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Human Growth Hormone(Somatropine) 100iu(10vial x 10iu)(Europe Pharmaceuticals)

Item 12749

Human Growth Hormone (HGH)
Replacement Therapy

It has been shown that as we age, our bodies' natural GH production decreases. Many of the effects of aging are seen as a result of this decrease. More important, clinical evidence and recent medical research clearly demonstrate that by replacing Human Growth Hormone in IGF-1 deficient adults, we can significantly eliminate these symptoms, reverse the biological effects of aging, reduce body fat, increase lean muscle mass, strengthen the heart and improve sexual performance. No other substance known to medical science has been shown continually to deter and reverse the process of aging.

 

In many cases, you can reasonably look to reverse ten to twenty years of age decline with one year of continual therapy.

 

Injectible Human Growth Hormone Available! Inquire for pricing


What is HGH?

Human Growth Hormone is an endocrine Hormone that is produced by the anterior portion of the pituitary gland. It is made up of 191 amino acids. Production of GH decreases as we age. Virtually every system in the human body is in some way dependent on HGH for proper functioning. Growth Hormone peaks during adolescence and decreases dramatically thereafter. At age 40, our GH production is only 40% of what it was at age 20. Levels are measured by IGF-1.


Benefits:

Abdominal Fat Reduction

Growth hormone promotes the action of insulin. When we use GH/ IGF-1 Precursor, it directs the action of insulin towards putting sugar into the cardiac, muscle and nerve cells, rather then into fat cells. By getting rid of abdominal fat, you can induce greater insulin sensitivity. Greater insulin sensitivity can help prevent, and in some cases reverse type 2 adult onset diabetes.


Increase Lean Muscle

There is an average increase of 9% in lean muscle mass in use of HGH for one year, as well as reduction of 14% in body fat in just six months of HGH use.


Sex Drive

The decline of the male and female libido is directly related to the age-related declines in Hgh and Testosterone in the body. A clinical study of 302 aging adults showed that HGH and/or Testosterone Replacement Therapy improved sexual potency and frequency in 75% of the men studied. Interviews with people on Hgh Replacement Therapy indicate that almost everyone, men and women, had improvement in sexual function.


Fewer Wrinkles

Growth hormone helps with the promotion of type-2 collagen which adds elasticity to the skin.


Healing Joints

GH also has an anabolic effect on soft tissue such as tendons, cartilage, and other connective tissue. This signifies that old injuries can repair at an accelerated rate and with more strength due to stronger connective tissue.


Metabolic Cascade

When we age without Rejuvenation, the efficiency of our overall endocrine system i.e., thyroid, pancreas, adrenal cortal, hypothalmic pituitary axis (HPA), etc. becomes tired and worn down.

 

In addition to this problem, a degenerative metabolic cascade takes place within yourself as less and less hormone/messengers are produced. The receptor sites also start to lag and some become switched off -- and as in menopause some disappear altogether. Thus the receptor sites target areas for some hormones messengers which are no longer there.
This problem demonstrates why some improperly administered HRT therapies are not effective.

 

GH has a very potent anabolic effect (protein synthesis/tissue building) which can cause an increase in the number of cells and the enlargement of muscle cells. The goal of restoring, retuning and maintaining youthful hormone levels helps to jumpstart tired worn receptors. Since GH/IGF-1 precursors rejuvenate on a cellular level/cell division, the overall effect of systemic endocrine rejuvenation has a long lasting list of benefits.

 

Thus it is essential that doctor administered protocols, with the help of doctors assistants for monitoring therapies are followed properly. Proper and timely Dosage Administration along with guidance in nutrition, adds a synergy with gratifying, satisfying results.

 

GH itself is not responsible for the majority of the effects seen from GH use. Actually it is only the precursor to the so called Good Stuff IGF-1.

Growth hormone treatment

Growth hormone treatment refers to the use of growth hormone (GH) as a prescription medication - it is one form of Hormone therapy. Growth hormone is a peptide hormone secreted by the pituitary gland that stimulates growth and cell reproduction. In the past, growth hormone was extracted from human pituitary glands. GH is now produced by recombinant DNA technology and is prescribed for a variety of reasons. GH therapy has been a focus of social and ethical controversies for 50 years.

This article describes the history of GH treatment, current uses and risks arising from GH use. Other articles describe GH physiology, diseases of GH excess (acromegaly and pituitary gigantism), deficiency, the recent phenomenon of HGH controversies, growth hormone in sports, and growth hormone for cows.

Medical uses

HGH deficiency in children

Growth hormone deficiency is treated by replacing GH.[1][2] [3] All GH prescribed in North America, Europe, and most of the rest of the world is a human GH, manufactured by recombinant DNA technology. As GH is a large peptide molecule, it must be injected into subcutaneous tissue or muscle to get it into the blood. Nearly painless insulin syringes make this less trying than is usually anticipated, but perceived discomfort is a subjective value.

When treated with GH, a deficient child will begin to grow faster within months. Other benefits may be noticed, such as increased strength, progress in motor development, and reduction of body fat. Side-effects of this type of physiologic replacement are quite rare. Known risks and unsettled issues are discussed below, but GH-deficient children receiving replacement doses are at the lowest risk for problems.[citation needed].

Still, costs of treatment in terms of money, effort, and perhaps quality of life are substantial. Treatment of children usually involves daily injections of growth hormone, usually for as long as the child is growing. Lifelong continuation may be recommended for those most severely deficient as adults. Most pediatric endocrinologists monitor growth and adjust dose every 3–4 months. Assessing the psychological value of treatment is difficult, but most children and families are enthusiastic once the physical benefits begin to be seen. Treatment costs vary by country and by size of child, but $US 10,000 to 30,000 a year is common.

Little except the cost of treating severely deficient children is controversial, and most children with severe growth hormone deficiency in the developed world are offered treatment. Most accept. The story is very different for adult deficiency.[citation needed]

HGH deficiency in adults

GH replacement therapy can provide a number of measurable benefits to GH-deficient adults.[1][2][3] These include improved bone density.[4] Increased Muscle mass, decrease of adipose tissue, faster hair and nail growth, strengthened immune system, increased circulatory system, and improved blood lipid levels, but long term mortality benefit has not yet been demonstrated.[5][6][7][8]

GH for severe adult deficiency is usually prescribed as daily injections at a weekly dose about 25% of children's doses and comparably lower cost. Despite the potential benefits, most adults with GH deficiency are not being treated due to a combination of factors such as unwillingness of some adults to seek medical care, unacceptability of injections, inadequate insurance coverage, and significantly lower rates of diagnosis and treatment offered by internist endocrinologists[citation needed].

A peer-review article published in 2010 indicates that "Growth hormone (GH) replacement unequivocally benefits growth, body composition, cardiovascular risk factors and quality of life. Less is known about the effects of GH on learning and memory."[9]

Other

As of 2004, GH has been approved by the U.S. Food and Drug Administration for treatment of other conditions:

  • Turner syndrome epitomizes the response of non-deficient shortness. At doses 20% higher than those used in GH deficiency, growth accelerates. With several years of treatment the median gain in adult height is about 2–3 in (5.1–7.6 cm) on this dose. The gains appear to be dose-dependent.[11] It has been used successfully in toddlers with Turner syndrome,[12] as well as in older girls.[13][1][2][3]
  • Chronic renal failure results in many problems, including growth failure. GH treatment for several years both before and after transplantation may prevent further deceleration of growth and may narrow the height deficit, though even with treatment net adult height loss may be about 4 in (10 cm)[1][2]
  • Prader-Willi syndrome, a generally non-hereditary genetic condition, is a case where GH is prescribed for benefits in addition to height. GH is one of the treatment options an experienced endocrinologist may use when treating a child with PWS.[14] GH can help children with PWS in height, weight, body mass, strength, and agility.[citation needed]. Reports have indicated increase of growth rate (especially in the first year of treatment) and a variety of other positive effects, including improved body composition (higher muscle mass, lower fat mass); improved weight management; increased energy and physical activity; improved strength, agility, and endurance; and improved respiratory function. The Prader-Willi Syndrome Association (USA) recommends that a sleep study be conducted before initiating GH treatment in a child with PWS. At this time there is no direct evidence of a causative link between growth hormone and the respiratory problems seen in PWS (among both those receiving and those not receiving GH treatment), including sudden death. A follow-up sleep study after one year of GH treatment may also be indicated. GH (specifically Pfizer's version, Genotropin) is the only treatment that has received an FDA indication for children with PWS. The FDA indication only applies to children.[3]
  • Children short because of intrauterine growth retardation are small for gestational age at birth for a variety of reasons. If early catch-up growth does not occur and their heights remain below the third percentile by 2 or 3 years of age, adult height is likely to be similarly low. High-dose GH treatment has been shown to accelerate growth, but data on long term benefits and risks are limited.[15][1][3]
  • Idiopathic short stature (ISS) is one of the most controversial indications for GH as pediatric endocrinologists do not agree on its definition, diagnostic criteria, or limits.[16] The term has been applied to children with severe unexplained shortness that will result in an adult height below the 3rd percentile. In the late 1990s, the pharmaceutical manufacturer Eli Lilly and Company sponsored trials of Humatrope (their brand of rHGH) in children with extreme ISS, those at least 2.25 standard deviations below mean (in the lowest 1.2 percent of the population). These boys and girls appeared to be headed toward heights of less than 63" (160 cm) and 59" (150 cm) respectively. They were treated for about 4 years and gained 1.5–3 in (3.8–7.6 cm) in adult height. Controversy has arisen as to whether all of these children were truly "short normal" children, since the average IGF1 was low. It was not surprising that approval for this extreme degree of shortness led to an increase in the number of parents seeking treatment to make otherwise healthy children a little taller.[17][1][2][3]

Research

Everything discussed in this section involves either studies to see if GH could be useful for other diseases or conditions, or off-label uses that doctors have developed in the course of their daily work. None of the uses described below have been approved by the FDA.

Some of the uses that have been explored relate to stunted growth due to various disorders.

Post-transplant growth failure sometimes improves with GH. Many children who suffer from chronic renal, liver, and heart disease grow poorly for years before a transplant is required (or available). While growth may improve after correction of organ function by successful transplantation, the immunosuppressive drugs taken to protect the transplanted organ may continue to interfere with growth. Growth hormone may help offset these effects and is sometimes offered in these circumstances.[citation needed]

X-linked hypophosphatemic rickets is an inherited disorder of phosphorus metabolism that results in growth failure and rickets. GH has been shown to accelerate growth modestly.[citation needed]

Inflammatory bowel disease (ulcerative colitis and Crohn's disease) can impair growth before producing obvious bowel symptoms. Children with inflammatory bowel disease and Crohn's disease have often GH and IGF-I deficiency and /or GH resistance.[18] Trials of GH have shown at least modest acceleration of growth, but it is unknown whether this actually leads to an increased adult height.[19] Similarly, Coeliac Disease can prevent children from reaching their expected growth potential, if it begins before growth is complete. Stunted growth can be a result of Coeliac Disease damaging the intestines and preventing proper nutrient absorption. Treatment involves a gluten-free diet. HGH treatment has been used in an attempt to recover lost growth due to this effect.[citation needed] A study in the New England Journal of Medicine suggested that HGH might be a beneficial treatment for patients with Crohn's disease.[20]

Poor growth is a part of Noonan syndrome and many other genetic syndromes. Many short children with various syndromes have been treated with GH. As a broad generalization, GH for several years usually produces faster growth, and perhaps 1–2 in (2.5–5.1 cm) of extra adult height.[citation needed]

Small numbers of children with various forms of bone dysplasia (dwarfism in common parlance) have been treated with GH with modest increases in short-term height velocity. No long-term studies have demonstrated increased adult height, and dwarfism due to bone dysplasia remains the prime example of extreme shortness considered not very amenable to GH treatment.[citation needed]

On occasion, GH has been used for other purposes than accelerating growth or replacing deficiency. Nearly every hormone available for administration has been given to non-deficient people in hope of obtaining improvement for various conditions for which other treatments are unsatisfactory. With a few exceptions, benefits are modest and side-effect risk is higher. Experience with GH has yielded the same results. The following is not an exclusive list.[citation needed]

Due to the immunostimulatory effect of GH,[21] it can enhance immunorecevory after radiation in mice and nonhuman primates.[22]

Neurodegenerative diseases (i.e. Alzheimer's disease) are connected with the decline of growth hormone levels,[23] therefore some authors suggest that it is necessary to evaluate the use GH as future antinuerodegenerative strategy.[24]

Other scientists have explored whether hGH treatment could be useful in adults that are not severely deficient in GH. Treatment of healthy, normally aging individuals found the only benefit to be a slight increase in muscle mass, with frequent side-effects and no evidence that it is safe to use long-term.[25]

GH has been given to attempt to promote healing of large burns by reducing the amount of protein breakdown during the early post-injury period.

GH has been used as an adjunct to caloric restriction to attempt to treat obesity. GH promotes lipolysis and reduces proteolysis. It was hoped that GH would reduce muscle breakdown without interfering with use and reduction of fat as the body shifted to a near-starvation economy. Results showed potential benefit, but this has not been widely adopted for a variety of reasons (cost, injections, potential aggravation of insulin resistance, etc.). Recent studies suggest that side-effects, in particular, insulin resistance, may outweigh the potential benefits of such therapy.[26]

Fibromyalgia and chronic fatigue syndrome are poorly understood and vaguely defined conditions with overlapping features. After demonstration of disordered GH secretion and higher rates of tissue breakdown in patients with these conditions, a few people tried growth hormone treatment to see whether energy or healing could be improved. Disturbances of GH secretion may be secondary phenomena and not causal. Despite anecdotal reports of improvement, no large, controlled trials have demonstrated significant, persistent improvement, and GH is not a common or standard treatment for either condition.[citation needed]

GH has been illegally taken by athletes wanting to increase recovery, strength, and power. Some scientific research has been conducted to determine whether such use could be safe and effective -- see Growth hormone in sports.

Adverse effects

The New England Journal of Medicine published two editorials in 2003 expressing concern about off-label uses of HGH and the proliferation of advertisements for "HGH-Releasing" dietary supplements, and emphasized that there is no evidence that use of HGH in healthy adults or in geriatric patients is safe and effective - and especially emphasized that risks of long-term HGH treatment are unknown. One editorial was by Jeffrey M. Drazen, M.D., the editor-in-chief of the journal; the other one was by Dr. Mary Lee Vance, who provided the NEJM's editorial original, cautious comment on a much cited 1990 study on the use of HGH in geriatric patients with low growth hormone levels.

A small but controlled study of GH given to severely ill adults in an intensive care unit setting for the purpose of increasing strength and reducing the muscle wasting of critical illness showed a higher mortality rate for the patients having received GH.[27] The reason is unknown, but GH is now rarely used in ICU patients unless they have severe growth hormone deficiency.

GH treatment usually decreases insulin sensitivity,[28] but some studies showed no evidence for increased diabetes incidence in GH-treated adult hypopituitary patients.[29]

In past it was believed that GH treatment could increase the cancer risk; a large study recently concluded that "With relatively short follow-up, the overall primary cancer risk in 6840 patients receiving GH as adults was not increased. Elevated SIRs (which is risk of getting cancer) were found for subgroups in the USA cohort defined by age <35 years or childhood onset GH deficiency."[30]

The FDA issued a Safety Alert in August 2011, communicating the fact that a French study found that persons with certain kinds of short stature (idiopathic growth hormone deficiency and idiopathic or gestational short stature) treated with recombinant human growth hormone during childhood and who were followed over a long period of time, were at a small increased risk of death when compared to individuals in the general population of France. [31]

History

Perhaps the most famous person who exemplified the appearance of untreated congenital growth hormone deficiency was Charles Sherwood Stratton (1838–1883), who was exhibited by P.T. Barnum as General Tom Thumb, and married Lavinia Warren. Pictures of the couple show the typical adult features of untreated severe growth hormone deficiency. Despite the severe shortness, limbs and trunks are proportional.

Like many other nineteenth-century medical terms that lost precise meaning as they gained wider currency, “midget,” as a term for someone with extreme proportional shortness, acquired pejorative connotations and is no longer used in medical contexts.

By the middle of the twentieth century, endocrinologists understood the clinical features of growth hormone deficiency. GH is a protein hormone, like insulin, which had been purified from pig and cow pancreases for treatment of type 1 diabetes since the 1920s. However, pig and cow GH did not work at all in humans, due to greater species-to-species variation of molecular structure (i.e., insulin is considered more "evolutionarily conserved" than GH).

Extraction for treatment

Extracted growth hormone was used since late 1950s until late 1980s when its use was replaced by recombinant GH.

In the late 1950s, Maurice Raben purified enough GH from human pituitary glands to successfully treat a GH-deficient boy. A few endocrinologists began to help parents of severely GH-deficient children to make arrangements with local pathologists to collect human pituitary glands after removal at autopsy. Parents would then contract with a biochemist to purify enough growth hormone to treat their child. Few families could manage such a complicated undertaking.

In 1960, the National Pituitary Agency was formed as a branch of the U.S. National Institutes of Health. The purpose of this agency was to supervise the collection of human pituitary glands when autopsies were performed, arrange for large-scale extraction and purification of GH, and distribute it to a limited number of pediatric endocrinologists for treating GH-deficient children under research protocols. Canada, UK, Australia, New Zealand, France, Israel, and other countries establish similar government-sponsored agencies to collect pituitaries, purify GH, and distribute it for treatment of severely GH-deficient children.

Supplies of this “cadaver growth hormone” were limited, and only the most severely deficient children were treated. From 1963 to 1985 about 7700 children in the U.S. and 27,000 children worldwide were given GH extracted from human pituitary glands to treat severe GH deficiency. Physicians trained in the relatively new specialty of pediatric endocrinology provided most of this care, but in the late 1960s there were only a hundred of these physicians in a few dozen of the largest university medical centers around the world.

In 1976, physicians became aware that Creutzfeldt-Jacob disease could be transmitted by neurosurgical procedures and cornea transplantation. CJD is a rapidly fatal dementing disease of the brain also known as spongiform encephalopathy, related to “mad cow disease”.

In 1977, the NPA GH extraction and purification procedure was refined and improved.

A shortage of available cadaver GH worsened in the late 1970s as the autopsy rate in the U.S. declined, while the number of pediatric endocrinologists able to diagnose and treat GH deficiency increased. GH was "rationed." Often, treatment would be stopped when a child reached an arbitrary minimal height, such as 5 ft 0 in (1.52 m). Children who were short for reasons other than severe GH deficiency were lied to and told that they would not benefit from treatment. Only those pediatric endocrinologists that remained at university medical centers with departments able to support a research program had access to NPA growth hormone.

In the late 1970s, a Swedish pharmaceutical company, Kabi, contracted with a number of hospitals in Europe to buy pituitary glands for the first commercial GH product, Crescormon. Although an additional source of GH was welcomed, Crescormon was greeted with ambivalence by pediatric endocrinologists in the United States. The first concern was that Kabi would begin to purchase pituitaries in the U.S., which would quickly undermine the NPA, which relied on a donation system like blood transfusion. As the number of autopsies continued to shrink, would pathologists sell pituitaries to a higher bidder? The second offense was Kabi-Pharmacia’s marketing campaign, which was directed at primary care physicians under the slogan, “Now, you determine the need,” implying that the services of a specialist were not needed for growth hormone treatment anymore and that any short child might be a candidate for treatment. Although the Crescormon controversy in the U.S. is long forgotten, Kabi’s pituitary purchase program continued to generate scandal in Europe as recently as 2000.

Recombinant human growth hormone (rHGH)

In 1981, the new American corporation Genentech, after collaboration with Kabi, developed and started trials of recombinant human growth hormone (rHGH) made by a new technology (recombinant DNA) in which human genes were inserted into bacteria so that they could produce unlimited amounts of the protein. Because this was new technology, approval was deferred as lengthy safety trials continued over the next four years.

In 1985, four young adults in the U.S. having received NPA growth hormone in the 1960s developed CJD (Creutzfeldt-Jacob disease). The connection was recognized within a few months, and use of human pituitary GH rapidly ceased. Between 1985 and 2003, a total of 26 cases of CJD occurred in adults having received NPA GH before 1977 (out of 7700), comparable numbers of cases occurred around the world. By 2003 there had been no cases in people who received only GH purified by the improved 1977 methods.

Discontinuation of human cadaver growth hormone led to rapid Food and Drug Administration approval of Genentech’s recombinant human growth hormone, which was introduced in 1985 as Protropin in the United States. Although this previously scarce commodity was suddenly available in “bucketfuls,” the price of treatment (US$10,000–30,000 per year) was the highest at the time. Genentech justified it by the prolonged research and development investment, orphan drug status, and a pioneering post-marketing surveillance registry for tracking safety and effectiveness (National Cooperative Growth Study).

Within a few years, GH treatment had become “big business” in more than one sense. Eli Lilly launched a competing natural sequence growth hormone (Humatrope[32]). Pharmacia (formerly Kabi, now Pfizer) introduced Genotropin[33]. Novo Nordisk introduced Norditropin[34]. Serono (now EMD Serono) introduced Saizen[35] and Serostim[36] and Serostim[37]. Ferring has introduced Zomacton [38]. Genentech eventually introduced another HGH product, Nutropin[39], and stopped making Protropin in 2004. Price competition has begun. Teva, which is primarily a generics company, has introduced Tev-tropin[40]. Chinese companies have entered the market as well and have introduced more pricing competition: NeoGenica BioScience Ltd. introduced Hypertropin/[41]; GeneScience Pharmaceutical Co., Ltd. has introduced Jintropin[42]; Anhui Anke Biotechnology has introduced Ansomone[43]. (There are reports of a product called Fintropin sold by the Chinese biotech firm, Kexing, but as of December 2011, their website does not report that they produce rHGH.[44]) These are all recombinant human growth hormone products and they have competed with various marketing strategies. Most children with severe deficiency in the developed world are now likely to have access to a pediatric endocrinologist and be diagnosed and offered treatment.

Pediatric endocrinology became a recognizable specialty in the 1950s, but did not reach board status in the U.S. until the late 1970s. Even 10 years later, as a cognitive, procedureless specialty dealing with mostly rare diseases, it was one of the smallest, lowest-paid, and more obscure of the medical specialities[citation needed]. Pediatric endocrinologists were the only physicians interested in the arcana of GH metabolism and children’s growth[citation needed], but their previously academic arguments took on new practical significance with major financial implications.

The major scientific arguments dated back to the days of GH scarcity:

  • Everyone agrees on the nature and diagnosis of severe GH deficiency, but what are the edges and variations?
  • How should marked constitutional delay be distinguished from partial GH deficiency?
  • To what extent is “normal shortness” a matter of short children naturally making less growth hormone?
  • Can a child make GH in response to a stimulation test but fail to make enough in “daily life” to grow normally?
  • If a stimulation test is used to define deficiency, what GH cutoff should be used to define normal?

It was the ethical questions that were new. Is GH not a wise use of finite healthcare resources, or is the physician’s primary responsibility to the patient? If GH is given to most extremely short children to make them taller, will the definition of “extremely short” simply rise, negating the expected social benefit? If GH is given to short children whose parents can afford it, will shortness become a permanent mark of lower social origins? More of these issues are outlined in the ethics section. Whole meetings were devoted to these questions; pediatric endocrinology had become a specialty with its own bioethics issues.

Despite the price, the 1990s became an era of experimentation to see what else growth hormone could help. The medical literature of the decade contains hundreds of reports of small trials of GH use in nearly every type of growth failure and shortness imaginable. In most cases, the growth responses were modest[citation needed]. For conditions with a large enough potential market, more rigorous trials were sponsored by pharmaceutical companies that were making growth hormone to achieve approval to market for those specific indications. Turner syndrome and chronic renal failure were the first of these “nonGH-deficient causes of shortness” to receive FDA approval for GH treatment, and Prader-Willi syndrome and intrauterine growth retardation followed. Similar expansion of use occurred in Europe.

One obvious potential market was adult GH deficiency. By the mid-1990s, several GH companies had sponsored or publicized research into the quality of life of adults with severe GH deficiency[citation needed]. Most were people having been treated with GH in childhood for severe deficiency[citation needed]. Although the injections are painless, many of them had been happy to leave injections behind as they reached final heights in the low-normal range[citation needed]. However, as adults in their 30s and 40s, these people, who had been children with growth hormone deficiency, were now adults with growth hormone deficiency and had more than their share of common adult problems: reduced physical, mental, and social energy, excess adipose and diminished muscle, diminished libido, poor bone density, higher cholesterol levels, and higher rates of cardiovascular disease. Research trials soon confirmed that a few months of GH could improve nearly all of these parameters. However, despite marketing efforts, most GH-deficient adults remain untreated.

Though GH use was slow to be accepted among adults with GH deficiency, similar research to see if GH treatment could slow or reverse some of the similar effects of aging attracted much public interest. The most publicized trial was reported by Daniel Rudman in 1990.[45] As with other types of hormone supplementation for aging (testosterone, estrogen, DHEA), confirmation of benefit and accurate understanding of risks has been only slowly evolving.

There are always entrepreneurs who do not need much evidence to see a business opportunity. In 1997, Ronald Klatz of the American Academy of Anti-Aging Medicine published Grow Young With HGH: The Amazing Medically Proven Plan To Reverse the Effects Of Aging,[46] an uncritical touting of GH as the answer to aging.[citation needed] This time, the internet amplified the proposition and spawned a hundred frauds and scams. However, their adoption of the "HGH" term has provided an easy way to distinguish the hype from the evidence. In 2003, growth hormone hit the news again, when the US FDA granted Eli Lilly approval to market Humatrope for the treatment of idiopathic short stature. The indication was controversial for several reasons, the primary one being the difficulty in defining extreme shortness with normal test results as a disease rather than the extreme end of the normal height range[citation needed]; in fact, the definition offered by Lilly for ISS is a height in the shortest 1.2% of the population. While this is an extreme degree of shortness, critics suggested that the company could afford to be extremely restrictive to earn approval, yet be confident that the definition, as well as actual use, would be driven upward by parents and physicians. Meanwhile, pediatric endocrinologists are still arguing about whether ISS is a "pathologic" or a statistical condition.

As of 2004, GH use continues to rise, though it is no longer the most expensive prescription drug in the formulary. Recombinant growth hormone available in the U.S. (and their manufacturers) included Nutropin (Genentech), Humatrope (Eli Lilly and Company), Genotropin (Pfizer), Norditropin (Novo Nordisk), Tev-Tropin (Teva) and Saizen (Merck Serono). The products are nearly identical in composition, efficacy, and cost, varying primarily in the formulations and delivery devices.

Terminology

Growth hormone (GH l) is also called somatotropin (British: somatotrophin). The human form of growth hormone is known as human growth hormone, or hGH (ovine growth hormone, or sheep growth hormone, is abbreviated oGH). GH can refer either to the natural hormone produced by the pituitary (somatotropin), or biosynthetic GH for therapy.

Cadaver growth hormone is the term for GH extracted from human pituitary glands between 1960 and 1985 for therapy of deficient children. In the U.S., cadaver GH, also referred to as NPA growth hormone, was provided by the National Pituitary Agency, and by other national programs and commercial firms as well. In 1985 it was associated with the development of Creutzfeldt-Jakob Disease, and was withdrawn from use.

rHGH refers to recombinant human growth hormone (somatropin). Its amino acid sequence is identical with that of endogenous human GH.

It is coincidental that rHGH also refers to rhesus monkey GH, using the accepted naming convention. Rhesus growth hormone was never used by physicians to treat human patients, but rhesus GH was part of the lore of the underground anabolic steroid community in those years, and fraudulent versions may have been bought and sold in gyms.

met-GH refers to methionyl-growth hormone. This was the first recombinant GH product marketed (Protropin by Genentech). It had the same amino acid sequence as human GH with an extra methionine at the end of the chain to facilitate the manufacturing process. It was discontinued in 2004. [47]

rBST refers to recombinant bovine somatropin (cow growth hormone), or recombinant bovine GH (rbGH).

References

1.       ^ a b c d e f g http://www.accessdata.fda.gov/drugsatfda_docs/label/2009/019640s068lbl.pdf

2.       ^ a b c d e http://www.gene.com/gene/products/information/opportunistic/nutropin/insert.jsp

3.       ^ a b c d e f http://www.pfizer.com/files/products/uspi_genotropin.pdf

4.       ^ Gotherstrom, G; Bengtsson, B-A; Bosaeus, I; Johannsson, G; Svensson, J (2007). "Ten-year GH replacement increases bone mineral density in hypopituitary patients with adult onset GH deficiency". European Journal of Endocrinology 156 (1): 55–64. doi:10.1530/eje.1.02317. PMID 17218726.

5.       ^ Alexopoulou, O; Abs, R; Maiter, D (2010). "Treatment of adult growth hormone deficiency: Who, why and how? A review". Acta clinica Belgica 65 (1): 13–22. PMID 20373593.

6.       ^ Ahmad, Aftab M.; Hopkins, Marion T.; Thomas, Joegi; Ibrahim, Hisham; Fraser, William D.; Vora, Jiten P. (2001). "Body composition and quality of life in adults with growth hormone deficiency; effects of low-dose growth hormone replacement". Clinical Endocrinology 54 (6): 709–17. doi:10.1046/j.1365-2265.2001.01275.x. PMID 11422104.

7.       ^ Savine, Richard; Sönksen, Peter (2000). "Growth Hormone – Hormone Replacement for the Somatopause?". Hormone Research 53: 37–41. doi:10.1159/000023531. PMID 10971102.

8.       ^ Gotherstrom, G.; Bengtsson, B.-A.; Bosaeus, I.; Johannsson, G.; Svensson, J. (2007). "A 10-Year, Prospective Study of the Metabolic Effects of Growth Hormone Replacement in Adults". Journal of Clinical Endocrinology & Metabolism 92 (4): 1442–5. doi:10.1210/jc.2006-1487.

9.       ^ Wass JA, Reddy R (November 2010). "Growth hormone and memory". J. Endocrinol. 207 (2): 125–6. doi:10.1677/JOE-10-0126. PMID 20696696.

10.   ^ http://www.serostim.com/Files/PDFs/Full_Prescribing_Information.pdf

11.   ^ Bolar, K.; Hoffman, A. R.; Maneatis, T.; Lippe, B. (2008). "Long-Term Safety of Recombinant Human Growth Hormone in Turner Syndrome". Journal of Clinical Endocrinology & Metabolism 93 (2): 344–51. doi:10.1210/jc.2007-1723. PMID 18000090.

12.   ^ Davenport, M. L.; Crowe, B. J.; Travers, S. H.; Rubin, K.; Ross, J. L.; Fechner, P. Y.; Gunther, D. F.; Liu, C. et al. (2007). "Growth Hormone Treatment of Early Growth Failure in Toddlers with Turner Syndrome: A Randomized, Controlled, Multicenter Trial". Journal of Clinical Endocrinology & Metabolism 92 (9): 3406–16. doi:10.1210/jc.2006-2874. PMID 17595258.

13.   ^ Backeljauw, Philippe (2007). "Does growth hormone therapy before 4 years of age enhance the linear growth of girls with Turner's syndrome?". Nature Clinical Practice Endocrinology & Metabolism 4 (2): 78–9. doi:10.1038/ncpendmet0678.

14.   ^ http://www.mayoclinic.com/health/prader-willi-syndrome/DS00922/DSECTION=treatments-and-drugs

15.   ^ Chatelain, P.; Carrascosa, A.; Bona, G.; Ferrandez-Longas, A.; Sippell, W. (2007). "Growth Hormone Therapy for Short Children Born Small for Gestational Age". Hormone Research 68 (6): 300–9. doi:10.1159/000107935. PMID 17823537.

16.   ^ Czernichow, Paul (2007). "Which children with idiopathic short stature should receive growth hormone therapy?". Nature Clinical Practice Endocrinology & Metabolism 4 (3): 118–9. doi:10.1038/ncpendmet0700.

17.   ^ Hannon, T. S.; Danadian, K.; Suprasongsin, C.; Arslanian, S. A. (2007). "Growth Hormone Treatment in Adolescent Males with Idiopathic Short Stature: Changes in Body Composition, Protein, Fat, and Glucose Metabolism". Journal of Clinical Endocrinology & Metabolism 92 (8): 3033–9. doi:10.1210/jc.2007-0308.

18.   ^ http://www.ncbi.nlm.nih.gov/pubmed/20184596

19.   ^ http://www.ncbi.nlm.nih.gov/pubmed/21470283

20.   ^ Slonim, Alfred E.; Bulone, Linda; Damore, Mary B.; Goldberg, Teresia; Wingertzahn, Mark A.; McKinley, Matthew J. (2000). "A Preliminary Study of Growth Hormone Therapy for Crohn's Disease". New England Journal of Medicine 342 (22): 4265–70. doi:10.1056/NEJM200006013422203. PMID 10833209.

21.   ^ http://www.ncbi.nlm.nih.gov/pubmed/2849979

22.   ^ http://www.ncbi.nlm.nih.gov/pubmed/20585403

23.   ^ Gómez, JM (2008). "Growth hormone and insulin-like growth factor-I as an endocrine axis in Alzheimer's disease". Endocrine, metabolic & immune disorders drug targets 8 (2): 143–51. doi:10.2174/187153008784534367. PMID 18537700.

24.   ^ Gasperi, M; Castellano, AE (2010). "Growth hormone/insulin-like growth factor I axis in neurodegenerative diseases". Journal of endocrinological investigation 33 (8): 587–91. PMID 20930497.

25.   ^ Liu, H; Bravata, DM; Olkin, I; Nayak, S; Roberts, B; Garber, AM; Hoffman, AR (2007). "Systematic review: The safety and efficacy of growth hormone in the healthy elderly". Annals of internal medicine 146 (2): 104–15. PMID 17227934.

26.   ^ Pasarica, M.; Zachwieja, J. J.; Dejonge, L.; Redman, S.; Smith, S. R. (2007). "Effect of Growth Hormone on Body Composition and Visceral Adiposity in Middle-Aged Men with Visceral Obesity". Journal of Clinical Endocrinology & Metabolism 92 (11): 4265–70. doi:10.1210/jc.2007-0786.

27.   ^ Takala, Jukka; Ruokonen, Esko; Webster, Nigel R.; Nielsen, Michael S.; Zandstra, Durk F.; Vundelinckx, Guy; Hinds, Charles J. (1999). "Increased Mortality Associated with Growth Hormone Treatment in Critically Ill Adults". New England Journal of Medicine 341 (11): 785–92. doi:10.1056/NEJM199909093411102. PMID 10477776.

28.   ^ Bramnert, M. (2003). "Growth Hormone Replacement Therapy Induces Insulin Resistance by Activating the Glucose-Fatty Acid Cycle". Journal of Clinical Endocrinology & Metabolism 88 (4): 1455–63. doi:10.1210/jc.2002-020542. PMID 12679422.

29.   ^ Attanasio, AF; Jung, H; Mo, D; Chanson, P; Bouillon, R; Ho, KK; Lamberts, SW; Clemmons, DR et al. (2011). "Prevalence and Incidence of Diabetes Mellitus in Adult Patients on Growth Hormone Replacement for Growth Hormone Deficiency: A Surveillance Database Analysis". The Journal of clinical endocrinology and metabolism 96 (7): 2255–61. doi:10.1210/jc.2011-0448. PMID 21543424.

30.   ^ Child, C; Zimmermann, A; Woodmansee, W; Green, D; Li, J; Jung, H; Erfurth, EM; Robison, L (2011). "Assessment of Primary Cancers in Growth Hormone-Treated Adult Hypopituitary Patients: An Analysis from the Hypopituitary Control and Complications Study (HypoCCS)". European Journal of Endocrinology 165 (2): 217–23. doi:10.1530/EJE-11-0286. PMC 3132593. PMID 21646285.

31.   ^ http://www.fda.gov/Safety/MedWatch/SafetyInformation/SafetyAlertsforHumanMedicalProducts/ucm237969.htm

32.   ^ http://www.humatrope.com/Pages/index.aspx

33.   ^ http://www.genotropin.com/

34.   ^ http://www.norditropin-us.com/

35.   ^ http://www.saizenus.com/

36.   ^ http://www.serostim.com/

37.   ^ http://www.emdserono.com/en/therapies/metabolic_endocrinology/zorbtive/zorbtive.html

38.   ^ http://www.ferring.com/en/therapeutic/endo

39.   ^ http://www.nutropin.com/index.jsp

40.   ^ http://www.tev-tropin.com/

41.   ^ http://www.hypertropin.com/

42.   ^ http://www.jintropin.cn/

43.   ^ http://www.ansomone.com/

44.   ^ http://www.sdkexing.com/

45.   ^ Rudman, Daniel; Feller, Axel G.; Nagraj, Hoskote S.; Gergans, Gregory A.; Lalitha, Pardee Y.; Goldberg, Allen F.; Schlenker, Robert A.; Cohn, Lester et al. (1990). "Effects of Human Growth Hormone in Men over 60 Years Old". New England Journal of Medicine 323 (1): 1–6. doi:10.1056/NEJM199007053230101. PMID 2355952.

46.   ^ New York: Harper-Collins[better source needed][page needed]

47.   ^ http://www.gene.com/gene/about/ir/historical/product-sales/nutropin.html

 

 



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