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 Table of Contents  
ORIGINAL ARTICLE
Year : 2016  |  Volume : 3  |  Issue : 3  |  Page : 203-206

Incidentally detected thyrotoxicosis-etiology and natural course: A study from Central Kerala


1 Department of Endocrinology, Pushpagiri Institute of Medical Sciences, Thiruvalla, India
2 Department of Nuclear Medicine, Bharath Hospital, Kottayam, Kerala, India
3 Department of Medicine, Pushpagiri Institute of Medical Sciences, Thiruvalla, India

Date of Web Publication9-Jun-2016

Correspondence Address:
Rajeev Philip
Department of Endocrinology, Pushpagiri Institute of Medical Sciences, Thiruvalla, Kerala
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2348-3334.183742

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  Abstract 

Context: Thyrotoxicosis is a common clinical problem, and the most common cause of thyrotoxicosis is Graves' disease and is 4 times more common than the other causes combined. Of late, the number of people incidentally detected to have biochemical thyrotoxicosis is increasing, and most patients are detected during health checkups, pregnancy planning, and surgical fitness. There are no data on the etiology and natural course of such cases and no guidelines for evaluation of such patients. Aims: The aim of this study is to evaluate the cause of thyrotoxicosis in patients incidentally detected to have biochemical thyrotoxicosis and to study the natural course of illness of these patients. Subjects and Methods: All patients who were incidentally detected to have biochemical thyrotoxicosis (during health checkups, pregnancy planning, and surgical fitness) were included and studied. Patients who had symptoms of thyrotoxicosis, or patients in whom thyrotoxicosis was suspected by the treating doctor were excluded from the study. All patients underwent an ultrasound thyroid and thyroid scan, and treatment was decided based on the results. All patients were followed up for a minimum period of 3 months. Results: A total of 57 patients were studied. The average age of the study population was 32.8 years, with male:female ratio of 1:3.3. Of 57 patients, 52 (91%) had subacute thyroiditis as the cause of thyrotoxicosis while Graves' disease was seen in 9%. None had toxic adenoma or toxic multinodular goiter. In the patients with subacute thyroiditis, 47 became euthyroid and 5 became subclinically hypothyroid (Stage b). Conclusions: The majority of patients with incidentally detected thyrotoxicosis had thyroiditis as the cause, which reverted to euthyroid state in most of the cases. Based on the study, it seems prudent to wait and follow up this group of patients rather than start antithyroid drugs, especially if facilities for uptake scan are not available or affordable.

Keywords: Graves′ disease, subacute thyroiditis, thyrotoxicosis, uptake scan


How to cite this article:
Philip R, Sivaraman Nair SA, Kuruvilla V, John SM, Amal D, Sankaran KC. Incidentally detected thyrotoxicosis-etiology and natural course: A study from Central Kerala. CHRISMED J Health Res 2016;3:203-6

How to cite this URL:
Philip R, Sivaraman Nair SA, Kuruvilla V, John SM, Amal D, Sankaran KC. Incidentally detected thyrotoxicosis-etiology and natural course: A study from Central Kerala. CHRISMED J Health Res [serial online] 2016 [cited 2019 Jul 22];3:203-6. Available from: http://www.cjhr.org/text.asp?2016/3/3/203/183742


  Introduction Top


Thyrotoxicois is a common clinical problem and is defined biochemically as low thyroid-stimulating hormone (TSH) in the presence of an elevated T3 or T4 or both. As per the thyroid epidemiological study, the prevalence of thyrotoxicosis is around 2% in India and includes both subclinical and overt thyrotoxicosis. [1]

As the awareness about thyroid diseases increases, thyroid function tests are done as part of health checkups or pregnancy planning. A lot of these tests turn out to be abnormal, with a percentage being thyrotoxic, and get referred for further evaluation. The American Thyroid Society (ATS) guidelines recommend a period of waiting before starting treatment for subclinically toxic patients, but there are no clear guidelines on evaluation of incidentally detected thyrotoxicosis. [2] Also, the etiology of incidentally detected thyrotoxicosis and its natural progression is not clear. This study aims to look into the causes and natural progression of incidentally detected thyrotoxicosis.

Aims and objectives

  • To evaluate the cause of thyrotoxicosis in patients incidentally detected to have biochemical thyrotoxicosis
  • To study the natural course of illness of these patients.



  Subjects and methods Top


All patients who were incidentally detected to have biochemical thyrotoxicosis and referred for evaluation to the Departments of Endocrinology and Medicine of Pushpagiri Institute of Medical Sciences, Thiruvalla, Kerala, were studied. This included patients detected during health checkups, pregnancy planning, preoperative evaluation for a nonthyroidal surgery, etc. The study period was from February 2014 to January 2015 (1 year).

Inclusion criteria

  • Patients with low TSH levels along with elevated T3 or T4 or both were included in the study.


Exclusion criteria

  • Patients who had symptoms of thyrotoxicosis
  • Patients in whom thyrotoxicosis was suspected by the treating doctor
  • Patients with history of thyroid disease or on treatment for thyroid disease
  • Patients who had pain and tenderness over the thyroid
  • Patients who were pregnant or in the postpartum period
  • Patients with subclinical hyperthyroidism.


Study design and procedure

This was a prospective study. All patients referred for evaluation of thyrotoxicosis, who satisfied the inclusion criteria underwent a thyroid uptake scan to look for the cause of thyrotoxicosis. Also an ultrasound thyroid was done in all patients to look for nodules. A diagnosis of Graves' disease was made if the uptake scan showed increased uptake which was homogenous. If ultrasound thyroid showed nodules and if uptake scan showed patchy increase in uptake, the diagnosis of toxic multinodular goiter (MNG) was made. If the uptake was low, the diagnosis of subacute thyroiditis was made. Thyroid peroxidase antibodies (TPO) were estimated in all patients to look for underlying autoimmunity and Hashitoxicosis. Patients received treatment based on the results. All patients were followed up for a minimum period of 3 months. A free T3, free T4, and TSH were repeated at 6 weeks and 3 months to look at the progression of the disease.


  Results Top


A total of 57 patients were studied. There was a significant female predominance, with 44 females (77.1%). The mean age was 32.8 years (range 21-69). Baseline demographic characters are listed in [Table 1]. The reason for checking thyroid functions varied, with maximum number of cases picked up from health checkups (45.6%). About 23.6% of cases were found when thyroid functions were evaluated as part of preoperative investigations. Around 5.2% of patients were found to have biochemical thyrotoxicosis during thyroid screening camps [Table 2].
Table 1: Demographic characteristics (n=57)

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Table 2: Reasons for checking thyroid functions

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All patients included in this study had significant thyrotoxicosis, with a mean TSH value of 0.06 μIU/mL (0.5-4.70). The mean free T4 value was 2.68 ng/dL (0.8-1.8), and the mean free T3 value was 4.8 pg/mL (2.3-4.2). Forty-one (71.9%) patients had elevated free T3 and free T4, 15 (26.3%) patients had elevated free T4 only, and one patient had isolated elevation of free T3. Anti-TPO was positive in 31.5% of the patients. Thyroid ultrasound was suggestive of thyroiditis in 37 patients (59.6%). Thyroid ultrasound was reported as normal in 5 (8.7%) patients whereas ultrasound was suggestive of MNG in 4 patients (7.1%). A single nodule of more than 1 cm was found in 11 patients (19.2%) [Table 3].
Table 3: Laboratory data

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As far as the etiology of thyrotoxicosis was concerned, majority of the patients had a decreased technetium uptake of the thyroid gland suggestive of subacute thyroiditis. Of the 57 patients studied, 52 (91.2%) had subacute thyroiditis. Only 5 patients (8.8%) had increased uptake on the thyroid scan, and all had homogenous uptake suggestive of Graves' disease. None of the patients had hyperfunctioning nodules as the cause of thyrotoxicosis [Figure 1].

Follow-up of patients who were diagnosed to have subacute thyroiditis was done and TFTs were done at 6 weeks and 3 months. Of the 52 patients who were diagnosed to have subacute thyroiditis, thyrotoxicosis resolved in 6 weeks in all patients with free T4 and free T3 normalizing and TSH becoming either normal or high. Nine patients had TSH high at 6-week follow-up, of which 6 had TSH between 4.7 and 10, and 3 had TSH above 10. On repeat follow-up, after 3 months of diagnosis, a total of 5 patients were subclinically hypothyroid. This included 2 from the 6 patients who had high TSH between 4.7 and 10 at 6 weeks, 2 from TSH >10 group, and 1 patient whose TSH was normal at 6 weeks. All patients who had not recovered at 3 months had TSH between 4.7 and 10 [Table 4].
Figure 1: Etiology of thyrotoxicosis

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Table 4: Follow-up of patients with thyroiditis

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  Discussion Top


Thyrotoxicosis is a common clinical problem in India with an average prevalence of 2% in general population. Of the 2% population with thyrotoxicosis, 1.27% have subclinical thyrotoxicosis and 0.67% have overt thyrotoxicosis. [1] Thyrotoxicosis has a female preponderance and is at least twice as common in females as compared to males. [1],[3] The number of cases of thyroid disorders picked up is increasing, because of increasing awareness about thyroid disorders and due to the inclusion of thyroid function tests in health checkup programs. Thyroid disorders are also picked up when thyroid functions estimated as part of prepregnancy screening and presurgical evaluation for nonthyroidal surgery. Many times, thyrotoxicosis gets diagnosed based on lab tests, with patients having no signs or symptoms suggestive of thyrotoxicosis or with no clinical clue to the cause of thyrotoxicosis. Even though the ATS/American Association of Clinical Endocrinology guidelines mention that it would be prudent to wait for 3-6 months before starting treatment for subclinical hyperthyroidism, the guideline does not mention how to specifically evaluate and follow up incidentally detected thyrotoxicosis and mentions the same protocol for incidentally detected thyrotoxicosis and symptomatic thyrotoxicosis. Also, there are no data on the etiology of this kind of thyrotoxicosis. This study looks into this particular subset of thyrotoxic patients.

Thyroid diseases, especially hyperthyroidism, have a definite female preponderance, [4] and our study also had a predominant female population. However, this may also be contributed by the fact that a lot of cases were picked up during pregnancy planning, and also female health checkups routinely include thyroid function tests. Our study population was predominantly young, partly because of the same selection bias. Most of the patients with thyrotoxicosis had a predominantly free T4 elevation than free 3, which probably relates to the higher incidence of subacute thyroiditis in the study group and may be due to the release of stored T4 from the thyroid. [5] The prevalence of nodules in this study (20%) (based on ultrasound) was slightly lesser than what is described in Indian literature but comparable to the western population and probably reflects the iodination status in Kerala. [6],[7],[8]

The most striking result of this study is the astoundingly high incidence of subacute thyroiditis as the cause of thyrotoxicosis. All studies looking into the etiology of thyrotoxicosis have found that Graves' disease is the most common cause of hyperthyroidism, with the incidence of toxic MNGs and adenomas increasing as the age advances. [9],[10] The incidence of painless thyroiditis as the cause of thyrotoxicosis is less, with the previously published data showing 10% of thyrotoxicosis due to painless thyroiditis. [11] However, our study has shown that the majority of the patients who had incidentally detected thyrotoxicosis had painless thyroiditis as the cause, and it amounted to a total of 90% of the study population. Such a high incidence of thyroiditis has not been reported in literature till date. Whether this phenomenon is restricted to our geographic area alone needs to be seen even though most of the nuclear medicine centers in Kerala are reporting relatively high incidences of subacute thyroiditis. [12]

As far as the follow-up of these patients with subacute thyroiditis was concerned, majority of the patients revert back to euthyroid status while a small group remaining subclinically hypothyroid.


  Conclusions Top


A majority of patients with incidentally detected thyrotoxicosis have subacute thyroiditis as the cause, which reverted to euthyroid state in most of the cases. Based on the study, it seems prudent to wait and follow up patients incidentally detected to have thyrotoxicosis rather than start antithyroid drugs, especially if facilities for uptake scan are not available or affordable.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
  References Top

1.
Unnikrishnan AG, Kalra S, Sahay RK, Bantwal G, John M, Tewari N. Prevalence of hypothyroidism in adults: An epidemiological study in eight cities of India. Indian J Endocrinol Metab 2013;17:647-52.  Back to cited text no. 1
    
2.
Bahn RS, Burch HB, Cooper DS, Garber JR, Greenlee MC, Klein I, et al. Hyperthyroidism and other causes of thyrotoxicosis: Management guidelines of the american thyroid association and american association of clinical endocrinologists. Endocr Pract 2011;17:3.  Back to cited text no. 2
    
3.
Unnikrishnan AG, Menon UV. Thyroid disorders in India: An epidemiological perspective. Indian J Endocrinol Metab 2011;15:S78-81.  Back to cited text no. 3
    
4.
Nayak B, Hodak SP. Hyperthyroidism. Endocrinol Metab Clin North Am 2007;36:617-56.  Back to cited text no. 4
    
5.
Mortoglou A, Candiloros H. The serum triiodothyronine to thyroxine (T3/T4) ratio in various thyroid disorders and after levothyroxine replacement therapy. Hormones (Athens) 2004;3:120-6.  Back to cited text no. 5
    
6.
Brahmbhatt SR, Brahmbhatt RM, Eastman CJ, Boyages SC. Thyroid ultrasonography consistently identifies goiter in adults over the age of 30 years despite a diminished response with aging of the thyroid gland to the effects of goitrogenesis. Sci World J 2001;1:243-53.  Back to cited text no. 6
    
7.
Marwaha RK, Tandon N, Ashraf GM, Ganguly SK, Batra A, Aggarwal R, et al. Ultrasound evaluation of thyroid size: A large nationwide study of schoolchildren in India. Natl Med J India 2008;21:69-74.  Back to cited text no. 7
    
8.
Marwaha RK, Tandon N, Gupta N, Karak AK, Verma K, Kochupillai N. Residual goitre in the postiodization phase: Iodine status, thiocyanate exposure and autoimmunity. Clin Endocrinol (Oxf) 2003;59:672-81.  Back to cited text no. 8
    
9.
Davis PJ, Davis FB. Hyperthyroidism in patients over the age of 60 years. Clinical features in 85 patients. Medicine (Baltimore) 1974;53:161-81.  Back to cited text no. 9
    
10.
Laurberg P, Pedersen KM, Vestergaard H, Sigurdsson G. High incidence of multinodular toxic goitre in the elderly population in a low iodine intake area vs. high incidence of Graves′ disease in the young in a high iodine intake area: Comparative surveys of thyrotoxicosis epidemiology in East-Jutland Denmark and Iceland. J Intern Med 1991;229:415-20.  Back to cited text no. 10
    
11.
Williams I, Ankrett VO, Lazarus JH, Volpe R. Aetiology of hyperthyroidism in Canada and Wales. J Epidemiol Community Health 1983;37:245-8.  Back to cited text no. 11
    
12.
Dev A, Philip R, Varkey K. Changing Spectrum of Thyrotoxicosis - A Study from Central Kerala Paper Presented at API Kerala Annual Conference Kochi, Kerala; February, 2015.  Back to cited text no. 12
    


    Figures

  [Figure 1]
 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4]



 

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