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Chronic Fatigue Syndrome
Objectives:
After completing this course the student will have an understanding of the
definition of Chronic Fatigue Syndrome, the possible causes, diagnosis,
and treatments.
What is CFS?
Chronic fatigue syndrome, or CFS, is a debilitating and complex
disorder characterized by profound fatigue that is not improved by bed
rest and that may be worsened by physical or mental activity. Persons with
CFS most often function at a substantially lower level of activity than
they were capable of before the onset of illness. In addition to these key
defining characteristics, patients report various nonspecific symptoms,
including weakness, muscle pain, impaired memory and/or mental
concentration, insomnia, and post-exertional fatigue lasting more than 24
hours. In some cases, CFS can persist for years. The cause or causes of
CFS have not been identified and no specific diagnostic tests are
available. Moreover, since many illnesses have incapacitating fatigue as a
symptom, care must be taken to exclude other known and often treatable
conditions before a diagnosis of CFS is made.
A. Definition of CFS
A great deal of debate has surrounded the issue of how best to define
CFS. In an effort to resolve these issues, an international panel of CFS
research experts convened in 1994 to draft a definition of CFS that
would be useful both to researchers studying the illness and to
clinicians diagnosing it. In essence, in order to receive a diagnosis of
chronic fatigue syndrome, a patient must satisfy two criteria:
1) Have severe chronic fatigue of six months or longer duration with
other known medical conditions excluded by clinical diagnosis;
and 2) concurrently have four or more of the following
symptoms: substantial impairment in short-term memory or concentration;
sore throat; tender lymph nodes; muscle pain; multi-joint pain without
swelling or redness; headaches of a new type, pattern or severity;
unrefreshing sleep; and post-exertional malaise lasting more than 24
hours. The symptoms must have persisted or recurred during six or more
consecutive months of illness and must not have predated the
fatigue.
B. Similar Medical Conditions
A number of illnesses have been described that have a similar spectrum
of symptoms to CFS. These include fibromyalgia syndrome, myalgic
encephalomyelitis, neurasthenia,
multiple chemical sensitivities, and chronic mononucleosis. Although
these illnesses may present with a primary symptom other than fatigue,
chronic fatigue is commonly associated with all of them.
C. Other Conditions That May Cause Similar Symptoms
In addition, there are a large number of clinically defined, frequently
treatable illnesses that can result in fatigue. Diagnosis of any of
these conditions would exclude a definition of CFS unless the condition
has been treated sufficiently and no longer explains the fatigue and
other symptoms. These include hypothyroidism, sleep apnea and
narcolepsy, major depressive disorders, chronic mononucleosis, bipolar
affective disorders, schizophrenia, eating disorders, cancer, autoimmune
disease, hormonal disorders, subacute infections, obesity, alcohol or
substance abuse, and reactions to prescribed medications.
D. Other Commonly Observed Symptoms in CFS
In addition to the eight primary defining symptoms of CFS, a number of
other symptoms have been reported by some CFS patients. The frequencies
of occurrence of these symptoms vary from 20% to 50% among CFS patients.
They include abdominal pain, alcohol intolerance, bloating, chest pain,
chronic cough, diarrhea, dizziness, dry eyes or mouth, earaches,
irregular heartbeat, jaw pain, morning stiffness, nausea, night sweats,
psychological problems (depression, irritability, anxiety, panic
attacks), shortness of breath, skin sensations, tingling sensations, and
weight loss.
* Not all hormonal aberrations necessarily exclude a diagnosis of CFS.
See Section 3C.
Demographics
Several studies have helped to establish the distribution and frequency of
occurrence of CFS. While no single study can be considered definitive —
each approach has inherent strengths and weaknesses — epidemiologic
studies have greatly improved our understanding of how common the disease
is, which individuals are the most susceptible to developing it, whether
it can be transmitted to others, and how the illness typically progresses
in individuals.
A. How Common Is CFS?
One of the earliest attempts to estimate the prevalence of CFS was
conducted by the Centers for Disease Control and Prevention (CDC) from
1989 to 1993. Physicians in four U.S. cities were asked to refer
possible CFS patients for clinical evaluation by medical personnel
participating in the study. The study estimated that between 4.0 and 8.7
per 100,000 persons 18 years of age or older have CFS and are under
medical care. However, these projections were underestimates and could
not be generalized to the U.S. population since the study did not
randomly select its sites. A more recent study of the Seattle area has
estimated that CFS affects between 75 and 265 people per 100,000
population. This estimate is similar to the prevalence observed in
another CDC study conducted in San Francisco, which put the occurrence
of CFS-like disease (not clinically diagnosed) at approximately 200 per
100,000 persons. In general, it is estimated that perhaps as many as
half a million persons in the United States have a CFS-like condition.
B. Who Gets CFS?
This question is complex and does not have a definitive answer. The
four-city surveillance study of CFS identified a population of patients
that was 98% Caucasian and 85% female, with an average age at onset of
30 years. More than 80% had advanced education and one-third were from
upper income families. However, these data included only patients who
were under a physician's care. There is now evidence that CFS affects
all racial and ethnic groups and both sexes. The Seattle study found
that 59% of the CFS patients were women. Eighty-three percent were
Caucasian, an underrepresentation, since over 90% of the patients in the
study were white. The San Francisco study found that CFS-like disease
was most prevalent among women, among persons with household annual
incomes of under $40,000, and among blacks, and was least common among
Asians and whites. Adolescents can have CFS, but few studies of
adolescents have been published. A recently published study
documented that adolescents 12 to 18 years of age had CFS significantly
less frequently than adults and did not identify CFS in children under
12 years of age. CFS-like illness has been reported in children under 12
by some investigators, although the symptom pattern varies somewhat from
that seen in adults and adolescents. The illness in adolescents has many
of the same characteristics as it has in adults. However, it is
particularly important that the unique problems of chronically ill
adolescents (e.g., family social and health interactions, education,
social interactions with peers) be considered as a part of their care.
Appropriate dissemination of CFS information to patients, their
families, and school authorities is also important. CDC and the National
Institutes of Health (NIH) are currently pursuing studies of CFS in
children and adolescents.
C. Is CFS Contagious?
There is no evidence to support the view that CFS is a contagious
disease. Contagious diseases typically occur in well-defined clusters,
otherwise known as outbreaks or epidemics. While some earlier studies,
such as investigations of fatiguing illness in Incline Village, Nev.,
and Punta Gorda, Fla., have been cited as evidence for CFS acting as a
contagious illness, they did not rigorously document the occurrence of
person-to-person transmission. In addition, none of these studies
included patients with clinically evaluated fatigue that fit the CFS
case definition; therefore, these clusters of cases cannot be construed
as outbreaks of CFS. CDC worked with state health departments to
investigate a number of reported outbreaks of fatiguing illness and has
yet to confirm a cluster of CFS cases. Implicit in any contagious
illness is an infectious cause for the disease.
Carefully designed case-control studies involving rigorously
classified CFS patients and controls have found no association between
CFS and a large number of human disease agents. Finally, none of the
behavioral characteristics typically associated with contagious disease,
such as intravenous drug use, exposure to animals, occupational or
travel history, or sexual behavior, have been associated with CFS in
case-control studies. It therefore seems unlikely that CFS is a
transmissible disease. Nevertheless, the lack of evidence for clustering
of CFS, the absence of associations between specific behavioral
characteristics and CFS, and the failure to detect evidence of infection
more commonly in CFS patients than in controls do not rule out the
possibility that infectious agents are involved in or reflect the
development of this illness. For example, important questions remain to
be answered concerning possible reactivation of latent viruses (such as
human herpesviruses) and a possible role for infectious agents in some
cases of CFS.
D. Clinical Course of CFS
It is vital to understand the clinical course of CFS. This knowledge is
required to facilitate communication between physicians and patients, to
evaluate possible new treatments, and to address insurance and
disability issues. The clinical course of CFS varies considerably among
persons who have the disorder; the actual percentage of patients who
recover is unknown, and even the definition of what should be considered
recovery is subject to debate. Some patients recover to the point that
they can resume work and other activities, but continue to experience
various or periodic CFS symptoms. Some patients recover completely with
time, and some grow progressively worse. CFS often follows a cyclical
course, alternating between periods of illness and relative well being.
CDC continues to monitor the patients enrolled in the four-city
surveillance study; recovery is defined by the patient and may not
reflect complete symptom-free recovery. Approximately 50% of patients
reported "recovery," and most recovered within the first 5
years after onset of illness. No characteristics were identified that
made one patient more likely to recover than another. At illness onset,
the most commonly reported CFS symptoms were sore throat, fever, muscle
pain, and muscle weakness. As the illness progressed, muscle pain and
forgetfulness increased and the reporting of depression decreased.
Possible Causes of CFS
The cause or causes of CFS remain unknown, despite a vigorous search.
While a single cause for CFS may yet be identified, another possibility is
that CFS represents a common endpoint of disease resulting from multiple
precipitating causes. As such, it should not be assumed that any of the
possible causes listed below has been formally excluded, or that these
largely unrelated possible causes are mutually exclusive. Conditions that
have been proposed to trigger the development of CFS include virus
infection or other transient traumatic conditions, stress, and
toxins.
A. Infectious Agents
Due in part to its similarity to chronic mononucleosis, CFS was
initially thought to be caused by a virus infection, most probably
Epstein-Barr virus (EBV). It now seems clear that CFS cannot be caused
exclusively by EBV or by any single recognized infectious disease agent.
No firm association between infection with any known human pathogen and
CFS has been established. The four-city surveillance study found no
association between CFS and infection by a wide variety of human
pathogens, including EBV, human retroviruses, human herpesvirus 6,
enteroviruses, rubella, Candida albicans, and more recently bornaviruses
and Mycoplasma. Taken together, these studies suggest that among
identified human pathogens, there appears to be no causal relationship
for CFS. However, the possibility remains that CFS may have multiple
causes leading to a common endpoint, in which case some viruses or other
infectious agents might have a contributory role for a subset of CFS
cases.
B. Immunology
It has been proposed that CFS may be caused by an immunologic
dysfunction, for example inappropriate production of cytokines, such as
interleukin-1, or altered capacity of certain immune functions. One
thing is certain at this juncture: there are no immune disorders in CFS
patients on the scale traditionally associated with disease. Some
investigators have observed anti-self antibodies and immune complexes in
many CFS patients, both of which are hallmarks of autoimmune disease.
However, no associated tissue damage typical of autoimmune disease has
been described in patients with CFS. The opportunistic infections or
increased risk for cancer observed in persons with immunodeficiency
diseases or in immunosuppressed individuals is also not observed in CFS.
Several investigators have reported lower numbers of natural killer
cells or decreased natural killer cell activity among CFS patients
compared with healthy controls, but others have found no differences
between patients and controls.
T-cell activation markers have also been reported to have
differential expression in groups of CFS patients compared with
controls, but again, not all investigators have consistently observed
these differences. One intriguing hypothesis is that various triggering
events, such as stress or a viral infection, may lead to the chronic
expression of cytokines and then to CFS. Administration of some
cytokines in therapeutic doses is known to cause fatigue, but no
characteristic pattern of chronic cytokine secretion has ever been
identified in CFS patients. In addition, some investigators have noted
clinical improvement in patients with continued high levels of
circulating cytokines; if a causal relationship exists between cytokines
and CFS, it is likely to be complex. Finally, several studies have shown
that CFS patients are more likely to have a history of allergies than
are healthy controls. Allergy could be one predisposing factor for CFS,
but it cannot be the only one, since not all CFS patients have it.
C. Hypothalamic-Pituitary Adrenal (HPA) Axis
Multiple laboratory studies have suggested that the central nervous
system may have an important role in CFS. Physical or emotional stress,
which is commonly reported as a pre-onset condition in CFS patients,
activates the hypothalamic-pituitary-adrenal axis, or HPA axis, leading
to increased release of cortisol and other hormones. Cortisol and
corticotrophin-releasing hormone (CRH), which are also produced during
the activation of the HPA axis, influence the immune system and many
other body systems. They may also affect several aspects of behavior.
Recent studies revealed that CFS patients often produce lower levels of
cortisol than do healthy controls. Similar hormonal abnormalities have
been observed by others in CFS patients and in persons with related
disorders like fibromyalgia. Cortisol suppresses inflammation and
cellular immune activation, and reduced levels might relax constraints
on inflammatory processes and immune cell activation. As with the
immunologic data, the altered cortisol levels noted in CFS cases fall
within the accepted range of normal, and only the average between cases
and controls allows the distinction to be made. Therefore, cortisol
levels cannot be used as a diagnostic marker for an individual with CFS.
A placebo-controlled trial, in which 70 CFS patients were randomized to
receive either just enough hydrocortisone each day to restore their
cortisol levels to normal or placebo pills for 12 weeks, concluded that
low levels of cortisol itself are not directly responsible for symptoms
of CFS, and that hormonal replacement is not an effective treatment.
However, additional research into other aspects of neuroendocrine
correlates of CFS is necessary to fully define this important, and
largely unexplored, field.
D. Neurally Mediated Hypotension
Rowe and coworkers conducted studies to determine whether disturbances
in the autonomic regulation of blood pressure and pulse (neurally
mediated hypotension, or NMH) were common in CFS patients. The
investigators were alerted to this possibility when they noticed an
overlap between their patients with CFS and those who had NMH. NMH can
be induced by using tilt table testing, which involves laying the
patient horizontally on a table and then tilting the table upright to 70
degrees for 45 minutes while monitoring blood pressure and heart rate.
Persons with NMH will develop lowered blood pressure under these
conditions, as well as other characteristic symptoms, such as
lightheadedness, visual dimming, or a slow response to verbal stimuli.
Many CFS patients experience lightheadedness or worsened fatigue when
they stand for prolonged periods or when in warm places, such as in a
hot shower. These conditions are also known to trigger NMH. One study
observed that 96% of adults with a clinical diagnosis of CFS developed
hypotension during tilt table testing, compared with 29% of healthy
controls. Tilt table testing also provoked characteristic CFS symptoms
in the patients. A study (not placebo-controlled) was conducted to
determine whether medications effective for the treatment of NMH would
benefit CFS patients. A subset of CFS patients reported a striking
improvement in symptoms, but not all patients improved. A
placebo-controlled trial of NMH medications for CFS patients is now in
progress.
F. Nutritional Deficiency
There is no published scientific evidence that CFS is caused by a
nutritional deficiency. Many patients do report intolerances for certain
substances that may be found in foods or over-the-counter medications,
such as alcohol or the artificial sweetener aspartame. While evidence is
currently lacking for nutritional defects in CFS patients, it should
also be added that a balanced diet can be conducive to better health in
general and would be expected to have beneficial effects in any chronic
illness.
Diagnosis of CFS
A. How Physicians Diagnose CFS
If a patient has had 6 or more consecutive months of severe fatigue that
is reported to be unrelieved by sufficient bed rest and that is
accompanied by nonspecific symptoms, including flu-like symptoms,
generalized pain, and memory problems, the physician should further
investigate the possibility that the patient may have CFS. The first
step in this investigation is obtaining a detailed medical history and
performing a complete physical examination of the patient. Initial
testing should include a mental status examination, which ordinarily
will involve a short discussion in the office or a brief oral test. A
standard series of laboratory tests of the patient's blood and urine
should be performed to help the physician identify other possible causes
of illness. If test results suggest an alternative explanation for the
patient's symptoms, additional tests may be performed to confirm that
possibility. If no cause for the symptoms is identified, the physician
may render a diagnosis of CFS if the other conditions of the case
definition are met. A diagnosis of idiopathic chronic fatigue could be
made if a patient has been fatigued for 6 months or more, but does not
meet the symptom criteria for CFS.
B. Appropriate Tests for Routine Diagnosis of CFS
While the number and type of tests performed may vary from physician to
physician, the following tests constitute a typical standard battery to
exclude other causes of fatiguing illness: alanine aminotransferase
(ALT), albumin, alkaline phosphatase (ALP), blood urea nitrogen (BUN),
calcium, complete blood count, creatinine, electrolytes, erythrocyte
sedimentation rate (ESR), globulin, glucose, phosphorus, thyroid
stimulating hormone (TSH), total protein, transferrin saturation, and
urinalysis. Further testing may be required to confirm a diagnosis for
illness other than CFS. For example, if a patient has low levels of
serum albumin together with an above-normal result for the blood urea
nitrogen test, kidney disease would be suspected. The physician may
choose to repeat the relevant tests and possibly add new ones aimed
specifically at diagnosing kidney disease. If autoimmune disease is
suspected on the basis of initial testing and physical examination, the
physician may request additional tests, such as for antinuclear
antibodies.
C. Psychological/Neuropsychological Testing
In some individuals it may be beneficial to assess the impact of
fatiguing illness on certain cognitive or reasoning skills, e.g.,
concentration, memory, and organization. This may be particularly
relevant in children and adolescents, where academic attendance,
performance, and specific educational needs should be addressed.
Personality assessment may assist in determining coping abilities and
whether there is a co-existing affective disorder requiring
treatment.
D. Theoretical and Experimental Tests
A number of tests, some of which are offered commercially, have no
demonstrated value for the diagnosis of CFS. These tests should not be
performed unless required for diagnosis of a suspected exclusionary
condition (e.g., MRI to rule out suspected multiple sclerosis) or unless
they are part of a scientific study. In the latter case, written
informed consent of the patient is required. No diagnostic tests for
infectious agents, such as Epstein-Barr virus, enteroviruses,
retroviruses, human herpesvirus 6, Candida albicans, and Mycoplasma
incognita, are diagnostic for CFS and as such should not be used (except
to identify an illness that would exclude a CFS diagnosis, such as
mononucleosis). In addition, no immunologic tests, including cell
profiling tests such as measurements of natural killer cell (NK) number
or function, cytokine tests (e.g., interleukin-1, interleukin-6, or
interferon), or cell marker tests (e.g., CD25 or CD16), have ever been
shown to have value for diagnosing CFS. Other tests that must be
regarded as experimental for making the diagnosis of CFS include the
tilt table test for NMH, and imaging techniques such as MRI,
PET-scan,
or SPECT-scan.
Reports of a pathway marker for CFS as well as a urine marker for CFS
are undergoing further study; however, neither is considered useful for
diagnosis at this time.
Careful Consideration of Information about CFS
Because the cause of CFS has not been identified and its effect on the
body is not well understood, periodically new unvalidated beliefs about
cures and causes of CFS are widely circulated. These may be based on one
or more recent reports from the peer-reviewed scientific literature, or
they may evolve from the anecdotal remarks of clinicians or scientists at
medical meetings. In some cases the origin is obscure. Even work that is
of sufficiently high caliber to be published in the scientific literature
is not without limitations and design flaws, and all published work needs
to be verified and expanded on by others before it can be applied with
confidence in clinical situations. With regard to some stories that are
currently circulating about CFS: (i) there is no evidence that CFS
patients lose their fingerprints; (ii) there is no scientific evidence of
any nutritional deficiency in CFS patients; and (iii) suicides of CFS
patients have been reported, but the rate of occurrence has not been
well-studied and it is not known whether the rate is higher or lower than
what would be expected in the general population. It is not practical to
address all of the information that circulates or emerges regarding CFS.
Simply be advised to be wary of information that points to sure cures or
that alludes to pathological damage as a consequence of CFS. Specific
questions should be discussed with the patient's physician, local or state
health department, CDC, or one of the national patient support
organizations.
Treatment
A
variety of vitamin supplements, medications, and other substances have
been described as having potential therapeutic benefits for chronic
fatigue syndrome (CFS) patients. Many of the treatments recommended for
CFS patients are intended to provide relief for symptoms of this
condition. However, some proposed treatments are unproven and potentially
dangerous. As a service to CFS patients and other interested persons, this
section provides some basic information about different therapies that
have been used for the treatment of CFS patients. These descriptions are
intended to be used only for general informational purposes.
Decisions regarding the use of these or
other treatments should be made only in consultation with a physician. If
you have doubts about a particular treatment, contact your local medical
society, university medical school, or another physician for additional
information.
Non-Pharmacologic Therapy
Since no cause for CFS has been identified, the therapies for this
disorder are directed at relief of symptoms. The physician, together with
the patient, will develop an individually tailored program that provides
the greatest perceived benefit, based on some combination of the therapies
discussed in this section.
Physical Activity
In general, physicians advise patients with CFS to pace themselves
carefully and encourage them to avoid unusual physical or emotional
stress. A regular, manageable daily routine helps avoid the
"push-crash" phenomenon characterized by overexertion during
periods of better health, followed by a relapse of symptoms perhaps
initiated by the excessive activity. Although patients should be as
active as possible, clinicians may need to explain the disorder to
employers and family members, advising them to make allowances as
possible. Modest regular exercise to avoid de-conditioning is important
and should be supervised by a physician or physical therapist.
Physical Activities and Therapy:
Non-pharmacologic therapies sometimes used by CFS patients include
acupuncture, aquatic therapy, chiropractic, cranial-sacral, light
exercise, massage, self-hypnosis, stretching, tai chi, therapeutic
touch, and yoga.
Psychotherapy and Supportive Counseling
Certain psychotherapies, such as cognitive behavior therapy, have
shown promise for facilitating patient coping and for alleviating some
of the distress associated with CFS. In addition, any chronic illness
can affect the patient caregivers and family. In such instances, family
therapy may foster good communication and reduce the adverse impact of
CFS on the family.
Pharmacologic Therapy
Pharmacologic therapy is directed toward the relief of specific
symptoms experienced by the individual patient. Patients with CFS appear
particularly sensitive to drugs, especially those that affect the central
nervous system. Thus, the usual treatment strategy is to begin with very
low doses and to escalate the dosage gradually as necessary.
Prescription Medications
Low-dose Tricyclic Agents: Tricyclic agents are
sometimes prescribed for CFS patients to improve sleep and to relieve
mild, generalized pain. Examples include doxepin (Adapin, Sinequan),
amitriptyline (Elavil, Etrafon, Limbitrol, Triavil), desipramine (Norpramin),
and nortriptyline (Pamelor). Some adverse reactions include dry mouth,
drowsiness, weight gain, and elevated heart rate.
Antidepressants: Antidepressants have been used to treat
depression in CFS patients, although non-depressed CFS patients
receiving treatment with serotonin reuptake inhibitors have been found
by some physicians to benefit from this treatment as well or better than
depressed patients. Examples of antidepressants used to treat CFS
include serotonin reuptake inhibitors such as fluoxetine (Prozac),
sertraline (Zoloft), and paroxetine (Paxil); venlafaxine (Effexor);
trazodone (Desyrel); and bupropion (Wellbutrin). A number of mild
adverse reactions, varying with the specific drug, may be experienced.
Anxiolytic agents: Anxiolytic agents are used to
treat panic disorder in CFS patients. Examples include alprazolam (Xanax),
clonazepam ( Klonopin), and lorazepam (Ativan). Common adverse reactions
include sedation, amnesia, and withdrawal symptoms (insomnia, abdominal
and muscle cramps, vomiting, sweating, tremors, and convulsions).
Nonsteroidal Antiinflammatory Drugs: These drugs may
be used to relieve pain and fever in CFS patients. Some are available as
over-the-counter medications. Examples include naproxen (Aleve, Anaprox,
Naprosen), ibuprofen (Advil, Bayer Select, Motrin, Nuprin), and
piroxicam (Feldene). These medications are generally safe when used as
directed, but can cause a variety of adverse effects, including kidney
damage, gastrointestinal bleeding, abdominal pain, nausea, and vomiting.
Antimicrobials: An infectious cause for CFS has not
been identified, and antimicrobial agents are not commonly prescribed
for CFS, unless of course the patient has been diagnosed with a
concurrent infection.. A controlled trial of the antiviral drug
acyclovir found no benefit for the treatment of patients with CFS.
Antiallergy Therapy: Some CFS patients have
histories of allergy, and these symptoms may flare periodically.
Non-sedating antihistamines may be helpful for CFS patients. Examples
include astemizole (Hismanal) and loratadine (Claritin). Some of the
more common adverse reactions associated with their use include
drowsiness, fatigue, and headache. Sedating antihistimines can also be
of benefit to patients at bedtime.
Antihypotensive Therapy: Fludrocortisone (Florinef)
has sometimes been prescribed for CFS patients who have had a positive
tilt table test. Florinef is currently being tested in controlled
studies for its efficacy in the treatment of CFS patients. Beta blockers
such as atenolol (Tenormin) have also been prescribed for patients with
a positive tilt table test. Increased salt and water intake is also
recommended for these patients. Adverse reactions include elevated blood
pressure and fluid retention.
Experimental Drugs and Treatments
Ampligen is a synthetic nucleic acid product that stimulates
the production of interferons, a family of immune response modifiers
that are also known to have anti-viral activity. One report of a
double-blinded, placebo-controlled study of CFS patients documented
modest improvements in cognition and performance among Ampligen
recipients compared with the placebo group. These preliminary results
will need to be confirmed by further study. Ampligen is not approved by
the Food and Drug Administration (FDA) for widespread use, and the
administration of this drug in CFS patients should be considered
experimental. Although the recipients of Ampligen in this study
tolerated the drug well, the adverse reactions of this material are
still incompletely characterized, and some participants did experience
reactions that might be attributable to Ampligen.
Dehydroepiandrosterone (DHEA) was reported in preliminary
studies to improve symptoms in some patients; however, this finding has
not been confirmed and the use of DHEA in patients should be regarded as
experimental.
Gamma globulin (Gammar) is pooled human immune globulin.
It contains antibody molecules directed against a broad range of common
infectious agents and is ordinarily used as a means for passively
immunizing persons whose immune system has been compromised, or who have
been exposed to an agent that might cause more serious disease in the
absense of immune globulin. Its use with CFS patients is experimental
and based on the unsubstantiated hypothesis that CFS is characterized by
an underlying immune disorder. Serious adverse reactions are uncommon,
although in rare instances gamma globulin may initiate anaphylactic
shock.
High colonic enemas have no demonstrated value in the
treatment of CFS. The procedure can promote intestinal disease.
Kutapressin is a crude extract from pig's liver. Its use
should be regarded as experimental in any clinical circumstance, and
there is no scientific evidence that it has any value in the treatment
of CFS patients. Kutapressin can elicit allergic reactions.
Dietary Supplements and Herbal Preparations
General Comments: A variety of dietary supplements and
herbal preparations are claimed to have potential benefits for CFS
patients. With few exceptions, the effectiveness of these remedies for
treating CFS patients has not been evaluated in controlled trials.
Contrary to common belief, the "natural" origin of a product
does not ensure safety. Dietary supplements and herbal preparations can
have potential side reactions and some can interfere or interact with
prescription medications. CFS patients should seek the advice of their
physician before using any unprescribed remedy.
Vitamins, Coenzymes, Minerals: Preparations that
have been claimed to have benefit for CFS patients include adenosine
monophosphate, coenzyme Q-10, germanium, glutathione, iron, magnesium
sulfate, melatonin, NADH, selenium, l-tryptophan, vitamins B12, C, and
A, and zinc. An early CFS study found reduced red blood cell magnesium
sulfate in CFS patients, but two subsequent studies have found no
difference between patients and healthy controls. The therapeutic value
of all these preparations has not been validated.
Herbal Preparations: Plants are known sources of
pharmacological materials. However, unrefined plant preparations contain
variable levels of the active compound as well as many irrelevant,
potentially harmful substances. Preparations that have been claimed to
have benefit to CFS patients include astralagus, borage seed oil,
bromelain, comfrey, echinacea, garlic, Ginkgo biloba, ginseng,
primrose oil, quercetin, St. John's wort, and Shiitake mushroom extract.
Only primrose oil was evaluated in a controlled study, and the
beneficial effects noted in CFS patients have not been independently
confirmed. Some herbal preparations, notably comfrey and high-dose
ginseng, have recognized harmful effects.
How to
Select a Support Group
Support groups are not appropriate for everyone, and some CFS patients
may find that a support group actually adds to their stress rather than
relieving it. Most support groups are free, collect voluntary donations,
or charge modest membership dues to cover basic expenses (e.g.
refreshments at meetings or photocopying costs).
A useful support group should include:
- Both newcomers and patients who have had CFS for longer periods of
time to provide a balance of perspectives for the group.
- People with whom the CFS patient feels comfortable.
- Leaders who empathize, gently draw out shy members, and keep
others from dominating, and who distill discussion into useful
information.
- A history indicating the group is stable and meeting the needs of
its members.
Some support groups may put their own interests before those of the
individual patient. Groups that engage in any of the following
activities should be avoided:
- Promise sure cures and quick solutions.
- Conduct meetings that are mainly "gripe" sessions.
- Urge patients to stop prescribed treatment and recommend a single
solution to their problem.
- Insist that patients reveal private or sensitive
information.
- Demand allegiance to a cult-like, charismatic leader.
- Charge high fees.
- Require patients to purchase products.
Careful Consideration of Information about CFS
Because the cause of CFS has not been identified and its effect on the
body is not well understood, periodically new unvalidated beliefs about
cures and causes of CFS are widely circulated. These may be based on one
or more recent reports from the peer-reviewed scientific literature, or
they may evolve from the anecdotal remarks of clinicians or scientists
at medical meetings. In some cases the origin is obscure. Even work that
is of sufficiently high caliber to be published in the scientific
literature is not without limitations and design flaws, and all
published work needs to be verified and expanded on by others before it
can be applied with confidence in clinical situations.
With regard to some stories that are currently circulating about CFS:
(i) there is no evidence that CFS patients lose their fingerprints; (ii)
there is no scientific evidence of any nutritional deficiency in CFS
patients; and (iii) suicides of CFS patients have been reported, but the
rate of occurrence has not been well-studied and it is not known whether
the rate is higher or lower than what would be expected in the general
population.
It is not practical to address all of the information that circulates
or emerges regarding CFS. Simply be advised to be wary of information
that points to sure cures or that alludes to pathological damage as a
consequence of CFS. Specific questions should be discussed with the
patient's physician, local or state health department, CDC, or one of
the national patient support organizations.
References:
Nisenbaum R, Jones AB, Jones JF, Reeves WC.
Longitudinal analysis of symptoms reported by patients with chronic
fatigue syndrome. Ann Epidemiol 10:458, 2000.
Reyes M, Dobbins JG, Nisenbaum R, Subedar N, Randall B, Reeves WC
Chronic Fatigue Syndrome Progression and Self-defined Recovery: Evidence
from the CDC Surveillance System.
Journal of Chronic Fatigue Syndrome, 1998 (in press).
Steele L, Dobbins JG, Fukuda K, Reyes M, Randall B, Koppelman M, Reeves
WC.
The epidemiology of chronic fatigue in San Francisco.
Am J Med 105(3A):83S-90S, 1998.
Fukuda K, Dobbins JG, Wilson LJ, Dunn RA, Wilcox K, Smallwood D.
An epidemiologic study of fatigue with relevance for the chronic fatigue
syndrome. Journal of Psychiatric Research, vol. 31, pages 19-29, 1997.
Fukuda K, Nisenbaum R, Stewart G, Thompson WW, Robin L,
Washko RM, Noah DL, Barrett DH, Randall B, Herwaldt BL, Mawle AC, Reeves
WC.
A Chronic Multisymptom Illness Affecting Air Force Veterans of the Persian
Gulf War. JAMA 280:981-988, 1998.
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