How do I know if I have endometriosis?
The leading symptom of endometriosis chronic pain, which is mostly localised in the lower abdomen, the pelvic area, but can also radiate to the waist. The relief of pain symptoms is the main reason why women with endometriosis consult a doctor.Interestingly, the degree of pain is not necessarily related to the size and extent of the endometriosis nodules. It mainly occurs during and before menstruation, but in more advanced cases it can occur at virtually any time.
Another typical symptom is irregular bleeding. There are women with endometriosis who have a menstrual cycle, "only" with unbearable pain, but a common complaint is that the menstrual period does not keep the cycle going and bleeding can occur completely independently. When menstruating very heavy, patchy bleeding and the period can last much longer than the normal 3-5 days, up to 10 to 14 days. In some cases, this can mean severe blood loss, so the condition can also lead to anaemia.
Sharp pain during sex or a gynaecological examination, but also pain during urination and defecation. The pain in these situations is not spasmodic, but sharp and shooting. It is a typical symptom in endometriosis. Unfortunately, it is often not taken seriously, for example, your partner may think you are trying to avoid intercourse. It's a vicious circle: the sicker you are, the more you go to the gynaecologist, but the more unpleasant the examination itself...
The baby is not coming...It is assumed that endometriosis is both mechanical (adhesions, tubal blockage, etc.),can also cause damage to eggs by inhibiting egg migration, fertilisation and implantation infertility.
Other complaints that may help to make a differential diagnosis: lower back pain, chronic fatigue, abdominal distention, crampy bowel movements, painful bowel movements, frequent diarrhoea, urinary complaints, renal colic, intestinal lacrimation, sputum suspicious for tuberculosis, coughing up blood, other organ-specific symptoms and complications. If the location of the endometriosis is extragenital, i.e. not affecting the genital organs, the complaints are specific to the organ concerned. Until endometriosis is confirmed, this can be a serious diagnostic problem.
Here you can find a general, shorter description of endometriosis. If you would like to know more, I recommend you subscribe to Endomail where I will send you the latest research results in Hungarian every week, and you can find out more interesting and up-to-date information.
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I went from doctor to doctor for four years, I was told to accept that being a woman meant being in pain every month. I've ended up in the emergency room, vomiting, fainting, especially on the first day of my period, I have negative ultrasound findings from those times. Later surgery revealed that I had endometriosis nodules practically everywhere.
I didn't have any symptoms, apart from the occasional bloating in my stomach. I put it down to food sensitivities and ignored it. But the baby didn't come for 4 years, and finally, because of that, I had an operation for diagnostic purposes, which is how I found out I had endometriosis.
Unfortunately, endometriosis can also increase the risk of malignant diseases.
Endometriosis significantly increases the chances of developing certain ovarian cancers, and endometriosis-associated ovarian cancer appears to be a completely separate disease: patients are younger, diagnosed at an early stage, have lower grade (roughly meaning less advanced) lesions and better survival. The genetic background to this may be that, by a certain molecular mechanism, endometriosis cells become inoperable antitumour genes (tumour suppressors) that would prevent the cells from degenerating into cancer (PTEN, TP53, in other studies ALID1, MMAC).
The exact mechanisms that promote malignant transformation of endometriosis are still unclear, despite several historical and genetic studies.Some have attributed the loss of heterozygosity (LOH) in the chromosomes of endometriosis nodules, others have attributed the early stages of malignant transformation to mutations in various tumour suppressor genes (PTEN, TP53, ALID1, MMAC).Many, however, believe that even so, the co-occurrence of endometriosis and cancer is still relatively low and do not consider endometriosis to be an explicit predictor of cancer.
In chocolate cysts, which very often develop following retrograde menstruation, the accumulation of haem (the iron-containing component of haemoglobin) and free iron ions from the blood exposes the immediate environment to high levels of oxidative stress, which is known to damage DNA and thus induce genetic changes.
The inflammation around endometrial nodules is particularly harmful for the patient, on the one hand, it creates a pathogen-free, sterile inflammation (often treated with strong antibiotics, of course, completely ineffective), and on the other hand, the compounds produced by immune cells that accumulate in the inflammatory reaction stimulate the embedding and growth of endometrial cell groups and create a direct link to the already malignant lesions.
Estrogen, a steroid hormone, is known to promote malignant ovarian cysts in high concentrations. Interestingly, the aromatase enzyme involved in the production of oestrogen is not found in healthy endometrium, but only in lesions, while the enzyme that inactivates oestrogen behaves in the opposite way: it is present in healthy tissue and absent in endometrial proliferations. Overall, this results in a locally hyperestrogenic state in the lesion area, which may be exacerbated by two additional factors: a relative resistance to the anti-estrogenic hormone progesterone is observed in endometrial lesions (the protein that inhibits the binding of the hormone is present while the one that stimulates it is absent), and in addition, estrogen itself stimulates its own production (through the COX2 gene and its product PGE2, a prostaglandin, further increasing the level of the aromatase enzyme). This explains why the commonly used progesterone-based therapy is ineffective in many cases. Furthermore, it is particularly important to note here that this also means that the lesion is dependent on the function of the aromatase enzyme, so if this enzyme can be inhibited - remember, it is not present in the healthy endometrium! - then the disease can lose its hyperestrogenic state, which can cause the lesion to stop growing or regress. This would be a very promising potential therapy for the future, as it would achieve the same positive effects as the drugs currently in use, but without the serious systemic side effects. At the level of the body, the oestrogenic effect would prevail, but the endometriosis implants would have much less access.
It is important to point out that research findings to date are often contradictory as to whether endometriosis is definitely a condition that precedes ovarian cancer. Recent findings (Wiegand et al.) suggest that ARID1A gene mutations (alterations) in people with endometriosis may indeed lead to certain ovarian cancers, but the number of people studied is small and it is not known exactly when the alteration in the gene itself occurred. Further studies will answer these questions and will help to decide whether to incorporate routine diagnostics of the ARID1A gene into patient care.
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