scholarly journals Intrauterine exposure to mild analgesics is a risk factor for development of male reproductive disorders in human and rat

2010 ◽  
Vol 26 (1) ◽  
pp. 235-244 ◽  
Author(s):  
David Møbjerg Kristensen ◽  
Ulla Hass ◽  
Laurianne Lesné ◽  
Grete Lottrup ◽  
Pernille Rosenskjold Jacobsen ◽  
...  
Keyword(s):  
Risk Factor ◽  
Reproductive Disorders ◽  
Intrauterine Exposure ◽  
Mild Analgesics

scholarly journals Ibuprofen alters human testicular physiology to produce a state of compensated hypogonadism

2018 ◽  
Vol 115 (4) ◽  
pp. E715-E724 ◽  
Author(s):  
David Møbjerg Kristensen ◽  
Christèle Desdoits-Lethimonier ◽  
Abigail L. Mackey ◽  
Marlene Danner Dalgaard ◽  
Federico De Masi ◽  
...  
Keyword(s):  
Sertoli Cells ◽  
Transcriptional Repression ◽  
Endocrine System ◽  
Western World ◽  
Fetal Life ◽  
Reproductive Disorders ◽  
Elderly Men ◽  
Steroidogenic Cell ◽  
Physical Disorders ◽  
Mild Analgesics

Concern has been raised over increased male reproductive disorders in the Western world, and the disruption of male endocrinology has been suggested to play a central role. Several studies have shown that mild analgesics exposure during fetal life is associated with antiandrogenic effects and congenital malformations, but the effects on the adult man remain largely unknown. Through a clinical trial with young men exposed to ibuprofen, we show that the analgesic resulted in the clinical condition named “compensated hypogonadism," a condition prevalent among elderly men and associated with reproductive and physical disorders. In the men, luteinizing hormone (LH) and ibuprofen plasma levels were positively correlated, and the testosterone/LH ratio decreased. Using adult testis explants exposed or not exposed to ibuprofen, we demonstrate that the endocrine capabilities from testicular Leydig and Sertoli cells, including testosterone production, were suppressed through transcriptional repression. This effect was also observed in a human steroidogenic cell line. Our data demonstrate that ibuprofen alters the endocrine system via selective transcriptional repression in the human testes, thereby inducing compensated hypogonadism.

Hypogonadotropic Hypogonadism Associated With Obesity: A Case Report

2021 ◽  
Author(s):  
Niloufar Johari Varnoosfaderani ◽  
Sahar Karimpour Reyhan ◽  
Mahsa Abbaszadeh ◽  
Nasim Khajavirad
Keyword(s):  
Adipose Tissue ◽  
Risk Factor ◽  
Hypogonadotropic Hypogonadism ◽  
Reproductive Disorders ◽  
Secondary Sexual Characteristics ◽  
Cardiovascular Comorbidities ◽  
Preventable Risk Factor ◽  
Sexual Characteristics ◽  
Different Levels ◽  
Significant Factors

One of the most significant factors with a broad impact on health is obesity. Besides cardiovascular comorbidities caused by obesity, its probable association with hypogonadotropic hypogonadism in men was discussed in this article. We described a severe obese boy, presenting with no secondary sexual characteristics and hypertension. The hypothalamus-hypophyseal-gonadal axis can be influenced by multiple mechanisms at different levels of the axis. Some of these pathophysiological mechanisms, related to our case, were explained aiming at explaining the association between obesity and accompanied reproductive disorders. Adipose tissue, as an essential influencer, insignificantly affects the metabolism of hormones secreted by other glands. Obesity, as a preventable risk factor, is valuable to be researched to decrease the burden of its induced morbidity and mortality. Thus, further studies should be conducted to exactly determine the complex network of characteristics impacting hormonal imbalances in obese individuals.

scholarly journals Intrauterine exposure to mild analgesics during pregnancy and the occurrence of cryptorchidism and hypospadia in the offspring: the Generation R Study

2012 ◽  
Vol 27 (4) ◽  
pp. 1191-1201 ◽  
Author(s):  
C. A. Snijder ◽  
A. Kortenkamp ◽  
E. A. P. Steegers ◽  
V. W. V. Jaddoe ◽  
A. Hofman ◽  
...  
Keyword(s):  
Intrauterine Exposure ◽  
Mild Analgesics

Intrauterine Exposure to Maternal Enterovirus Infection as a Risk Factor for Development of Autoimmune Thyroiditis During Childhood and Adolescence

Thyroid ◽  
2004 ◽  
Vol 14 (5) ◽  
pp. 367-370 ◽  
Author(s):  
Johan Svensson ◽  
Bengt Lindberg ◽  
Björn Jonsson ◽  
Ulla-Britt Ericsson ◽  
Per Olofsson ◽  
...  
Keyword(s):  
Risk Factor ◽  
Autoimmune Thyroiditis ◽  
Childhood And Adolescence ◽  
Enterovirus Infection ◽  
Intrauterine Exposure

Clinical aspects of reactive oxygen and nitrogen species

2004 ◽  
Vol 71 ◽  
pp. 121-133 ◽  
Author(s):  
Ascan Warnholtz ◽  
Maria Wendt ◽  
Michael August ◽  
Thomas Münzel
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Risk Factor ◽  
Endothelial Dysfunction ◽  
Vascular Tissue ◽  
Rapid Development ◽  
Reactive Oxygen ◽  
Clinical Aspects ◽  
No Production ◽  
Oxygen Species

Endothelial dysfunction in the setting of cardiovascular risk factors, such as hypercholesterolaemia, hypertension, diabetes mellitus and chronic smoking, as well as in the setting of heart failure, has been shown to be at least partly dependent on the production of reactive oxygen species in endothelial and/or smooth muscle cells and the adventitia, and the subsequent decrease in vascular bioavailability of NO. Superoxide-producing enzymes involved in increased oxidative stress within vascular tissue include NAD(P)H-oxidase, xanthine oxidase and endothelial nitric oxide synthase in an uncoupled state. Recent studies indicate that endothelial dysfunction of peripheral and coronary resistance and conductance vessels represents a strong and independent risk factor for future cardiovascular events. Ways to reduce endothelial dysfunction include risk-factor modification and treatment with substances that have been shown to reduce oxidative stress and, simultaneously, to stimulate endothelial NO production, such as inhibitors of angiotensin-converting enzyme or the statins. In contrast, in conditions where increased production of reactive oxygen species, such as superoxide, in vascular tissue is established, treatment with NO, e.g. via administration of nitroglycerin, results in a rapid development of endothelial dysfunction, which may worsen the prognosis in patients with established coronary artery disease.

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