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Fibromyalgia and HCV 

Biopsies of Chronic Inflammatory Muscle Disease Show Enterovirus RNA
By Will Boggs, MD

NEW YORK (Reuters Health) Jan 02 - The presence of enterovirus RNA in muscle biopsies from patients with chronic inflammatory muscle disease or fibromyalgia favors a persistent infection involving defective viral replication, according to a new report. Enterovirus RNA was detected in 20% of patients with chronic inflammatory muscle diseases, 13.3% of patients with fibromyalgia/chronic fatigue syndrome, and no healthy volunteers.

"The persistence of defective or infectious enteroviruses is well established for a lot of organs, including myocardium (with possible involvement in idiopathic dilated myocardiopathy), Langerhans' islets (with possible involvement in juvenile diabetes mellitus), and central nervous system (with possible involvement in post-polio syndrome and Charcot disease)," Dr. Bruno Pozzetto from CHU de Saint-Etienne, France told Reuters Health. "However, the link between these diseases, as well as chronic inflammatory muscle diseases, and viral persistence is not clear."

Dr. Pozzetto and colleagues investigated the presence of enterovirus in skeletal muscle biopsies from 15 patients with chronic inflammatory muscle diseases, 30 patients with fibromyalgia/chronic fatigue syndrome, and 29 healthy subjects to test their hypothesis that skeletal muscle may host enteroviral persistent infection.

The study is reported in the December 2003 Journal of Medical Virology.

The signals expressed in the three positive patients with chronic inflammatory muscle disease were higher than those found in the four positive patients with fibromyalgia/chronic fatigue syndrome, the report indicates, though the PCR test used in this assay was not quantitative.

None of the muscle biopsies in this study contained the VP-1 structural protein, the researchers note, which "suggests a defective viral replication, as evidenced by previous results obtained both in chronic fatigue syndrome patients and in a murine model of chronic inflammatory myopathy."

"The results of this study, although of small size, are not in favor of an enteroviral reservoir in the muscle compartment for virus persistence since no virus RNA was found in the control group (made of healthy subjects)," Dr. Pozzetto said. "However, the mean age of the control group was significantly lower than patients, and it cannot be excluded that the accumulation of enterovirus RNA in muscle occurs later during life."

It is too early to derive therapeutic implications from these results, Dr. Pozzetto said.

"However, coxsackieviruses B seem to play a key role in enteroviral myocardial and possibly muscular persistent infections," he said. "To prevent this persistence, an inactivated vaccine directed towards these viruses could be indicated. Pleconaril, an antiviral agent acting during the early phases of the viral cycle, could also be useful in muscular diseases clearly associated with enterovirus. Such an approach is under investigation for idiopathic dilated myocardiopathy. However, it is too early to answer for muscular diseases."

J Med Virol 2003;71:540-547.


Fibromyalgia syndrome in patients with hepatitis C infection.

Rheumatol Int. 2003 Sep;23(5):248-51. Epub 2003 Mar 18.

Kozanoglu E, Canataroglu A, Abayli B, Colakoglu S, Goncu K.

Department of Physical Medicine and Rehabilitation, Cukurova University
Faculty of Medicine, Adana, Turkey

PMID: 14504918


Fibromyalgia syndrome (FS) is characterized by widespread pain and tenderness at Specific anatomic sites. Different theories have been proposed in the etiopathogenesis of this syndrome, and besides genetic, neuroendocrine, psychologic, and traumatic causes, infections have also been reported. The aim of the present study was to evaluate the presence of FS in patients with hepatitis C virus (HCV) infection.

Ninety-five patients with chronic HCV infection and 95 healthy controls were enrolled in the study. The 1990 American College of Rheumatology classification criteria were used for the diagnosis of FS. Tender point count, pain intensity, sleep disturbance, stiffness, headache, paresthesia, fatigue, irritable bowel syndrome (IBS), and sicca- and Raynaud-like symptoms were assessed.

Fibromyalgia was found in 18.9% of patients and 5.3% of healthy controls. Mean tender point count, pain intensity scored on a visual analog scale (VAS), sleep disturbance, stiffness, paresthesia, and fatigue were higher in the HCV group. No significant relationship was observed between the two groups regarding headache, IBS, and sicca- and Raynaud-like symptoms. In addition, mean tender point count and pain intensity scores were also significantly higher in HCV patients with FS than in control subjects with FS. All of the symptoms except stiffness were not statistically significant
between the HCV and control groups with FS.

Our results demonstrate a tendency toward higher prevalence of FS in patients with HCV infection. Besides various extrahepatic features, musculoskeletal disorders including fibromyalgia might be expected in the progression of HCV infection. Detailed examination of the patients helps to differentiate FS from other musculoskeletal complications of HCV infection. This will provide appropriate management approaches and better quality of life for them.

Fibromyalgia in men found more severe although less frequent

An Israeli study of fibromyalgia that compared 40 men to 40 women
matched by age and educational status has found that the condition is
worse in the males.  The authors report: "Men with FMS reported more
severe symptoms than women, decreased physical function, and lower
quality of life. Women had lower tender thresholds than men; however
their mean point counts were similar."  They concluded "Although FMS
is uncommon in men, its health outcome in our study population was
worse than in women.  Further studies in larger samples and in
diverse ethnocultural populations are needed to confirm this
observation.

See this paper as:
   Buskila D, Neumann L, Alhoashle A, Abu-Shakra M.  Fibromyalgia
   syndrome in men.  Semin Arthritis Rheum. 2000 Aug;30(1):47-51.
   PMID: 10966212; UI: 20419396




 

Hepatitis C Virus Might Induce Fibromyalgia

By Nelle Nix Exclusive to SHN

Source: "Fibromyalgia: A prominent feature in patients with musculoskeletal problems in chronic hepatitis C, A report of 12 patients,"
by A. Barkhuizen, G.S. Schoepflin, and R.M. Bennett,
Journal of Clinical Rheumatology, Vol. 2, No. 4, August 1996.

October 17, 1996 -- A Portland, Ore. study suggests hepatitis C may trigger fibromyalgia. The study is the first to show a link between the two illnesses.

Fibromyalgia often arises after a traumatic event or an illness. Several infections have previously been proposed as potential inciters of fibromyalgia, including Lyme disease and the human herpes virus-6.

Published in the Journal of Clinical Rheumatology's August issue, the 12 patient study determined that the relationship between hepatitis C virus and fibromyalgia followed three distinct patterns:

•In nine patients, fibromyalgia developed as a long-term complication of the hepatitis, arising on average 13.4 years after the virus was acquired.

•In two patients, fibromyalgia arose simultaneously with the hepatitis C infection.

•In one patient, pre-existing fibromyalgia was significantly worsened by the hepatitis C.

Six of the 12 patients were diagnosed with fibromyalgia after initial evaluations for musculoskeletal complaints. All had the chance of contracting hepatitis C through either blood or body fluid exposure. Three used intravenous blood products, one experienced an occupational needle stick, three had tattoos, three used intravenous drugs, and two engaged in promiscuous sexual practices.

The reason for the link between hepatitis C virus and fibromyalgia is unknown. The authors propose, however, that hepatitis C causes chronic activation of the immune system that leads to muscle aching, fatigue, mental changes, sleep abnormalities, and alterations of the neuroendocrine system.

The patients with both hepatitis C and fibromyalgia could be distinguished from most other patients with fibromyalgia alone because they had symptoms unusual to fibromyalgia. These symptoms included synovitis (inflammation of the membrane around a joint, bursa, or tendon) and vasculitis (inflammation of a blood or lymph vessel). In addition, laboratory findings pointed to a disease process other than fibromyalgia.

The study was conducted at Oregon Health Sciences University and Portland Adventist Hospital.

Fibromyalgia in hepatitis C virus infection. Another infectious disease relationship. 

Buskila D. Shnaider A. Neumann L. Zilberman D. Hilzenrat N. Sikuler E. Archives of Internal Medicine. 157(21):2497-500, 1997 Nov 24. The objective was to determine whether there might be an association between hepatitis C virus (HCV) chronic infection and fibromyalgia (FM). We determined the prevalence of HCV infection in 112 FM patients, in comparison with matched rheumatoid arthritis (RA) patients from the out-patient clinic of a teaching tertiary care general hospital. Furthermore, we looked for evidence of FM in 58 patients diagnosed with chronic hepatitis due to HCV, compared with matched surgery clinic patients. HCV antibodies were determined by enzyme-linked immunosorbent assay (ELISA) and recombinant immunoblot assay (RIBA). Serum RNA of HCV (HCV-RNA) was determined by polymerase chain reaction. In the group of FM patients, HCV antibodies were found by ELISA in 17 (15.2%) patients and in six (5.3%) of the RA controls (P less than 0.05). RIBA was positive in 16 and indeterminate in one of the FM patients. Serum HCV-RNA was found in 13 of these FM patients. In eight (47%) FM patients, alanine aminotransferase (ALT) was normal, although HCV-RNA was detected in four (50%) of them. In the group of patients with chronic hepatitis due to HCV, all patients had HCV antibodies and the presence of HCV- RNA in serum. Within these patients, 31 (53%) had diffuse musculoskeletal pain, while six (10%) fulfilled FM diagnostic criteria. In the control group, 13/58 (22%) had diffuse musculoskeletal pain (P less than 0.001), whereas only one female patient (1.7%) fulfilled FM criteria (P less than 0.05). Serum ALT was 51.7 +/- 38.4 in FM patients, whereas it was 122 +/- 76.3 in patients with HCV chronic hepatitis but without FM (P less than 0.001). There were no statistical differences in autoimmune markers between patients with and without FM. These data suggest that there exists an association between FM and active HCV infection in some of our patients. FM is not associated with liver damage or autoimmune markers in these patients. HCV infection should be considered in FM patients even though ALT elevations were absent.

 Fibromyalgia-associated hepatitis C virus infection. 

AUTHORS: Buskila D, Shnaider A, Neumann L, Zilberman D, Hilzenrat N, Sikuler E; SOURCE: Arch Intern Med 1997 Nov 24;157(21):2497-2500

BACKGROUND: Fibromyalgia syndrome (FS) is a common disorder of diffuse pain in the muscles or joints accompanied by tenderness at specific tender points and a constellation of related symptoms. The potential role of infections in the pathogenesis of FS has only recently been investigated.

OBJECTIVES: To evaluate the prevalence of FS and to assess tenderness thresholds in patients infected with hepatitis C virus (HCV).

METHODS: The study included 90 patients with HCV, 128 healthy, anti-HCV-negative controls, and 32 patients with non-HCV-related cirrhosis. Tenderness was measured by manual palpation (18 tender points) and with a dolorimeter. Fibromyalgia syndrome was diagnosed according to the 1990 American College of Rheumatology criteria.

RESULTS: The diagnosis of FS was established in 14 patients (16%) with HCV, in 1 patient (3%) with non-HCV- related cirrhosis, and in none of the healthy controls (P less than .001). Thirteen of the HCV-positive patients with FS were women. The patients with HCV had significantly (P less than .01) more tender points (mean [+/- SD] 3.6 +/- 5.3) than the healthy controls (0.1 +/- 0.5) and the patients with non-HCV-related cirrhosis (1.2 +/- 2.7). Specifically, the patients with cirrhosis were most tender on both tenderness measures owing to the high proportion of women in this group. Patients with FS were significantly more tender than those without FS: their dolorimetry thresholds were 2.9 kg vs 6.0 kg (P less than .001).

CONCLUSIONS: A high prevalence of FS was observed in patients infected with HCV, especially women. Recognizing FS in patients with HCV will prevent misinterpretation of FS symptoms as part of the liver disease and will enable the physician to reassure the patient about these symptoms and to alleviate them. AUTHORS: Buskila D, Shnaider A, Neumann L, Zilberman D, Hilzenrat N, Sikuler E; SOURCE: Arch Intern Med 1997 Nov 24;157(21):2497-2500

TECTONIC CHANGES IN DISABILITY LAW

By Joshua Potter, Esq., Pasadena, CA

There have been tectonic changes in the disability environment. By this, I mean that since the publication of the 1990 fibromyalgia syndrome criteria by the American College of Rheumatology, and the 1994 statement for chronic fatigue syndrome by Dr. Fakuda and others at the Center for Disease Control (CDC), little has changed in the disability landscape. There have been judicial skirmishes, insurance refinements, but the largest impact has been in the area of policy interpretation.

The last year of this decade has seen interesting, but only minor changes in the way the disability programs address the FMS and CFS communities. As early as October of 1998, there were signs within the Social Security Administration (SSA) that some Screening Attorneys were favorably disposed to granting disability for well-defined claims based on CFS/FMS. Just one month later, some Long Term Disability policies were beginning to pay initial claims for FMS and CFS, providing that the documentation was sufficiently strong. These events were no more than the seismic precursors to momentous changes which have now been realized in 1999.

On the last day of April, 1999, the SSA issued new regulations which are as staggering as the initial ACR statement and the later Fukuda statement. Social Security Ruling 99-2p (referred to as SSR-99-2p) has caused more than a mere earthquake. It will shatter the entire landscape of disability for individuals afflicted with CFS and FMS. SSR 99-2p boldly announces that these syndromes "are medically determinable conditions." This simple concept represents a vast breakthrough in appreciation. It is a bold declaration that legitimizes the clinical diagnosis. The requirements for SSR-99-2p are provided in the section below, "Medically Determinable Impairment Requirements for CFS and FMS."

During the last decade, patients have argued with uneven success that the pain and fatigue cycles against which they struggle are legitimate and real. They have struggled against professional gainsayers who have asserted that in the absence of a serological test or scan, the condition is merely a psychiatric manifestation and has nothing to do with clinical medicine. These practitioners, insurance companies, and judges who have invested themselves in the flat denial that illness can exist absent serologic studies must now reassess their position. As a matter of regulation within the SSA, CFS and FMS exist as a disease process. As such, these conditions can result in a finding of disability. SSR-99-2p is not the most complex regulation drafted, but it will require careful reading to appreciate.

SSR-99-2p will not open the floodgates for claims before Social Security. It will serve to exclude more than it includes at first. SSR 99-2p will need superior charting and greater attention to detail, especially by physicians as well as patients. Testimony will have to be more concise and narrowly focused. Within Social Security there will no doubt be some lag time in the application of the new regulation, but greater problems will occur in the mountains of charting which already exist and cannot be altered. It is in the future that the greatest change will occur. This new piece of regulation, as momentous as it is, nests within a series of other complex rules and regulations and its application depends on demonstrating that the other regulations have been satisfied.

The only way that this most modest requirement can be accommodated is by having complete and thorough charting. Charting means historical medical records that detail the tracking of failed therapies as well as the documentation of symptoms and function. It will not only include one's medical history, but also work history. Reliance on a shorthand in which the diagnosis appears unsubstantiated and unexplained throughout the chart will simply be unacceptable. The medical community must take heart that the Federal Government has taken this momentous step. Physicians who make the diagnosis of FMS or CFS should no longer be subject to derision by their colleagues. But more important to the patient is that the constellation of symptoms needs to be featured within the chart. This is because the symptoms themselves play an important role in any disability determination, whether Federal or Private.

A patient's chart will be considered incomplete if it merely recites the diagnosis and the medications prescribed. Not only must the chart demonstrate that the patient meets the American College of Rheumatology criteria for FMS or the Fukuda Standard in the case of CFS, but more importantly, what are the symptoms and complaints associated with that diagnosis? The diagnosis by itself is not the equivalent of disability and will never support a doctor's comment that the individual is or is not disabled. The legal-medical-vocational amalgam of the sundry facts are what the disability system is predicated on.

As the SSA adjusts to the new rules and judges become more familiar with SSR-99-2p, so too must the private long-term disability (LTD) carriers. Though the implications of SSR-99-2p are profound to Social Security, they will be revolutionary to the private insurance industry. The great LTD carriers will rapidly have to readjust their positions in light of the new law. LTD carriers will need to look squarely at the functional impact of FMS and CFS because the great debate over the meaning of "medically determinable" has finally been settled.

We stand at the threshold of a new environment. It is imperative that physicians and patients work together to provide clear and concise charting. These are exciting times in which we operate. It's now time to focus on the diagnosis and consequences of these conditions. The battle to make FMS and CFS medically determinable diseases by the SSA has been won. Take the steps necessary to ensure that you and your health care team are complying with the documentation requirements set forth in SSR-99-2p, just in case you might need to rely upon this new ruling in years to come. Read the final section of this article for more information on what this documentation should include.

Medically Determinable Impairment Requirements for CFS and FMS

One or more of the following must be documented for at least six consecutive months:

a.. Palpably swollen or tender lymph nodes on exam
b.. Nonexudative pharyngitis (sore throat without signs of inflamation)
c.. Persistent, reproducible muscle tenderness on repeated examinations, including the presence of positive tender points
d.. There is considerable overlap of symptoms between CFS and FMS, but individuals with CFS who have tender points have a medically determinable impairment. Individuals with impairments that fulfill the ACR criteria for FMS (which includes the minimum number of tender points) may also fulfill the criteria for CFS. However, individuals with CFS who do not have the specified number of tender points to establish FMS may still be found to have a medically determinable impairment.

The following tests may be used to help establish a medically determinable impairment in individuals with CFS (and FMS if they meet the criteria):

a.. Elevated antibody to EBV capsid antigen equal to or greater than 1:5120, or early antigen equal to or greater than 1:640
b.. An abnormal MRI scan of the brain
c.. Neurally mediated hypotension as shown by tilt table testing or another clinically acceptable form of testing
d.. Others tests, such as abnormal sleep studies or exercise intolerance

Documentation

...view it as an insurance policy

Not to sound pessimistic, but you never know what the future holds. If you take steps now to regularly document your health and work status to meet the requirements of SSR-99-2p, then at least you won't have any regrets later if you are overtaken by ill health. More often than not, FMS is triggered by unexpected events such as auto-accidents, infections or the onset of another illness. These same events can also lead to a serious decrement in function from which your body may not fully recover.

Once you have endured a setback in your health, it is usually too late to start thinking about issues of documentation. The SSA will look at your medical records for the past 12 months and weigh that information against their template. If your physician writes a complete chart, it is possible that disability will be paid. Unfortunately for you and your physician, this scenario is not common these days.

The new SSA ruling will allow an interested reviewer to also take into consideration the personal records of a person with FMS/CFS, such as a journal, diary or notes that describe one's impairment(s) and its associated impact on function over time. Again, the SSA will be looking at relevant evidence for the 12-month period preceding the month of application to them.

What about LTD carriers and insurance cases involving motor vehicle accidents of people who have previously been diagnosed with FMS or CFS? Chances are, they will apply standards as strict as SSR-99-2p.

If you don't want to find yourself at the mercy of the court system and government-paid Independent Medical Examiners who may not realize how functionally impacting FMS/CFS can be, start taking the following precautions now:

a.. Visit your FMS/CFS physician at least three times a year. During each visit, bring with you a list (preferably typed) of your dominant symptoms and any significant problems that you are having with function (work, house chores and social activities). Make sure that this gets incorporated into your medical record and keep a copy for yourself. If you have done your job of getting right to the point of the visit, then you shouldn't feel awkward about asking what he or she will be writing in your record.
b.. Whenever you visit any health care provider (gynocologist, naturopath, chiropractor, physical therapist, occupational therapist, counselor, etc.), try to follow through with the same recommendations as given above for physicians.
c.. Keep your own journal, diary or notes.
d.. -----------------------------------------------------------------------------------------------------------------------------------------------------------------------------------
e.. I KNOW I went thru getting SSA about 10yrs ago ,but needed a Lawyers assistance as my condition was complex,but mainly I was to weak and Bad Brainfog along with all the Emotions you go Thru...I Honestly luved my Job and couldn't think of not working and being a Burden to my Wife with also knowing I couldn't work in my Condition...My wife has a very Stressful job so it was hard for Her to do all the Paperwork,so we decided on using a Lawyer.....
f.. Whether or not your applying for SSA or SSI you have to read and really think about your answer,because there are some guestions like can you lift 10 lbs'.,but doesn't ask the outcome of you doing so or can you do it all day...Sheesh I know I'd end up in Bed....So think your answers thru.........

Does FMS worsen over time?

Does FMS worsen over time? This is a common question A six-year follow-up study of 45 FMS patients indicates that symptoms typically remain stable. Patients who participated in this study had rated the severity of their symptoms during an earlier study, and were asked to rate them again six years later. The authors of this study found no change in sleep quality, morning stiffness, amount of medications used per week, functional ability, anxiety, or perceived severity of overall symptoms. Pain did increase, but patients expressed improved vitality and control over their symptoms, enabling them to cope better with the condition.

This study reinforces what four expert advisors had to say in the October 2002 issue about FMS/CFS: symptoms will persist over time, but in general, they should not worsen. If you are experiencing a persistent decline in health, it is usually caused by another disorder that is developing and needs treatment, rather than the FMS/CFS itself. The symptoms of pain and fatigue are found in many other conditions, and that is why we asked the experts how physicians are supposed to select out conditions that may mimic your FMS/CFS, as well as offer advice to patients regarding what symptoms should not be construed as part of their FMS/CFS.

A study linking the symptom of dizziness (or lightheadedness) to problems in the renin-angiotensin-aldosterone (RAA) system. It's one of many neuroendocrine systems in the body. Abnormalities in multiple hormones have been identified in FMS patients. With the exception of low growth hormone, however, they are usually mild in nature unless tested under a stressful response. For example, during exercise, the body is supposed to produce a several fold increase in its production of growth hormone, epinephrine and norepinephrine, but this does not happen in people with FMS. Also, the autonomic nervous system appears to be limping along, and several research studies indicate it is under-responsive to many different types of challenges

Summarizing the meaning of the many hormonal abnormalities in FMS, Gail Adler, M.D., Ph.D., of Boston, MA, writes: "A combination of multiple, mildly impaired responses may lead to more profound physiologic and clinical consequences as compared with a defect in only one system, and could contribute to the symptoms of fibromyalgia." Adler is unsure whether these alterations are the primary cause of FMS or whether they may be appearing as a result of the development of the condition. In either case, she suggests that effective therapy must be multifaceted in nature to target the many neuroendocrine abnormalities.

Restless legs syndrome (RLS) and its cousin, periodic limb movements during sleep (PLMS), may occur in roughly 50% of FMS patients and a new medication called Mirapex (pramipexole) might be beneficial But, how can you be sure if a new treatment prescribed for sleep is actually helping your sleep, or better yet, reducing your limb movements during the night? A study using actigraphy, which involves wearing a device the size of a wrist watch that attaches around a person's nondominant arm, indicates that this technique my be used in the future to help you and your physician determine if and how a given therapy is working.(6) It may also help determine if your daytime fatigue levels are due to your sleep disorder or something else. Actigraphy is a natural way to study the activity and sleep patterns of patients in their own home environment.

The actigraphy study lasted six days and was led by Ania Korszun, M.D., of the United Kingdom. It consisted of four groups of people: 16 FMS patients without depression; 6 FMS patients just diagnosed with concurrent depression but not yet treated for this condition; 28 healthy controls without any signs of pain, fatigue, or depression; and 9 depressed patients who were not responding to the anti-depressant drug intervention. FMS patients who did not have any evidence of depression (the majority of the patients) and those who were found to have depression at the time of recruitment for the study were compared in an effort to find out the effects of concurrent depression on the symptoms of FMS. For additional comparison purposes, the authors looked at a control group of healthy people attending the clinic for other reasons and previously documented depressed patients who had returned to the clinic because their prescribed therapies were not working (in other words, they still had significant symptoms of major depression).

The controls showed the regular sleep/wake cycle, demonstrating a high level of activity during the day and virtually no movements during sleep. The FMS "only" group showed levels of daytime activity similar to those of healthy people, but during the night they experienced significantly increased levels of activity. The depression "only" group also showed increased levels of nighttime activity. FMS patients who were also experiencing depression at the time of the study showed the most impairment according to the actigraphy measures. They were less active during the daytime and at night, the amount of their movement was greater than either the depressed patients or the FMS "only" patients. Although FMS is not caused by depression, it appears to significantly impair function in people with FMS. The authors state that their next step might be to re-evaluate the patients with both FMS and depression after they have been effectively treated for their depression to determine if daytime function and quality of sleep improve.

A better understanding of what is going on in FMS and CFS is definitely needed, along with a marker that can identify these syndromes which are thought by many researchers to be the same. A distinctive marker to separate FMS/CFS patients from healthy people and from those who are depressed, would be a dream come true, particularly for the many patients who have been told that their symptoms are due to depression. As the acitgraphy study above indicated, roughly one-third of FMS patients attending a clinic for treatment are also depressed. This means that 65% of patients are not depressed.

A research team in Milan, Italy, conducted a study to look at the beta-endorphin levels in the immune cells of 17 patients with CFS, 5 patients with FMS, 10 patients with depression and 8 healthy control subjects. Beta-endorphin is the opioid produced by the body to fight pain. Its level in the central nervous system (CNS) is believed to be low in patients with FMS/CFS. Brain levels of the opioid cannot be easily analyzed in humans, so the study analyzed special cells in the immune system (peripheral blood mononuclear cells or PBMCs) because they are believed to reflect the beta-endorphin concentrations in the brain. Explaining why the research team used this study design, they wrote in their report: "In the CNS, beta-endorphin is involved in stress responses, analgesia, and mood disorders." They also state that the CNS and PBMNC levels of beta-endorphin exert an inhibitory action on the immune system. So, if beta-endorphin levels in the brain are high, then the immune system is suppressed (which has been shown to be the case in patients with HIV/AIDS).

One would expect that in chronic painful conditions, such as FMS and CFS, that the PBMNC levels of the body's opioid control system (i.e., beta-endorphin) would be low, which could result in an activation of the immune system. Although FMS/CFS are not considered to be like the classic autoimmune disorders such as lupus and rheumatoid arthritis, evidence of the immune system's activation of pro-inflammatory cytokines has been documented. The actual blood or plasma beta-endorphin levels do not appear to be elevated in FMS, but this finding would be expected if FMS/CFS really are diseases of the CNS.

The results of the Italian researchers are both interesting and promising. The PBMNC levels of beta-endorphin in both the CFS and FMS patient groups were close to half that of the healthy control group. As for the depressed patients, the beta-endorphin levels were twice that of the healthy controls (meaning that they were almost four times that of the CFS and FMS patients). The authors of the study admit that a larger number of patients need to be evaluated, but their results strongly suggest that PBMNC beta-endorphin levels might offer a new diagnostic tool for CFS and FMS as well as for their differentiation from depression.
 

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