Introduction Decrease in effective testosterone levels as result of decreased free concentration often as result of decreased production (Leydig and pituitary dysfunction) also result of increased synthesis of SHBG decreased activity at receptor often as result of androgen receptor deficiency May be primary or secondary primary hypogonadism / hypergonadotropic hypogonadism ↓ function of Leydig cells results in ↓ testosterone synthesis any dysfunction isolated to Sertoli cells/seminiferous tubules does not result in ↓ testosterone synthesis if testes are cryptorchid, testosterone production is normal because Leydig cells are not affected by ↑ temperature loss of negative feedback of testosterone results in ↑ LH FSH levels are variable based on presence of inhibin ↑ FSH if seminiferous tubule dysfunction is also present inhibin normally released by Sertoli cells to inhibit FSH if damaged that feedback is lost normal FSH if dysfunction is limited to Leydig cells etiologies include alcoholic liver disease damage to Leydig cells as result of trauma, toxins, inflammation, and irradiation secondary hypogonadism / hypogonadotropic hypogonadism ↓ function of hypothalamus/pituitary results in ↓ LH and FSH synthesis and consequent ↓ testosterone synthesis etiologies include craniopharyngioma pituitary adenoma Presentation Symptoms ↓ secondary male characteristics osteoporosis result of dysregulated osteoclast activity (normally ↓ by testosterone) infertility ↓ sperm count impotence Treatment Testosterone administration Formulations Topical Intramuscular Subcutaneous Contraindications Prostate cancer Breast cancer