SWAlexander
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This is the first complete research that confirms my long-standing theory.
This is a long paper, though reading is worth it.
ME/CFS, FM, RA, SS, POTS, PVACS, Lyme: THERAPEUTIC TEST AND FIRST TREATMENT REGIME, WITH FIBRINOLYTICS AND FAMOTIDINE FOR PATIENTS WITH CHRONIC FATIGUE AND/OR PAIN TO ASSIST THE DIAGNOSIS OF PERSISTENT MICROCLOTS AND HYPOPERFUSION.
Abstract and Figures
For patients with Myalgic Encephalomyelitis/Chronic Fatigue Syndrome, Fibromyalgia, Rheumatoid Arthritis, Sjögren Syndrome, POTS, Long COVID or PACS, Post-Vaccine COVID Syndrome (PVACS), Chronic Lyme, EBV, others. BACKGROUND. The symptoms of Chronic Fatigue and Brain Fog are associated more frequently with Endothelial Dysfunction and less Blood Flow. Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) and Fibromyalgia (FM) affects many people, and often in addition to fatigue, patients present with various neurological symptoms known collectively as Brain Fog. Several studies have been published in which it is evidenced that, both in Chronic Fatigue Syndrome and in the so-called Brain Fog, there is less blood flow and/or long-term dysfunction (inadequate functioning) at the level of the endothelial cells that make up the blood vessel walls [1-8]. Presence of hypercoagulability, alteration in hematological parameters and increased risk of thrombosis in CFS/ME and FM. In patients with CFS/ME, the presence of hypercoagulability and thrombophilia has been identified in about 80% of cases [9,10]. In the case of FM, there are also publications that associate it with a prothrombotic state [11]. In addition, the alteration in some hematological parameters has been identified, such as elevation of the Mean Platelet Volume [12], greater erythrocyte deformability and faster erythrocyte aggregation [13]. And studies have been published that conclude that FM patients have a higher risk of stroke [14] and coronary heart disease [15,16]. Presence of hypercoagulability and thrombophilia in Rheumatoid Arthritis (RA) and Sjögren's Syndrome (SS). Several studies indicate that thrombotic events, hypercoagulability, endothelial dysfunction, platelet hyperactivity, and elevated von Willebrand factor are common in RA patients [17-22]. In Sjögren's Syndrome (SS) higher levels of serum viscosity [23,24], erythrocyte sedimentation rate and Immunoglobulin G [24] and a higher risk of thromboembolism [25] have been shown. Presence of hypercoagulability and microclots in Long COVID/PACS and PVACS. In patients with Long COVID or Post COVID Acute Syndrome (PACS), several studies show very high frequency the presence of platelet hyperactivity and microclots, observing a significant improvement in symptoms with the use of anticoagulants, antiplatelets and fibrinolytics [26]. While in Post-Vaccine against COVID Syndrome (PVACS) o Post-Vaccine Syndrome, affected patients frequently manifest persistent symptoms associated with hypoperfusion, hypercoagulability and microclots (HHM). Platelet infection, vascular injury, and hypercoagulability in Lyme. In Lyme disease, it has been shown that the causal agent, the Borrelia bacterium, is highly concentrated in the platelets, which is why it is pointed out that these would be a refuge or reservoir where they can remain persistently, it was also identified that it infects erythrocytes, but to a lesser degree [27]. On the other hand, several cases of thrombosis, ischemic stroke, transient ischemic attack and cerebral vasculitis have been reported in patients with Lyme disease, especially those who develop neuroborreliosis [28,29]. Presence of Antiphospholipid Antibodies and hypercoagulability in POTS (Postural Orthostatic Tachycardia Syndrome), Dysautonomia. In patients with POTS, published studies have identified the presence of persistent Antiphospholipid Antibodies, which are associated with a state of hypercoagulability and thrombophilia [31,32]. This has also been identified in Long COVID patients with POTS and MCAS [33]. Subgroups of CFS/ME, FM, RA, SS, POTS, PVACS, Lyme, and other diseases associated with Hypoperfusion, Hypercoagulability and Microclots (HHM).
Our approach is that in CFS/ME, FM, RA, SS, POTS, PVACS, Lyme and in other diseases and syndromes that cause fatigue and/or chronic pain, several Subgroups are included according to their pathophysiology and the causes that originate the symptoms, being the main Subgroups, to which most of the patients belong, the Subgroups of diagnoses associated with HHM due to chronic Endotheliitis (inflammation of the endothelial cells) that entails a dysfunction or inadequate functioning of the walls of the blood vessels accompanied by a state of long-term hypercoagulability, slowing or stasis of blood flow, and the presence of persistent microclots with a high content of amyloid fibrin. Other Subgroups of CFS/ME, FM, AR, SS, POTS, PVACS, Lyme. In addition to the most frequent Subgroups that are associated with HHM, there are other Subgroups within CFS/ME, FM, RA, SS, POTS and Chronic Lyme such as that associated with Dysbiosis, SIBO or alteration of the Intestinal Microbiota and the presence of Biofilms at intestinal level, a situation in which D-Lactate is increased. There is another Subgroup associated with alteration of the Oral Microbiota and presence of Dental Biofilms, a Subgroup associated with alteration of the Renal microbiota with the presence of Biofilms at this level and a Subgroup associated with alteration of microbiota and Biofilms from other locations. There are also Subgroups associated with Vitamin Depletion (especially of the B complex and Vitamin D), with Mineral (such as magnesium, copper, iron, selenium), and other Nutrients Depletion, and Subgroups associated with a decrease in hormones, especially thyroid and adrenal hormones such as cortisol. It should be taken into account that patients who have years with the aforementioned pathologies frequently present symptoms associated with several of the aforementioned Subgroups, observing in several cases that symptoms of HHM and Endothelial Inflammation, Dysbiosis or SIBO and Biofilms are presented at the same time. Depletion of Vitamins, Minerals and other Nutrients, Decrease of hormones and other substances. Implications of tissue hypoperfusion. Long-term inflammation of the endothelial cells causes the presence of persistent microclots and a decrease in the perfusion of fluids from the bloodstream to the cells and tissues, which is called hypoperfusion, which implies a lower contribution to the cells and tissues. of: - Oxygen (generating cellular hypoxia). - Vitamins. - Minerals and other Nutrients. - Hormones. - Other substances. Long-term tissue hypoperfusion affects the normal functioning of organs and systems, especially those that require a greater supply of oxygen and nutrients, which are mainly the musculoskeletal system and the brain. Chronic endotheliitis, persistent clots and hypoperfusion are not detectable with routine tests. Chronic Endotheliitis, the inadequate functioning of the endothelial cells (inflammation and endothelial dysfunction) and tissue hypoperfusion cause various organs and systems to not respond adequately when they are required, but it is a problem in the functioning that usually does not produce obvious tissue damage This is why most of the ancillary tests that are ordered routinely tend to be normal, such as X-rays, CT scans and routine laboratory tests. Persistent bioclots as a refuge for viruses and other microorganisms. We have also explained that viruses and other organisms that cause persistent intracellular infections take refuge in persistent clots that are high in fibrin amyloid fibrin [34,35,36,37]. Because these clots perform similar functions to Biofilms, we have named them Bioclots. It has been shown in publications that the persistence of viruses and other microorganisms is associated with platelet hyperactivity and the presence of persistent clots.
SYNDROMES AND CHRONIC DISEASES THAT PRESENT CHRONIC FATIGUE OR PAIN AND FREQUENTLY ALSO BRAIN FOG. There are several syndromes and chronic or persistent diseases that present fatigue or chronic pain and often also brain fog, and whose causal or etiological agent is not clearly identified, and in several of these cases the co-existence of 2 or more causal agents may exist. The most frequent and well-known are named below: Chronic Fatigue Syndrome/Myalgic encephalomyelitis (CFC/ME). Fibromyalgia. Rheumatoid arthritis. Long COVID or Post Acute COVID Syndrome (PACS) or Persistent Symptoms Post Acute COVID or Chronic COVID. Post-Vaccine against COVID Syndrome (PVACS) o Post-Vaccine Syndrome (PVS), and Persistent Symptoms Post-Vaccine against COVID. Hyperviscosity syndrome. Restless legs syndrome or Willis-Ekbom disease. Seated Immobility Thromboembolism (SIT) syndrome. Benign fasciculation syndrome and cramp fasciculation syndrome. Rheumatoid Arthritis. Sjögren Syndrome. Amplified Musculoskeletal Pain Syndrome (AMPS) or Amplified Pain Syndrome. Chronic myofascial pain. Functional Neurological Disorders (FND). Gulf War Illness (GWI). Post-viral syndromes. Postural Orthostatic Tachycardia Syndrome (POTS), and orthostatic intolerance. Histaminosis, histamine intolerance, MAO dysfunction and Mast Cell Activation Syndrome (MCAS) or Mast Cell Activation Disorder (MCAD). EDS (Ehlers-Danlos Syndrome). Bing-Neel syndrome. Thrombotic thrombocytopenic purpura. Hypothyroidism. Chronic depression. Alzheimer's disease and dementias. Psychosis and Schizophrenia.
PERSISTENT INFECTIONS THAT PRESENT FATIGUE OR CHRONIC PAIN AND FREQUENTLY ALSO MENTAL FOG. On the other hand, there are several persistent infections that present chronic fatigue or pain and often also mental fogginess. These infections are generally caused or associated with the presence of persistent intracellular microorganisms. The most frequent and well-known are: PERSISTENT VIRUS INFECTIONS: Viruses of the Herpesviridae family: - Herpes Simplex Virus 1 and 2 (HSV1 and HSV2). - Herpes-Zoster Virus (VZV). - Epstein-Barr Virus (EBV). - Cytomegalovirus (CMV). - Human Herpesvirus 6 and 7 (HHV-6 and HHV-7). - Human Herpesvirus 8 (HHV8) or Kaposi's Sarcoma virus. SARS CoV-2 virus (Chronic COVID, Long COVID or Persistent COVID). Human parvovirus B19. Enterovirus. Coxsackievirus B3. H1N1/09 influenza. Ebola virus. Dengue. Chikungunya. Human Papillomavirus (HPV). Adenovirus 2 Human retroviruses. Hepatitis B Virus (HBV) and Hepatitis C Virus (HCV). Human Type 1 T-cell Lymphotropic Virus (HTLV-1), West Nile Virus. Polio virus. Ross River Virus (RRV). Other viruses.
PERSISTENT INFECTIONS BY BACTERIA AND OTHER MICROORGANISMS: Chronic Lyme disease and Post-treatment Lyme disease syndrome (PTLDS), caused by the bacteria Borrelia burgdorferi and Borrelia mayonii. Bartonellosis (caused by the gram-negative bacteria Bartonella). Babesiosis (caused by the protozoan Babesia). Mollicutes or Mycoplasma diseases. They are bacteria that lack a cell wall. The pathogenic species are Mycoplasma pneumoniae, Mycoplasma genitalium and Ureaplasma urealyticum. Ehrlichiosis and Anaplasmosis (caused by bacteria of the rickettsiae family: Ehrlichia and Anaplasma). Neoehrlichia. Other Rickettsiosis (they are intracellular pleomorphic bacteria). Q fever by Coxiella burnetti. Candida and other mycoses. Chronic Typhoid Fever (or Chronic Paratyphoid), caused by Salmonella Typhi or Salmonella Paratyphi A, B and C. Chronic Chagas disease (caused by the Trypanosoma cruzi parasite). Toxoplasmosis. Mycobacterial diseases. Tuberculosis. Giardia lamblia Helicobacter pylori. Microorganisms that persist in oral, intestinal, renal and other biofilms. Microorganisms of the microbiota that overgrow. Other bacteria or microorganisms. In all these Syndromes and Persistent Infections that present chronic fatigue and brain fog, there may be endothelial dysfunction, persistent clots and tissue hypoperfusion, for which we recommend D-Dimer analysis and the application of the Therapeutic Test and first treatment regime to assist the diagnosis of Persistent Microclots and Hypoperfusion.
D-DIMER ANALYSIS FOR THE DIAGNOSIS OF PERSISTENT CLOTS. D-dimer is a breakdown product of fibrin, which is the main component of persistent clots. It is generally accepted that the normal value is less than 0.5 ug/ml. The D-dimer is considered a sensitive test, and it rises within a few hours of initiating the breakdown of clots. Elevated D-dimer in ME/CFS, FM, RA, SS, POTS, Long COVID/PACS, PVACS, Lyme. If an elevated D-dimer is identified in a patient with any of the aforementioned pathologies, it is interpreted that there is the presence of persistent clots. The higher the D-Dimer is, it is interpreted that the breakdown of a greater number of clots is taking place. Normal D-dimer in ME/CFS, FM, RA, SS, POTS, Long COVID/PACS, PVACS, Lyme, POTS. It should be clear that the D-Dimer does not measure the formation of clots, what it measures is the decomposition or fibrinolysis of the clots present in the body. So, if there are persistent clots, and the patient with any of the aforementioned pathologies is not taking any medication, supplement or food with an anticoagulant or fibrinolytic effect, the D-dimer may be normal.
VENOUS BLOOD GASES (VBG) MEASUREMENT FOR THE DIAGNOSIS OF HYPOXEMIA, WHICH IS CORRELATED TO THE SEVERITY OF HHM SYMPTOMS. A non-complex and low-cost test used to diagnose hypoxemia, which correlates with the severity of HHM symptoms, is the Venous Oxygen Saturation (SvO2 or Sat vO2) blood test, for which which is required to ask the patient for a Venous Blood Gas Measurement (VBG), since SvO2 is part of this auxiliary test. The SvO2 tells us what is the level or amount of oxygen in the blood when it returns to the heart. A low SvO2 value equates to Hypoxemia, which generally indicates increased oxygen demand (consumption). And when there is hypoxemia there is cellular hypoxia, the supply of oxygen to the tissues by the blood is decreased. However, it must be taken into account that there are patients with CFS/ME and other of the mentioned pathologies that may present a normal or even high SvO2, which is more frequently associated with a lower extraction of oxygen from the blood, which It can be caused by mitochondrial dysfunction and microthrombosis at the capillary level, in addition to other factors. Fibrinogen, Blood Viscosity and Cortisol. These are other tests that are also recommended, since the elevation of fibrinogen and blood viscosity correlates with the presence of HHM. In the case of Cortisol, what occurs is a decrease in this hormone, which would be associated with less blood flow to the adrenal glands that generate this hormone.
THERAPEUTIC TEST TO ASSIST THE DIAGNOSIS OF PERSISTENT MICROCLOTS AND HYPOPERFUSION. If a patient with persistent microclots is given medications or supplements with fibrinolytic, anticoagulant and/or antiplatelet effects, these will cause the clots to break down, which in turn will cause a significant elevation of the D-dimer. Taking into account the aforementioned, we have developed a Therapeutic Test to aid in the Diagnosis of Persistent Microclots and Tissue Hypoperfusion. This Test, as an aid to diagnosis, is indicated for patients who present a normal D-Dimer. If the patient already has a high D-dimer result, and has fatigue and other symptoms associated with HHM, then the diagnosis has already been confirmed that the symptoms they present are due to HHM and endothelial inflammation, and what must be applied is a Protocol or Treatment Regime, which includes, in addition to fibrinolytics and antiplatelets, medications and procedures against the microbial load. Objectives of the Therapeutic Test for Persistent Microclots and Hypoperfusion. This Test has the following objectives and utilities: 1) Identify a significant improvement in Symptoms associated with HHM, which is useful in supporting the existence of symptoms of HHM, which is almost always caused by endothelial inflammation, in turn triggered by persistent infections. 2) Identify a significant elevation of D-Dimer, which is useful for laboratory diagnosis of the existence of persistent clots, which are associated with the presence of a persistent infection that affects the walls of the blood vessels. 3) If possible, a venous blood gas analysis should be performed, with the aim of identifying a significant improvement in SvO2, which would be useful in supporting the existence of hypoxemia and cellular hypoxia, and that these findings were associated with presence of HHM. Sequence of activities to follow for the application of Therapeutic Test. For the application of this Therapeutic Test for Persistent Bioclots and Hypoperfusion, the following sequence of activities must be followed: 1) Assess the patient for symptoms of HHM. An easy-to-apply test is being developed so that the patient or their relatives can easily assess the presence and severity of HHM symptoms. 2) Evaluate the presence of symptoms of Histaminosis, MCAS, Allergies and Hyperreactivity. If this occurs, 2 H1 Blockers, 1 First Generation and 1 Second or Third Generation, and also Quercetin should be included in the treatment regime. 3) It is indicated to suspend any medication, supplement, herb or food with an effect on coagulation for at least 3 days before starting the "Therapeutic Trial". 4) Perform D-Dimer analysis. This step is optional, because in several countries there are inconveniences to be able to carry out analysis. In the cases in which several analyzes can be carried out, if possible, VBG, fibrinogen and cortisol should also be carried out. 5) Start taking the medications or supplements of the Test, which are taken for 6 days. 6) On the 7th day, evaluate the therapeutic response based on the clinical improvement of the symptoms associated with HHM. To evaluate the answer, a scale of 1 to 10 points, or in percentage, can be used. 7) In the same way, on the 7th day, the D-Dimer analysis should be performed, to evaluate the therapeutic response based on the percentage elevation of the D-Dimer value. 8) If possible, VBGanalysis should also be performed.
MEDICATIONS AND SUPPLEMENTS INCLUDED IN THE THERAPEUTIC TEST FOR PERSISTENT MICROCLOTS AND HYPOPERFUSION.
This Therapeutic Test includes 2 medications or nutritional supplements with effects of contributing to the breakdown of clots, and as a third medication Famotidine is included, which reduces the risk of gastrointestinal bleeding, is anti-inflammatory and reduces histamine levels, among other effects. beneficial. So, in a generic way, this Therapeutic Test includes: 1) A drug or supplement with an antiplatelet and/or anticoagulant effect. 2) A Supplement that has fibrinolytic effects. 3) Famotidine. Table 1 shows the names of the medications or supplements included in this Therapeutic Trial and their alternatives.
https://www.researchgate.net/public...O_ASSIST_THE_DIAGNOSIS_OF_PERSISTENT_MICROCLO
This is a long paper, though reading is worth it.
ME/CFS, FM, RA, SS, POTS, PVACS, Lyme: THERAPEUTIC TEST AND FIRST TREATMENT REGIME, WITH FIBRINOLYTICS AND FAMOTIDINE FOR PATIENTS WITH CHRONIC FATIGUE AND/OR PAIN TO ASSIST THE DIAGNOSIS OF PERSISTENT MICROCLOTS AND HYPOPERFUSION.
Abstract and Figures
For patients with Myalgic Encephalomyelitis/Chronic Fatigue Syndrome, Fibromyalgia, Rheumatoid Arthritis, Sjögren Syndrome, POTS, Long COVID or PACS, Post-Vaccine COVID Syndrome (PVACS), Chronic Lyme, EBV, others. BACKGROUND. The symptoms of Chronic Fatigue and Brain Fog are associated more frequently with Endothelial Dysfunction and less Blood Flow. Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) and Fibromyalgia (FM) affects many people, and often in addition to fatigue, patients present with various neurological symptoms known collectively as Brain Fog. Several studies have been published in which it is evidenced that, both in Chronic Fatigue Syndrome and in the so-called Brain Fog, there is less blood flow and/or long-term dysfunction (inadequate functioning) at the level of the endothelial cells that make up the blood vessel walls [1-8]. Presence of hypercoagulability, alteration in hematological parameters and increased risk of thrombosis in CFS/ME and FM. In patients with CFS/ME, the presence of hypercoagulability and thrombophilia has been identified in about 80% of cases [9,10]. In the case of FM, there are also publications that associate it with a prothrombotic state [11]. In addition, the alteration in some hematological parameters has been identified, such as elevation of the Mean Platelet Volume [12], greater erythrocyte deformability and faster erythrocyte aggregation [13]. And studies have been published that conclude that FM patients have a higher risk of stroke [14] and coronary heart disease [15,16]. Presence of hypercoagulability and thrombophilia in Rheumatoid Arthritis (RA) and Sjögren's Syndrome (SS). Several studies indicate that thrombotic events, hypercoagulability, endothelial dysfunction, platelet hyperactivity, and elevated von Willebrand factor are common in RA patients [17-22]. In Sjögren's Syndrome (SS) higher levels of serum viscosity [23,24], erythrocyte sedimentation rate and Immunoglobulin G [24] and a higher risk of thromboembolism [25] have been shown. Presence of hypercoagulability and microclots in Long COVID/PACS and PVACS. In patients with Long COVID or Post COVID Acute Syndrome (PACS), several studies show very high frequency the presence of platelet hyperactivity and microclots, observing a significant improvement in symptoms with the use of anticoagulants, antiplatelets and fibrinolytics [26]. While in Post-Vaccine against COVID Syndrome (PVACS) o Post-Vaccine Syndrome, affected patients frequently manifest persistent symptoms associated with hypoperfusion, hypercoagulability and microclots (HHM). Platelet infection, vascular injury, and hypercoagulability in Lyme. In Lyme disease, it has been shown that the causal agent, the Borrelia bacterium, is highly concentrated in the platelets, which is why it is pointed out that these would be a refuge or reservoir where they can remain persistently, it was also identified that it infects erythrocytes, but to a lesser degree [27]. On the other hand, several cases of thrombosis, ischemic stroke, transient ischemic attack and cerebral vasculitis have been reported in patients with Lyme disease, especially those who develop neuroborreliosis [28,29]. Presence of Antiphospholipid Antibodies and hypercoagulability in POTS (Postural Orthostatic Tachycardia Syndrome), Dysautonomia. In patients with POTS, published studies have identified the presence of persistent Antiphospholipid Antibodies, which are associated with a state of hypercoagulability and thrombophilia [31,32]. This has also been identified in Long COVID patients with POTS and MCAS [33]. Subgroups of CFS/ME, FM, RA, SS, POTS, PVACS, Lyme, and other diseases associated with Hypoperfusion, Hypercoagulability and Microclots (HHM).
Our approach is that in CFS/ME, FM, RA, SS, POTS, PVACS, Lyme and in other diseases and syndromes that cause fatigue and/or chronic pain, several Subgroups are included according to their pathophysiology and the causes that originate the symptoms, being the main Subgroups, to which most of the patients belong, the Subgroups of diagnoses associated with HHM due to chronic Endotheliitis (inflammation of the endothelial cells) that entails a dysfunction or inadequate functioning of the walls of the blood vessels accompanied by a state of long-term hypercoagulability, slowing or stasis of blood flow, and the presence of persistent microclots with a high content of amyloid fibrin. Other Subgroups of CFS/ME, FM, AR, SS, POTS, PVACS, Lyme. In addition to the most frequent Subgroups that are associated with HHM, there are other Subgroups within CFS/ME, FM, RA, SS, POTS and Chronic Lyme such as that associated with Dysbiosis, SIBO or alteration of the Intestinal Microbiota and the presence of Biofilms at intestinal level, a situation in which D-Lactate is increased. There is another Subgroup associated with alteration of the Oral Microbiota and presence of Dental Biofilms, a Subgroup associated with alteration of the Renal microbiota with the presence of Biofilms at this level and a Subgroup associated with alteration of microbiota and Biofilms from other locations. There are also Subgroups associated with Vitamin Depletion (especially of the B complex and Vitamin D), with Mineral (such as magnesium, copper, iron, selenium), and other Nutrients Depletion, and Subgroups associated with a decrease in hormones, especially thyroid and adrenal hormones such as cortisol. It should be taken into account that patients who have years with the aforementioned pathologies frequently present symptoms associated with several of the aforementioned Subgroups, observing in several cases that symptoms of HHM and Endothelial Inflammation, Dysbiosis or SIBO and Biofilms are presented at the same time. Depletion of Vitamins, Minerals and other Nutrients, Decrease of hormones and other substances. Implications of tissue hypoperfusion. Long-term inflammation of the endothelial cells causes the presence of persistent microclots and a decrease in the perfusion of fluids from the bloodstream to the cells and tissues, which is called hypoperfusion, which implies a lower contribution to the cells and tissues. of: - Oxygen (generating cellular hypoxia). - Vitamins. - Minerals and other Nutrients. - Hormones. - Other substances. Long-term tissue hypoperfusion affects the normal functioning of organs and systems, especially those that require a greater supply of oxygen and nutrients, which are mainly the musculoskeletal system and the brain. Chronic endotheliitis, persistent clots and hypoperfusion are not detectable with routine tests. Chronic Endotheliitis, the inadequate functioning of the endothelial cells (inflammation and endothelial dysfunction) and tissue hypoperfusion cause various organs and systems to not respond adequately when they are required, but it is a problem in the functioning that usually does not produce obvious tissue damage This is why most of the ancillary tests that are ordered routinely tend to be normal, such as X-rays, CT scans and routine laboratory tests. Persistent bioclots as a refuge for viruses and other microorganisms. We have also explained that viruses and other organisms that cause persistent intracellular infections take refuge in persistent clots that are high in fibrin amyloid fibrin [34,35,36,37]. Because these clots perform similar functions to Biofilms, we have named them Bioclots. It has been shown in publications that the persistence of viruses and other microorganisms is associated with platelet hyperactivity and the presence of persistent clots.
SYNDROMES AND CHRONIC DISEASES THAT PRESENT CHRONIC FATIGUE OR PAIN AND FREQUENTLY ALSO BRAIN FOG. There are several syndromes and chronic or persistent diseases that present fatigue or chronic pain and often also brain fog, and whose causal or etiological agent is not clearly identified, and in several of these cases the co-existence of 2 or more causal agents may exist. The most frequent and well-known are named below: Chronic Fatigue Syndrome/Myalgic encephalomyelitis (CFC/ME). Fibromyalgia. Rheumatoid arthritis. Long COVID or Post Acute COVID Syndrome (PACS) or Persistent Symptoms Post Acute COVID or Chronic COVID. Post-Vaccine against COVID Syndrome (PVACS) o Post-Vaccine Syndrome (PVS), and Persistent Symptoms Post-Vaccine against COVID. Hyperviscosity syndrome. Restless legs syndrome or Willis-Ekbom disease. Seated Immobility Thromboembolism (SIT) syndrome. Benign fasciculation syndrome and cramp fasciculation syndrome. Rheumatoid Arthritis. Sjögren Syndrome. Amplified Musculoskeletal Pain Syndrome (AMPS) or Amplified Pain Syndrome. Chronic myofascial pain. Functional Neurological Disorders (FND). Gulf War Illness (GWI). Post-viral syndromes. Postural Orthostatic Tachycardia Syndrome (POTS), and orthostatic intolerance. Histaminosis, histamine intolerance, MAO dysfunction and Mast Cell Activation Syndrome (MCAS) or Mast Cell Activation Disorder (MCAD). EDS (Ehlers-Danlos Syndrome). Bing-Neel syndrome. Thrombotic thrombocytopenic purpura. Hypothyroidism. Chronic depression. Alzheimer's disease and dementias. Psychosis and Schizophrenia.
PERSISTENT INFECTIONS THAT PRESENT FATIGUE OR CHRONIC PAIN AND FREQUENTLY ALSO MENTAL FOG. On the other hand, there are several persistent infections that present chronic fatigue or pain and often also mental fogginess. These infections are generally caused or associated with the presence of persistent intracellular microorganisms. The most frequent and well-known are: PERSISTENT VIRUS INFECTIONS: Viruses of the Herpesviridae family: - Herpes Simplex Virus 1 and 2 (HSV1 and HSV2). - Herpes-Zoster Virus (VZV). - Epstein-Barr Virus (EBV). - Cytomegalovirus (CMV). - Human Herpesvirus 6 and 7 (HHV-6 and HHV-7). - Human Herpesvirus 8 (HHV8) or Kaposi's Sarcoma virus. SARS CoV-2 virus (Chronic COVID, Long COVID or Persistent COVID). Human parvovirus B19. Enterovirus. Coxsackievirus B3. H1N1/09 influenza. Ebola virus. Dengue. Chikungunya. Human Papillomavirus (HPV). Adenovirus 2 Human retroviruses. Hepatitis B Virus (HBV) and Hepatitis C Virus (HCV). Human Type 1 T-cell Lymphotropic Virus (HTLV-1), West Nile Virus. Polio virus. Ross River Virus (RRV). Other viruses.
PERSISTENT INFECTIONS BY BACTERIA AND OTHER MICROORGANISMS: Chronic Lyme disease and Post-treatment Lyme disease syndrome (PTLDS), caused by the bacteria Borrelia burgdorferi and Borrelia mayonii. Bartonellosis (caused by the gram-negative bacteria Bartonella). Babesiosis (caused by the protozoan Babesia). Mollicutes or Mycoplasma diseases. They are bacteria that lack a cell wall. The pathogenic species are Mycoplasma pneumoniae, Mycoplasma genitalium and Ureaplasma urealyticum. Ehrlichiosis and Anaplasmosis (caused by bacteria of the rickettsiae family: Ehrlichia and Anaplasma). Neoehrlichia. Other Rickettsiosis (they are intracellular pleomorphic bacteria). Q fever by Coxiella burnetti. Candida and other mycoses. Chronic Typhoid Fever (or Chronic Paratyphoid), caused by Salmonella Typhi or Salmonella Paratyphi A, B and C. Chronic Chagas disease (caused by the Trypanosoma cruzi parasite). Toxoplasmosis. Mycobacterial diseases. Tuberculosis. Giardia lamblia Helicobacter pylori. Microorganisms that persist in oral, intestinal, renal and other biofilms. Microorganisms of the microbiota that overgrow. Other bacteria or microorganisms. In all these Syndromes and Persistent Infections that present chronic fatigue and brain fog, there may be endothelial dysfunction, persistent clots and tissue hypoperfusion, for which we recommend D-Dimer analysis and the application of the Therapeutic Test and first treatment regime to assist the diagnosis of Persistent Microclots and Hypoperfusion.
D-DIMER ANALYSIS FOR THE DIAGNOSIS OF PERSISTENT CLOTS. D-dimer is a breakdown product of fibrin, which is the main component of persistent clots. It is generally accepted that the normal value is less than 0.5 ug/ml. The D-dimer is considered a sensitive test, and it rises within a few hours of initiating the breakdown of clots. Elevated D-dimer in ME/CFS, FM, RA, SS, POTS, Long COVID/PACS, PVACS, Lyme. If an elevated D-dimer is identified in a patient with any of the aforementioned pathologies, it is interpreted that there is the presence of persistent clots. The higher the D-Dimer is, it is interpreted that the breakdown of a greater number of clots is taking place. Normal D-dimer in ME/CFS, FM, RA, SS, POTS, Long COVID/PACS, PVACS, Lyme, POTS. It should be clear that the D-Dimer does not measure the formation of clots, what it measures is the decomposition or fibrinolysis of the clots present in the body. So, if there are persistent clots, and the patient with any of the aforementioned pathologies is not taking any medication, supplement or food with an anticoagulant or fibrinolytic effect, the D-dimer may be normal.
VENOUS BLOOD GASES (VBG) MEASUREMENT FOR THE DIAGNOSIS OF HYPOXEMIA, WHICH IS CORRELATED TO THE SEVERITY OF HHM SYMPTOMS. A non-complex and low-cost test used to diagnose hypoxemia, which correlates with the severity of HHM symptoms, is the Venous Oxygen Saturation (SvO2 or Sat vO2) blood test, for which which is required to ask the patient for a Venous Blood Gas Measurement (VBG), since SvO2 is part of this auxiliary test. The SvO2 tells us what is the level or amount of oxygen in the blood when it returns to the heart. A low SvO2 value equates to Hypoxemia, which generally indicates increased oxygen demand (consumption). And when there is hypoxemia there is cellular hypoxia, the supply of oxygen to the tissues by the blood is decreased. However, it must be taken into account that there are patients with CFS/ME and other of the mentioned pathologies that may present a normal or even high SvO2, which is more frequently associated with a lower extraction of oxygen from the blood, which It can be caused by mitochondrial dysfunction and microthrombosis at the capillary level, in addition to other factors. Fibrinogen, Blood Viscosity and Cortisol. These are other tests that are also recommended, since the elevation of fibrinogen and blood viscosity correlates with the presence of HHM. In the case of Cortisol, what occurs is a decrease in this hormone, which would be associated with less blood flow to the adrenal glands that generate this hormone.
THERAPEUTIC TEST TO ASSIST THE DIAGNOSIS OF PERSISTENT MICROCLOTS AND HYPOPERFUSION. If a patient with persistent microclots is given medications or supplements with fibrinolytic, anticoagulant and/or antiplatelet effects, these will cause the clots to break down, which in turn will cause a significant elevation of the D-dimer. Taking into account the aforementioned, we have developed a Therapeutic Test to aid in the Diagnosis of Persistent Microclots and Tissue Hypoperfusion. This Test, as an aid to diagnosis, is indicated for patients who present a normal D-Dimer. If the patient already has a high D-dimer result, and has fatigue and other symptoms associated with HHM, then the diagnosis has already been confirmed that the symptoms they present are due to HHM and endothelial inflammation, and what must be applied is a Protocol or Treatment Regime, which includes, in addition to fibrinolytics and antiplatelets, medications and procedures against the microbial load. Objectives of the Therapeutic Test for Persistent Microclots and Hypoperfusion. This Test has the following objectives and utilities: 1) Identify a significant improvement in Symptoms associated with HHM, which is useful in supporting the existence of symptoms of HHM, which is almost always caused by endothelial inflammation, in turn triggered by persistent infections. 2) Identify a significant elevation of D-Dimer, which is useful for laboratory diagnosis of the existence of persistent clots, which are associated with the presence of a persistent infection that affects the walls of the blood vessels. 3) If possible, a venous blood gas analysis should be performed, with the aim of identifying a significant improvement in SvO2, which would be useful in supporting the existence of hypoxemia and cellular hypoxia, and that these findings were associated with presence of HHM. Sequence of activities to follow for the application of Therapeutic Test. For the application of this Therapeutic Test for Persistent Bioclots and Hypoperfusion, the following sequence of activities must be followed: 1) Assess the patient for symptoms of HHM. An easy-to-apply test is being developed so that the patient or their relatives can easily assess the presence and severity of HHM symptoms. 2) Evaluate the presence of symptoms of Histaminosis, MCAS, Allergies and Hyperreactivity. If this occurs, 2 H1 Blockers, 1 First Generation and 1 Second or Third Generation, and also Quercetin should be included in the treatment regime. 3) It is indicated to suspend any medication, supplement, herb or food with an effect on coagulation for at least 3 days before starting the "Therapeutic Trial". 4) Perform D-Dimer analysis. This step is optional, because in several countries there are inconveniences to be able to carry out analysis. In the cases in which several analyzes can be carried out, if possible, VBG, fibrinogen and cortisol should also be carried out. 5) Start taking the medications or supplements of the Test, which are taken for 6 days. 6) On the 7th day, evaluate the therapeutic response based on the clinical improvement of the symptoms associated with HHM. To evaluate the answer, a scale of 1 to 10 points, or in percentage, can be used. 7) In the same way, on the 7th day, the D-Dimer analysis should be performed, to evaluate the therapeutic response based on the percentage elevation of the D-Dimer value. 8) If possible, VBGanalysis should also be performed.
MEDICATIONS AND SUPPLEMENTS INCLUDED IN THE THERAPEUTIC TEST FOR PERSISTENT MICROCLOTS AND HYPOPERFUSION.
This Therapeutic Test includes 2 medications or nutritional supplements with effects of contributing to the breakdown of clots, and as a third medication Famotidine is included, which reduces the risk of gastrointestinal bleeding, is anti-inflammatory and reduces histamine levels, among other effects. beneficial. So, in a generic way, this Therapeutic Test includes: 1) A drug or supplement with an antiplatelet and/or anticoagulant effect. 2) A Supplement that has fibrinolytic effects. 3) Famotidine. Table 1 shows the names of the medications or supplements included in this Therapeutic Trial and their alternatives.
https://www.researchgate.net/public...O_ASSIST_THE_DIAGNOSIS_OF_PERSISTENT_MICROCLO
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I mean I can understand apple and others but grapes. I even eat grapes with the seedsin it. watermellon too.