in the 1960s developed cjd (creutzfeldt–jakob 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 more common and competitors entered the market. eli lilly launched a competing natural sequence growth hormone (humatrope). pharmacia (formerly kabi, now pfizer) introduced genotropin. novo nordisk introduced norditropin. serono (now emd serono) introduced saizen and serostim. ferring has introduced zomacton. genentech eventually introduced another hgh product, nutropin, and stopped making protropin in 2004. price competition had begun. teva, which is primarily a generics company, has introduced tev-tropin. chinese companies have entered the market as well and have introduced more pricing competition: neogenica bioscience ltd. introduced hypertropin, genescience introduced jintropin, anhui anke biotechnology introduced ansomone, shanghai united kefei biotechnology introduced kefei hgh, and hygene biopharm introduced hygetropin. 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. pediatric endocrinologists were the only physicians interested in the arcana of gh metabolism and children's growth , 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. 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 kidney 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. most were people having been treated with gh in childhood for severe deficiency. 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. 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. 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. 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, an uncritical touting of gh as the answer to aging. 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 recombinant growth hormone available in the u.s. (and their manufacturers) include 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. somapacitan-beco (sogroya) is first once-per week subcutaneous human growth hormone (hgh) therapy that was approved in the united states. it was approved for medical use in the united states in august 2020. 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 the pituitary glands of human cadavers 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 (rhgh, rhgh) refers to recombinant human growth hormone, that is, somatropin (inn). its amino acid sequence is identical with that of endogenous human gh. it is coincidental that rhgh also refers to rhesus monkey gh (rhgh), using the accepted naming convention of rh for rhesus. 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, that is, somatrem (inn). this was the first recombinant gh product marketed (trade name 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. rbst refers to recombinant bovine somatotropin (cow growth hormone), or recombinant bovine gh (rbgh, rbgh).