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Hypercoagulation, Fibromylagia, and Chronic Fatigue Syndrome

Recent research in patients with fibromyalgia (FM) and chronic fatigue/immune dysfunction syndrome (CFIDS) suggests that pain, fatigue, and a range of other symptoms may be related to the development of a hypercoagulable state. In plain language, here is what we think happens, and what it means.

With almost any form of severe or prolonged physical, mental, and or emotional trauma, the body produces high levels of stress hormones and immune system mediators. When this happens in patients with FM or CFIDS, it may trigger an abnormal cascade of coagulation proteins. The trauma responsible for triggering a hypercoagulable state could be an accident (such as a fall or a car accident), a flu-like illness, surgery, a gauntlet of stress, or literally any form of intense or sustained stress on one's physical or mental health.

When this happens inpatients with FM or CFIDS, a coagulation protein called fibrin has been shown to accumulate in the microcirculation (where the smallest arteries are turning into capillaries). Fibrin is a stiff protein that functions as scaffolding for blood clots. In this instance, blood clots do not form, but the fibrin itself forms a meshwork, or screen, slowing down the blood flow to those cells supplied by the vessels containing too much fibrin. The accumulating fibrin also promotes the accumulation of additional protein debris. This means less oxygen and nutrients are reaching the cells, and less waste products are being carried away from the cells. The result is chronic pain, fatigue, and a host of other symptoms and signs of a body that is not functioning normally.

This appears to happen for genetic reasons. Some people have genes causing them to produce too much of the raw material that will eventually turn into fibrin, while others have genes that result in lower amounts of the enzymes that clear fibrin away. Some people can have both types of genes, predisposing to even more fibrin accumulation.

Treating with low dose anticoagulants, such as Heparin or Coumadin, is proving helpful in selected patients who generate too much thrombin-related raw material. Treating with enzymes that clear away fibrin, such as Nattokinase, is proving helping in selected patients who can't clear away fibrin well enough on their own. The use of proteolytic enzyme blends can also help clear protein debris from the blood and the lymph circulations.

The biochemistry of coagulation is fairly complicated. There are many laboratory tests available to help identify coagulation abnormalities. The use of these tests in determining which patients with FM or CFIDS will best respond to therapies is being investigated.

There is much yet to learn about which types of stress or trauma, combined with which type of genetic picture, result in which type of hypercoagulable state, let alone which forms of treatment work best. Early reports of success using fibrin-clearing enzymes are promising. It will take time for well-designed clinical studies to answer these questions, but enough is already known about safety to proceed with trials of therapy using enzymes to control a hypercoagulable state.

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