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Hypercoagulation & Lyme


Dr. Charles Crist's Report

Treatment for Hypercoagulation - Located Here.

"Hypercoagulation, or thrombophilia, may be defined as reduced capillary blood flow or a greater tendency than normal for blood to coagulate, or clot. 

Of approximately 900 borreliosis [Munch's note: med term for Lyme infection] patients that I have tested, 90 percent have hypercoagulation. Comparatively, only five percent of the general healthy population has hypercoagulation.  

Two major aspects of hypercoagulation are infections and hereditary or genetic abnormalities. Chronic infections such as borreliosis, Epstein-Barr virus, cytomegalovirus, human herpes virus 6 and mycoplasma have all been associated with hypercoagulation.  

These infections appear to be the driving force behind the greater tendency to form blood clots. Infections may elevate levels of fibrinogen, fibrin, thrombin/antithrombin complexes, fragment 1+2, and Factor II (prothrombin) activity which may decrease capillary blood flow.  

When you get a cut, the fibrinogen in your blood converts into fibrin, which in turn forms a mesh to create a blood clot to help stop the bleeding. Antithrombin binds to thrombin to form a complex to prevent thrombin from causing blood to clot. Antithrombin protects against too much clotting, when it binds thrombin.  

When thrombin is forming a clot it produces fragment 1+2. Prothrombin (Factor II) converts into thrombin, which causes blood to clot. When these coagulation components are high, it indicates that the blood has a greater tendency to clot., and may inhibit blood circulation in capillaries.

Inherited or genetic disorders may also predispose to blood clotting. Some of these hereditary defects include antithrombin activity deficiency, protein C activity deficiency, protein S activity deficiency, Factor II gene mutation, APC resistance (Activated Protein C resistance is also called Factor V Leiden deficiency), elevated lipoprotein(a) or Lp(a), elevated PAI-1 (Plasminogen Activator Inhibiter-1), and elevated homocysteine.  

Hereditary hypercoagulation test panels are abnormal in 66 percent of borreliosis patients, as opposed to about 25 percent of the general healthy population.

Treatment for hypercoagulation caused by infections is heparin, which is a blood thinner. Typically, heparin is given subcutaneously (under the skin) by injection twice a day in low doses for not more than nine months. It can also be compounded into a troche that dissolves in the mouth, but that is usually more expensive and is often less effective than injections.

Symptoms that improve with heparin are pain, fatigue, cognitive problems and neurological problems. About 80 percent of borreliosis patients feel better with heparin, and it has been a safe treatment so far. One patient did develop bleeding from the rectum, but then a colonoscopy revealed a colon cancer that had not yet spread to the local lymph nodes. In other words, the heparin unmasked a hidden malignancy, so in this case the side effect was a blessing.

Heparin is not only a blood thinner, it is also anti-inflammatory, antiviral, antibacterial, and may even be anti-cancer (unproven). Therapy with heparin usually lowers the level of the coagulation components fibrinogen, fibrin, thrombin/antithrombin complexes, fragment 1+2 and Factor II activity. This is desirable, because elevated levels of these coagulation components can cause decreased capillary blood flow, if they are high enough.  

Capillaries are microscopic blood vessels that are about eight microns wide. A normal red blood cell, which travels through the capillaries, is about seven microns wide. When elevation of coagulation components occur, they could conceivably attach to the inside surface (endothelial surface) of capillaries, thereby narrowing them.  

For example, fibrinogen attached to the inside surface could make it harder for a seven-micron-wide red blood cell to squeeze through the narrowed capillary. Reduced blood flow in capillaries would in turn reduce oxygen and nutrients, and reduce removal of toxins from tissues. It stands to reason that if heparin could improve blood flow, antibiotics and hormones would be more effective because they could pass through capillaries easier.  

Life is in the blood. Less blood flow means less “life,” and possibly more symptoms and diseases -- perhaps even death.

Hypercoagulation is associated with other chronic diseases, not just borreliosis. It is my opinion that how hypercoagulation is treated will become a paradigm shift in medicine, once further research has been accomplished.

© 2006 Dr. Charles L. Crist, MD. All Rights Reserved. 

More Information

Q&A with Dr. Burrascano

Q: What about hypercoagulation and Heparin?
A: Hypercoagulation is also seen in Babesia. Dr. Burrascano finds that heparin helps the same things as Babesia treatment and thus may not be warranted if Babesia is [successfully] addressed.

Link Here.

Lyme Treatment Guidelines

  • Hypercoaguable states are often associated with Babesia infections. 

    Link Here.

 



More info: 
http://www.immunesupport.com/library/showarticle.cfm/ID/3110/e/1/T/CFIDS_FM/

When adding in heparin to your protocol you will herx! 

Source: http://lassesen.com/cfids/herxheimer.htm

+The Jarisch-Herxheimer reaction (referred to as "Herx") is caused by organisms (bacteria) dying off and releasing toxins into the body faster than the body may comfortably handle it. 



Hypercoagulation and Babesia

Clin Infect Dis. 2001 Apr 15;32(8):1117-25. Epub 2001 Mar 26.

Severe babesiosis in Long Island: review of 34 cases and their complications.

Abstract

Thirty-four consecutive patients were hospitalized with diagnosis of severe Babesia infection over the course of 13 years. The average time from onset of symptoms to diagnosis was 15 days. When compared with uninfected febrile control patients, affected patients complained significantly more often of malaise, arthralgias and myalgias, and shortness of breath (P<.05), and they more often had thrombocytopenia and abnormal liver function (P<.05). 

Forty-one percent of patients with Babesia developed complications such as acute respiratory failure, disseminated intravascular coagulation, congestive heart failure, and renal failure. Analysis of data revealed that complicated babesiosis was more commonly associated with the presence of severe anemia (hemoglobin level <10 g/dL; P=.01) and higher parasitemia levels (>10%; P=.08). Patients were treated with a combination of drugs that included clindamycin, quinine, atovaquone, or azithromycin. Despite treatment, parasitemia persisted for an average of 8.5 days (range, 3--21 days). Exchange transfusion was performed for 7 patients, and it effectively reduced the high levels of parasitemia. Three patients died. Improved outcomes may result with prompt recognition and treatment of babesiosis.

PMID:
 
11283800
 
[PubMed - indexed for MEDLINE] 
Free full text





Coinfection should be considered in patients who present with more-severe initial symptoms than are commonly observed with Lyme disease alone, especially in those who have high-grade fever for >48 h, despite receiving antibiotic therapy appropriate for Lyme disease, or who have unexplained leukopenia, thrombocytopenia, or anemia (A-III). 

Suspicion of HGA is based on the acute onset of unexplained fever, chills, and headache, often in association with thrombocytopenia, leukopenia, and/or increased liver enzyme levels in patients with exposure to I. scapularis or I. pacificus ticks within the prior 3 weeks.

[Spotted Fever]-  Laboratory features may include leukopenia, lymphopenia, thrombocytopenia, and mild elevation of liver enzyme levels. 





Eur J Haematol. 2018 Jul 30. doi: 10.1111/ejh.13156. [Epub ahead of print]

Recommendations for the diagnosis and treatment of patients with polycythaemia vera.

Author information

1
Clinic of Hematology and Blood Transfusion, University Hospital, Faculty of Medicine, Medical School Comenius University, Slovak Medical University, Bratislava, Slovakia.
2
Clinical Section, Institute of Hematology and Blood Transfusion and Institute of Clinical and Experimental Hematology, Charles University, Prague, Czechia.
3
Clinic for Hematology Clinical Center of Serbia, Medical Faculty University of Belgrade, Belgrade, Serbia.
4
Department of Clinical Hematology, Masaryk University Hospital, Brno, Czechia.
5
Department of Hematology, Dubrava University Hospital, University of Zagreb, Medical School, Zagreb, Croatia.
6
Department of Hematology, Somogy Country Mór Kaposi General Hospital Kaposvár, Hungary.
7
Department of Hematology, Oncology and Palliative Medicine, Johannes Wesling Academic Medical Center, Minden, Germany.
8
University Clinic for Hematology, Oncology and Palliative Medicine, Johannes Wesling Medical Center Minden, University of Bochum, Germany.
9
Department of Hematology, Blood Neoplasms and Bone Marrow Transplantation, Wróclaw Medical University, Wróclaw, Poland.
10
Department of Hematology and Transplantology, Medical University Hospital, Gdaňsk, Poland.
11
Department of Medical Genetics, State Institution National Research Center for Radiation Medicine of National Academy of Medical Sciences of Ukraine, Kyiv, Ukraine.
12
Provita Diagnosis and Treatment Center, Bucharest, Romania.
13
Ludwig-Maximilian's University and Hematology Oncology Center Munich, Munich, Germany.
14
Department of cancer Prevention, Public School of Health, Silesian Medical University, Katowice, Poland.
15
Department of Hematology, University Clinical Center, Ljubljana, Slovenia.
16
Division of Hematology, University Clinic of Medicine, Kantonsspital Aarau, Switzerland.
17
Institute of Pathology, University of Cologne, Cologne, Germany.
18
Department of Internal Medicine V, Hematology& Oncology, Innsbruck Medical University, Innsbruck, Austria.
19
Medical Clinic 3, Oncology, Hematology and Rheumatology, University Hospital of Bonn, Bonn, Germany.
20
Department of Internal Medicine I, Division of Hematology and Blood Coagulation, Medical University of Vienna Hospital, Vienna, Austria.

Abstract

OBJECTIVES: 

To present the Central European Myeloproliferative Neoplasm Organisation (CEMPO) treatment recommendations for polycythaemia vera (PV).

METHODS: 

During meetings held from 2015 through 2017, CEMPO discussed PV, and its treatment and recent data.

RESULTS: 

PV is associated with increased risks of thrombosis/thrombo-haemorrhagic complications, fibrotic progression, and leukaemic transformation. Presence of Janus kinase (JAK)-2 gene mutations is a diagnostic marker and standard diagnostic criterion. World Health Organization 2016 diagnostic criteria for PV, focusing on haemoglobin levels and bone marrow morphology, are mandatory. 

PV therapy aims at managing long-term risks of vascular complications and progression towards transformation to acute myeloid leukaemia and myelodysplastic syndrome. Risk stratification for thrombotic complications guides therapeutic decisions. 

Low-risk patients are treated first line with low-dose aspirin and phlebotomy. 

Cytoreduction is considered for low-risk (phlebotomy intolerance, severe/progressive symptoms, cardiovascular risk factors) and high-risk patients. Hydroxyurea is suspected of leukaemogenic potential. IFN-α has demonstrated efficacy in many clinical trials; its pegylated form is best tolerated, enabling less-frequent administration than standard interferon. Ropeginterferon alfa -2b has been shown to be more efficacious than hydroxyurea. JAK1/JAK2-inhibitor ruxolitinib is approved for hydroxyurea resistant/intolerant patients.

CONCLUSIONS: 

Greater understanding of PV is serving as a platform for new therapy development and treatment response predictors. This article is protected by copyright. All rights reserved.

This article is protected by copyright. All rights reserved.

KEYWORDS: 

cytoreductive therapy; diagnosis; management; myeloproliferative neoplasms; polycythaemia vera; recommendations

PMID:
 
30058088
 
DOI:
 
10.1111/ejh.13156
]

Link Here




Lyme & Polycythemia


Pennsylvania Study on Polycythemia vera











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