Endometriosis

Published on 09/03/2015 by admin

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Chapter 4 Endometriosis

Gary Swift

Definition. Endometriosis is defined as the presence of endometrial-like tissue outside the uterus, which induces a chronic inflammatory reaction and is associated with pain, subfertility and impaired quality of life.

Cyclical bleeding into deposits causes inflammation, scarring and adhesions, leading to pain, anatomical distortion and pelvic organ dysfunction. Dysmenorrhoea, dyspareunia, non-cyclical pelvic pain, dysuria, dyschezia and infertility result from the disease, though it may be asymptomatic in a minority. Symptoms in women subsequently found to have endometriosis may commence soon after menarche, with the disease varying widely in severity, symptomatology, and clinical and social impact. The disease ranges from relatively trivial superficial deposits causing few symptoms to severe deep infiltrating endometriosis (DIE) affecting the muscularis of pelvic viscera and/or the rectovaginal septum with associated quality of life implications.

Prevalence. An estimated 10% of reproductive-age women, in all social and ethnic groups, have endometriosis; 30% of women presenting with infertility have endometriosis; 50%–60% of women presenting with pelvic pain have endometriosis.

Risk factors

• higher risk with early menarche, short cycles and heavy menstrual flow (>8 days relative risk (RR) 2.4)
• reduced incidence with smoking (reduced oestrogen) and exercise (increased sex hormone-binding globulin (SHBG) and reduced luteal oestrogen levels)
• relative risk greatly increased with first-degree relative afflicted
• dietary factors: reduced risk with high fruit (odds ratio (OR) 0.6) and vegetable (OR 0.3) intake and fish oil (animal studies); increased risk with high red meat consumption (OR 2.0).
• increased risk with higher levels of vitamin D
• inverse association between endometriosis and body mass index (BMI)
• possible increased risk with alcohol, caffeine, and polychlorinated biphenyls (PCB) and dioxin exposure

Aetiology

The exact aetiology is still not known. The most widely accepted theory is related to viable endometrial cells reaching the peritoneal cavity through retrograde menstruation along the fallopian tubes (Sampson 1927). At least 90% of women with patent fallopian tubes will have evidence of retrograde menstruation; yet, in the majority, the menstrual debris is rapidly and efficiently cleared, by macrophages and natural killer (NK) cells.

Alternative theories of ‘coelomic metaplasia’ and ‘embryonic cell rests’ are less favoured.

Increased susceptibility is possibly related to:

• increased exposure to menstrual debris
• abnormal eutopic endometrium
• altered peritoneal environment
• reduced immune surveillance
• increased angiogenic capacity

Genetics

Genes influence susceptibility to endometriosis.

• considered to be a complex heritable trait with many genes contributing to risk, with the contribution of any one individual gene likely to be small
• genomic linkages found on chromosomes 7, 10 and 20 so far
• relative increased risk with sibling affected: 2.34 to 15 times (higher risk in more severe forms of the disease)

Pathology

The lesions of endometriosis vary from superficial to deep and in appearance from clear to white to red to black in proportion to degree of inflammation, vascularity and haemosiderin deposition. Newly formed lesions tend to be clear to red, with older lesions more deeply pigmented, with variable proportions of pale scarring and fibrosis. With increasing fibrosis, lesions become nodular. Lesions in postmenopausal or hormonally suppressed women will tend to be paler.

The inflammation and fibrosis leads to adhesions and anatomical distortion. Shortening and thickening of uterosacral ligaments reduces uterine mobility and causes fixed retroversion. Shortening and thickening of ovarian ligaments displaces ovaries medially. Pouch of Douglas obliteration follows involvement of rectal serosa and sometimes muscularis.

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