Hypothyroidism is not a chronic disease in Canada. Why not?

Thyroid disease is chronic, not cured

Why is hypothyroidism missing from Canada’s chronic diseases list?

The infographic copied above is not the official list.

Here is the current list of links on the Chronic Diseases page, under the jurisdiction of the Public Health Agency of Canada (PHAC):

  1. Arthritis
  2. Cancer
  3. Chronic Respiratory Diseases
  4. Dementia
  5. Diabetes
  6. Heart (Cardiovascular) Disease
  7. Inflammatory bowel disease (IBD)
  8. Mental Illness
  9. Neurological Conditions
  10. Osteoporosis

The exclusion of thyroid disease is a problem for thyroid patients and for our healthcare system.

  • Chronic diseases are often targeted for research funding.
  • Health Canada keeps statistics on official chronic diseases.

Because thyroid diseases are not on this list,

  • We currently have no idea how many people suffer from the various types and degrees of thyroid disease in all provinces and across Canada. Thyroid patients are invisible.
  • Errors in diagnosis and treatment that go beyond superficial TSH normalization are not being monitored by third parties who care for citizens’ well being and health outcomes.
  • Health care expenditures as a result of poorly treated thyroid diseases are not measured.
  • Thyroid disease and its treatments are rarely included in lists of comorbidities that influence the progression of another chronic disease.

Not every disease can be included on this list, but consider why some are and others aren’t. It’s a choice. It’s influenced by medical biases and trends in health care.

  • What makes a disease worthy of being on Canada’s list of chronic diseases?
  • What does it mean for citizens who have that disease to have their disease on that list?
  • What does it mean for doctors and researchers, or for society?

Is Canada’s omission due to the World Health Organization’s omission?

Canada often tends to follow the lead of more powerful countries and large organizations with high status. With a history of colonialism, we may tend to be deferential. Are we not thinking for ourselves?

Sub-pages of Canada’s chronic disease pages refer to the World Health Organization (WHO).

The WHO calls chronic diseases “noncommunicable diseases.” This is how they are defined on their website:

“Noncommunicable diseases (NCDs), also known as chronic diseases, tend to be of long duration and are the result of a combination of genetic, physiological, environmental and behavioural factors.

The main types of NCD are cardiovascular diseases (such as heart attacks and stroke), cancers, chronic respiratory diseases (such as chronic obstructive pulmonary disease and asthma) and diabetes.”

(WHO, “Noncommunicable diseases” page)

The 2014 report “Noncommunicable Diseases Global Monitoring Framework” includes these as targets for member states:

  • A 25% relative reduction in the overall mortality from cardiovascular diseases, cancer, diabetes, or chronic respiratory diseases
  • Halt the rise in diabetes and obesity

However, the word “thyroid” is nowhere in this 41-page report.

Search the WHO’s entire website, and thyroid disease rarely comes up. The WHO’s priorities may be taken as a reflection of its member states’ interests.

BUT Does it have to be a chronic disease on the WHO’s list to be on Canada’s list?

NO. Canada’s chronic disease list is far more comprehensive than the WHO’s. Canada adds arthritis and even inflammatory bowel disease.

Canadians can take the lead when tracking chronic diseases.

Does it always have to be chronic to be included?

Apparently not.

  • Some people do recover from hypertension if its cause can be removed or treated.
  • Many people do not require lifelong treatment for mood disorders or mental health problems.

Among the various types of thyroid disease, some are truly “chronic” while others are not.

  • Infectious thyroiditis is temporary, and some forms of postpartum thyroiditis are temporary.
  • Some patients with autoimmune Graves’ hyperthyroidism can permanently go into remission after a year of anti-thyroid treatment.
  • When thyroid cancer is treated, the “cancer” part of the problem may be removed and controlled.

However, once a hyperthyroid person or thyroid cancer patient permanently loses enough thyroid gland function to require lifelong treatment, they now technically have a chronic disease.

What makes a chronic disease eligible to be on this list?

Does it have to be a public health crisis of increasing prevalence? We might be in crisis if someone kept stats on its rising prevalence in Canada. Thyroid disease rates are rising in other parts of the world that do keep stats. We are ignorant.

Does it have a significant amount of people? We are just as numerous and possibly more numerous as many who have diseases on this list. How many are being prescribed more than 25 mcg of thyroid hormones per day?

The problem is that incidence rates may be tracked for one high-status type of thyroid disease (thyroid cancers) and not others presumed to be rare (atrophic thyroiditis or central hypothyroidism).

Is hypothyroidism not chronic enough or not disease-ish enough?

Boy do patients have something to say on that matter. Myths to dispel. Does our condition not cause a reduction in quality of life and ability to function even when it is treated well?

Are some of us actually “disabled” by our thyroid disorder, unable to work? Yes, absolutely. But endocrinology organizations will prefer to blame other chronic diseases, especially mental illness, for the sake of defending our untreated, normal TSH — or our TSH-normalized therapy.

Is our omission partly caused by obsession with our normalized TSH?

Perhaps endocrinologists have told people we no longer have hypothyroidism when TSH is normalized, or when TSH is normal and FT4 is not low. We are no longer “hypothyroid” by the TSH-based definitions. Our condition has been erased. We are now supposedly “well managed.”

However, this is not more to boast about than saying that diabetes can be controlled, heart disease biomarkers can be lowered, and cancer deaths can be delayed.

Every chronic disease has its trendy treatment targets, and many may meet them. Nobody boasts that diabetes, heart disease, or cancer are now crossed off the list of chronic diseases.

No one should ever dare to claim that medicine has conquered thyroid disease by means of a simple recipe of TSH-normalized T4 therapy if they haven’t yet asked about the decades of experience of patients who had to flee from this recipe to save their own lives.

Why is it that so many find relief from symptoms and improved health by means of old-fashioned T3-inclusive therapies that do not make TSH their tyrant? When a marriage breaks down, do you prefer to blame the victim rather than the abuser? What happens when the abuser is your favorite child?

Chronic disease lists ensure that vulnerable people are identified and protected by society.

Thyroid patients should not be left to the mercy of medical specialists or primary care physicians or pharmaceutical companies whose interests are served by declaring us well treated when we aren’t.

Governments have to monitor and oversee those endocrinologists and question the objectivity of science that conveniently reinforces treatment guidelines.

If endocrinologists truly cared for the fate of all thyroid patients, they would have fought for thyroid disease’s status as a chronic disease. They wouldn’t have been satisfied with average treatment effect and mere statistical significance. They would have sought out the statistical outliers, the patients falling through the cracks of thyroid treatment guidelines, especially those thyroid patients whose diabetes, heart diseases, or cancer were not doing so well while FT3 fell into the low end of reference. They would have pointed at for people who weren’t recruited for clinical trials because their health was too poor or TSH too unmanageable to meet inclusion criteria and said — “Thyroid disease isn’t conquered yet.”

Protecting vulnerable patients is not accomplished by a long series of kangaroo clinical trials comparing standard LT4 therapy to a single T4-T3 combination recipe, carelessly normalizing both therapies to anywhere in TSH reference range, finding neither superior or inferior to the other based on statistical averages, and then declaring standard therapy the victor because of its familiarity. Such designs are uninterested in discovering subgroups at risk under each therapy.

How many clinical trials compare two thyroid therapies under the conditions of physiological stress or acute distress?

Why is it that no matter what thyroid therapy works when things are going well, something beyond medical control can still destabilize treatment?

People who have lost a vital gland’s function, like a thyroid’s secretion of T4 and T3, or a pancreas’s secretion of insulin, are vulnerable.

Even if we have perfectly optimized pharmaceutical support, including T3-inclusive therapies, our thyroid hormone metabolism is rigidly controlled by medication, an artificial and static daily dose, not a living, adjusting gland.

Therefore, we cannot adapt as easily to insults that will inevitably cause thyroid hormone shifts — such as

  • cold climate,
  • pregnancy,
  • menopause,
  • diabetes and insulin resistance, and
  • estrogen dysregulation.

To the degree that some still depend on partial thyroid gland function, we are also at the mercy of environmental toxins (endocrine disruptors) like fluoride that can interfere with thyroid hormone synthesis.

As for our lifelong disease progression, autoimmune thyroid disease does not stop progressing or shifting for the rest of our lives.

As I’ve said before, we may have had a thyroidectomy, but there’s no such thing as an antibody-ectomy, and thyroid antibodies continue to cause thyroid damage. Those of us with autoimmune hypothyroidism do continue to lose thyroid gland tissue over the course of our lives.

TSH-receptor antibodies, even after a total thyroidectomy, can cause serious metabolic distortions and TSH distortions.

  • In Hashimoto’s, high TPO-antibody flares are associated with more severe symptoms throughout the body.
  • In Graves’ disease, the TSH receptor antibodies can cause thyroid eye disease (TED, Graves’ ophthalmopathy) even after the thyroid gland is gone.
  • TSH receptor antibodies can interfere with TSH-receptor co-regulation of pituitary TSH secretion via the “ultrashort feedback loop.” This causes incorrect management of hypothyroidism when TSH is incorrectly high or low due to pituitary interference.

Does a chronic disease qualify for its status by putting life at risk? Thyroid disease qualifies.

Look up the consequences of severe hypothyroidism, or myxedema coma, which has high death rates, and can even occur during poorly monitored thyroid treatment.

But since the published incidence rates of myxedema coma are low, consider next the medical tragedy of non-recovery from “non-thyroidal illness” or “low T3 syndrome.”

As chronic hypothyroid people, we may not be able to recover from a car accident or massive burn injuries or kidney failure if our T3 drops low and all we’re given in hospital is T4.

T4 hormone won’t convert to T3 sufficiently when the D3 enzyme is upregulated by organs and tissues in severe crisis. In the early phases of low T3 syndrome, the body lowers the metabolic rate by dumping T3. At a certain point, the loss of T3 becomes pathological, and people do die, not necessarily from the severity of acute, short-term T3 loss, but the inability to mount a timely T3 recovery.

During critical illness, low T3 is often the strongest predictor of death, not obesity, not smoking status, not diabetes status, and not age. Low T3 often equal in predictive power to cardiovascular risk scores, but Low T3 is easier to measure.

We don’t always recover naturally. Natural recovery occurs by means of a swift escalation of TSH stimulation of a healthy thyroid. If we had even a fragment of a living thyroid gland that could be stimulated to produce T3, we could recover T3 with the aid of this natural TSH-driven T3 engine. But many of us can’t obtain TSH-stimulated T3 secretion to aid recovery. We recover only insofar as our treatment and our metabolic ability enables us to recover.

Some of us suffer low T3 chronically BEFORE we become ill, and it becomes LOWER when we are ill.

It is mind-boggling but true that few scientists have bothered to research how often we die from non-thyroidal illness due to inability to recover T3 during thyroid treatment: Treated thyroid patients are excluded from almost all of studies of nonthryoidal illness syndrome.

Why? Because we take thyroid hormone and we are blindly assumed to be ok when our TSH is normal.

But deaths due to low T3 also occur in thyroid-healthy populations when TSH is normal. The normal or low TSH is part of the definition of Low T3 syndrome.

Normal TSH prevents no one from dying of failure to recover from a low T3.

The science on NTIS recovery via TSH-stimulated T3 would leave a lot of room to hypothesize that no, people with little to no thyroidal T3 secretion ability are vulnerable to death — or extended recovery, which is a cost burden.

Are there any downsides to having hypothyroidism listed here as a chronic disease?

Yes, potentially. Here is a challenge of being on the list. It’s a minor annoyance compared to the “chronic ignorance” I’ve just outlined.

Chronic diseases are often seen as largely preventable with public health campaigns on lifestyle and diet.

The chronic diseases section of the Government of Canada is under the jurisdiction of public health, whose portfolio includes prevention, not just management.

Few types of thyroid diseases are preventable.

Mistaking thyroid disease as largely preventable would be one undesirable side-effect of being included in a list side by side with Type 2 diabetes, which often carries the unfortunate stigma of being partly caused by the patient.

Although diet and lifestyle interventions do affect both antibodies and hormone metabolism, and they can always help to tweak and minimize the harms of poor pharmaceutical treatment of hypothyroidism, diet and lifestyle interventions CANNOT cure dead or missing thyroid gland tissue. To believe otherwise is to be unscientific and believe in magic.

But being non-preventable should not disqualify thyroid disease from being included in the list.

A large part of the portfolio of Public Health includes disease prevention. But no one thinks all cancers, all heart diseases, or all types of arthritis are preventable.

Type 1 diabetes is, like permanent primary or secondary hypothyroidism, a disease that cannot be prevented or cured by diet and lifestyle alone.

Like diabetes, individualized pharmaceutical intervention, based on appropriate testing and ongoing medical education, is the foundation of our lifelong chronic disease management.

This is something that the Diabetes community likely continues to struggle with — the lack of public understanding of the distinction between type 1 and type 2.

Severely and permanently hypothyroid citizens are just as dependent on medication as a Type 1 diabetic is. An essential organ has failed and it’s not the patient’s fault. Just like a Type 1 diabetic, our medication does not cure us. We remain at the mercy of pharmaceutical intervention for the rest of our lives, and our medication is too often maladjusted to our body’s needs.

Canadian health policy is wrong to overlook thyroid disease.

Advocacy on this front is something we want to pursue as we develop our campaign into a registered nonprofit organization, and then into a patient-led charity.

For thyroid therapy to advance and protect all vulnerable citizens, we do need the support of chronic disease status.

YES, Hypothyroidism is a chronic disease, just as much as any of those listed.

We are not cured.

Our disease is often poorly managed by TSH alone, and this renders our medical system blind and neglectful:

  • Blind to thyroid metabolic problems causing some people severely reduced T4-T3 conversion beyond the hypothalamus and pituitary during standard LT4 therapy, which is easy to identify with a chronically low FT3:FT4 ratio.
  • Blind to acquired central hypothyroidism (pituitary TSH secretion dysfunction) that may occur during treatment, which makes a policy of TSH normalization cause chronic underdose in the undiagnosed treated patient with central hypo,
  • Blind to the impact of Graves’ disease TSH-receptor antibody flares and TSH receptor-blocking antibodies on manipulating TSH levels and causing fluctuations during hypothyroid therapy,
  • Blind to the fact that functional thyroid nodules (5-10% of thyroid nodules) can destabilize thyroid hormone metabolism even when TSH is in range,
  • Blind to T3 hormone loss during severe winters in Canada, when significant losses are seen in treated thyroid patients in Sicily,
  • Neglectful of the impact of thyroid antibodies on the progression of thyroid damage in Hashimoto’s or thyroid atrophy in Atrophic Thyroiditis, making an increased T4 dosage the only response, while the benefits of having TSH stimulation of a partly functional thyroid gland are progressively lost.
  • Neglectful of the effects on our thyroid hormone dosing and metabolism caused by other chronic illnesses and their treatments — such as diabetes, heart disease, kidney and liver disease and gastrointestinal dysfunction, and
  • Neglectful of treated patients’ risk of death and increased length of recovery from low T3 induced by acute nonthyroidal illness syndrome (NTIS), especially in people with no thyroid function or pituitary dysfunction. Treated patients are routinely excluded from studies of NTIS and its treatment.

Let’s do it better. Protect citizens with thyroid disease and hold endocrinologists accountable for working harder to defend every patient’s individual life, health, and well being.

Further information from the government

Canada: A-Z Chronic Diseases (list)

Canada: Chronic Diseases

Canada: Chronic Disease Data and Indicators (research, stats)


In several sections


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Bunevicius, R., Velickiene, D., & Prange, A. J. (2005). Mood and anxiety disorders in women with treated hyperthyroidism and ophthalmopathy caused by Graves’ disease. General Hospital Psychiatry, 27(2), 133–139. https://doi.org/10.1016/j.genhosppsych.2004.10.002

Chung, Y. J., Lee, B. W., Kim, J.-Y., Jung, J. H., Min, Y.-K., Lee, M.-S., … Chung, J. H. (2006). Continued suppression of serum TSH level may be attributed to TSH receptor antibody activity as well as the severity of thyrotoxicosis and the time to recovery of thyroid hormone in treated euthyroid Graves’ patients. Thyroid: Official Journal of the American Thyroid Association, 16(12), 1251–1257. https://doi.org/10.1089/thy.2006.16.1251

Han, Y., Mao, L.-J., Ge, X., Huang, K., Yan, S.-Q., Ren, L.-L., … Tao, F.-B. (2018). Thyroid autoantibodies in pregnancy are associated with hypertensive disorders of pregnancy: Ma’anshan Birth Cohort Study. Clinical Endocrinology, 88(6), 928–935. https://doi.org/10.1111/cen.13590

Khoo, D. H., Eng, P. H., Ho, S. C., Tai, E. S., Morgenthaler, N. G., Seah, L. L., … Aw, S. E. (2000). Graves’ ophthalmopathy in the absence of elevated free thyroxine and triiodothyronine levels: prevalence, natural history, and thyrotropin receptor antibody levels. Thyroid: Official Journal of the American Thyroid Association, 10(12), 1093–1100. https://doi.org/10.1089/thy.2000.10.1093

Polovina, S. P., Miljic, D., Zivojinovic, S., Milic, N., Micic, D., & Popovic Brkic, V. (2017). The impact of thyroid autoimmunity (TPOAb) on bone density and fracture risk in postmenopausal women. Hormones (Athens, Greece), 16(1), 54–61. https://doi.org/10.14310/horm.2002.1719


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Ataoğlu, H. E., Ahbab, S., Serez, M. K., Yamak, M., Kayaş, D., Canbaz, E. T., … Yenigün, M. (2018a). Prognostic significance of high free T4 and low free T3 levels in non-thyroidal illness syndrome. European Journal of Internal Medicine, 57, 91–95. https://doi.org/10.1016/j.ejim.2018.07.018

Bertoli, A., Valentini, A., Cianfarani, M. A., Gasbarra, E., Tarantino, U., & Federici, M. (2017). Low FT3: a possible marker of frailty in the elderly. Clinical Interventions in Aging, 12, 335–341. https://doi.org/10.2147/CIA.S125934

Brent, G. A., & Hershman, J. M. (1986). Thyroxine therapy in patients with severe nonthyroidal illnesses and low serum thyroxine concentration. The Journal of Clinical Endocrinology and Metabolism, 63(1), 1–8. https://doi.org/10.1210/jcem-63-1-1

  • Quote from abstract: “T4 therapy was not beneficial in this population of intensive care unit patients, and by inhibiting TSH secretion, it may suppress an important mechanism for normalization of thyroid function during recovery.”

Bunevicius, A., Iervasi, G., & Bunevicius, R. (2015). Neuroprotective actions of thyroid hormones and low-T3 syndrome as a biomarker in acute cerebrovascular disorders. Expert Review of Neurotherapeutics, 15(3), 315–326. https://doi.org/10.1586/14737175.2015.1013465

Bunevičius, R. (2009). Low Triiodothyronine Syndrome and Depression in Patients with Chronic Heart Failure. In G. Iervasi & A. Pingitore (Eds.), Thyroid and Heart Failure (pp. 203–212). Retrieved from http://www.springerlink.com/index/10.1007/978-88-470-1143-4_18

Cerillo, A. G., Storti, S., Kallushi, E., & Haxhiademi, D. (2014). The low triiodothyronine syndrome: a strong predictor of low cardiac output and death in patients undergoing coronary artery bypass grafting. The Annals of Thoracic Surgery, 97(6), 2089.

Fragidis, S., Sombolos, K., Thodis, E., Panagoutsos, S., Mourvati, E., Pikilidou, M., … Vargemezis, V. (2015). Low T3 syndrome and long-term mortality in chronic hemodialysis patients. World Journal of Nephrology, 4(3), 415–422. https://doi.org/10.5527/wjn.v4.i3.415

Gangemi, E. N., Garino, F., Berchialla, P., & Martinese, M. (2008). Low triiodothyronine serum levels as a predictor of poor prognosis in burn patients. Burns, 34(6), 817–824. https://doi.org/10.1016/j.burns.2007.10.002

Gao, R., Chen, R.-Z., Xia, Y., Liang, J.-H., Wang, L., Zhu, H.-Y., … Xu, W. (2018). Low T3 syndrome as a predictor of poor prognosis in chronic lymphocytic leukemia. International Journal of Cancer, 143(3), 466–477. https://doi.org/10.1002/ijc.31327

Gao, R., Liang, J.-H., Wang, L., Zhu, H.-Y., Wu, W., Wu, J.-Z., … Xu, W. (2017). Low T3 syndrome is a strong prognostic predictor in diffuse large B cell lymphoma. British Journal of Haematology, 177(1), 95–105. https://doi.org/10.1111/bjh.14528

Horácek, J., Sulková, S. D., Kubisová, M., & Safránek, R. (2012). Thyroid Hormone Abnormalities in Hemodialyzed Patients: Low Triiodothyronine As Well As High Reverse Triiodothyronine Are Associated With Increased Mortality. Physiological Research, 61(5), 495.

Iervasi, G., Pingitore, A., Landi, P., & Raciti, M. (2003). Low-T3 syndrome: a strong prognostic predictor of death in patients with heart disease. Circulation, 107(5), 708.

Iglesias, P., Muñoz, A., Prado, F., Guerrero, M. T., Macías, M. C., Ridruejo, E., … Díez, J. J. (2010). Serum thyrotropin concentration is an early marker of normalization of low triiodothyronine syndrome in aged hospitalized patients after discharge. Journal of Endocrinological Investigation, 33(9), 607–611. https://doi.org/10.1007/BF03346657

Katzeff, H. L., Powell, S. R., & Ojamaa, K. (1997). Alterations in cardiac contractility and gene expression during low-T3 syndrome: prevention with T3. The American Journal of Physiology, 273(5 Pt 1), E951-956.

Kohno, A., & Hara, Y. (2001). Severe Myocardial lschemia following Hormone Replacement in Two Cases of Hypothyroidism with Normal Coronary Arteriogram. Endocrine Journal, 48(5), 565–572. Retrieved from https://www.jstage.jst.go.jp/article/endocrj1993/48/5/48_5_565/_pdf

  • Abstract is worth quoting:  Two cases of hypothyroidism with cardiac attack (acute myocardial infarction, AMI) following thyroxine [T4] replacement were reported. Neither of these cases showed any major coronary artery disease. The first case was a 58 year-old male who was treated with L-thyroxine (initial dose 0.025 mg/day) for hypothyroidism due to Hashimoto’s disease. The dose was increased up to 0.1 mg/day within 2 weeks. Acute myocardial infarction occurred 6 weeks after the replacement was started. Angiographical study showed no notable pathological change in major coronary arteries, but echocardiography demonstrated diffuse hypokinesis of the left ventricular wall. The second case was a 61-year-old female who suffered from Graves’ disease and had been treated with thiamazole (2.5 mg/day) for 15 years. Later, she became hypothyroid and was treated with thyroxine. At first, 0.05 mg/day of L-thyroxine was given, and then the dose was increased up to 0.1 mg/day after the 7th week. Acute myocardial infarction occurred 3 weeks after the dose was increased. Angiographic study of the coronary arteries revealed no abnormality. Possible causes of AMI in thyroxine replacement were discussed in relation to vascular spasm and small vessel disease of the heart. Importance of echocardiographic study before hormone replacement therapy is stressed, particularly for middle/old-aged patients with long-term hypothyroidism.

Kumar, K. V. S. H., Kapoor, U., Kalia, R., Chandra, N. S. A., Singh, P., & Nangia, R. (2013). Low triiodothyronine predicts mortality in critically ill patients. Indian Journal of Endocrinology and Metabolism, 17(2), 285–288. https://doi.org/10.4103/2230-8210.109715

Lee, Y.-M., Ki, Y.-J., Choi, D.-H., & Kim, B.-B. (2015). Value of Low Triiodothyronine and Subclinical Myocardial Injury for Clinical Outcomes in Chest Pain. The American Journal of the Medical Sciences, 350(5), 393.

Lin, C., Lin, K., Guo, Y., You, Z., Zheng, W., Lin, F., … Zhu, P. (2019). Low free triiodothyronine is associated with contrast-induced acute kidney injury and long-term outcome in elderly patients who underwent percutaneous coronary intervention. Anatolian Journal of Cardiology, 21(2), 60–67. https://doi.org/10.14744/AnatolJCardiol.2018.38228

Liu, Jinliang, Wu, X., Lu, F., Zhao, L., Shi, L., & Xu, F. (2016). Low T3 syndrome is a strong predictor of poor outcomes in patients with community-acquired pneumonia. Scientific Reports, 6. https://doi.org/10.1038/srep22271

Meyer, S., Schuetz, P., Wieland, M., & Nusbaumer, C. (2011). Low triiodothyronine syndrome: a prognostic marker for outcome in sepsis? Endocrine, 39(2), 167–174. https://doi.org/10.1007/s12020-010-9431-4

Pingitore, A., Galli, E., Barison, A., & Iervasi, A. (2008). Acute effects of triiodothyronine (T3) replacement therapy in patients with chronic heart failure and low-T3 syndrome: a randomized, placebo-controlled study. The Journal of Clinical Endocrinology and Metabolism, 93(4), 1351.

Pingitore, A., Landi, P., Taddei, M. C., & Ripoli, A. (2005). Triiodothyronine levels for risk stratification of patients with chronic heart failure. The American Journal of Medicine, 118(2), 132–136. https://doi.org/10.1016/j.amjmed.2004.07.052

Preoperative low tri-iodothyronine concentration is associated with worse health status and shorter five year survival of primary brain tumor patients – Semantic Scholar. (n.d.). Retrieved June 12, 2018, from /paper/Preoperative-low-tri-iodothyronine-concentration-is-Bunevicius-Deltuva/49b81aa04281dbebcb6e1497581b91352da0eb89

Qiu, M., Fang, M., & Liu, X. (2017). Low free triiodothyronine levels predict symptomatic intracranial hemorrhage and worse short-term outcome of thrombolysis in patients with acute ischemia stroke. Medicine, 96(45). https://doi.org/10.1097/MD.0000000000008539

Rhee, C. M., Brent, G. A., Kovesdy, C. P., Soldin, O. P., Nguyen, D., Budoff, M. J., … Kalantar-Zadeh, K. (2015). Thyroid functional disease: an under-recognized cardiovascular risk factor in kidney disease patients. Nephrology Dialysis Transplantation, 30(5), 724–737. https://doi.org/10.1093/ndt/gfu024

Ruiz-Núñez, B., Tarasse, R., Vogelaar, E. F., Dijck-Brouwer, J., A, D., & Muskiet, F. A. J. (2018). Higher Prevalence of “Low T3 Syndrome” in Patients With Chronic Fatigue Syndrome: A Case–Control Study. Frontiers in Endocrinology, 9. https://doi.org/10.3389/fendo.2018.00097

Sato, Y., Yoshihisa, A., Kimishima, Y., Kiko, T., Kanno, Y., Yokokawa, T., … Takeishi, Y. (2019). Low T3 Syndrome Is Associated With High Mortality in Hospitalized Patients With Heart Failure. Journal of Cardiac Failure, 25(3), 195–203. https://doi.org/10.1016/j.cardfail.2019.01.007

Su, Wen, Zhao, X.-Q., Wang, M., Chen, H., & Li, H.-W. (2018). Low T3 syndrome improves risk prediction of in-hospital cardiovascular death in patients with acute myocardial infarction. Journal of Cardiology, 72(3), 215–219. https://doi.org/10.1016/j.jjcc.2018.02.013

Suda, S., Shimoyama, T., Nagai, K., Arakawa, M., Aoki, J., Kanamaru, T., … Kimura, K. (2018). Low Free Triiodothyronine Predicts 3-Month Poor Outcome After Acute Stroke. Journal of Stroke and Cerebrovascular Diseases: The Official Journal of National Stroke Association, 27(10), 2804–2809. https://doi.org/10.1016/j.jstrokecerebrovasdis.2018.06.009

Yazıcı, S., Kırış, T., Ceylan, U. S., Terzi, S., Erdem, A., Atasoy, I., … Yeşilçimen, K. (2017a). Relation of Low T3 to One-Year Mortality in Non-ST-Elevation Acute Coronary Syndrome Patients. Journal of Clinical Laboratory Analysis, 31(2). https://doi.org/10.1002/jcla.22036


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Gullo, D., Latina, A., Frasca, F., Squatrito, S., Belfiore, A., & Vigneri, R. (2017). Seasonal variations in TSH serum levels in athyreotic patients under L-thyroxine replacement monotherapy. Clinical Endocrinology, 87(2), 207–215. https://doi.org/10.1111/cen.13351

Han, Y., Mao, L.-J., Ge, X., Huang, K., Yan, S.-Q., Ren, L.-L., … Tao, F.-B. (2018). Thyroid autoantibodies in pregnancy are associated with hypertensive disorders of pregnancy: Ma’anshan Birth Cohort Study. Clinical Endocrinology, 88(6), 928–935. https://doi.org/10.1111/cen.13590

Karakosta, P., Alegakis, D., Georgiou, V., Roumeliotaki, T., Fthenou, E., Vassilaki, M., … Chatzi, L. (2012). Thyroid Dysfunction and Autoantibodies in Early Pregnancy Are Associated with Increased Risk of Gestational Diabetes and Adverse Birth Outcomes. The Journal of Clinical Endocrinology & Metabolism, 97(12), 4464–4472. https://doi.org/10.1210/jc.2012-2540

Li, Jia, Shen, J., & Qin, L. (2017). Effects of Levothyroxine on Pregnancy Outcomes in Women With Thyroid Dysfunction: A Meta-analysis of Randomized Controlled Trials. Alternative Therapies in Health and Medicine, 23(2), 49–58.

Nazarpour, S., Tehrani, F. R., Simbar, M., Tohidi, M., Majd, H. A., & Azizi, F. (2017). Effects of levothyroxine treatment on pregnancy outcomes in pregnant women with autoimmune thyroid disease. European Journal of Endocrinology, 176(2), 253–265. https://doi.org/10.1530/EJE-16-0548

Resetkova, E., Notenboom, R., Arreaza, G., Mukuta, T., Yoshikawa, N., & Volpé, R. (1994). Seroreactivity to Bacterial Antigens Is Not a Unique Phenomenon in Patients with Autoimmune Thyroid Diseases in Canada. Thyroid, 4(3), 269–274. https://doi.org/10.1089/thy.1994.4.269

Schoutens, A., Laurent, E., Markowicz, E., & Lisart, J. (1991). Serum triiodothyronine, bone turnover, and bone mass changes in euthyroid pre- and postmenopausal women. Calcified Tissue International, 49(2), 95.

Franklyn, J. a., Betteridge, J., Holder, R., & Sheppard, M. c. (1995). Effect of Estrogen Replacement Therapy upon Bone Mineral Density in Thyroxine-Treated Postmenopausal Women with a Past History of Thyrotoxicosis. Thyroid, 5(5), 359–363. https://doi.org/10.1089/thy.1995.5.359

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Categories: Health Canada, Health care system

1 reply

  1. i didnt read the whole article but technically the definition of chronic is “life-long / lasted more than 3 months, and usually isn’t cured”… and the types of thyroid stuff i see being listed in the article exclude congenital hypothyroidism,,? how so?

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