In males, LH stimulates testosterone production by testicular interstitial cells (Leydig cells.) FSH stimulates testicular growth and enhances the production of androgen-binding proteins via supporting cells (Sertoli cells). Androgen-binding proteins can cause high levels of testosterone in the vicinity of the spermatozoa, an important influence in normal sperm development. Thus, FSH and LH are required for sperm maturation. One of the most common abnormalities seen in the clinical management of male patients when examining their hormone panel of six is the manifestation of high FSH in men. These patients are often accompanied by abnormal semen tests. So, what are the main causes of increased FSH? This is briefly summarized below. Causes of high FSH: This can be congenital or acquired Congenital: mainly due to genetic mutations, chromosomal abnormalities, cryptorchidism, specific lack of testicular support cells and other factors. These causes can be identified through medical means such as chromosome examination, physical examination, male ultrasound and testicular puncture. Acquired: Some men who have had children, or even had normal semen tests a few years ago, show semen abnormalities in several recent tests. Acquired factors leading to this condition are: 1. Infection: the most common is mumps orchitis. The seminiferous tubules are almost always severely affected, often leading to infertility, especially with bilateral testicular involvement.Leydig cells may also be damaged, leading to decreased production of testosterone with high LH levels. 2. Radiation: This mainly damages the seminiferous tubules or ovaries. The degree of damage is proportional to the level of radiation exposure. 3, Antitumor drugs: Cyclophosphamide, nitrogen mustard phenylbutyrate, cisplatin and carboplatin can reduce sperm counts by damaging the seminiferous tubules. Less commonly, testosterone production also declines. Recovery may occur over time. Similarly, in women, chemotherapy may lead to ovarian failure. 4. Chemicals: Chemicals such as dibromodichloropropane can reduce spermatogenesis. 5, Glucocorticoids: These can lead to hypogonadism by suppressing the pituitary gland and testes. 6, Ketoconazole: This is an antifungal drug that inhibits testosterone biosynthesis. 7, Sulforaphane: this is an antiparasitic drug that can block testosterone synthesis in Leydig cells. 8, trauma: the injury can be severe enough to damage the seminiferous tubules and Leydig cells. 9. Testicular torsion: Torsion lasting longer than 8 hours may result in low sperm counts. Both testes may be damaged even if the torsion involves only 1 testis; the mechanism is unknown. 10. Chronic systemic diseases: Cirrhosis, chronic renal failure, and AIDS may lead to primary and secondary hypogonadism. Bilateral femoral artery anastomosis in men may lead to reduced blood supply to the testes, mainly affecting the seminiferous tubules. 11, Autoimmune damage: This is due to anti-sperm antibodies. It can be part of autoimmune polyglandular syndrome. 12. Idiopathic: Many men and women with primary hypogonadism suffer from idiopathic disease, the cause of which has never been recognized. The cause may be autoimmune. 13. Gonadal adenomas: These are the most common pituitary macroadenomas. They usually do not cause a recognizable clinical endocrine syndrome. They present with optic nerve damage, headaches, and pituitary hormone deficiency due to compression of non-adenomatous pituitary cells by the macroadenoma. Gonadal adenomas themselves can overproduce FSH, LH or one of the subunits (alpha or beta). All of the above factors can lead to altered male fertility. Congenital factors can be examined and clarified under the guidance of a physician; acquired factors need to be prevented and if they occur, a reproductive physician needs to be consulted for treatment.