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In medicine, hypothyroidism is "a syndrome that results from abnormally low secretion of thyroid hormones from the thyroid gland, leading to a decrease in basal metabolic rate. In its most severe form, there is accumulation of mucopolysaccharides in the skin and edema, known as myxedema."[1]

Thyroid stimulating hormone levels of less than 10 may not be important.[2]


Because the manifestations of hypothyroidism in the typical patient do no present the physician with a specific set of signs and symptoms, diagnosis of the disease usually requires laboratory tests.

Primary hypothyroidism

If the initiating pathological process greatly affects the thyroid gland as its primary target, the thyroid hormone, thyroxin (T4), will show abnormally low concentrations in blood, while the pituitary hormone, thyrotropin (TSH), which normally stimulates the thyroid gland to secrete thyroid hormones, shows abnormally high concentrations in the blood, due to lack of the normal physiological feedback inhibition of TSH secretion by T4. In a sense, the pituitary gland, through excess TSH secretion 'tries' to compensate for the the low blood T4 concentrations by excess stimulation of the diseased thyroid gland.

If the elevated TSH concentration can maintain a normal or near normal T4 concentration, the diagnosis is subclinical hypothyroidism.

Central hypothyroidism

in some cases of hypothyroidism, referred to as central hypothyroidism, the hypothalamus, which normally produces a hormone, thyrotropin-releasing hormone (TRH), that stimulates the pituitary gland to secrete TSH, is abnormal, in which case the laboratory results will show and abnormally low T4 concentration in the blood without an appropriate compensatory increase in TSH concentration. In other cases of so-called central hypothyroidism, the primary problem may reside in the pituitary gland itself, also giving on laboratory testing a low T4 concentration and an inappropriately high TSH concentration.


Symptoms may not be accurate.[3][4] The symptoms that may be distinguish between hypothyroid and normal patients are hoarse voice, dry skin, and muscle cramps.[4]


Canaris and colleagues studied more than 25,000 participants of a state health fair in Colorado, and reported the following:[5]

Results: The prevalence of elevated TSH levels (normal range, 0.3-5.1 mIU/L) in this population was 9.5%, and the prevalence of decreased TSH levels was 2.2%. Forty percent of patients taking thyroid medications had abnormal TSH levels. Lipid levels increased in a graded fashion as thyroid function declined. Also, the mean total cholesterol and low-density lipoprotein cholesterol levels of subjects with TSH values between 5.1 and 10 mIU/L were significantly greater than the corresponding mean lipid levels in euthyroid subjects. Symptoms were reported more often in hypothyroid vs euthyroid individuals, but individual symptom sensitivities were low.

Conclusions: The prevalence of abnormal biochemical thyroid function reported here is substantial and confirms previous reports in smaller populations. Among patients taking thyroid medication, only 60% were within the normal range of TSH. Modest elevations of TSH corresponded to changes in lipid levels that may affect cardiovascular health. Individual symptoms were not very sensitive, but patients who report multiple thyroid symptoms warrant serum thyroid testing. These results confirm that thyroid dysfunction is common, may often go undetected, and may be associated with adverse health outcomes that can be avoided by serum TSH measurement.

Causes of primary hypothyroidism


About thirty[6] to forty[3][7] percent of patients taking thyroid hormone replacement may not have appropriate values of thyroid stimulating hormone (TSH).

Taking replacement hormone at night may be better.[8]


  1. Anonymous (2023), Hypothyroidism (English). Medical Subject Headings. U.S. National Library of Medicine.
  2. Rodondi N, den Elzen WP, Bauer DC, Cappola AR, Razvi S, Walsh JP et al. (2010). "Subclinical hypothyroidism and the risk of coronary heart disease and mortality.". JAMA 304 (12): 1365-74. DOI:10.1001/jama.2010.1361. PMID 20858880. Research Blogging.
  3. 3.0 3.1 Canaris GJ, Manowitz NR, Mayor G, Ridgway EC (2000). "The Colorado thyroid disease prevalence study.". Arch Intern Med 160 (4): 526-34. PMID 10695693[e]
  4. 4.0 4.1 Canaris GJ, Steiner JF, Ridgway EC (1997). "Do traditional symptoms of hypothyroidism correlate with biochemical disease?". J Gen Intern Med 12 (9): 544-50. DOI:10.1046/j.1525-1497.1997.07109.x. PMID 9294788. PMC PMC1497160. Research Blogging.
  5. Canaris GJ, Manowitiz NR, Mayor G, Chester-Ridgeway E. (2003 The Colorado Thyroid Disease Prevalence Study. Arch Intern Med. 160:526-534.
  6. Ross DS, Daniels GH, Gouveia D (1990). "The use and limitations of a chemiluminescent thyrotropin assay as a single thyroid function test in an out-patient endocrine clinic.". J Clin Endocrinol Metab 71 (3): 764-9. PMID 2394778[e]
  7. Okosieme OE, Belludi G, Spittle K, Kadiyala R, Richards J (2011). "Adequacy of thyroid hormone replacement in a general population.". QJM 104 (5): 395-401. DOI:10.1093/qjmed/hcq222. PMID 21109503. Research Blogging.
  8. Bolk N, Visser TJ, Nijman J, Jongste IJ, Tijssen JG, Berghout A (2010). "Effects of evening vs morning levothyroxine intake: a randomized double-blind crossover trial.". Arch Intern Med 170 (22): 1996-2003. DOI:10.1001/archinternmed.2010.436. PMID 21149757. Research Blogging.