Tuesday 12 August 2008

Late Onset Hypogonadism, ADAM, Andropause: What Is It And What Is The Treatment?

�UroToday.com - Late-onset hypogonadism (LOH), or androgen refuse in the aging male person, is a syndrome caused by the well-known go down in gonadal production of androgens in males that occurs with aging. It is characterized by clinical symptoms that accompany downcast serum androgen levels. LOH affects a wide reach of organ systems and has a broad harshness of clinical presentations. Sexual dysfunction, including erectile disfunction (ED), decreased libido, difficulty achieving climax, and decreased penile sensation, is normally the presenting complaint, although fatigue, grim mood, impaired cognition, and decreased heftiness mass are other common symptoms. If these symptoms are found in conjunction with low serum testosterone (T), a diagnosis of LOH may be made. Universally recognised guidelines for a level of T to define or treat LOH have not been established. In general, when the T level is found to be at or beneath the lower limit of normal, in conjunction with symptoms, treatment is appropriate.


The incidence of LOH is rising. Serum T levels decrease with years and according to U.S. Census data from 2000, the U.S. population of men 65 years of age and older is projected to double by the yr 2030. An extrapolation from the Massachusetts Male Aging Study set up a prevalence of LOH of nigh half a million fresh cases per year in men in their fifth, sixth, and seventh decades of life. The principal treatment for LOH is androgen successor, also known as testosterone replacement therapy (TRT). With the rising incidence of LOH and better agreement of treatment benefits, the use of TRT has been steadily increasing in recent years. This come up is evidenced by a 500% step-up in prescription sales of T since 1993.


The benefits of TRT are easily recognized, primarily because as levels of blood serum T anneal, desired improvements in sexual function, libido, and temper, as advantageously as in overall quality of biography are reached. TRT also has a positive effect on cardiovascular health; one well-documented effect of TRT is a decrease in total cholesterol and low-density lipoprotein (LDL)1. Recent studies have shown a nexus between hypogonadism and a high-risk and increasingly rife syndrome called metabolic syndrome, also known as insulin resistance syndrome, or syndrome X. Metabolic syndrome is characterized by at least 3 of the following: abdominal obesity, hypertriglyceridemia, low high-density lipoprotein (HDL), hyperglycemia, and hypertension2. Laaksonen and colleagues experience suggested that hypogonadism is an element of metabolic syndrome based on their large population-based study. Treatment of LOH with TRT may ameliorate the symptoms of metabolic syndrome, and vice versa, treatment of metabolic syndrome may improve the symptoms of LOH.



Despite its benefits, TRT has a number of contraindications, and questions remain regarding its personal effects on prostate health. Benign prostatic hyperplasia (BPH) is an androgen-sensitive disease which is accelerated by endogenous and exogenous T. The incidence of BPH increases with eld, and prostate volume is decreased in hypogonadal workforce compared to men with normal blood serum T. Prostate volumes of men with LOH undergoing TRT increase up to the levels of age-matched controls, merely TRT has not been shown to drastically addition prostate intensity beyond that of eugonadal men of the same age. Similar to BPH, prostate cancer the Crab (CaP) is exquisitely androgenic hormone sensitive. First-line treatment for metastatic CaP is androgen deprivation, either through bilaterally symmetric orchiectomy or medical castration with gonadotropin-releasing hormone agonists. While numerous studies have failed to show that exogenous T is a direct cause of CaP, the fact that CaP is androgenic hormone sensitive raises the doubtfulness of whether T can buoy awaken a clinically insignificant CaP or augment a CaP into a higher Gleason level.


Short-term changes in prostate-specific antigen (PSA) levels during TRT stimulate been reported. Much of this information is derived from relatively small, oft retrospective studies. A classic double-blind, randomized, placebo-controlled study on the effect TRT has on PSA has yet to be published. A systematic review of 18 studies of short-run TRT for men with LOH performed in 2003 found an average PSA increase of 0.3 ng/mL, and a taxonomical review of 6 other published studies of TRT in slenderly older work force with LOH found a slightly higher average PSA increase of 0.43 ng/mL. The long-term effects TRT has on PSA, however, experience yet to be reported.

References:


1. Muller M, van der Schouw Y, Thijssen JHH: Endogenous sexual urge hormones and cardiovascular disease. J Clin Endocrinol Metab 2003; 88:5076-5086.

2. Expert Panel on Detection Evaluation and Treatment of High Blood Cholesterol in Adults: Executive Summary of The Third Report of The National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, And Treatment of High Blood Cholesterol In Adults (Adult Treatment Panel III). JAMA, 285: 2486, 2001.


Presented by: Culley C. Carson, MD, at the Masters in Urology Meeting - July 31, 2008 - August 2, 2008, Elbow Beach Resort, Bermuda

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