Hypertrophy of the limbs: It is caused by excessive secretion of growth hormone (GH) by the pituitary gland. In adolescents, gigantism is formed when the epiphysis is not closed; after puberty, the epiphysis has fused, then acromegaly is formed; in a few cases, the disease starts in adolescence and continues to develop in adulthood to form acromegaly gigantism. So, what is the cause of hypertrophy of the limbs? The main effects of GH are to promote the growth of bone tissue, muscle, connective tissue and internal organs, to promote DNA and RNA synthesis, to counteract insulin to promote water and sodium retention, and to stimulate the secretion of some peptides, such as growth interferon, in the body. such as growth interferon. GH has both insulin-like and anti-insulin-like effects on glucose metabolism, with the former occurring earlier and the latter later; GH also has a direct effect on pancreatic islet B cells, and about 1/4 of patients can develop diabetes at the same time. Growth interferon (somatomedin, SM) is derived from the liver and can increase cartilage growth through its effect on DNA and RNA protein synthesis. Growth interferon A (SmA) stimulates collagen and non-collagen synthesis, growth interferon C (SmC) stimulates collagen synthesis in osteoblasts, and BGP acts as a result of GH action through SmA. Excess GH accelerates bone formation and maturation and promotes bone growth. Bone remodeling is increased and bone conversion is accelerated. In pituitary dwarfism, the growth and development of bone is halted or delayed due to GH deficiency. In humans, GH increases intestinal calcium absorption, bone formation, and bone mineralization and increases bone mass, while in vitro, it does not directly stimulate bone matrix formation. Growth mediators have growth-promoting effects on various tissues and can mediate the effects of GH on bone growth, both in bone and cartilage. GH can alter the circadian rhythm changes of serum phosphorus, which increases blood phosphorus, and can also increase TRP, which alters the maximum renal phosphorus reabsorption/glomerular filtration rate ratio (TMP/GFR), further increasing blood phosphorus.