scholarly journals Compound Heterozygous Mutations in theGNASGene of a Boy with Morbid Obesity, Thyroid-Stimulating Hormone Resistance, Pseudohypoparathyroidism, and a Prothrombotic State

2008 ◽  
Vol 93 (12) ◽  
pp. 4844-4849 ◽  
Author(s):  
Kathleen Freson ◽  
Benedetta Izzi ◽  
Jaak Jaeken ◽  
Monique Van Helvoirt ◽  
Chantal Thys ◽  
...  
2015 ◽  
Vol 8 (1) ◽  
pp. 32-33
Author(s):  
SM Ashrafuzzaman ◽  
Zafar A Latif

Resistance to thyrotropin or thyroid stimulating hormone (RTSH) can be defined as decreased responsiveness to thyroid stimulating hormone (TSH) characterized by high TSH with normal but occasionally low T4 and T3 usually in absence of goiter or ectopic thyroid. It can be diagnosed when TSH is >30 mIU/L but free T4 (FT4) is within normal limit. Patient usually presents in euthyroid state with abnormally high TSH but may also present with mild to overt hypothyroidism. The precise prevalence is not known, but 20-30% infants may show transient mild RTSH. In adults it is rare.Here we report a case of RTSH in which a 19 years old young girl presented in euthyroid state with mild goiter.Ibrahim Med. Coll. J. 2014; 8(1): 32-33


1982 ◽  
Vol 243 (1) ◽  
pp. E37-E42
Author(s):  
A. M. Spiegel ◽  
M. A. Levine ◽  
G. D. Aurbach ◽  
R. W. Downs ◽  
S. J. Marx ◽  
...  

Pseudohypoparathyroidism is an inherited disorder associated with resistance to the action of several hormones, including parathyroid hormone, thyroid-stimulating hormone, follicle-stimulating hormone, and luteinizing hormone. The disorders described under this designation are heterogeneous in regard to the underlying genetic defects, the phenotypic manifestation, and the severity of the defects in hormone action. The majority of affected individuals who also have the characteristic skeletal changes (heredity osteodystrophy) have a defect in the guanine nucleotide regulatory protein (G protein) that is essential for coupling certain cell-surface hormone receptors to the adenylate cyclase system. This defect is probably the cause for resistance to the action of multiple hormones. In the remaining patients the cause for hormone resistance has not been identified.


Nutrients ◽  
2019 ◽  
Vol 11 (5) ◽  
pp. 1121 ◽  
Author(s):  
Paula Juiz-Valiña ◽  
Elena Outeiriño-Blanco ◽  
Sonia Pértega ◽  
Bárbara María Varela-Rodriguez ◽  
María García-Brao ◽  
...  

Obesity is associated with several endocrine abnormalities, including thyroid dysfunction. The objective of this study was to investigate the effect of weight loss after bariatric surgery on thyroid-stimulating hormone (TSH) levels in euthyroid patients with morbid obesity. We performed an observational study, evaluating patients with morbid obesity submitted to bariatric surgery. We included 129 patients (92 women) and 31 controls (21 women). Clinical, anthropometric, biochemical, and hormonal parameters were evaluated. The primary endpoint was circulating TSH (µU/mL). Fasting TSH levels were higher in the obese group (3.3 ± 0.2) than in the control group (2.1 ± 0.2). The mean excessive body mass index (BMI) loss (EBMIL) 12 months after bariatric surgery was 72.7 ± 2.1%. TSH levels significantly decreased in the obese patients after surgery; 3.3 ± 0.2 vs. 2.1 ± 0.2 before and 12 months after surgery, respectively. Free thyroxine (T4) (ng/dL) levels significantly decreased in the obese patients after surgery; 1.47 ± 0.02 vs. 1.12 ± 0.02 before and 12 months after surgery, respectively. TSH decreased significantly over time, and the decrement was associated with the EBMIL. In euthyroid patients with morbid obesity, weight loss induced by bariatric surgery promotes a significant decline of the increased TSH levels. This decrement of TSH is progressive over time after surgery and significantly associated with excess BMI loss.


1961 ◽  
Vol 38 (4) ◽  
pp. 577-584 ◽  
Author(s):  
Sven Erik Björkman ◽  
Torsten Denneberg ◽  
Inge Hedenskog

ABSTRACT A method for demonstrating the presence of a thyroid stimulating factor in the blood of patients with progressive exophthalmos after thyroidectomy or after treatment with radioiodine is described. The method consists of transfusing freshly drawn blood from the patients to euthyroid recipients and subsequently following the PBI level of the recipients at regular intervals. Six exophthalmic patients tested in this manner were found to have such a factor in their circulating blood. After transfusion of their blood a significant rise in the PBI level of the recipients could be demonstrated. Two other patients, one with exophthalmos of long duration did not show this response nor did it occur after transfusion of blood from two control subjects. In one case the action of this factor was compared with that of animal thyrotrophin and found to be of the same magnitude.


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