1/16. Potent thyrotrophin receptor-blocking antibodies: a cause of transient congenital hypothyroidism and delayed thyroid development.OBJECTIVE: We describe an infant with surprisingly severe neonatal hypothyroidism due to transplacental passage of thyrotrophin receptor (TSH-R)-blocking antibodies (TBAb). DESIGN AND methods: TBAb were detected using a cell line which stably expresses the human TSH-R and a cAMP-responsive luciferase reporter by their ability to inhibit TSH-stimulated luciferase expression. Potent TBAb were detected in maternal serum and initially in the infant's serum but, in the latter, TBAb decreased over time to within the reference range by 3-4 months of age, illustrating the transient nature of this condition. RESULTS: The thyroid function of this child did not return to normal on withdrawal of thyroxine therapy at 16 months of age when he developed transient compensated hypothyroidism. CONCLUSIONS: We propose that the presence of potent TBAb in utero and in the first weeks of life may have implications for the development of a normally sized thyroid gland. We have demonstrated the presence of TBAb in the mother's milk and, as far as we are aware, this is the first such report. However, the TBAb in the milk probably did not contribute significantly to hypothyroidism in the child, given the reducing antibody titre in his circulation.- - - - - - - - - - ranking = 1keywords = nature (Clic here for more details about this article) |
2/16. Acute mania in the setting of severe hypothyroidism.Although the associations between depression and hypothyroidism and between mania and hyperthyroidism are well described, mania in the setting of hypothyroidism is unusual. The authors present the case of a patient whose acute mania appears to have been precipitated by hypothyroidism secondary to postpartum thyroiditis. This case underscores the importance of thyroid screening in patients with mood and psychotic disorders, including patients who lack the classical psychiatric features of thyroid dysfunction. Further investigation is required on the nature of the relationship between thyroid function and bipolar disorder and any implications it may have for the diagnosis and treatment of this illness.- - - - - - - - - - ranking = 1keywords = nature (Clic here for more details about this article) |
3/16. Hypothyroidism after sunitinib treatment for patients with gastrointestinal stromal tumors.BACKGROUND: Sunitinib malate is an oral tyrosine kinase inhibitor recently approved for the treatment of gastrointestinal stromal tumors and renal cell carcinoma. Because the ret proto-oncogene is also inhibited by this agent, clinical evaluation of thyroid function was performed. OBJECTIVE: To describe the prevalence and clinical presentation of thyroid dysfunction related to sunitinib therapy. DESIGN: Prospective, observational cohort study. SETTING: Tertiary care hospital. patients: 42 patients treated for a median of 37 weeks (range, 10 to 167 weeks). MEASUREMENTS: Following analysis of serial thyroid-stimulating hormone (TSH) measurements collected prospectively during a clinical trial of sunitinib, the authors determined the proportion of patients with thyroid dysfunction. RESULTS: Abnormal serum TSH concentrations were documented in 26 of 42 patients (62%): 15 (36%) developed persistent, primary hypothyroidism; 4 (10%) developed isolated TSH suppression; and 7 (17%) experienced transient, mild TSH elevations. The risk for hypothyroidism increased with the duration of sunitinib therapy. Six of 15 (40%) hypothyroid patients had suppressed TSH concentrations before developing hypothyroidism, suggesting thyroiditis. Two hypothyroid patients evaluated with thyroid ultrasonography had no visualized thyroid tissue despite normal baseline thyroid function. LIMITATIONS: The exploratory nature of this study precluded more frequent biochemical and sonographic analysis that may better define the mechanism of sunitinib-associated thyroid dysfunction. CONCLUSION: Hypothyroidism is a frequent complication of sunitinib therapy. Regular surveillance of thyroid function is warranted in patients receiving the drug. Although the mechanism by which this complication occurs is unknown, the observations of preceding TSH suppression and subsequent absence of visualized thyroid tissue in some patients suggest that sunitinib may induce a destructive thyroiditis through follicular cell apoptosis. This provides a rationale for further investigation of sunitinib treatment in patients with advanced thyroid cancer.- - - - - - - - - - ranking = 1keywords = nature (Clic here for more details about this article) |
4/16. Basophilic bodies of skeletal muscle in hypothyroidism: enzyme histochemical and ultrastructural studies.Basophilic bodies of skeletal muscles from two patients with hypothyroidism were examined by enzyme histochemistry and ultrastructural study of ultrathin sections stained with periodic-acid-thiocarbohydrazide-silver proteinate for polysaccharides. Some additional characterizations of basophilic bodies were observed: basophilic bodies were found exclusively in type 1 fiber; basophilic bodies were devoid of myofibrillary adenosine triphosphatase, oxidative enzymes, and phosphorylase; and both fibrillary and granular components of basophilic bodies stained strongly for polysaccharides. The polysaccharide nature of basophilic bodies is in keeping with the previous suggestion that the formation of basophilic bodies in hypothyroid patients is related to an impairment of carbohydrate metabolism. Their selective involvement of type 1 fiber and preferential occurrence at the myotendinous junction remain obscure.- - - - - - - - - - ranking = 1keywords = nature (Clic here for more details about this article) |
5/16. Transient neonatal 'athyreosis' resulting from thyrotropin-binding inhibitory immunoglobulins.Recognition of transient forms of neonatal hypothyroidism is difficult because of the urgency of thyroxine treatment. In the present report the first child born to a mother with Graves' disease developed transient hyperthyroidism during the newborn period. The mother underwent radioactive iodine treatment and was maintained euthyroid on l-thyroxine. Two subsequent children were detected by newborn thyroid screen to have low thyroxine and markedly elevated serum thyrotropin (TSH) levels. technetium 99 metastable and iodine 123 scans at 22 days of age showed the second child to be athyreotic. The third child was not scanned. All three children were nongoitrous at birth. patients 2 and 3 had continuous TSH suppression with thyroxine therapy for 3 and 4 years. Thyroid function measurements after discontinuation of therapy for 8 weeks were normal, and both children had normal 123I thyroid scans. The mother was found to have potent TSH-binding inhibitory immunoglobulin (TBII) levels in her serum (85.5%). A fourth child with low thyroxine and elevated TSH was born to a mother on a regimen of l-thyroxine for hypothyroidism. 99mTc scan at 26 days of age showed no thyroid tissue and was normal at 3 months. TBII activity was 35% in the maternal serum and absent in the infant's serum. The above laboratory and clinical data are compatible with the blocking nature of TBII, resulting in transient newborn hypothyroidism and an athyreotic appearance on scan. The TBII measurement can be a useful predictor of neonatal hypothyroidism as well as confirm the transient nature of the disease in newborns.- - - - - - - - - - ranking = 2keywords = nature (Clic here for more details about this article) |
6/16. Spinal epidural lipomatosis: report of a case secondary to hypothyroidism and review of literature.Epidural lipomatosis usually occurs as a complication of steroid therapy. This report includes the first description of a case secondary to hypothyroidism. Adults in all age groups can be affected and present with progressive signs and symptoms of spinal cord or cauda equina compression. The dorsal aspect of the thoracic spine is most commonly involved, usually in its total extent. spine radiographs are normal and myelography poorly delineates the nature and extent of abnormality. While computed tomography can provide information about the nature of the spinal mass, magnetic resonance imaging is the investigation of choice. Extensive decompressive laminectomy is useful but the results are variable. Correction of underlying endocrine abnormality can reverse the process. The need for early diagnosis of this disorder is therefore emphasized.- - - - - - - - - - ranking = 2keywords = nature (Clic here for more details about this article) |
7/16. Evolution of hypothyroidism in familial goitre due to deiodinase deficiency: report of a family and review of the literature.We studied two sisters who developed large non-toxic goitres in adolescence. Deiodinase deficiency was diagnosed by a rapid thyroid uptake of radioactive iodine (RAI) at 2 hours associated with a marked fall in thyroidal 131I by 24 hours. Serial RAI scans in the second patient documented evolution of the iodine-deficient state. Conservation of intra-thyroidal iodine stores was maintained by avid iodine uptake and failure to release organified 131I. With progressive loss of inorganic iodine, hypothyroidism developed, associated with a rise in serum TSH which further exacerbated the loss of iodine. Treatment with L-thyroxine resulted in an improvement of thyroid function, but normalization was achieved only after small doses of Lugol's iodine were administered. These studies illustrate the variable nature and late onset of an inborn error of thyroid metabolism. This family supports an autosomal recessive mode of inheritance for deiodinase deficiency. We have documented progression from a euthyroid to hypothyroid state resulting from decompensation of iodine conservation mechanisms.- - - - - - - - - - ranking = 1keywords = nature (Clic here for more details about this article) |
8/16. Relapse of Graves' disease 23 years after treatment with radioactive iodine (131I).The use of radioactive iodine (131I) in the treatment of Graves' disease results frequently in hypothyroidism requiring thyroid hormone supplementation. Relapse of Graves' disease months after inadequate treatment with 131I is well-recognized. However, late relapse of Graves' disease in a patient rendered hypothyroid by 131I years after therapy has not been reported. The authors discuss a patient who had a relapse of his Graves' disease 23 yr after treatment with 131I. Over the interval the patient had been on 1-thyroxine replacement for hypothyroidism and had persistently high levels of long acting thyroid stimulator or thyroid stimulating antibody. The authors speculate that the immune nature of Graves' disease may play a role in the observed clinical response to 131I.- - - - - - - - - - ranking = 1keywords = nature (Clic here for more details about this article) |
9/16. Hypothyroid Graves' disease.Graves' disease has recently been shown to exist in a euthyroid form in untreated patients. Sporadic reports of a hypothyroid form are beginning to emerge, thus illustrating the multifaceted nature of this disorder, with thyrotoxicosis at one end of the spectrum and hypothyroidism at the other. Three patients with nonthyrotoxic Graves' disease and concomitant hypothyroidism were seen at Emory University Hospital in one year, and deatailed studies were made to help elucidate the nature of this unusual combination. Results of these studies are reported and briefly discussed. It is suggested that, until more is known about this intriguing aspect of the Graves' disease spectrum, the label "hypothyroid Graves' disease" is justifiable.- - - - - - - - - - ranking = 2keywords = nature (Clic here for more details about this article) |
10/16. Thyroid disease with monoclonal (immunoglobulin g lambda) antibody to triiodothyronine and thyroxine.A man with previous Graves' disease spontaneously developed hypothyroidism. He became euthyroid with T4 therapy, but developed inappropriately elevated serum levels of T3 and, to a lesser extent, T4. Gel filtration analysis (Sephadex G-150) of serum trace-labeled with [125I]T3 revealed binding to a high molecular weight fraction, distinct from normal T3-binding proteins. This abnormal activity cochromatographed with serum immunoglobulin g (IgG) by deae-cellulose chromatography and gel filtration, and was retained by the F(ab)2 fragment of IgG, indicating its true antibody nature. By isoelectric focussing, there was restricted heterogeneity of the [125I]T3-antibody complex (pI 9.0-9.1), and the antibody was identified as an IgG (lambda) monoclonal Ig by immune precipitation. Antigenic cross-reactivity with T4 was demonstrated by inhibition of hapten binding. The affinity of the antibody for T3 was high (Ka = 0.9 x 10(9) liter mol-1), and the T3 binding capacity of the antibody in serum was estimated as 1132 ng/dl, equivalent to 1.39 mg T3-specific IgG/liter (0.014% of the total serum IgG). This binding capacity was similar to the serum T3 values (1100-1300 ng/dl) at which transition from hypothyroid to euthyroid states was observed, as judged by clinical examination and measurement of serum TSH levels.- - - - - - - - - - ranking = 1keywords = nature (Clic here for more details about this article) |
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