Endometriosis is a common gynecological disease affecting 10% of women in reproductive age.

Women, at risk for developing the disease are – young age group, presence of uterine anomalies, nulliparous and those with a family history especially in the first degree relatives.

The presenting symptoms in endometriosis includes dysmenorrheoa, dyspareunia, dyschesia, chronic pelvic pain and infertility.

Its incidence among infertile women is 25 to 50 % .

In endometriosis women have a lower fecundity rate compared to normal couples – 0.02 – 0.1 per month and 0.15 – 0.20 per month respectively and also have lower live birth rates.

Endometriosis is a progressive and a recurrent disease. The disease progresses from red vesicular – active lesions , which respond to cyclical changes of sex steroids and then powder burn and finally fibrotic phase, where adhesion formation happens within the structures in the pelvis , thus altering normal anatomy

How endometriosis affects fertility ?

  1. Inflammatory reaction : affects the function of oocyte, sperm, embryo, and fallopian tube.
    • Peritoneal fluid in endometriosis shows an increase in  number of activated macrophages and TNF-α, IL-1β, IL-6, IL-8, RANTES, and monocyte chemotactic protein-1 and these cytokines increase COX -2 activity, thus increasing PGE2 and PGF2a and promotes angiogenesis  and adhesion formation.
  1. Distorted pelvic anatomy – Due to Pelvic adhesions or peritubal adhesions
    • Disturbs the tubo-ovarian relation and tube patency which impairs oocyte release from the ovary, inhibit ovum pickup, or impede ovum transport.
  1. Endocrine and ovulatory disorders:
    • Luteinized unruptured follicle syndrome, impaired folliculogenesis and  luteal phase defect. Increased expression of aromatase enzymes in ectopic endometrium, increases estrogen milieu in the peritoneum and also shows progesterone resistance evidenced  by absence of progesterone receptor B Dysregulation of progesterone responsive genes in the luteal phase, thus causing an incomplete transition of endometrium from the proliferative to secretory phase
  1. Affects endometrial receptivity and embryo implantation:
    • Elevated levels of IgG and IgA antibodies and lymphocytes in the eutopic endometrium.
    • Altered expression of a5B3 integrin and L seclectin in the endometrium.
    • Impaired NK cell function and increased expression of IL -6 in eutopic endometrium.
    • Increased prostaglandins promotes abnormal uterine contraction.

Treatment of endometriosis associated infertility:

According to EHRE guidelines –  A combination of conservative surgery along with artificial reproductive techniques(IUI or IVF)  with or without hormonal adjuvant therapy, is suggested.

The choice of treatment depends on stage of the disease, ovarian reserve, tubal status and male factor.

Stage I/II – Ablation of endometriotic lesions along with adhesiolysis followed by ovulation induction with  IUI – 3 to 4 cycles

Stage III/IV – requires multidisciplinary approach, a combination of surgery and or hormonal therapy along with In vitro fertilization. But in case of previous surgery, surgical treatment should be carefully planned, because multiple surgeries may cause damage to normal ovarian tissue thus reducing the reserve.

Laparoscopic cystectomy considered :

  • Endometriomas > 4cm , complete excision of cyst wall or fulgurations of cyst wall, here CO2 laser preferred over monoplolar cautery.
  • Improve access to follicles

IVF indications:

– Affected tubal function

– Severe male factor infertility

– Stage III/IV endometriosis : GnRH agonist 3 months prior to IVF is known to increase oocyte quality and embryo implantation.

Endometriosis requires early detection and systematic  management to achieve a pregnancy. Though the woman is young, ART should be considered rather than expectant management. Hence endometriotic patients requires thorough counseling regarding the disease behavior and its implication on fertility and the importance of artificial reproductive techniques