Description
HUMAN CHORIONIC GONADOTROPIN (HCG 5000 iu) INJECTION
HUMAN CHORIONIC GONADOTROPIN (HCG 5000 iu) INJECTION Human chorionic gonadotropin (HCG) and a recombinant formulation, called choriogonadotropin alfa (r-HCG), is a gonad-stimulating polypeptide hormone normally secreted by the placenta during pregnancy. The non-recombinant products are obtained from the urine of pregnant women. Recombinant-HCG is produced via recombinant DNA techniques in Chinese Hamster Ovary (CHO) cells. The pharmacological actions of HCG and of r-HCG are similar and resemble those of luteinizing hormone (LH); HCG is generally used as a substitute for LH. HCG has been used to treat cryptorchidism or hypogonadotropic hypogonadism in males, sometimes in combination with menotropins or follitropin. Interestingly, HCG was introduced for the treatment of cryptorchidism in 1931, and remained the only hormonal agent available to treat the condition until the 1970’s, when gonadotropin-releasing hormone (GnRH) analogs also became a treatment option. Human chorionic gonadotropin (HCG) is used in controlled ovarian hyperstimulation protocols for infertility in females. Intralesional HCG has been utilized for the treatment of Kaposi’s sarcoma, but further clinical trials are required to prove efficacy. Human chorionic gonadotropin is banned from use in competitive sport; some male athletes have used HCG to stimulate testosterone production or to prevent testicular atrophy resulting from the abuse of anabolic steroids and androgens. Urine-derived HCG was first approved by the FDA in 1939, and received subsequent approval for additional indications in 1973.
Mechanism of Action
The mechanism of action of human chorionic gonadotropin (HCG) depends upon the purpose for which it is being used, the sex of the patient, and the level of maturity of the patient to whom it is administered.
Adult females: In select females with infertility , human chorionic gonadotropin has actions essentially identical to those of luteinizing hormone (LH). Human chorionic gonadotropin (HCG) also appears to have additional, though minimal, follicle-stimulating hormone (FSH) activity. By administering HCG after follitropin, menotropins, or clomiphene, the normal LH surge that precedes ovulation can be mimicked. Human chorionic gonadotropin (HCG) promotes the development and maintenance of the corpus lutetium and the production of progesterone. Following HCG administration, final luteinization or maturation of the oocytes occurs and either ovulation can ensue for timed insemination techniques, or oocyte retrieval can take place for assisted reproductive technology (ART) procedures such as in vitro fertilization (IVF). Once pregnancy takes place, endogenous HCG is normally secreted by the placenta to support the continued secretion of female hormones and the corpus luteum.
Adult and adolescent males: In adult and adolescent men with hypogonadotropic hypogonadism, HCG acts like LH and stimulates testosterone production in the Leydig cells and spermatogenesis in the seminiferous tubules. Stimulation of androgen production by HCG causes development of secondary sex characteristics in males (e.g., deepening of voice, facial hair, etc.). Human chorionic gonadotropin (HCG) also stimulates the Leydig cells to produce estrogens; increased estrogen levels may produce gynecomastia in some males. Once HCG is initiated, it takes at least 70—80 days for germ cells to reach the spermatozoal stage. Response to treatment is also noted by the development of masculine features and the normalization of serum testosterone levels. Induction of testicular growth and increased sperm volumes may help to restore fertility in these men after many months to years of treatment, which is then sometimes combined with the use of either menotropins or follitropin.
Male infants and children: In the male infant, normal testicular descent is complete by 3 months of age. Testicular descent occurs secondary to an endogenous testosterone surge stimulated by pituitary gonadotropins in response to the discontinued exposure to maternal circulating estrogens upon birth; this testosterone surge peaks within 60 days postnatally. In male infants and children with cryptorchidism, HCG acts like LH and causes the Leydig cells of the testes to produce a testosterone surge and induce the descent of palpable testes. The hormonal stimulation by HCG may result in an early pseudopuberty, and in some cases, the response to hormonal therapy may be temporary in 10—20% of cases. Hormonal therapies like HCG have not replaced the primary surgical treatment for the condition, which is orchiopexy within the first 1—2 years of life. Early animal studies have suggested that HCG may be used as an adjunct to orchiopexy to help preserve fertility, but human data is lacking.
