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.
This IL-33/ST2 signaling pathway has been found to be one of the main genetic determinants in bronchial asthma pathogenesis, and because of the pathological linkage between asthma and rhinitis, the experimental focus of IL-33 has now turned to its role in the development of allergic rhinitis in humans and mouse models. Recently, it was found that allergic rhinitis patients expressed higher levels of IL-33 in their nasal epithelium and had a higher concentration of ST2 serum in nasal passageways following their exposure to pollen and other allergens, indicating that this gene and its associated receptor are expressed at a higher rate in allergic rhinitis patients. In a 2020 study on polymorphisms of the IL-33 gene and their link to allergic rhinitis within the Han Chinese population, researchers found that five SNPs specifically contributed to the pathogenesis of allergic rhinitis, with three of those five SNPs previously identified as genetic determinants for asthma.Another study focusing on Han Chinese children found that certain SNPs in the protein tyrosine phosphatase non-receptor 22 (PTPN22) gene and cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4) gene can be associated with childhood allergic rhinitis and allergic asthma. The encoded PTPN22 protein, which is found primarily in lymphoid tissue, acts as a post-translational regulator by removing phosphate groups from targeted proteins. Importantly, PTPN22 can affect the phosphorylation of T cell responses, and thus the subsequent proliferation of the T cells.