Treatment of Long Covid with Enoxaparin, 2025, Wright, Ciara PhD, Kell, Douglas PhD, Pretorius, Resia PhD. Putrino, David PhD Abstract Background and Purpose: Long COVID is a complex multisystemic disease state, which represents a huge economic and health burden worldwide. Hypercoagulation and the formation of fibrinaloid microclots have been proposed as an underlying pathology, which may underpin a wide variety of presenting symptoms, via reduced blood flow and cellular energy production. Postexertional malaise (PEM) is common and exercise therapy should not be recommended without addressing the underlying pathology. Case Presentation: Patient was female, 43, with Long COVID for 21 months characterized primarily by extreme fatigue, exercise intolerance, PEM, cognitive dysfunction, and postural orthostatic tachycardia syndrome. She was unable to work or leave the house unless for essential medical appointments. Before her initial severe acute respiratory syndrome coronavirus 2 infection, she had no prior health conditions or comorbidities, a body mass index of 20.8, and engaged in regular vigorous exercise. Intervention: This case report describes a patient treated with enoxaparin, a low molecular weight heparin, at 20 mg per day subcutaneously, with assessment at 8 weeks. Outcomes: The patient's function and quality of life improved markedly, as reported subjectively, and with objective measurements at 8 weeks. Levels of activity improved markedly with no adverse events. The severity of PEM decreased dramatically, and postural orthostatic tachycardia syndrome was better controlled. The FUNCAP score, used to measure functional capacity, increased from 3.3 (moderately affected) to 5.07 (mildly affected) after treatment. Discussion: It is recommended that this treatment should be further investigated to elucidate the role of enoxaparin in addressing underlying pathology in Long COVID, including hypercoagulation and microclots. LINK
I wonder what other medication she took with the LMW anticoagulant. When we were tested the protocol included Fragmin and a anti-viral/immune modulator.
The patient in this study is the first author. I'm not sure that it is good practice to do this without mentioning the fact.
Doxycycline & #PEM - My experience since starting doxy (3wks), either threshold for PEM has markedly increased or it is just not triggering. Been wayyy over the ‘too much’ recently (family stuff &work), go to sleep, wake up RESTED ready to go. Actual MAGIC Yes it treated a possible Bartonella (high IgM) but it hardly solved that in a week. A swollen lump in my throat for the past yr has gone tho. But this PEM change seems like a non-antibiotic mechanism eg glutamine/ glutamate. 2 days left so will see what happens after https://twitter.com/user/status/1868246760109584520
This is possibly an important factor for a subset of pwME. I actually had some revealing blood tests recently that were surprising. Had surgery in Nov and during the pre-op testing they found a coagulation abnormality in my blood, my APTT (also called PTT) was very high. Then they ran a bunch of coagulation tests to find I am positive for lupus anticoagulant. Then they ran antiphospholipid antibody syndrome tests and I’m positive for two APS antibodies, anti-beta 2 glycoprotein 1 and anti-phosphatidylserine prothrombin complex. Though I’ve never had a thrombosis/clotting event yet. Now they are going to do all the lupus diagnostic blood tests. I’ve also had a positive ANA with homogeneous pattern for years now and they measured it again it to confirm. These results have me thinking how long have I had this? Did it develop due to ME or have I had it since long before and it was as a major contributing factor? Or do I have lupus since lupus can take many years to develop and often doesn’t present with typical symptoms? Lupus and APS are closely linked autoimmune disorders. My former ME doctor (Dr Levine) only ever tested ANA and anti-cardiolipin antibodies over the years and with my terrible luck my cardiolipin antibodies are negative. It’s only one of the three important APS antibodies. It goes to show how missing one test and failing to be comprehensive can result in many years going by without having really important actionable information. Even without any clotting events yet the hematologist said some of the ME symptoms could actually be driven by these autoantibodies. So after going through the lupus dx profiling I’m going to start hydroxychloroquine and I’ve already started low dose aspirin. Both are standard of care for APS for people without clotting events but at high risk and hcq is also soc for lupus. Since hcq can affect antibodies I have to wait until after the dx bloodwork is done to start it.
I really hope HCQ will make some difference in my ME symptoms. I’ve never trialed it. Even if I test positive for lupus and am diagnosed with lupus the soc is also HCQ unless it by itself can’t control flare ups and organ damage. But if I do have lupus so many ME symptoms overlap with lupus symptoms I have no idea what is causing what now. HCQ can take 3 months of dosing to start showing benefit
One thing to mention is one worry I have about HCQ is that it can cause herpesvirus reactivation. I’m in the subset with definite lab evidence suggestive of viral reactivation. It’s the age old ME question, for those of us with evidence of herpesviral (EBV, CMV, HHV-6) reactivation (in my case since the beginning of our ME) will immunosuppressive medications make us worse? Or is it actually the autoantibodies and downstream pathophysiological effects that are causing the reactivations and counterintuitively will suppressing this actually reduce herpesviral activity and reactivations? As we’ve seen in countless research papers in recent years, herpesviruses are implicated in multiple autoimmune disorders and I’ve always wondered is immunosuppression a double edged sword? Is it improving symptoms in the short term only to make things worse by promoting viral reactivation long term?
