scholarly journals Hypogonadotropic and Hypergonadotropic Hypogonadism

Testosterone ◽  
2017 ◽  
pp. 133-145
Author(s):  
Vijaya Surampudi ◽  
Ronald S. Swerdloff
2014 ◽  
Author(s):  
Murat Sahin ◽  
Ayten Oguz ◽  
Selda Yilmaz ◽  
Elif Inanc ◽  
Murat Ozdemir ◽  
...  

2011 ◽  
Vol 155 (2) ◽  
pp. 403-408 ◽  
Author(s):  
D. Misceo ◽  
O.K. Rødningen ◽  
T. Barøy ◽  
H. Sorte ◽  
J.R. Mellembakken ◽  
...  

PEDIATRICS ◽  
1984 ◽  
Vol 73 (5) ◽  
pp. 741-741
Author(s):  
HAROLD K. MARDER ◽  
LAXMI S. SRIVASTAVA ◽  
STEPHEN BURSTEIN

In Reply.— We thank Nishi et al for outlining the role that has been suggested for zinc in normal testicular function and the speculation that zinc deficiency might contribute to the hypergonadotropic hypogonadism found in males with chronic renal failure. We have no data concerning zinc levels in our patients, and so we felt we could offer no further insight into the possibility that zinc deficiency might play a role in the etiology of the hypergonadotropism we described.


2020 ◽  
Author(s):  
Amanda French

Although common, delayed puberty can be distressing to patients and families.   Careful assessment is necessary to ensure appropriate physical and social development in patients that require intervention to reach pubertal milestones and achieve optimal growth.  Most pubertal delay is from lack of activation of the hypothalamic-pituitary-gonadal axis which then results in a functional or physiologic GnRH deficiency.  The delay may be temporary or permanent.  Constitutional delay (CDGP), also referred to as self-limited delayed puberty (DP), describes children on the extreme end of normal pubertal timing and is the most common cause of delayed puberty, representing about one third of cases.  Hypergonadotropic hypogonadism (primary hypogonadism) results from a failure of the gonad itself, and hypogonadotropic hypogonadism (secondary hypogonadism) results from a failure of the hypothalamic-pituitary axis, which is usually caused by another process, often systemic.  Diagnosis is based on history and examination.  Treatment is based on the underlying cause of pubertal delay and may include hormone replacement.  Involving a pediatric endocrinologist should be considered.  Appropriate counseling and ongoing support are important for all patients and families, regardless of underlying disease process.   This review contains 4 figures, 4 tables, and 32 references. Keywords: puberty, delayed puberty, hypogonadism, hypogonadotropic hypogonadism, hypergonadotropic hypogonadism, menarche, thelarche, constitutional delay and growth in puberty, Turner syndrome


Author(s):  
Gerard S. Conway ◽  
Jacqueline Doyle ◽  
Melanie C. Melanie

The average age of menopause, denoted by the last menstrual period, occurs at an average age of 50.7 years in the western world (1) and this age has been found to be constant across generations, although one group have reported a secular trend to advancing menopausal age (2). The age of menopause in an individual is determined by both genetic and environmental factors (1, 3). Menopause before the age of 40 is most commonly taken to be the definition of ‘premature ovarian failure’ and this coincides approximately with youngest one percent of the frequency distribution of the age of menopause (Fig. 8.1.5.1). For every decade before 40 the prevalence of POF is estimated to decrease by a factor of 10. Thus, in presence of normal karyotype, 1:1000 of women at 30 has POF, 1:10 000 at 20 and 1:100 000 of women will present with gonadal failure and primary amenorrhoea. In terms of the mode of presentation, premature ovarian failure (POF) is the aetiology of 20% of cases with primary amenorrhoea and 10% of those with secondary amenorrhoea. Premature ovarian failure (POF) refers to the cessation of ovarian function at an earlier than expected age due to ovarian pathology. Primary ovarian failure is used in two contexts—to describe very early onset ovarian failure presenting with primary amenorrhoea and also to differentiate ovarian pathology from secondary ovarian failure, which refers to lack of ovarian activity as a result of gonadotropin deficiency. Primary ovarian insufficiency is recently favoured as an all-encompassing term that accounts for the variable course and occasional remission (4). The term hypergonadotropic hypogonadism is also used to emphasize ovarian origin. Resistant ovary syndrome (ROS) is an obsolete term, used to describe the coexistence of hypergonadotropic hypogonadism with normal ovarian follicles on histology of the ovary. It was soon realized that women with ROS progressed to complete ovarian failure and that ovarian follicles on histology were commonly found in established ovarian failure, negating the usefulness of this diagnostic label. Very early onset ovarian failure with a known genetic cause is often labelled inaccurately as ‘gonadal dysgenesis’ as in most situations it is thought that early ovarian development is normal.


Sign in / Sign up

Export Citation Format

Share Document