Male Endometriosis

The first published case of a human male with endometriosis occurred in 1971. (1) Since then, a few sporadic cases have been published. But how is it possible for a human male to develop endometriosis?  In our database search of publications to date, all cases but one have common characteristics that suggest stimulation of dormant cells from early  embryo development well before birth.

During early embryo development, the capacity to become both male and female is present. The reproductive organs and genitalia of females develop from Mullerian Ducts (MD). Around the second month of embryo development, a substance is released which prevents further development of the reproductive organs and genitalia of the opposite sex.  This substance is called MIS or AMH, (Mullerian Inhibiting Substance or Anti Mullerian Hormone).  If there are genetic defects which prevent secretion of MIS/AMH or the Mullerian Ducts cannot detect the substance, this leads to Persistent Mullerian Duct Syndrome (PMDS) in which a male develops a uterus and fallopian tubes.

All cases presented to date, with exception of one, (2) were exposed to high levels of circulating estrogen. It is theorized that elevated estrogen levels stimulated these dormant Mullerian Ducts to develop into female tissues and organs. What creates an environment of elevated estrogen?  Three different scenarios all create elevated estrogen levels.

  • Males with history of estrogen therapies to treat prostate cancer (3,4)
  • Males with liver cirrhosis (liver is unable to breakdown estradiols in foods) (5)
  • Males with Morbid Obesity (high body fat levels = higher estrogen levels) (6)

A case of a 27 year old male did not fit the profile of all other cases of male endometriosis. All other cases were over the age of 50 years and presented with one of the three scenarios listed above for elevated estrogen levels which are theorized to reactivate Mullerian Rests of cells that had been dormant throughout life, stimulated to begin development into female reproductive tissues.  The lack of estrogen exposure, normal endocrine function and hormone levels and an absence of any genetic mutation(s) (46, XY) could not explain the development of cystic endometriosis among the epididymis of this otherwise healthy young man. (2)  The only remote theory the authors proposed was that exposure of environmental endocrine disruptors while the man was still in the womb at early embryogenesis, caused a delay in the production and release of MIS (Mullerian Inhibiting Substance). The delay in the substance allowed both male and female tissues to begin evolving from the Mullerian Ducts. However, at some point, progression of female reproductive tissues ceased and only male features continued.

46, XY Disorder of sexual development (DSD):  A genetic mutation known as 46 XY leads to development of smaller, oft nonfunctional female reproductive organs and tissues internally, and male reproductive organs and tissues.

Male Endometriosis Citations

 

 

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