The Potential of Non-Invasive Biomarkers for Early Diagnosis of Asymptomatic Patients with Endometriosis, 2021, Kimber-Trojnar et al.

The Potential of Non-Invasive Biomarkers for Early Diagnosis of Asymptomatic Patients with Endometriosis
Kimber-Trojnar, Żaneta; Pilszyk, Aleksandra; Niebrzydowska, Magdalena; Pilszyk, Zuzanna; Ruszała, Monika; Leszczyńska-Gorzelak, Bożena

Endometriosis is a disease that affects women of reproductive age and has a significantly negative impact on their well-being. The main symptoms are dysmenorrhoea, chronic pelvic pain and infertility. In many patients the diagnostic process is very long and can take up to 8–12 years. Laparoscopy, an invasive method, is still necessary to confirm the diagnosis. Therefore, development of more effective diagnostic markers appears to be of the utmost importance for early diagnosis of endometriosis and provision of appropriate treatment.

From a clinical point of view, detection of early-stage endometriosis in asymptomatic patients is an ideal situation since early diagnosis of endometriosis may delay the onset of symptoms as well as prevent progression and complications. In the meantime, Cancer Antigen 125 (CA-125) is still the most frequently studied and used marker. Other glycoproteins, growth factors and immune markers seem to play an important role. However, the search for an ideal endometriosis marker is still underway. Further studies into the pathogenesis of endometriosis will help to identify biomarkers or sets of biomarkers with the potential to improve and speed up the diagnostic process in a non-invasive way.

Link | PDF (Journal of Clinical Medicine)

 

Recording a couple of quotes as endometriosis and dysregulated menstrual cycles seem to be reported in ME and LC —

 

I keep seeing menstrual dysregulation and pelvic pain in patient discussions, though I think it's not talked about more widely due to social constraints. It's also common to hear that LC symptoms worsen with menses. I haven't looked to see if it's been discussed or informally polled on S4ME. I suspect it's more widespread than we realise.

The hypotheses to explain endo have never been satisfactory. The explanation has to account for spread in the peritoneal cavity - OK - that's potentially direct spread in one body compartment. But then to the chest in the pleural space (catamenial pneumothorax) - well sure sometimes there are defects in the diaphragm and you can get pleural accumulations of CSF from a ventriculoperitoneal shunt. But then actually in the lungs or brain - now you have to surmise pseudometastatic spread or stem cells.

To my mind there seems to be symptomatic overlap and co-morbiidity between ME/LC and pelvic pain, endometriosis, polycystic ovarian disease, interstitial cystitis. Then you have drug findings like metformin being used in endometriosis and PCOS. It all suggests a hidden uniting aetiology relating to metabolism and in particular immunometabolism and resulting immune dysregulation and inflammation.

And the NK cell hypofunction, well that could be causal or simply an association with endo, but it seems like a well established observation in ME.

See Endometriosis as a Comorbid Condition in Chronic Fatigue Syndrome (CFS): Secondary Analysis of Data From a CFS Case-Control Study (2019, Frontiers in Pediatrics)

which concluded —

 

From Wikipedia —

From Transforming Growth Factor-β Induced Warburg-Like Metabolic Reprogramming May Underpin the Development of Peritoneal Endometriosis (2014) —

Would be interesting to see if EBV/HHV-6 have been implicated in endometriosis, as dUTPase-induced upregulation of activin A could relate.

 

I saw this being reported with such high frequency I couldn't imagine it wouldn't get researched. It's reported many ways: more problems, fewer problems, longer, shorter. Many changes, all over the place. Hard to study, for sure, but it's hard to imagine scientists going "meh" over this, and simply not bothering.

I clearly lack imagination about the many ways people will fuck everything up. I can only remember a single study and it was about the effect of vaccines, obviously dismissing everything as psychological. It hasn't been studied at all. No one is even keeping track, there is no recorded data anywhere on this, so it's not even possible to look back retroactively on anything.

As an information specialist, I am baffled at how much data medicine just doesn't bother looking at, don't even want to record it in the first place. And almost everything they look at is selective. There is no more investigative research anymore, it's like the entire research paradigm has ended. It feels more like theology at times, only looking at familiar words, and barely at that.

Most crap companies selling garbage products out there with decades of customer, sales and production data. Kept everything just in case. All of this is being leveraged using machine learning. Meanwhile I guess that medicine really wants to save up on disk space, or something like that. Can't have large bases of data, too long to backup, I guess.

 

From Aviation and healthcare: a comparative review with implications for patient safety (2015, J Royal Soc Med) —

 

I could post that paper in a separate thread.

ETA: https://www.s4me.info/threads/aviat...ns-for-patient-safety-2016-kapur-et-al.32716/

 

Related potential biomarkers for endometriosis —

Fibronectin Molecular Status in Plasma of Women with Endometriosis and Fertility Disorders (2021, International Journal of Molecular Sciences)

Plasma and Peritoneal Fluid Fibronectin and Collagen IV Levels as Potential Biomarkers of Endometriosis (2022, International Journal of Molecular Sciences)

 

Fibronectin and thrombosis: Fibronectin maintains the balance between hemostasis and thrombosis (2016, Cellular and Molecular Life Sciences)

So would elevated fibronectin be associated with more likelihood of thromboembolic disease in endometriosis? There doesn't seem to be much literature on endometriosis and thrombo-embolic disease that I could find, which suggests that it hasn't been on people's radar. However, perhaps elevated fibronectin might be generally protective against venous thromboembolism, as there are subtleties in how fibronectin interacts which could make it less likely (see first paper).

Endometriosis and thrombosis: Risk of venous thromboembolism in women with endometriosis (2022, Thrombosis Research)

Which concluded no significantly increased risk.

However note the methodology —

533 consecutive women with a diagnosis of severe endometriosis based on histological and surgical criteria and whom all underwent laparoscopic surgery between January 2015 and December 2019. At time of surgery, all women were using hormonal therapy for management or pain alleviation of endometriosis. Follow-up started after surgery and ended if a VTE occurred or patients were lost to follow-up.

Eleven patients with a personal VTE history before the surgery were excluded.​

Excluding those who have already demonstrated a propensity to VTE might then under-represent the risk.