0021-972x/92/7502-0343$03.00/0 Journal of Clinical Endocrinology and Metabolism Copyright 0 1992 by The Endocrine Society

Editorial: Secretion

Vol. 75, No. 2

Printed

Non-Thyrotropin-Dependent

in U.S.A.

Thyroid

regarding the relative lack of a decline in serum thyroglobulin with T4 suppression when basal TSH values are below 0.1 mU/L (7), we have also observed alterations in serum thyroglobulin values in some thyroid cancer patients at serum TSH levels lOO-fold lower (unpublished data). Whether such patients have a different serum TSH-thyroglobulin doseresponse pattern than is present in the nonresponsive patients is unclear. Further, not all serieshave found that the T4 replacement of autoimmune hypothyroidism significantly differs from patients with complete thyroid gland ablation (8). In any regard, the authors have eloquently stated their position and it is for others to determine the validity of their findings. With the recent availability of increasingly more sensitive methods for serum TSH measurement, hopefully a definitive answer to the important question as to the biological relevance of subnormal serum TSH levels in normal and pathologic thyroid stateswill soon be forthcoming. John T. Nicoloff Carole A. Spencer University of Southern California School of Medicine

The article published in the present issue of the journal by Buirmeister et al. (1) demonstrates that systematically larger doses of oral T4 therapy are required when employing serum TSH as a therapeutic endpoint in patients with thyroid ablation for thyroid cancer as compared to other hypothyroid subjects in whom a functional thyroid remnant is likely to be present. Although thyroid remnant secretion may be explained by continued immunoglobulin stimulation in treated toxic Graves’ disease patients (unfortunately not measured in this study), the apparent TSH-independent thyroid hormone secretion occurring in other forms of hypothyroidism has no such simple explanation. It is the authors contention that autonomous non-TSH-dependent secretion by the thyroid remnant provides the most likely cause for this phenomenon. As pointed out by the authors, the concept of autonomous thyroid secretion independent of TSH is not a new one (2). Indeed, it has been previously demonstrated that the normal thyroid gland can sustain about one third of its basal T4 output when serum TSH levels are suppressed by exogenous liothyronine therapy (3). Such apparent TSH-independent function may have broad implications relative to the possible benefit of thyroid hormone therapy in a wide spectrum of thyroid disease. Indeed, recent evidence suggests that thyroid hormone suppressive therapy is relatively ineffective as a treatment for nontoxic goiter (4) as well as benign thyroid neoplasias (5). The data provided in the present report also suggests that in patients with TSH dependent thyroid cancers serum thyroglobulin values are unaffected by T4 suppression if serum TSH values are less than 0.4 mu/L. This leads one to the provocative conclusion that TSH suppression with T4 therapy is likely to be of no particular benefit in the treatment of either benign or malignant thyroid disorders! Before making such a sweeping conclusion, however, we should pause for a moment of reflection. First of all, there appears no doubt that the pituitary gland, presumably acting via TSH, is essential for maintenance, growth, and secretion of the normal thyroid gland. Indeed, without it, the thyroid gland is unable to sustain any secretion and it will eventually atrophy (3, 5). Although we have reported similar findings

References 1. Burmeister LA, Goumaz MO, Mariash CN, Oppenheimer JH. 1992 Levothyroxine dose requirements for thyrotropin suppression in the treatment of differentiated thyroid cancer. J Clin Endocrinol Metab. 75:344-50. 2. Duick DS, Stein RB, Warren DW, Nicoloff JT. 1975 Significance of partial suppressibility of serum thyroxine by triiodothyronine administration in euthyroid man. J Clin Endocrinol Metab. 41:22934. 3. Nicoloff JT. 1986 Assessment of thyroid function in patients receiving replacement therapy. In: lngbar SH, Braverman LE, eds. The Thyroid. 5th ed. Philadelphia: Lippincott; 1445-52. 4. Edmonds C. 1992 Treatment of sporadic goiter with thyroxine. Clin Endocrinol (Oxf). 36:21-3. 5. Reverter JL, Lucas A, Salinas I, Andi L, Foz M, Sanmarti A. 1992 Suppressive therapy with levothyroxine for solitary thyroid nodules. Clin Endocrinol (Oxf). 36:25-8. 6. Singer PA, Nicoloff JT, Stein RB, Jaramillo J. 1978 Transient monotrophic thyrotropin (TSH) deficiency associated with thyroid hormone therapy. J Clin Endocrinol Metab. 47:512-K 7. Spencer CA, Lai-Rosenfeld AO, Guttler RB, et al. 1986 Thyrotropin secretion in thyrotoxic and thyroxine-treated patients: assessment bv a sensitive immunoenzvmometric assav. , , 1, Clin Endocrinol Metab..63:349-55. 8. Bearcroft CP, Toms GC, Williams SJ, Noonan K, Monsom JP. 1991 Thyroxine replacement in post-radioiodine hypothyroidism. Clin Endocrinol (Oxf). 34:115-S.

Received March 1, 1992. Address requests for reprints to: John T. Nicoloff, University of Southern California, School of Medicine, 2025 Zonal Avenue, Room 18415, Los Angeles, California 90033.

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Non-thyrotropin-dependent thyroid secretion.

0021-972x/92/7502-0343$03.00/0 Journal of Clinical Endocrinology and Metabolism Copyright 0 1992 by The Endocrine Society Editorial: Secretion Vol...
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