scholarly journals Precocious Puberty with Primary Hypothyroidism due to Autoimmune Thyroiditis

2016 ◽  
Vol 34 (1) ◽  
pp. 45-47
Author(s):  
Setara Binte Kasem
Keyword(s):  
Precocious Puberty ◽  
Autoimmune Thyroiditis ◽  
Vaginal Bleeding ◽  
Linear Growth ◽  
Pubertal Development ◽  
Hormone Replacement ◽  
Primary Hypothyroidism ◽  
Thyroid Hormone Replacement ◽  
Rare Association ◽  
Characteristic Features

Children with hypothyroidism generally have delayed pubertal development. Rare association with precocious puberty may occur especially in long standing untreated patients. The cardinal features of hypothyroidism induced pseudoprecocious pubertal development include thelarche, galactorrhoea & menarche . Other characteristic features are absence of sexual hair & retardation of linear growth. In this report a rare case of vaginal bleeding, large multicystic ovaries, precocious puberty, slow physical & mental growth in a seven and half years old girl with hypothyroidism due to autoimmune thyroiditis is described. It is important to recognize this syndrome because initiating simple thyroid hormone replacement completely resolves symptoms and hormone abnormalities, avoiding unnecessary investigations for malignancies or surgical intervention.J Bangladesh Coll Phys Surg 2016; 34(1): 45-47

scholarly journals Premature Menarche Associated with Primary Hypothyroidism in a 5.5-Year-Old Girl

2011 ◽  
Vol 2011 ◽  
pp. 1-3
Author(s):  
Dhrubajyoti Sharma ◽  
Devi Dayal ◽  
Anju Gupta ◽  
Akshay Saxena
Keyword(s):  
Precocious Puberty ◽  
Vaginal Bleeding ◽  
Linear Growth ◽  
Pubertal Development ◽  
Primary Hypothyroidism ◽  
Autoimmune Hypothyroidism ◽  
Rare Association ◽  
History Of ◽  
Multiple Cysts

Children with hypothyroidism generally have delayed pubertal development. Rare association with precocious puberty may occur especially in long standing untreated patients. The cardinal features of hypothyroidism induced pseudo precocious pubertal development include thelarche, galactorrhea and menarche. Other characteristics features are an absence of sexual hair and retardation of linear growth. Its manifestation as isolated menarche has been rarely reported. Recently, a five and half year old girl presented to us with history of one episode of vaginal bleeding. A pelvic ultrasonogram revealed multiple cysts in both ovaries and subsequent investigations led to a diagnosis of autoimmune hypothyroidism.

scholarly journals Persistence of hyperprolactinemia after treatment of primary hypothyroidism and withdrawal of long term use of estrogen: are the tuberoinfundibular dopaminergic neurons permanently lesioned?

2005 ◽  
Vol 49 (3) ◽  
pp. 468-472 ◽  
Author(s):  
Luiz Augusto Casulari ◽  
Fábio Celotti ◽  
Luciana A. Naves ◽  
Lucília Domingues ◽  
Carla Papadia
Keyword(s):  
Dopaminergic Neurons ◽  
Hormone Replacement ◽  
Hormonal Contraceptive ◽  
Primary Hypothyroidism ◽  
Trh Test ◽  
Pituitary Mass ◽  
Thyroid Hormone Replacement ◽  
Before And After ◽  
High Doses

Long term use of high doses of estrogen and the presence of chronic hyperprolactinemia may, at least in the rat, provoke lesions in the tuberoinfundibular dopaminergic (TIDA) neurons responsible for the control of prolactin (Prl) secretion. This occurrence, which is not yet well documented in humans, may have taken place in a patient on chronic oral hormonal contraceptive (OC) treatment who was seen for primary hypothyroidism, hyperprolactinemia and a pituitary mass. After thyroid hormone replacement, OC withdrawn and bromocriptine treatment, this patient could not maintain normal Prl levels, unless continuously treated with a dopaminergic agonist even when MRI was indicative of a normal situation. Function of TIDA neurons was investigated by TRH test (200µg IV) performed before and after treatment with 25mg carbidopa plus 250mg L-dopa every 4 hours for one day. Basal TSH was normal (3.9µU/mL) whereas basal Prl was high (67.5 ng/mL); both TSH and Prl levels appropriately increased after TRH: peaks 31.8µU/mL and 157.8 ng/mL, respectively. After treatment with carbidopa/L-dopa, basal TSH (1.6µU/mL) and Prl (34ng/mL) decreased and the response to TRH was partially blocked (10.3µU/mL and 61ng/mL, respectively). In spite of a normal response, we discuss the possibility that the persistence of hyperprolactinemia is due to lesion of the TIDA neurons produced by the long term use of high doses of estrogens and by the presence of chronic hyperprolactinemia.

scholarly journals Unusual Presentation of Precocious Puberty Associated with Primary Hypothyroidism in a 8.5 Years Old Girl

2018 ◽  
Vol 6 (2) ◽  
pp. 102-105
Author(s):  
Shamsun Naher Rikta ◽  
Fatema Ashraf ◽  
Samira Areen
Keyword(s):  
Precocious Puberty ◽  
Rare Complication ◽  
Pubertal Development ◽  
Thyroid Function Test ◽  
Ovarian Tumour ◽  
Primary Hypothyroidism ◽  
Monthly Interval ◽  
Close Monitoring ◽  
College Hospital ◽  
Ovarian Volume

Precocious puberty is one of the gynaecological problems in childhood. Children with hypothyroidism generally have delayed pubertal development. But primary hypothyroidism is one of the rare causes of precocious puberty especially in long standing untreated patients. Bilateral ovarian enlargement due to multiple cystic ovaries is a rare complication of primary hypothyroidism. For ovarian enlargement no treatment is required at all. This is a case report of an 8.5 years old girl diagnosed as a case of precocious puberty with benign ovarian tumour at a peripheral hospital and was being prepared to undergo laparotomy. When patient was admitted at Shaheed Suhrawardy Medical College Hospital (ShSMCH), Dhaka, Bangladesh, after thorough investigations primary hypothyroidism was diagnosed. She was given thyroxin replacement and close monitoring was done by doing USG of uterus and adnexae, thyroid function test at monthly interval. USG after 2 months revealed significant reduction of ovarian volume and at 6 month ovarian volume reduced to normal. It was also noticed that the rate of reduction of ovarian volume corresponds to the rate of reduction of serum TSH level measured serially at every 2 months interval.Delta Med Col J. Jan 2018 6(2): 102-105

scholarly journals Hypothyroidism with Ascites

1970 ◽  
Vol 10 (2) ◽  
pp. 121-123
Author(s):  
Md Titu Miah ◽  
Raihan Rotap Khan ◽  
Zannatun Nur ◽  
Syed Mohammad Ali Romel ◽  
Md Kamal Hossain Patwary ◽  
...  
Keyword(s):  
Replacement Therapy ◽  
Complete Resolution ◽  
Hormone Replacement ◽  
Primary Hypothyroidism ◽  
Thyroid Hormone Replacement ◽  
Thyroid Hormone Replacement Therapy ◽  
Unnecessary Procedures ◽  
Liver Biopsies ◽  
High Index Of Suspicion ◽  
Key Words Ascites

Primary hypothyroidism is a common clinical condition. Ascites caused by hypothyroidism is rare. So its diagnosis is often delayed and patients frequently receive unnecessary procedures such as liver biopsies and exploratory laparotomies. We report a male person of 58 years with hypothyroidism with ascites who responded well with thyroid hormone replacement therapy with complete resolution of ascites. Analyses of ascites from patients in this condition usually shows exudative ascites with high protein (>2.5 g/dL) and SAAG < 1.1 gm/dl. High index of suspicion is required to reach at such diagnosis. Though it is a rare but prognosis is excellent with replacement therapy. Key words: Ascites, Hypothyroidism.   doi: 10.3329/jom.v10i2.2828   J MEDICINE 2009; 10 : 121-123

scholarly journals Effect of Adequate Thyroid Hormone Replacement on the Hypothalamo-Pituitary-Gonadal Axis in Premenopausal Women with Primary Hypothyroidism

2019 ◽  
Vol 8 (3) ◽  
pp. 152-158
Author(s):  
Bharath Bachimanchi ◽  
Suresh Vaikkakara ◽  
Alok Sachan ◽  
Ganji Praveen Kumar ◽  
Ashok Venkatanarasu ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Hormone Replacement ◽  
Premenopausal Women ◽  
Primary Hypothyroidism ◽  
Thyroid Hormone Replacement

Precocious Puberty

2006 ◽  
Vol 00 (02) ◽  
Author(s):  
Paul B Kaplowitz
Keyword(s):  
Precocious Puberty ◽  
Linear Growth ◽  
Pubertal Development ◽  
Black Girls ◽  
Pubic Hair ◽  
Growth Spurt ◽  
Tall Stature ◽  
Early Puberty ◽  
Bone Maturation ◽  
Early Appearance

Precocious puberty refers to the appearance of physical and hormonal signs of pubertal development at an earlier age than is considered normal.Although traditionally, any signs of puberty in girls prior to age eight years have been considered abnormal, recent studies indicate that signs of early puberty (breasts and pubic hair) are often present in girls (particularly black girls) between ages 6–8 years.The early growth spurt initially can cause tall stature, but rapid bone maturation can cause linear growth to cease too early and result in short adult stature.The early appearance of breasts or menses in girls and increased libido in boys can cause emotional distress for some children.

Inherited primary hypothyroidism with thyrotrophin resistance in Japanese cats

1991 ◽  
Vol 129 (2) ◽  
pp. 245-NP ◽  
Author(s):  
H. Tanase ◽  
K. Kudo ◽  
H. Horikoshi ◽  
H. Mizushima ◽  
T. Okazaki ◽  
...  
Keyword(s):  
Autosomal Recessive ◽  
Hormone Replacement ◽  
Primary Hypothyroidism ◽  
Serum Concentrations ◽  
Laboratory Studies ◽  
Thyroid Hormone Replacement ◽  
Threefold Increase ◽  
Thyroid Glands ◽  
Mild Anaemia ◽  
Autosomal Recessive Manner

ABSTRACT Mutant cats were developed with non-goitrous primary hypothyroidism. They were clinically characterized by severely retarded growth, mild anaemia and high mortality in the young. They responded markedly to thyroid hormone replacement. Thyroid glands in the mutants were normal in position but slightly reduced in size. Laboratory studies revealed low serum concentrations of thyroxine (T4) and tri-iodothyronine (T3), and increased serum concentrations of TSH. Administration of TRH induced no further increase in TSH. Administration of exogenous TSH after suppression of endogenous TSH by T3 did not increase the serum concentration of T4 in the mutants, in sharp contrast with the threefold increase in serum T4 observed in the normal litter-mates. These findings suggest that the underlying pathogenesis of this disorder is unresponsive to TSH. Moreover, we found that the mutants were transmitted in an autosomal recessive manner. Journal of Endocrinology (1991) 129, 245–251

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