|Year : 2017 | Volume
| Issue : 3 | Page : 491-492
Papillary thyroid cancer: Why the increase and what can be done?
Professor (Retired), Government Medical College, Kozhikode, Kerala, India
|Date of Web Publication||24-May-2018|
K P Aravindan
Professor (Retired), Government Medical College, Kozhikode, Kerala, India
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Aravindan K P. Papillary thyroid cancer: Why the increase and what can be done?. Indian J Cancer 2017;54:491-2
The article by Rao et al. in this issue of the journal highlights the clinicopathological profile of papillary thyroid cancer (PTC), the most common among thyroid malignancies. This tumor is important in that its incidence is increasing rapidly around the world. It is debatable whether the rise in incidence is due to increased detection of smaller clinically insignificant lesions or due to environmental factors. It could also be a combination of both. Kerala has the highest incidence of this tumor in India. As per the Trivandrum cancer registry, in 1982–1986, thyroid cancer was placed fifth in 35- to 64-year-old women, accounting for 2.5% of cancers. By 2007–2011 it had become the second most common cancer, accounting for 10.2%. In the 15–34-year age group, it has replaced breast cancer (19.4%) to take the first place (35.6%).
It has been argued that the increase in incidence is no mere diagnostic artifact because large tumors have also increased in number and that gender differences and birth cohort effects are present. In addition, thyroid cancer mortality has increased despite early diagnosis and better treatment.,
If there are environmental factors in play in global increase in thyroid cancer, what are they? Among the potential risk factors for thyroid cancers, three have shown a rising trend in the recent decades. They are medical diagnostic radiation, iodine intake, and thyroid autoimmunity.
| » Radiation and Papillary Thyroid Cancer|| |
The link between thyroid cancer and radiation is well-known. There was a large increase in PTC among the cohort of children exposed to radiation after the Chernobyl accident. Childhood exposure to diagnostic radiation has also increased in the past few decades, especially after the advent of computed tomography scan. It has been argued that this coincides with the rise in PTC incidence and that it could be a contributing factor. Guidelines to limit excessive use of diagnostic radiation exposure in children need to be widely implemented.
High background radiation from thorium containing sand was considered a risk factor for cancer in the coastal areas of southern Kerala and parts of China. Studies from both these areas show no such causative link in existence.
| » Thyroid Autoimmunity|| |
Thyroid autoimmunity and chronic lymphocytic thyroiditis have shown a concomitant rise along with PTC over the years. The possibility of autoimmune thyroiditis (AIT) as a predisposing factor for papillary thyroid carcinoma has been suggested. The lymphocytic infiltration in PTC could either be a risk factor for papillary carcinoma or it could be a reaction to the tumor. In a study of papillary carcinoma of the thyroid, the grade of thyroiditis in the area within 2 cm and away from 2 cm did not show significant difference, indicating that lymphocytic thyroiditis is probably not a local immune response to papillary cancer. This leaves the possibility that papillary carcinoma tends to develop in thyroids having lymphocytic thyroiditis.
| » Biological Link of Iodine and Thyroiditis|| |
Enhancement of autoimmunogenic properties of thyroglobulin was first demonstrated by Roitt and Cooke. Increased binding enhances stability of thyroglobulin and reduces its susceptibility to proteolytic cathepsins of thyroid, thus increasing auto-antigenicity. It was also found that T cells from humans with chronic lymphocytic thyroiditis proliferate in the presence of iodinated thyroglobulin. On adding iodine to drinking water, in non-obese diabetic NOD-H2 mice, the prevalence and severity of thyroid lesions increased markedly. It was also shown that iodine intake significantly affected the incidence of spontaneous lymphocytic thyroiditis in young genetically predisposed rats.
| » Dietary Iodine, Thyroid Autoimmunity, and Cancer|| |
It was observed that there was an increase in the prevalence of AIT with increasing iodide intake in China in cohorts from three regions with different levels of iodine intake. Similar findings were reported in small-scale comparative epidemiologic studies by Laurberg et al. and Sczaboles et al. High iodine intake may trigger and exacerbate AIT increasing the likelihood of overt hypothyroidism., The administration of iodized oil to patients with nontoxic goiter in an iodine-replete area was accompanied by the development of abnormal levels of thyroid autoantibodies and increase in thyroid lymphocytic infiltration.
| » Thyroiditis and Papillary Thyroid Cancer After Salt Iodization Programs|| |
Increase in AIT and PTC has been observed in many studies. In studies done over many phases of iodine prophylaxis, in Salta, Argentina, it was seen that increased iodine intake is associated with an increased incidence of PTC and AIT. A former iodine-deficient goiter endemic region in Austria during a period of 1984–2001 after the introduction of iodine prophylaxis (1991) noted increased incidence of thyroid carcinoma. A host of studies from China indicate increase in the two diseases after iodized salt was introduced.,, There are similar studies from Sri Lanka, Slovenia, and Iran.
Even in the post-iodization phase, goiter has persisted in India with a prevalence of 23% according to a country-wide study in 2003. The median urinary iodine excretion (UIE) in goitrous subjects (2–53 mmol/L) was significantly higher than in controls (2–24 mmol/L; P < 0.001). We now realize that there are factors other than iodine deficiency responsible for goiters in India.
It is increasingly becoming evident that diseases due to excess of iodine may be becoming a public health problem calling for a fresh calibration of strategy. It is suggested that although iodine supplementation should be implemented to prevent and treat iodine deficiency disorders, supplementation should be maintained at a safe level. Levels that are more than adequate (median UIE 200–299 μg/L) or excessive (median UIE >300 μg/L) do not appear to be safe, especially for susceptible populations. Supplementation programs should be tailored to each particular region. Generally, no iodine supplementation should be provided for regions in which iodine intake is sufficient, whereas salt in regions in which iodine intake is deficient should be supplemented with iodine according to the degree of iodine deficiency.
| » References|| |
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