Testosterone -The Effects
You have sent too many requests causing Linguee to block your computerCompared with survivors with normal testosterone levels, survivors with low testosterone levels were more likely to have a range of chronic health problems, including sy,ptoms blood pressure, diabetes, erectile dysfunction, and anxiety or depression. Low testosterone levels can be present at the time of a testicular cancer diagnosis or develop as a side effect of surgery or chemotherapy. Although it has been known that low testosterone levels occur in a significant proportion of testicular cancer survivors, this is one of the first studies testosterone symptoms high examine its relationship with long-term health complications in North American patients. This analysis comes from the first patients enrolled in The Platinum Studywhich aims to be the largest study of testicular cancer survivors worldwide, with over 1, survivors already enrolled and still actively testosterone symptoms high. All patients received chemotherapy and were younger than age 55 when they were diagnosed with cancer. The median age testosterone symptoms high clinical evaluation was 38 years. The goal testosterone symptoms high the Tsetosterone Study is to follow the lifelong health of men who received testosterone enanthate dangers chemotherapy for testicular cancer.
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Nature and Physiology of Growth Hormone top. Growth hormone is a major body system-wide metabolic hormone that regulates protein, lipid fat , and carbohydrate homeostasis balance. In addition to being an anabolic hormone, it also has fat mobilizing diabetogenic properties i. The body produces several kinds of growth hormone. The principal form of growth hormone in humans is a complex protein that weighs 22 kd kilodaltons and contains amino acids.
It is known as somatotrope; and, what is usually reference when discussing growth horomone GH. GH is produced by growth hormone cells, known as somatotropes, which are located in the anterior lobe of the pituitary located in the brain. Growth hormone GH is required for growth, development, and maintenance of the body and mind of humans and many other forms of life from conception through the end of life. The hypothalamus gland is located in the brain just above the pituitary.
The pituitary branches into two lobes; and, is connected to the hypothalamus by a pituitary stalk. The pituitary stalk is the pathway through which the hypothalamus transmits neuroendocrine signals or messages to the pituitary. In turn, the pituitary mediates or regulates the production of numerous hormones by various glands.
The hypothalamic neuroendocrine messenger that directs the anterior lobe of the pituitary to produce GH is called growth hormone releasing hormone GHRH.
GH is mediated or regulated by a hormone called somatostatin,; which is also made by the hypothalamus. Somatostatin is produced by the hypothalamus on an intermittent basis. When somatostatin is not present, the hypothalamus produces GHRH. This relationship between somatostatin and GHRH is principally responsible for the pulsatile secretion of approximately 6 to 10 random bursts of GH during a 24 hour period.
The bursts of GH differ in frequency, amplitude, and duration. The pattern of GH secretion is chiefly a function of developmental state, nutritional state, sleep state, stress, and exercise, and metabolic clearance. The maximum amplitude of GH bursts occurs at the onset of the first slow-wave sleep stages III and IV , which usually takes place during the first hour of sleep.
GH stays within the body for only minutes. During its short life, is distributed to various organs and tissues of the body,including the liver. It is IGF-I that is proximately responsible for commencing the metabolic functions that result in building bone, muscle, and tissue, including linear growth in children. In addition to performing certain independent endocrine functions, growth hormone is the principal means of producing IGF-I. Classification of Growth Hormone Deficiency top.
Growth hormone deficiency GHD may be classified broadly into four categories based on the source of the GH deficiency: Pituitary GHD is the incapacity of the pituitary to produce growth hormone. Child-onset GHD is caused by different genetic defects in various genetic components and by Prader-Willi syndrome a congenital disorder characterized by obesity, short stature, lack of muscle tone, hypogonadism, and central nervous dysfunction ; associated brain structural defects, and associated mid-line facial defects.
It is possible that a significant number of patients develope hypothalamic radiation-induced damage to the GHRH secreting neurons, which results in the pituitary gland developing decreased responsiveness to GHRH following CI in childhood. In the transition period from GH in childhood to adulthood, the emphasis is on completion of the development of bone and muscles.
There is increasing recognition of the need to continue GH therapy beyond final height in young adults with severe GHD on retesting. In the middle years, adult acquired onset is caused by trauma at or soon after birth, central nervous system infection, tumors of the hypothalamus or pituitary glands, infiltrative or granulomatous disease, cranial irradation, surgery; or, from idiopathic causes.
The chief concerns are increased cardiovascular risk risk involving GHD-related dyslipidemia, increased fat mass, reduced insulin sensitivity, and increased mortality markers, especially in women as compared with the general population. In the elderly,GHD becomes manifest in decreased quality of life, fatigue, and alteration of body composition differently than in normal persons.
Abnormalities in body composition, bone metabolism, and lipid profile in GH-deficient and hypopituitary adults are distinct from those that occur as the result of normal aging. Thus, growth hormone has significant benefits in adults with GHD or hypopituitarism throughout each stage of adult life.
Epidemiolgy of Growth Hormone Deficiency top. Since then, similar, but not identical brands, of rhGH have come to the marketplace. In the last 15 years, it has been recognized that growth hormone deficiency GHD in the adult leads to increased morbidity metabolic syndrome, osteoporosis, muscle wasting, impaired quality of life and increased incidence of cardiovascular events, a main cause of the increased mortality observed in this population.
Pituitary adenomas and their treatment surgery, radiation are the most common cause of GHD in adults. In the United States, it is estimated that the incidence of growth hormone deficiency in children is between 1 in 4, and 1 in 10, More than 50, adults in the United States are growth hormone deficient, and 6, new cases are reported each year, including GHD children who transition to GHD as an adult.
Diagnosis of Adult Growth Hormone Deficiency top. Until several years ago, the growth hormone stimulation test GHST , which measures the capacity of the pituitary to produce growth, was considered the principal biochemical test for the diagnosis of AGHD. During the past several years, the accuracy of the GHST to determine whether a person has AGHD has been increasingly questioned because of test variability and increasing acceptance of IGF-I being of significant diagnostic value in combination with the GHST, the phenotype physical and mental characteristics, the medical history, as described above; and, increased understanding that, in the absence of a clearly defined organic cause for AGHD, the unique physiology of each person being evaluated, makes the diagnosis of AGHD complex and varied.
Adult growth hormone deficiency GHD is a multifactorial disorder in which pituitary dysfunction associated with pituitary adenomas or their treatment plays a major role. The concept of partial GHD, recognized by paediatric endocrinologists for many years, is being now being examined in adults for an association between hypothalamic-pituitary disease and metabolic and anthropometric abnormalities in persons whose GH range from severe GHD to non-GHD levels.
Partial GHD, however, becomes more difficult to diagnosis in the presence of obesity, increasing age, and in the absence of additional pituitary hormone deficits. Adults with GHD can have a variety of signs and symptoms, which include abnormality body composition with increased fat mass especially central adiposity , decreased lean muscle mass, extracellular fluid volumn, dimished muscle strength, physical energy and stamina, lack of motivation, lethargy, lability changes in mood , depression, and impairment of congitive functions.
Comprehensive biochemical testing may reveal the following conditions that are also markers for AGHD: An MRI scan may reveal a structural abnormality or tumor in the brain. A pulmonary function test may reveal diminished lung respiratory muscle capacity. All those conditions are consistent with AGHD.
Hypopituitarism and GHD are associated with an increased mortality. Comprehensive biochemical testing initally includes, but is not limited to: Biochemical testing can also reveal deficiences in thyroxin, testosterone, and androgenic steriods DHEAS and androstenedione , diseases and disorders of metabolism, and genetic defects that can interfere with the secretion, uptake, and utilization of GH and IGF-I.
When the IGF-I is low, further investigation is warranted to determine the cause of the low IGF-I, which can include 1 the testing of IGF-II, and the IGF binding proteins; 2 growth hormone stimulation tests to determine whether the pituitary has the capacity to produce growth hormone; 3 the levels of zinc, magnesium, and selenium, which minerals are necessary for the proper functioning of certain enzymes that are essential for the metabolic processes involved in with IGF-I and its various binding proteins; and, possibly testing for metabolic diseases and disorders.
The diagnosis of AGHD is often challenging because of the absence of growth parameters as diagnostic factors in addition factor, and the effects of other disorders that adults acquire over time.
Other markers are therefore needed to identify adults who have GHD and could potentially benefit from GH replacement therapy. Consensus guidelines for the diagnosis and treatment of adult GHD include patients who have evidence of hypothalamic-pituitary disease or disorder, patients with childhood-onset GHD, and patients who have undergone cranial ablation, or have a history of head trauma.
Suspicion of GHD is also heightened in the presence of other pituitary hormone deficits. Tests for GHD include measurement of GH upon conducting growth hormone stimulation tests GHSTs with provoking agents that have high sensitivity and sensitivity including, but not limited to, the insulin tolerance test ITT. The results of several studies have found that non-stimulated serum or urine measurements of GH levels do not reliably predict deficiency in adults.
Also, the ITT has some potential risks involved its administration and is of questionable reproducibility, which have prompted the development of the previously mentioned tests. The signs and symptoms of growth hormone deficiency can be masked by testosterone or thyroxin; or caused by deficiencies in those hormones or by other hormone dysfunction or by metabolic disorders. In such cases, rhGH can cause other hormone deficiencies. For example, cortisol, or in combination with testosterone in males, can cause secondary polycythemia via the hormone erythropietin, resulting in serious and even grave conditions, such as hemochromotosis, cardiac infarction, stroke and paralysis, liver damage.
Food and Drug Administration. Although made by various manufacturers, rhGH contains DNA sequencing that is identical to natural GH, regardless of the source material from which it is made. Therefore, with the possibility of a minimal difference bioequivalancy among the rhGH products, all those products and their delivery devices are safe and efficacious.
Generally, rhGH treatment is monitored by testing a periodic intervals determined by the endocrinologist, changes in body composition, and bone remodeling, and lipid values. Based on patient experience in recent years, with minor but aggravating adverse events such as edema and joint pain, lower doses have been found to be efficacious, but safer, with a reduction in the IGF-I levels.
These estimates are consistent with the dosage regimens found to be adequate in recent studies on dosage regimen. Benefits of Treatment with Recombinant Growth Hormone top. One daily subcutaneous injection of rhGH can reverse many of the symptoms and signs of growth hormone deficiency.
The pathophysiology for this positive results appears to be the natural mediatory and regulatory effects of rhGH on the neurotransmitters of the central nervous system CNS , which seem to perform better than psychotropic drugs. After 3 and 6 months of rhGH treatment in the closed label phase a significant improvement of attentional performance was observed compared to baseline in the rhGH group but not in the placebo group. After 6 months scores of attention were significantly different between rhGH and placebo treatment for the digit cancellation test and marginally different for the trail-making test.
In contrast, long-term verbal memory and non-verbal intelligence did not improve compared to baseline during therapy and short-term memory improved both in the GH and the placebo group after 3 and 6 months.
This was considered as a placebo or practice effect. In the open-label phase a further improvement of attention was found in the GH group and subsequent treatment with rhGH for 3 and 6 months in the placebo group also significantly improved attentional performance supporting the results of the rhGH group in the first 6 months of the double-blind phase. RhGH treatment appears to have a beneficial effect on attentional performance in adult hypopituitary patients with GH deficiency when treated for at least 3 months.
Our study does not support a role for GH in influencing verbal memory or non-verbal intelligence. The introduction of recombinant growth hormone GH for the treatment of GHD has opened up new treatment avenues but has also raised concerns about possible untoward long-term metabolic effects of GH, such as the potential effect of GH on insulin sensitivity and a deterioration in glucose tolerance. Research has shown that GH induces insulin resistance by the stimulation of lipolysis and a concomitant switch from oxidation of glucose to oxidation of lipids, during both acute and chronic treatment.
However, although this is a consistent effect of GH therapy, it does not mean per se that it leads to abnormal glucose tolerance and diabetes mellitus. This article discusses this and other potential long-term metabolic effects of GH, and raises a number of questions to be addressed by future research.
LDL-cholesterol abnormalities appear to improve with GH replacement even if maintained within physiological dose range; the greatest improvement occurs in those subjects with higher baseline total and LDL cholesterol values and in female patients with adult onset GHD compared with male patients with childhood onset GHD. In contrast, hypertriglyceridaemia is not corrected by GH replacement. The majority of the reports suggest GH replacement increases Lipoprotein-a levels. Long-term observation will be required to determine whether GH replacement reduces cardiovascular morbidity and mortality in GHD adults.
The reduced muscle mass and strength associated with GHD has been shown to improve after GH replacement. GH treatment also improves maximal and sub-maximal exercise performance in GHD adults.
The effects on protein metabolism, energy expenditure and thyroid metabolism in GHD adults are also critical. GH replacement has a long-term beneficial effect on muscle mass and function in patients with GHD of all ages, although there appears to be a greater effect in normalizing muscle mass and function in young males and in adults with adult-onset GHD compared with those with childhood-onset GHD.
Results also suggest that concomitant exercise training might further improve the outcome of GH replacement therapy. Karger AG, Basel Vol.
The beneficial effects of rhGH replacement, described after short-term rhGH replacement, are sustained in the long term up to 7 years. Understanding the mechanisms by which GH antagonizes insulin-stimulated glucose disposal in muscle is an important future research field, with implications for a variety of clinical conditions ranging from malnutrition to obesity and type 2 diabetes mellitus.
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