement decreases oxidant status and increases antioxidant status following the 6 months of Levothyroxine replacement in hypothyroidism that develops in accordance with the HT.
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The impact of Levothyroxine sodium treatment on oxidative stress in Hashimoto’s thyroiditis
European Journal of Endocrinology, 2016Co-Authors: Ihsan Ates, Mustafa Altay, Fatma Meric Yilmaz, Canan Topcuoglu, Nisbet Yilmaz, Dilek Berker, Serdar GulerAbstract:OBJECTIVE: Although several studies reported increased oxidative stress in Hashimoto's thyroiditis (HT), the effect of Levothyroxine treatment on oxidative status is not studied extensively. Therefore, we conducted this study to investigate the effects of Levothyroxine replacement on oxidative stress in HT. DESIGN AND METHODS: Thirty-six patients recently diagnosed with HT-related hypothyroidism and 36 healthy controls were included in the study. Levothyroxine replacement was started to patients with hypothyroidism, and had been followed-up for 6 months. RESULTS: Mean basal serum total antioxidant status (TAS), total thiol, arylesterase, and paraoxonase 1 (PON1) levels were significantly lower, and serum total oxidant status (TOS) and oxidative stress index (OSI) were significantly higher in the patients with hypothyroid than the controls. In the hypothyroid group serum TAS, total thiol, arylesterase, and PON1 levels increased and serum TOS and OSI levels decreased significantly after Levothyroxine treatment. Pretreatment serum TAS, total thiol, PON1, and arylesterase levels were positively correlated with free Levothyroxine (fT4) and negatively correlated with thyroid-stimulating hormone (TSH), antithyroid peroxidase (anti-TPO), and antithyroglobulin (anti-TG) levels. Also, pretreatment serum TOS and OSI levels were negatively correlated with fT4 levels and positively correlated with TSH, anti-TPO, and anti-TG. We have also found that the fT4 and anti-TPO levels are independent predictors of the oxidative stress parameters in stepwise multivariable linear regression analysis. CONCLUSION: This study suggests that Levothyroxine replacement decreases oxidant status and increases antioxidant status following the 6 months of Levothyroxine replacement in hypothyroidism that develops in accordance with the HT.
Jacqueline Jonklaas - One of the best experts on this subject based on the ideXlab platform.
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Levothyroxine Dose Adjustment to Optimise Therapy Throughout a Patient’s Lifetime
Advances in Therapy, 2019Co-Authors: Leonidas H. Duntas, Jacqueline JonklaasAbstract:Levothyroxine is the standard therapy for patients with hypothyroidism, a condition that affects up to 5% of people worldwide. While Levothyroxine therapy has substantially improved the lives of millions of hypothyroid patients since its introduction in 1949, the complexity of maintaining biochemical and clinical euthyroidism in patients undergoing treatment with Levothyroxine cannot be underestimated. Initial dosing of Levothyroxine can vary greatly and may be based on the amount of residual thyroid function retained by the patient, the body weight or lean body mass of the patient, and thyroid-stimulating hormone levels. As Levothyroxine is usually administered over a patient’s lifetime, physiological changes throughout life will affect the dose of Levothyroxine required to maintain euthyroidism. Furthermore, dose adjustments may need to be made in patients with concomitant medical conditions, in patients taking certain medications, as well as in elderly patients. Patients who have undergone any weight or hormonal changes may require dose adjustments, and the majority of pregnant women require increased doses of Levothyroxine. Optimal treatment of hypothyroidism requires a partnership between patient and physician. The physician is tasked with vigilant appraisal of the patient’s status based on a thorough clinical and laboratory assessment and appropriate adjustment of their Levothyroxine therapy. The patient in turn is tasked with medication adherence and reporting of symptomatology and any changes in their medical situation. The goal is consistent maintenance of euthyroidism, without the patient experiencing the adverse events and negative health consequences of under- or overtreatment. Funding Merck. Plain Language Summary Plain language summary available for this article.
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Levothyroxine Dose Adjustment to Optimise Therapy Throughout a Patient's Lifetime.
Advances in Therapy, 2019Co-Authors: Leonidas H. Duntas, Jacqueline JonklaasAbstract:Levothyroxine is the standard therapy for patients with hypothyroidism, a condition that affects up to 5% of people worldwide. While Levothyroxine therapy has substantially improved the lives of millions of hypothyroid patients since its introduction in 1949, the complexity of maintaining biochemical and clinical euthyroidism in patients undergoing treatment with Levothyroxine cannot be underestimated. Initial dosing of Levothyroxine can vary greatly and may be based on the amount of residual thyroid function retained by the patient, the body weight or lean body mass of the patient, and thyroid-stimulating hormone levels. As Levothyroxine is usually administered over a patient's lifetime, physiological changes throughout life will affect the dose of Levothyroxine required to maintain euthyroidism. Furthermore, dose adjustments may need to be made in patients with concomitant medical conditions, in patients taking certain medications, as well as in elderly patients. Patients who have undergone any weight or hormonal changes may require dose adjustments, and the majority of pregnant women require increased doses of Levothyroxine. Optimal treatment of hypothyroidism requires a partnership between patient and physician. The physician is tasked with vigilant appraisal of the patient's status based on a thorough clinical and laboratory assessment and appropriate adjustment of their Levothyroxine therapy. The patient in turn is tasked with medication adherence and reporting of symptomatology and any changes in their medical situation. The goal is consistent maintenance of euthyroidism, without the patient experiencing the adverse events and negative health consequences of under- or overtreatment.Funding Merck.Plain Language Summary Plain language summary available for this article.
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timing of Levothyroxine administration affects serum thyrotropin concentration
The Journal of Clinical Endocrinology and Metabolism, 2009Co-Authors: Thiengiang Bachhuynh, Bindu Nayak, Jennifer Loh, Steven J Soldin, Jacqueline JonklaasAbstract:Context: Patients treated with Levothyroxine typically ingest it in a fasting state to prevent food impairing its absorption. The serum thyrotropin concentration is the therapeutic index of Levothyroxine action. Objective: The study objective was to determine the effect of the timing of Levothyroxine administration in relationship to food on serum thyrotropin levels. Design: Participants were randomized to one of six sequences, each consisting of three 8-wk regimens in a three-period crossover design. These regimens were in a fasting state, at bedtime, and with breakfast. The concentrations of TSH, free T4, and total T3 during each of the three timing regimens were documented. The primary outcome was the difference between serum TSH concentrations under fasting conditions compared with concentrations during the other 8-wk regimens. Setting: The study was conducted in an academic medical center. Participants: Study participants were receiving Levothyroxine for treatment of hypothyroidism or thyroid cancer. Results: Sixty-five patients completed the study. The mean thyrotropin concentration was 1.06 ± 1.23 mIU/liter when Levothyroxine was administered in the fasting state. When Levothyroxine was taken with breakfast, the serum thyrotropin concentration was significantly higher (2.93 ± 3.29 mIU/liter). When Levothyroxine was taken at bedtime, the serum TSH concentration was also significantly higher (2.19 ± 2.66 mIU/liter). Conclusion: Nonfasting regimens of Levothyroxine administration are associated with higher and more variable serum TSH concentrations. If a specific serum TSH goal is desired, thereby avoiding iatrogenic subclinical thyroid disease, then fasting ingestion of Levothyroxine ensures that TSH concentrations remain within the narrowest target range.
Ihsan Ates - One of the best experts on this subject based on the ideXlab platform.
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the impact of Levothyroxine sodium treatment on oxidative stress in hashimoto s thyroiditis
European Journal of Endocrinology, 2016Co-Authors: Ihsan Ates, Mustafa Altay, Fatma Meric Yilmaz, Canan Topcuoglu, Nisbet Yilmaz, Dilek Berker, Serdar GulerAbstract:OBJECTIVE: Although several studies reported increased oxidative stress in Hashimoto's thyroiditis (HT), the effect of Levothyroxine treatment on oxidative status is not studied extensively. Therefore, we conducted this study to investigate the effects of Levothyroxine replacement on oxidative stress in HT. DESIGN AND METHODS: Thirty-six patients recently diagnosed with HT-related hypothyroidism and 36 healthy controls were included in the study. Levothyroxine replacement was started to patients with hypothyroidism, and had been followed-up for 6 months. RESULTS: Mean basal serum total antioxidant status (TAS), total thiol, arylesterase, and paraoxonase 1 (PON1) levels were significantly lower, and serum total oxidant status (TOS) and oxidative stress index (OSI) were significantly higher in the patients with hypothyroid than the controls. In the hypothyroid group serum TAS, total thiol, arylesterase, and PON1 levels increased and serum TOS and OSI levels decreased significantly after Levothyroxine treatment. Pretreatment serum TAS, total thiol, PON1, and arylesterase levels were positively correlated with free Levothyroxine (fT4) and negatively correlated with thyroid-stimulating hormone (TSH), antithyroid peroxidase (anti-TPO), and antithyroglobulin (anti-TG) levels. Also, pretreatment serum TOS and OSI levels were negatively correlated with fT4 levels and positively correlated with TSH, anti-TPO, and anti-TG. We have also found that the fT4 and anti-TPO levels are independent predictors of the oxidative stress parameters in stepwise multivariable linear regression analysis. CONCLUSION: This study suggests that Levothyroxine replacement decreases oxidant status and increases antioxidant status following the 6 months of Levothyroxine replacement in hypothyroidism that develops in accordance with the HT.
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The impact of Levothyroxine sodium treatment on oxidative stress in Hashimoto’s thyroiditis
European Journal of Endocrinology, 2016Co-Authors: Ihsan Ates, Mustafa Altay, Fatma Meric Yilmaz, Canan Topcuoglu, Nisbet Yilmaz, Dilek Berker, Serdar GulerAbstract:OBJECTIVE: Although several studies reported increased oxidative stress in Hashimoto's thyroiditis (HT), the effect of Levothyroxine treatment on oxidative status is not studied extensively. Therefore, we conducted this study to investigate the effects of Levothyroxine replacement on oxidative stress in HT. DESIGN AND METHODS: Thirty-six patients recently diagnosed with HT-related hypothyroidism and 36 healthy controls were included in the study. Levothyroxine replacement was started to patients with hypothyroidism, and had been followed-up for 6 months. RESULTS: Mean basal serum total antioxidant status (TAS), total thiol, arylesterase, and paraoxonase 1 (PON1) levels were significantly lower, and serum total oxidant status (TOS) and oxidative stress index (OSI) were significantly higher in the patients with hypothyroid than the controls. In the hypothyroid group serum TAS, total thiol, arylesterase, and PON1 levels increased and serum TOS and OSI levels decreased significantly after Levothyroxine treatment. Pretreatment serum TAS, total thiol, PON1, and arylesterase levels were positively correlated with free Levothyroxine (fT4) and negatively correlated with thyroid-stimulating hormone (TSH), antithyroid peroxidase (anti-TPO), and antithyroglobulin (anti-TG) levels. Also, pretreatment serum TOS and OSI levels were negatively correlated with fT4 levels and positively correlated with TSH, anti-TPO, and anti-TG. We have also found that the fT4 and anti-TPO levels are independent predictors of the oxidative stress parameters in stepwise multivariable linear regression analysis. CONCLUSION: This study suggests that Levothyroxine replacement decreases oxidant status and increases antioxidant status following the 6 months of Levothyroxine replacement in hypothyroidism that develops in accordance with the HT.