Effects of long-term, high-dose bovine thyrotropin administration on human thyroid tissues from patients with graves’ disease and normal subjects xenografted into nude mice

1990 ◽  
Vol 1 (4) ◽  
pp. 220-227 ◽  
Author(s):  
Yoshio Kasuga ◽  
Sunao Matsubayashi ◽  
Fumito Akasu ◽  
Naomi Miller ◽  
Christopher Jamieson ◽  
...  
Keyword(s):  
Nude Mice ◽  
Normal Subjects ◽  
Human Thyroid ◽  
Graves Disease ◽  
High Dose

scholarly journals Preserved activation of thyrotropin receptor antibody to stimulate thyroid function despite long-term treatment in euthyroid patients with Graves' disease

1998 ◽  
pp. 281-285 ◽  
Author(s):  
M Akuzawa ◽  
M Murakami ◽  
M Yamada ◽  
T Satoh ◽  
H Shimizu ◽  
...  
Keyword(s):  
Thyroid Function ◽  
Normal Subjects ◽  
Term Treatment ◽  
Graves Disease ◽  
Thyrotropin Receptor ◽  
Receptor Antibody ◽  
Thyrotropin Receptor Antibody ◽  
Long Term Treatment ◽  
Tsh Levels

Clinical evaluation was conducted to ascertain whether thyrotropin receptor antibody (TRAb) in the normal range may still be involved in the regulation of thyroid function after prolonged treatment for Graves' disease. All patients (n = 33) were treated with antithyroid drugs for an average of 10.6 years and were under euthyroid conditions in which normal blood levels of tri-iodothyronine (T3) were significantly correlated with blood thyrotropin (TSH) levels, but not with titers of TRAb. A significant correlation was observed between TRAb titer and thyroid-stimulating antibody (TSAb) activity. In contrast, this correlation was not found in normal subjects. After administration of T3 (75 microg daily for 8 days), the patients showed increased levels of T3 with concomitant suppression of TSH levels. Under these conditions, linear regression analysis showed significant correlations of TRAb titer and TSAb activity with 24-h thyroid radioiodine uptake (r = 0.641 and 0.621 respectively, P < 0.01), in contrast to declining blood thyroxine levels. Moreover, the immunoglobulin G (IgG) of the patients precipitated to a greater extent than IgG from normal subjects a peptide consisting of the amino acid sequence near the terminus of the human TSH receptor. These findings indicated that TRAb at normal levels possessed significant unremitting activities on thyroid function despite long-term treatment in euthyroid patients with Graves' disease.

Antibody-dependent cell-mediated growth inhibition of rat thyroid cells, FRTL-5, in patients with autoimmune thyroid diseases

1988 ◽  
Vol 118 (4) ◽  
pp. 580-586 ◽  
Author(s):  
Yasuhiro Iida ◽  
Kanji Kasagi ◽  
Yasutaka Tokuda ◽  
Keisuke Arai ◽  
Takashi Misaki ◽  
...  
Keyword(s):  
Growth Inhibition ◽  
Mononuclear Cell ◽  
Thymidine Incorporation ◽  
Normal Subjects ◽  
Human Thyroid ◽  
Graves Disease ◽  
Thyroid Cell ◽  
Chronic Thyroiditis ◽  
Thyroid Cells ◽  
Rat Thyroid

Abstract. We studied antibody-dependent mononuclear cell-mediated growth inhibition of thyroid cells in 18 untreated patients with Graves' disease, 18 patients with chronic thyroiditis, and 15 normal subjects by measuring the ability of their sera to inhibit [3H]thymidine incorporation into DNA in a rat thyroid cell line, FRTL-5, in the presence of normal mononuclear cells. [3H]thymidine incorporation was significantly inhibited in the presence of sera from patients with Graves' disease and chronic thyroiditis (P <0.001), whereas it was not affected in normal subjects. A significant correlation was observed between the inhibition of [3H]thymidine incorporation and the titre of anti-microsomal antibodies (P <0.05). The inhibitory effect on [3H]thymidine incorporation was significantly abolished when serum pre-absorbed with human thyroid membranes was used (P <0.005). These inhibitory effects on [3H]thymidine incorporation significantly correlated with those obtained by using IgG fractions (P <0.01). These data indicate that antibody-dependent mononuclear cell-mediated growth inhibtion may play a role in thyroid cell growth regulation in patients with autoimune thyroid disease.

Immunoglobulins from Graves' disease patients stimulate phospholipase A2 and C systems in FRTL-5 and human thyroid cells

1996 ◽  
Vol 135 (3) ◽  
pp. 322-327 ◽  
Author(s):  
Mohamed A Atwa ◽  
Robert C Smallridge ◽  
Henry B Burch ◽  
Irene D Gist ◽  
Rui Lu ◽  
...  
Keyword(s):  
Immunoglobulin G ◽  
Normal Subjects ◽  
Phospholipase A ◽  
Human Thyroid ◽  
Graves Disease ◽  
Washington Dc ◽  
Dependent Manner ◽  
Thyroid Cells ◽  
Dose Dependent ◽  
External Calcium

Atwa MA, Smallridge RC, Burch HB, Gist ID, Lu R, Abo-Hashem EM, El-Kannishy MH, Burman KD. Immunoglobulins from Graves' disease patients stimulate phospholipase A2 and C systems in FRTL-5 and human thyroid cells. Eur J Endocrinol 1996;135:322–7. ISSN 0804–4643 We have studied the effects of immunoglobulin G from Graves' disease patients on phospholipase A2 (PLA2) and C (PLC) systems in FRTL-5 and human thyroid cells. Immunoglobulin G (IgG) from Graves' disease patients stimulated arachidonic acid (AA) release in a time- and dose-dependent manner. In FRTL-5 thyroid cells, removal of external calcium had no significant effect on the IgG (20 μg/ml)-induced AA release in FRTL-5 thyroid cells. U-73122 (3 μmol/l), a PLC inhibitor, and quinacrine (100 μmol/l) but not U-26384 (5 μmol/l), PLA2 inhibitors, blocked the IgG-induced (20 μg/ml) AA release in FRTL-5 thyroid cells. Immunoglobulin G (100 μg/ml) also stimulated accumulation of inositol-1,4,5-triphosphate (IP3) in a time- and dose-dependent (20–300 μg/ml) manner in FRTL-5 cells. Immunoglobulin G from Graves' disease patients induced a significant increase of IP3 production (p = 0.01) compared to IgG from normal subjects. Removal of external calcium had no significant effect on the IgG-induced IP3 production. The PLC inhibitor U-73122 completely blocked IgG-induced IP3 production from FRTL-5 thyroid cells. Also, in human thyroid cells, IgG from Graves' disease patients induced a significant increase of AA release (p = 0.001) and IP3 production (p = 0.004) compared to the IgG from normal subjects. These data indicate that IgG from Graves' disease patients induced PLA2 activity that was PLC dependent, a pattern referred to as sequential activation. Our studies suggest that IgG from Graves' disease patients activates PLA2 and PLC systems in FRTL-5 and human thyroid cells. These signal transduction pathways could be involved in the pathogenesis of Graves' disease and future studies are warranted to investigate this area. Kenneth D Burman, Endocrine Section, Washington Hospital Center, 110 Irving St. NW, Washington, DC 20010, USA

Short- and Long-Term Results of Total vs Subtotal Thyroid- ectomies in the Surgical Treatment of Graves' Disease

Swiss Surgery ◽  
2001 ◽  
Vol 7 (1) ◽  
pp. 20-24 ◽  
Author(s):  
Robert ◽  
Mariéthoz ◽  
Pache ◽  
Bertin ◽  
Caulfield ◽  
...  
Keyword(s):  
Recurrent Laryngeal Nerve ◽  
Nerve Palsy ◽  
Recurrent Laryngeal Nerve Palsy ◽  
Laryngeal Nerve ◽  
Long Term Results ◽  
Graves Disease ◽  
Laryngeal Nerve Palsy ◽  
Short And Long Term

Objective: Approximately one out of five patients with Graves' disease (GD) undergoes a thyroidectomy after a mean period of 18 months of medical treatment. This retrospective and non-randomized study from a teaching hospital compares short- and long-term results of total (TT) and subtotal thyroidectomies (ST) for this disease. Methods: From 1987 to 1997, 94 patients were operated for GD. Thirty-three patients underwent a TT (mostly since 1993) and 61 a ST (keeping 4 to 8 grams of thyroid tissue - mean 6 g). All patients had received propylthiouracil and/or neo-mercazole and were in a euthyroid state at the time of surgery; they also took potassium iodide (lugol) for ten days before surgery. Results: There were no deaths. Transient hypocalcemia (< 3 months) occurred in 32 patients (15 TT and 17 ST) and persistent hypocalcemia in 8 having had TT. Two patients developed transient recurrent laryngeal nerve palsy after ST (< 3 months). After a median follow-up period of seven years (1-15) with five patients lost to follow-up, 41 patients having had a ST are in a hypothyroid state (73%), thirteen are euthyroid (23%), and two suffered recurrent hyperthyroidism, requiring completion of thyroidectomy. All 33 patients having had TT - with follow-ups averaging two years (0.5-8) - are receiving thyroxin substitution. Conclusions: There were no instances of persistent recurrent laryngeal nerve palsy in either group, but persistent hypoparathyroidism occurred more frequently after TT. Long after ST, hypothyroidism developed in nearly three of four cases, whereas euthyroidy was maintained in only one-fourth; recurrent hyperthyroidy was rare.

[18F]Fluoride PET Indicates Reduced Bone Formation in Severe Glucocorticoid-induced Osteoporosis

1998 ◽  
Vol 37 (02) ◽  
pp. 76-79 ◽  
Author(s):  
T. D. Kirchhoff ◽  
W. Burchert ◽  
J. v. d. Hoff ◽  
H. Zeidler ◽  
H. Hundeshagen ◽  
...  
Keyword(s):  
Bone Formation ◽  
Multiple Organ ◽  
High Dose ◽  
Multiple Fractures ◽  
Glucocorticoid Treatment ◽  
Organ Manifestations ◽  
Diagnostic Benefit ◽  
Sharp Syndrome ◽  
18F Fluoride

SummaryA 61-year-old female patient presenting with mixed connective tissue disease (Sharp syndrome), underwent a long-term high dose glucocorticoid treatment because of multiple organ manifestations. Under steroid therapy she developed severe osteoporosis resulting in multiple fractures. A dynamic [18F]fluoride PET study in this patient revealed reduced fluoride influx in non-fractured vertebrae. This finding corresponds to pathogenetic concepts which propose an inhibition of bone formation as major cause of glucocorticoid-induced osteoporosis. In the light of the presented case it seems to be promising to evaluate the diagnostic benefit of [18F]fluoride PET in osteoporosis.

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