Diabetes mellitus in a girl with thyroid hormone resistance syndrome: a little recognized interaction between the two diseases

The syndrome of resistance to thyroid hormone (RTH) is characterized by elevated serum free thyroid hormones (FT4 and FT3) in the presence of unsuppressed TSH levels, reflecting resistance to the normal negative feedback mechanisms in the hypothalamus and pituitary. The degree of resistance within peripheral tissues determines whether thyrotoxic clinical features are associated with this condition. Classic features include attention deficit hyperactivity disorder, growth delay, tachycardia, and goiter. However, other features, such as frequent ear, nose and throat infections, hearing deficit, and decreased bone mass have recently been recognized. The phenotype of RTH is variable, with most patients presenting with mild to moderate symptoms. In this report we describe a girl with familiar RTH and diabetes mellitus. This is, to our knowledge, the first report regarding this association. Nearly one year after long-term triiodothyroacetic acid (Triac) therapy, we observed a reduction of thyroid hormone levels with an amelioration of insulin resistance. The possible interactions between these disorders are discussed.

[1]  R. Coppari,et al.  Leptin revisited: its mechanism of action and potential for treating diabetes , 2012, Nature Reviews Drug Discovery.

[2]  K. Petersen,et al.  Resistance to thyroid hormone is associated with raised energy expenditure, muscle mitochondrial uncoupling, and hyperphagia. , 2010, The Journal of clinical investigation.

[3]  A. Colao,et al.  Secondary diabetes associated with principal endocrinopathies: the impact of new treatment modalities , 2009, Acta Diabetologica.

[4]  M. Patti,et al.  Links between thyroid hormone action, oxidative metabolism, and diabetes risk? , 2008, Thyroid : official journal of the American Thyroid Association.

[5]  T. Cheetham,et al.  Prolonged honeymoon phase in an adolescent with diabetes and thyrotoxicosis provides support for the accelerator hypothesis. , 2008, Pediatric diabetes.

[6]  M. Roden,et al.  Mitochondrial function and endocrine diseases , 2007 .

[7]  M. Roden,et al.  ESCI Award 2006. Mitochondrial function and endocrine diseases. , 2007, European journal of clinical investigation.

[8]  V. Toscano,et al.  Thyroid hormone receptor TRbeta1 mediates Akt activation by T3 in pancreatic beta cells. , 2007, Journal of molecular endocrinology.

[9]  E. Spada,et al.  Italian cross-sectional growth charts for height, weight and BMI (2 to 20 yr) , 2006, Journal of endocrinological investigation.

[10]  M. Obregon,et al.  T3 and Triac inhibit leptin secretion and expression in brown and white rat adipocytes. , 2004, Biochimica et biophysica acta.

[11]  R. Walther,et al.  Expression of Thyroid Hormone Receptor Isoform α1 in Pancreatic Islets , 2003 .

[12]  R. Walther,et al.  Expression of thyroid hormone receptor isoform alpha1 in pancreatic islets. , 2003, Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association.

[13]  Sheue-yann Cheng,et al.  Differential expression of thyroid hormone receptor isoforms dictates the dominant negative activity of mutant Beta receptor. , 2002, Molecular endocrinology.

[14]  N. Takasu,et al.  Evidence for a deficient pancreatic beta-cell response in a rat model of hyperthyroidism. , 2002, Life sciences.

[15]  O Rajanayagam,et al.  Three novel mutations at serine 314 in the thyroid hormone beta receptor differentially impair ligand binding in the syndrome of resistance to thyroid hormone. , 1999, Endocrinology.

[16]  A. Pinchera,et al.  Three Novel Mutations at Serine 314 in the Thyroid Hormone β Receptor Differentially Impair Ligand Binding in the Syndrome of Resistance to Thyroid Hormone1. , 1999, Endocrinology.

[17]  S. Refetoff Resistance to thyroid hormone. , 1993, Current therapy in endocrinology and metabolism.

[18]  F. Wondisford,et al.  Isoform variable action among thyroid hormone receptor mutants provides insight into pituitary resistance to thyroid hormone. , 1997, Molecular endocrinology.

[19]  P. Kopp,et al.  Syndrome of Resistance to Thyroid Hormone: Insights into Thyroid Hormone Action , 1996, Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine.

[20]  E. Eldrup,et al.  β‐Cell function and glucose and lipid oxidation in Graves’ disease , 1996, Clinical endocrinology.

[21]  T. Takeda,et al.  Triiodothyroacetic acid has unique potential for therapy of resistance to thyroid hormone. , 1995, The Journal of clinical endocrinology and metabolism.

[22]  S. Ohguni,et al.  Correlation of plasma free thyroxine levels with insulin sensitivity and metabolic clearance rate of insulin in patients with hyperthyroid Graves' disease. , 1995, Internal medicine.

[23]  P. Beck‐Peccoz,et al.  The variable clinical phenotype in thyroid hormone resistance syndrome. , 1994, Thyroid : official journal of the American Thyroid Association.

[24]  R. Weiss,et al.  The syndromes of resistance to thyroid hormone. , 1993, Endocrine reviews.

[25]  S. Refetoff,et al.  Recessive inheritance of thyroid hormone resistance caused by complete deletion of the protein-coding region of the thyroid hormone receptor-beta gene. , 1992, The Journal of clinical endocrinology and metabolism.

[26]  C. Hales,et al.  THE EFFECT OF THYROID DISEASE ON PROINSULIN AND C‐PEPTIDE LEVELS , 1989, Clinical endocrinology.

[27]  J. Orgiazzi,et al.  Hyperthyroidism due to selective pituitary resistance to thyroid hormones in a 15-month-old boy: efficacy of D-thyroxine therapy. , 1988, The Journal of clinical endocrinology and metabolism.

[28]  B. Weintraub,et al.  Absence of thyroid-binding immunoglobulins in patients with thyrotropin-mediated hyperthyroidism. , 1980, The Journal of clinical endocrinology and metabolism.

[29]  S. Refetoff,et al.  Familial syndrome combining deaf-mutism, stuppled epiphyses, goiter and abnormally high PBI: possible target organ refractoriness to thyroid hormone. , 1967, The Journal of clinical endocrinology and metabolism.