This study was a continuation of a previous study. In the previous study, the authors found that the three main treatments for Graves’ Disease (surgical treatment, radioiodine treatment, and anti-thyroid drug treatment) all resulted in a similar long-term quality-of-life. Although the three treatments didn’t differ from each other, Graves’ disease patients reported an overall lower quality-of-life than did healthy control subjects of similar age and sex.
The authors examined whether the patients’ current TSH, T3 or T4 levels could explain the low quality-of-life reported by GD patients. There examined a total of 91 patients who had either received surgery (n=38), medication (n=17) or radioiodine (n=27). Additionally, 9 patients had received multiple treatments. Every participant had their TSH, T3, and T4 levels measured, and answered a questionnaire that evaluated their physical and mental health.
The study found that most of the patients with low physical and mental health scores had low TSH levels. However, there were exceptions. A few low-TSH patients had high physical and mental health scores. Physical and mental health scores didn’t differ among the three treatment types. Forty-four patients (48%) had TSH within the reference range. Forty-three patients (47%) had suppressed TSH. Only a few patients had high TSH levels.
Of the 91 patients who took supplemental thyroid hormone (thyroxine), approximately half had normal serum TSH, while the rest had high serum TSH. Physical and mental health scores were similar, regardless of TSH level.
The only blood value that was correlated with improved physical or mental health scores was free-T3. Patients with higher free T3 values had improved mental health scores.
The authors conclude by saying “the absent [of a] relation between the thyroid hormonal state and the [quality of life] scores indicates that the diminished [quality of life of long-term Graves’ Disease patients] are not related to the thyroid hormone levels and therefore may have other explanations.”.
What I took away from this paper was that many GD patients have poorly managed thyroid levels, as seen by TSH and serum values. 47% of patients after treatment STILL had suppressed TSH? That’s too high. Nearly half of the patients taking supplemental thyroid hormone had elevated levels – again, too many. I don’t know whether it is doctors’ failure to treat effectively or patients’ failure to adhere to treatment regimes, but there were too many “treated” people out of “normal range”.
The authors also conclude by saying that GD patients may have poor responses (or exaggerated responses) to stress, since stress can cause GD. They say that the reduced quality-of-life in GD patients may have nothing to do with the thyroid, but be related to stress-management in patients. I don’t feel that my GD was brought on by stress, nor do I lead a particularly stressful life, so I can’t speak to this. It’s hard not to take a little offense at being told my GD is my poor reaction to stress, but it’s a reasonable explanation for why else GD patients who have normal thyroid levels still have poorer quality of life than normal folks. Perhaps their next study will be a survey of our stress-coping mechanisms.
Abraham-Nordling, M., Wallin, G., Lundell, G. & Torring, O. (2007) Thyroid hormone state and quality of life at long-term follow-up after randomized treatment of Graves’ disease. Eur J Endocrinol, 156, 173-179.
In a 14-21 year follow-up of health-related quality of life (HRQL) outcome of 179 patients after randomized treatment of Graves’ disease (GD) with surgical, medical or radioiodine, we found no differences. The HRQL for Graves’ patients, however, was lower compared with a large age- and sex-matched Swedish reference population. We have now studied whether the reported HRQL-scores by Medical Outcome Study 36-item Short-Form Health Status Survey (SF36) and quality of life 2004 (QoL2004) answers were related to the thyroid hormone state of the patient. Methods: This report comprises 91 of the original patients in which both the results of SF36 and QoL2004 questionnaire as well as serum thyroid hormones and current use of L-thyroxine treatment were available. Results: A large number of the patients had low or undetectable serum TSH concentrations. SF36 scores and answers to QoL2004 questionnaires were not correlated to TSH levels or associated with suppressed TSH. A low free triiodothyronine was weakly associated with a low GH score (P < 0.02) and elevated thyrotropin receptor antibody with a low physical component summary (P < 0.02). Conclusion: HRQL do not seem to be influenced by the thyroid hormone state of the patient including subclinical thyrotoxicosis. It is possible that the personality of GD patients as such may have resulted both in the development of GD and lower HQRL scores later on in life. Alternatively, the generic SF36 may not be a proper instrument to detect relevant differences in HRQL related to the thyroid state.