Research Topic

The Male HPG Axis and Chronic Diseases

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Background
Serum testosterone (T) concentration is reduced in the presence of chronic or acute diseases such as diabetes, obesity, polypharmacy, hypertension, cardiac, hepatic or renal failure, chronic obstructive lung disease, rheumatologic conditions, cancer, HIV positivity, myocardial infarction, ...

Background
Serum testosterone (T) concentration is reduced in the presence of chronic or acute diseases such as diabetes, obesity, polypharmacy, hypertension, cardiac, hepatic or renal failure, chronic obstructive lung disease, rheumatologic conditions, cancer, HIV positivity, myocardial infarction, burns, inflammatory bowel disease, sepsis, ICU admission. It is not clear whether the association of hypotestosteronemia with these conditions is a physiologic adaptation (e.g. is explainable because all non-vital functions, including reproductive functions, are shut off to minimize expenditure of energy that is not utilized for recovery or survival), or is rather a maladaptation, which may place the patient at increased risk by inducing a spectrum of catabolic states such as fatigue, change in body composition, frailty, sarcopenia, increased risk of falling, or cachexia.

Details for Authors:
While the concept that certain acute or chronic conditions are associated with hypotestosteronemia is fairly- well established, a comprehensive review of this topic is missing and is expected to shed light on important lingering questions. For instance, what is the overall prevalence of hypogonadism among these individuals? Are all these conditions responsible for a specific type of hypogonadism, (e.g. primary or secondary)? If it is a primary etiology, what is the mechanism responsible, is the process affecting only T release by Leydig cells, or is affecting also sperm formation? If it is a form of secondary hypogonadism, is the process mediated by abnormalities in the pituitary or hypothalamus and what is the mechanism? If the primary culprit is lack of GnRH release, is the process affecting GnRH neurons or rather a signaling pathway proximal to GnRH production? If it is a pituitary abnormality, are other pituitary hormones affected? Many of these acute or chronic illnesses are associated with an increased inflammatory phenotype, hence, do we know whether activities of inflammatory markers cause dysfunctions of the central structures, or of the interstitial or germinal compartments of the gonad? Many of these chronic conditions are associated with a constellation of catabolic states, hence, is it known whether treating these individuals with T is beneficial in reversing these catabolic manifestations similarly to what has been observed in men affected by classic hypogonadism treated with T.

A general way to organize review papers on this topic could follow this advice: 1. Citation and review of all papers that have addressed the epidemiology of hypotestosteronemia in the selected chronic (or acute) condition. 2. Does hypotestosteronemia affect the outcome of these conditions, i.e. facilitates a certain clinical end point, makes the individual more prone to develop certain complications or to die. 3. Review of the known and potential mechanisms. 4. Are published RCT or observational trials addressing the question of whether supplementation with T affects recovery of these patients. 5. For each condition, what are the unanswered questions, and what should be done to increase knowledge in terms of recognition, physiopathology and treatment.


Keywords: HPG axis, hypogonadism, COPD, CHF, Obesity, CKD, Chronic Liver Disease


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