How many people die from hyperthyroidism

Thyroxine T 4 : the major hormone produced by the thyroid gland. T 4 gets converted to the active hormone T 3 in various tissues in the body. In an effort to answer the question, this study was designed to examine the association between thyroid disease and death and cardiovascular risk in a large Danish population. Subclinical and overt thyroid dysfunction and risk of all-cause mortality and cardiovascular events: a large population study.

J Clin Endocrinol Metab. March 21, [Epub ahead of print]. Patients taking thyroid hormones or antithyroid drugs or had had a heart attack, stroke, heart failure, or cancer were excluded.

They compared levels of thyroxine in blood samples of the adults with how many of them died of sudden cardiac death. Heart attacks: What you should know. They discovered that higher levels of thyroxine were associated with an increased risk of sudden cardiac death, independent of other cardiovascular risk factors. The researchers indicated that their findings probably would be similar in the United States.

Why are higher levels of the thyroid-stimulating hormone associated with an increased risk of sudden cardiac death? However, "we were surprised to see that when we control our analyses for these factors, the association remained similar, suggesting that other pathways could play a role," she added.

This could lead to better assessment of individual risk and identify possible prevention targets. What tests you really need and when. A time-dependent Cox proportional hazards-regression model was used to evaluate the prognostic influence of T 4 therapy and of serum thyrotropin measurements on survival. We also investigated differences in risk associated with subclinical thyroid dysfunction recorded during follow-up before initiation of T 4 therapy for overt hypothyroidism.

For this, we considered both the first recorded thyrotropin measurement as a single time-constant categorical variable low, normal, or high serum thyrotropin levels , as well as repeated measures of serum thyrotropin considered as time-dependent categorical variables.

These models were adjusted for patient age at entry in 5-year age groups , sex, and interval between radioiodine treatment and date of first serum thyrotropin measurement.

Before presenting results from the Cox models, we tested the proportional hazard assumption by introducing constructed time-dependent variables for all covariates and tested for their significance. Kaplan-Meier curves were constructed for survival from ischemic heart disease during the period of follow-up prior to T 4 therapy and predicted by the first recorded serum thyrotropin measurement low, normal, or high.

Data were analyzed using SAS version 8. All P values were 2-sided. Characteristics of the patients in the study are shown in Table 1. Their median age at first measurement of serum thyrotropin was 62 years range, years and The baseline characteristics of men and women were similar Table 1.

Of the patients, died before the end of the study. The expected number of deaths for the total number of person-years at risk 15 years was , leading to a relative risk of 1.

The risks of death due to endocrine and metabolic disorders and circulatory diseases were significantly greater than what they were in the general population and together accounted for 47 of the 67 excess deaths observed. The risk of death from other major causes, including cancer and respiratory diseases, were not increased significantly Table 2.

Excess deaths from circulatory diseases were confined to cardiovascular deaths SMR, 1. There were also small and nonsignificant increases in the number of deaths from ischemic heart disease and cerebrovascular disease. When mortality among men and women was considered separately, the increase in all-cause, circulatory, and cardiovascular risk was confined to women; in men an increase in deaths from respiratory diseases was apparent Table 2.

Mortality was compared during follow-up specifically associated with no T 4 therapy ie, in those never overtly hypothyroid and requiring T 4 or prior to development of overt hypothyroidism with follow-up specifically during treatment with T 4 for overt hypothyroidism.

All-cause mortality was increased in the cohort compared with the background population of England and Wales when not taking, or before commencement of, T 4 therapy. This excess mortality was no longer evident when risk of death for the cohort compared with the background population was considered for the period of follow-up during T 4 therapy Table 3. This difference largely reflected a difference in risk of death from circulatory diseases, and specifically from death due to cardiovascular diseases, especially the subcategory that included deaths from dysrhythmias and heart failure, as well as cerebrovascular diseases Table 3.

A similar pattern was observed when mortality was examined in men and women Table 3 and when the cohort was stratified according to age data available on request.

Age-specific mortality rates for all causes of death and for both sexes, compared with the background population of England and Wales, for the period of follow-up prior to, or not requiring, T 4 and follow-up associated with T 4 therapy are shown in Figure 1. This illustrates an increase in all-cause mortality associated with follow-up prior to T 4 , not evident during follow-up associated with T 4 therapy.

The absence of increased risk of death from all causes or from vascular diseases in the cohort when taking T 4 therapy was sustained, being evident both in the first 5 years after starting T 4 circulatory disease SMR, 0. The results were similar when comparison within the cohort was performed using a multivariable Cox proportional hazards regression model including T 4 therapy as a time-dependent covariable Table 4. All-cause mortality was decreased during follow-up of patients receiving T 4 therapy compared with risk during follow-up when not taking T 4 therapy hazard ratio, 0.

This was largely accounted for by reduced risk of death from circulatory disorders while taking T 4 hazards ratio, 0. Significant differences in mortality from respiratory causes and causes of death other than due to cancer, circulatory, or respiratory diseases were also observed.

Reductions in all-cause and circulatory mortality during T 4 therapy compared with no T 4 , or before, T 4 therapy were observed in both men and women when analyzed separately Table 4.

All-cause mortality as predicted from the overall SMR of 1. Circulatory disease mortality followed a similar pattern, being significantly increased compared with the background population for follow-up associated with normal serum thyrotropin circulatory disease SMRs associated with low [SMR, 1.

Ischemic heart disease mortality was nonsignificantly increased in all thyrotropin subgroups, the highest SMR being associated with high serum thyrotropin ischemic heart disease SMRs associated with low [SMR, 1. Comparison according to serum thyrotropin was also performed within the cohort during follow-up when not requiring or before T 4 therapy.

Outcome was considered in relation to both first recorded measurement of serum thyrotropin during long-term follow-up and in relation to repeated measures of serum thyrotropin Table 5. During this period, the presence of high serum thyrotropin was not associated with significant differences in all-cause or circulatory mortality overall compared with normal thyrotropin values. However, an increased risk of death from ischemic heart disease was found, both when high thyrotropin was considered as a single measure first recorded measurement on the register; Figure 2 or as a repeated finding recorded during follow-up Table 5.

No relationship was evident when mortality was investigated according to recorded serum free T 4 concentrations data available on request. We have found an increased risk of all-cause and circulatory mortality in a cohort of patients treated with radioiodine from through These findings were similar to those reported previously from our follow-up of a cohort treated with radioiodine from through , 3 our results indicating that despite perception of earlier or better diagnosis and treatment for overt hyperthyroidism, increased risk of death persists in this disorder in a contemporary cohort.

We found significant increases in the risk of death attributed to endocrine disorders, especially thyroid disease, as expected, and all forms of cardiovascular disease especially deaths due to dysrhythmias and cardiac failure , without significant effects on other major causes of mortality, such as cancer, again in agreement with previous results. A significant excess of deaths due to respiratory disease was confined to men, a finding reported previously in Sweden.

Because hypothyroidism frequently develops during long-term follow-up of patients treated for hyperthyroidism with radioiodine, 10 we wished to determine whether treatment of overt hypothyroidism with T 4 might affect the adverse influence of hyperthyroidism on mortality seen in this and previous studies.

One study of women with idiopathic hypothyroidism described increased mortality from all causes, 15 which may have reflected hyperlipidemia, diastolic hypertension, or diastolic left ventricular dysfunction known to be associated with overt hypothyroidism.

In the present study, we found that cardiovascular risk was increased compared with the background population in those who received treatment for hyperthyroidism and survived hyperthyroidism. During follow-up of individuals not taking T 4 therapy, the increased risk of mortality persisted compared with the background population.

This increase in risk compared with the background population was no longer evident during follow-up of individuals taking T 4 replacement. These findings may reflect the fact that development of overt hypothyroidism requiring T 4 therapy after radioiodine is the best indicator of effective cure of hyperthyroidism and is thus associated with the greatest likelihood of amelioration of the adverse effects of thyroid hormone excess on the vascular system.

Atrial fibrillation is considered one of the major risk factors for morbidity and mortality associated with hyperthyroidism. You can view a filtered list of clinical studies on hyperthyroidism that are open and recruiting at www.

You can expand or narrow the list to include clinical studies from industry, universities, and individuals; however, the NIH does not review these studies and cannot ensure they are safe.

Always talk with your health care provider before you participate in a clinical study. The NIDDK translates and disseminates research findings to increase knowledge and understanding about health and disease among patients, health professionals, and the public.

Hoang, D. How common is hyperthyroidism? Who is more likely to develop hyperthyroidism? Is hyperthyroidism during pregnancy a problem? What are the complications of hyperthyroidism? What are the symptoms of hyperthyroidism? What causes hyperthyroidism? How do doctors diagnose hyperthyroidism? How do doctors treat hyperthyroidism?

How does eating, diet, and nutrition affect hyperthyroidism? Clinical Trials for Hyperthyroidism What is hyperthyroidism? The thyroid is a small gland in your neck that makes thyroid hormones. About 1 out of Americans ages 12 years and older have hyperthyroidism. Be sure your hyperthyroidism is under control before becoming pregnant. Symptoms of hyperthyroidism can vary from person to person and may include 4 weight loss despite an increased appetite rapid or irregular heartbeat nervousness, irritability, trouble sleeping, fatigue shaky hands, muscle weakness sweating or trouble tolerating heat frequent bowel movements an enlargement in the neck, called a goiter In older adults, hyperthyroidism is sometimes mistaken for depression or dementia.

Overactive thyroid nodules Overactive thyroid nodules, or lumps in your thyroid, are common and usually not cancerous. Thyroiditis Thyroiditis is inflammation of your thyroid gland. The types of thyroiditis that can cause hyperthyroidism include subacute thyroiditis, which involves a painfully inflamed and enlarged thyroid. Your thyroid may be enlarged. Experts think painless thyroiditis is probably an autoimmune condition.

Too much iodine Your thyroid uses iodine to make thyroid hormone. Too much thyroid hormone medicine Some people who take thyroid hormone medicine for hypothyroidism may take too much.