Endometriosis is an oestrogen-mediated benign inflammatory disease affecting about 10 - 15 % of reproductive aged women.

• Incidence peaks at 40 - 44 years.

• Prevalence increases to about 30 % in women with infertility and to 45 % in those with chronic pelvic pain .

• Approximately 70 % of menstruating women exhibit bleeding reflux, but only a small percentage develop endometriosis.

 • Characterised by the presence of endometrial cells outside the uterus, especially in the pelvic peritoneum.

• Many studies show an altered immune response involving macrophages, T cells, B cells and inflammatory cytokines.

• Specifically natural killer (NK) cells appear to play an important role in the pathogenesis of endometriosis.

• Reduced cytotoxic function of NK cells has been observed in the peritoneal fluid (PF) of women with endometriosis.

• This may allow endometrial fragments to survive in the peritoneum.

• Macrophage numbers are increased in the PF of women with endometriosis, but they fail to act as scavengers or endometrial tissue.

• Macrophages are the primary contributors to the increase in pro-inflammatory mediators in the area.


• Differentiation of mesothelial cells into endometrium-like tissue within the peritoneal cavity.

• Menstrual tissue from the endometrial cavity reaches other body sites through veins or lymphatic vessels.

• Circulating blood cells originating from bone marrow differentiate into endometriotic tissue at various body sites.

• Other locations include the ovaries and retrovaginal septum, intestines and rectum.

 Characterised by a variety of symptoms:

  • Cyclic pain • Dysmenorrhoea • Mittelschmerz (pain on ovulation) • Heavy or long uncontrollable menstrual periods with small or large blood clots • Premenstrual spotting • Metrorrhagia • Menstrual spotting post intercourse Reproductive • Chronic pelvic pain • Dyspareunia • Infertility • Vaginal thrush (esp. pre-menstrually) • Hot flushes prior to menstruation • Hot flushes at ovulation • Hot flushes at conception and / or implantation. Diarrhoea (esp. with menses) • Constipation (esp. pre-menstrually) • Vomiting • Headaches • Chronic fatigue • Pain in the legs, thighs, back pains.• Anaemia (iron deficiency).

Can cause adhesions between the ovaries, intestines, rectum and bladder.

The only way to make a diagnosis is with a laparoscopy or laparotomy.

There will be a blood test that will soon be available to make the diagnoses.

• Increased (local) production of oestrogen, cytokines, prostaglandins and metalloproteinases .

• A defective immune system fails to clear implants off the peritoneal surface.

Genetic factors :Ten-fold excess in female relatives compared with husband’s female relatives.

Endometriosis is a chronic inflammatory disease involving secondary inflammatory mediators : Primary inflammatory mediators, e.g. bacterial endotoxin or lipopolysaccharide (LPS), trigger the secretion of various secondary inflammatory mediators, such as cytokines, chemokines, and growth factors, by mature/activated macrophages in the pelvis.

• Results from several studies point to bacterial contamination of the endometrium as a potential new factor in the establishment of endometriosis.

• In addition to the individual action of 17β-oestradiol (E2) and lipopolysaccharide (LPS) in promoting inflammatory response and growth of endometriosis, an additive effect between E2 and LPS might be involved in further worsening of pelvic inflammation and growth of endometriosis.

• If we consider the internal milieu of the pelvic environment, a substantial amount of E2 and endotoxin in the pelvis of women with endometriosis may jointly trigger this detrimental effect.

• Studies have suggested that exposure to dioxins in sanitary pads may be a cause of endometriosis

 • It suggests that environmental factors, as well as hormonal ones, might be associated with the risk of endometriosis.

The inflammatory process in endometriosis:

• May stimulate nerve endings in the pelvis to cause pain.

• Impairs function of the fallopian tubes.

• Decreases receptivity of the endometrium.

 • Negatively affects development of the oocyte and embryo.

• Inflammation is a hallmark of endometriotic tissue that overproduces prostaglandins, metalloproteinases, cytokines, and chemokines.

• Increased levels of acute inflammatory cytokines such as interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumour necrosis factor-alpha (TNF-α) likely enhance adhesion of tissue fragments on peritoneal surfaces.

• Hypo methylation appears to be an integral component of endometriosis:

• Associated with increased oestradiol, progesterone resistance and inflammation1.

• Stromal cells of endometriosis lesions have altered patterns of DNA methylation, compared to stromal cells in normal endometrium.

• These changes affect genes with roles in cell signalling, proliferation and migration, nerve development and immunity.

• Altered mast cell activity results in excessive pro-inflammatory cytokine release, increasing inflammation and promoting neuronal pain sensitivity.

• Pro-inflammatory cascade further promotes cell proliferation and angiogenesis, driving growth of endometriosis.

• Compared to the general  population, women with endometriosis had significantly higher rates of: • Hypothyroidism • Rheumatoid arthritis • Systemic lupus erythematosus • Sjogren's syndrome • Multiple sclerosis • Also fibromyalgia, chronic fatigue syndrome.

Treatments include:

Liver detox.

Cod liver oil packs, hot water bottle and remedies to alleviate the pain.

Herbal remedies to reduce the inflammation, improve methylation and control the autoimmune condition.

Diet changes.

Reduce the mast cell activation with an antihistamine diet and herbal remedies.

Improve the microcirculation as there is a drop of oxygen in the tissues from the spasms.

Prevent the formation of adhesions.


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