Response to Dr. Paul Drinka

May 24, 2017 | Autor: Graziano Ceresini | Categoria: Aging, Humans, Thyroid gland, Iodine, Female, Male
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208

LETTERS TO THE EDITOR

To the Editor: I enjoyed reading “Thyroid Status and 6-Year Mortality in Elderly People Living in a Mildly Iodine-Deficient Area: The Aging in the Chianti Area Study” by Ceresini and colleagues. Subclinical hyperthyroidism was defined as a thyrotropin level of less than 0.46 mIU/L, free thyroxine (FT4) of 0.77 to 2.19 ng/dL, and free triiodothyronine (FT3) of 2.77 to 5.27 pg/mL. Low T3 syndrome, or nonthyroidal illness, was diagnosed when FT3 was less than 2.77 pg/mL with normal thyrotropin. After adjusting for multiple confounders, participants with subclinical hyperthyroidism (hazard ratio = 1.65) had significantly greater all-cause mortality than those with normal thyroid function. The discussion states that interleukin (IL)-6 and tumor necrosis factor alpha (TNF-a) measurements gave further support to the exclusion of nonthyroidal illness in the group with subclinical hyperthyroidism. The specific data regarding IL6 and TNF-a values in subclinical hyperthyroidism were not included.1 I must admit that I have not kept up on this field, although it is my understanding that nonthyroidal illness, medications (e.g., glucocorticoids), and hypothalamicpituitary disease can also suppress thyrotropin levels.2 I would be surprised if these situations are always associated with low FT3 or FT4 levels during a single blood draw. It is difficult to label all the individuals with low thyrotropin and normal levels of thyroid hormone as having endogenous subclinical hyperthyroidism with overproduction of thyroid hormone without further testing or follow-up. A review states “Confronted with a low serum level of thyrotropin, physicians should not jump to the conclusion that it is due to a hyperthyroid state.”3 Perhaps some or many of the individuals with biochemically defined “subclinical hyperthyroidism” did not have endogenous thyroid disease and simply had a nonthyroidal illness that increased all-cause mortality and lowered thyrotropin levels. I would appreciate the authors’ recommendations regarding assessment and follow-up of individuals with biochemical evidence of “subclinical hyperthyroidism” with a single blood draw. How can the practitioner determine the cause of the low thyrotropin value in an individual?

Paul Drinka, MD, AGSF Department of Internal Medicine/Geriatrics, University of Wisconsin–Madison, Madison, Wisconsin

ACKNOWLEDGMENTS Conflict of Interest: The editor in chief has reviewed the conflict of interest checklist provided by the author and has determined that the author has no financial or any other kind of personal conflicts with this paper. Author Contributions: I am the sole author. Sponsor’s Role: There was no sponsor.

REFERENCES 1. Ceresini G, Ceda GP, Lauretani F et al. Thyroid status and 6-year mortality in elderly people living in a mildly iodine-deficient area: The Aging in the Chianti Area Study. J Am Geriatr Soc 2013;61:868–874.

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2. Drinka PJ, Amberson J, Voeks SK et al. Low TSH levels in nursing home residents not taking thyroid hormone. J Am Geriatr Soc 1996;44: 573–577. 3. Pantalone KM, Nasr C. Approach to a low TSH level: Patience is a virtue. Cleve Clin J Med 2010;77:803–811.

RESPONSE TO DR. PAUL DRINKA To the Editor: We thank Dr. Drinka for his letter1 in response to our recent article2 and welcome the opportunity to provide additional details. There were no differences in interleukin (IL)-6 or tumor necrosis factor alpha (TNF-a) levels between euthyroid participants and individuals with subclinical hyperthyroidism (for IL-6: median 1.45 pg/mL, interquartile range (IQR) 0.85–2.24 pg/mL vs median 1.53 pg/mL, IQR 0.83–2.15 pg/mL; logtransformed age- and sex-adjusted P = .85; for TNF-a: median 4.64 pg/mL, IQR 3.34–6.23 pg/mL vs median 4.76 pg/mL, IQR 3.24–5.66 pg/mL; log-transformed age- and sex-adjusted P = .37). In Model 2 of the multivariate analysis,2 subclinical hyperthyroidism remained a significant independent risk factor for all-cause mortality when data were adjusted for log IL-6 (hazard ratio (HR) = 1.75, 95% confidence interval (CI) = 1.13–2.73, P = .01) or log TNF-a (HR = 1.6, 95% CI = 1.02–2.51, P = .04). We agree on the difficulty of correctly diagnosing subclinical hyperthyroidism based on a single result of low circulating levels of thyrotropin with normal thyroid hormone concentrations, because numerous conditions that characterize the so-called nonthyroidal illness, along with some pharmacological agents, may lead to low circulating thyrotropin.3 We also agree that repeating a thyroid function test would help in the diagnosis. As we stated in the comment of our article, only baseline thyroid function tests determined on a single blood withdrawal were available in our study. This could be a limitation of our results, which many epidemiological studies share, but the fact that IL-6 and TNF-a were comparable between euthyroid subjects and those with subclinical hyperthyroidism and the exclusion of subjects with low circulating concentrations of free triiodothyronine (T3) in our analysis further suggest that a nonthyroidal illness is unlikely to be the explanation for low thyrotropin levels in our subjects. Because inflammatory markers are not routinely measured in clinical practice, they cannot be considered as common tools for excluding the effect of a nonthyroidal illness in the diagnosis of subclinical hyperthyroidism. We rather believe that an accurate history of the patients, aimed at the identification of any underlying thyroid disease and potential clinical conditions (or therapeutic agents) that may result in low thyrotropin, be mandatory before a diagnosis of subclinical hyperthyroidism is made. In some cases, a further thyroid function test and measurements of free T3 circulating concentrations may help. On the other hand, a correct diagnosis of subclinical hyperthyroidism should not be missed, because this thyroid disorder may be associated with other negative clinical outcomes,4 and its treatment has been advocated, especially in elderly subjects.5

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Graziano Ceresini, MD, PhD Gian P. Ceda, MD Geriatric Endocrine Unit, Department Clinical and Experimental Medicine, University Hospital of Parma, Parma, Italy Fulvio Lauretani, MD Geriatric Unit, University Hospital of Parma, Parma, Italy Marcello Maggio, MD, PhD Elisa Usberti, MD Michela Marina, MD Geriatric Endocrine Unit, Department Clinical and Experimental Medicine, University Hospital of Parma, Parma, Italy Stefania Bandinelli, MD Geriatric Unit, ASF Toscana, Firenze, Italy Jack M. Guralnik, MD Laboratory of Epidemiology, Demography, and Biometry, National Institute on Aging, Baltimore, Maryland Giorgio Valenti, MD Geriatric Endocrine Unit, Department Clinical and Experimental Medicine, University Hospital of Parma, Parma, Italy

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LETTERS TO THE EDITOR

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Luigi Ferrucci, MD, PhD National Institute on Aging, Baltimore, Maryland

ACKNOWLEDGEMENTS Conflict of Interest: The editor in chief has reviewed the conflict of interest checklist provided by the authors and has determined that the authors have no financial or any other kind of personal conflicts with this paper. Author Contributions: The authors contributed equally to the manuscript. Sponsor’s Role: There was no sponsor.

REFERENCES 1. Drinka PJ.Low thyrotropin from nonthyroidal illness? J Am Geriatr Soc 2014;62:207–208. 2. Ceresini G, Ceda GP, Lauretani F et al. Thyroid status and 6-year mortality in elderly people living in a mildly iodine-deficient area: The Aging in the Chianti Area Study. J Am Geriatr Soc 2013;61:868–874. 3. Drinka PJ, Amberson J, Voeks SK et al. Low TSH levels in nursing home residents not taking thyroid hormone. J Am Geriatr Soc 1996;44:573–577. 4. Ceresini G, Lauretani F, Maggio M et al. Thyroid function abnormalities and cognitive impairment in elderly people: Results of the Invecchiare in Chianti Study. J Am Geriatr Soc 2009;57:89–93. 5. Bahn RS, Burch HB, Cooper DS et al. ATA/AACE taskforce on hyperthyroidism and other causes of thyrotoxicosis. Thyroid 2011;6:593–647.

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