CFS – it’s worse than Multiple Sclerosis

Posted on 04/27/2018 by wames

Health rising blog post, by Cort Johnson, 16 April 2018: Chronic Fatigue Syndrome – It’s Worse than Multiple Sclerosis – and Fibromyalgia is No Walk in the Park Either

Multiple sclerosis (MS) is a dreaded disease. About ten years into having chronic fatigue syndrome (ME/CFS), I still remember being tested for it and how thankful I was that I didn’t have it.

MS does things to people that ME/CFS doesn’t. For one thing, it kills more people and in a horrible way. According to one site, the average lifespan after an MS diagnosis is about 25 -35 years.

When people with MS die, they usually do so because they either kill themselves, or from an inability to carry out basic functions such as breathing or swallowing. Respiratory failure, pneumonia, sepsis and/or uremia are often listed as contributing causes on their death certificates. As in ME/CFS, a bedridden state increases the risk of all of these.

MS and chronic fatigue syndrome (ME/CFS) are both considered to be amongst the most fatiguing of all diseases. In fact, for many with MS, fatigue is their most debilitating symptom. Alan Light’s ME/CFS/MS study suggests that people with MS may be more fatigued than people with ME/CFS, but experience much less post-exertional malaise.

The scientific literature suggests that many people with ME/CFS plateau at some point while a subset gets worse over time. Suicide rates appear to be elevated – two people with ME/CFS have committed suicide in the last month – and while some severely ill patients do die, studies suggest that death rates probably don’t nearly reach those in MS.

How then to explain Leonard Jason’s study which found that people with ME/CFS were not just more functionally limited than MS patients but were significantly more limited?

Jason’s web-based study included 106 people with MS and 269 people with ME or CFS who were recruited online. The DePaul Symptom Questionnaire (DSQ) and Medical Outcomes Short Forms Health Survey (SF-36) were used to assess symptom severity and functional capacity.

Insights Biomed. 2017;2(2). pii: 11. doi: 10.21767/2572-5610.10027. Epub 2017 Jun 12. Differentiating Multiple Sclerosis from Myalgic Encephalomyelitis and Chronic Fatigue Syndrome. Jason LA1, Ohanian D1, Brown A1, Sunnquist M1, McManimen S1, Klebek L1, Fox P1, Sorenson M1.

Results
Some basic demographic factors separated the two groups; the ME/CFS group was older, less likely to be married and more likely to be on disability.

Functionally, the ME/CFS group was significantly more impaired than the MS patients. This wasn’t a case of subtle statistical differences. Except for on the emotional and mental functional scales – which were similar – the ME/CFS group scored far lower (lower is worse; higher is better in the SF-36) than the MS group.

The MS group reported twice the level of physical functioning (54 for MS, 26 for ME/CFS), scored ten times better on role physical (20.6, 2.6), were in considerably less pain (56.5, 36.0), had poor, but still greatly increased, vitality compared to the ME/CFS patients (26.3, 10.1), and were considerably less held back socially by their illness than the ME/CFS patients (54.0, 19.8).

Despite their significantly decreased functioning in all areas, the ME/CFS patients had similar “role emotional” and “role mental” scores as the MS patients.

The symptom assessments bore out the harsher world chronic fatigue syndrome (ME/CFS) patients face. Of the 54 symptoms assessed, 38 were significantly worse in the ME/CFS patients. (None were significantly worse for the MS patients.) The MS patients did experience significant post-exertional malaise but not to the extent that ME/CFS did, who generally reported about 50% higher scores.

Sleep problems where common in both diseases and, except for worsened unrefreshing sleep and insomnia in the ME/CFS group, were similar. Every pain symptom was significantly worse in the ME/CFS group. Even the neurocognitive symptoms were significantly increased in the ME/CFS group with particular issues with sensitivities to noise and bright lights.

Cort goes on to discuss the severe burden that FM also puts on patients and comments:

Remarkably, these findings have made little to no difference in the research funding each disease gets. The NIH – the biggest medical research funder in the world (@$36 billion/year) – spent $11 million on FM and $8 million on ME/CFS this year. Compare that to its spending on some of the diseases studies have shown place less of a burden on patients.

  • Rheumatoid arthritis – $94 million
  • Osteoarthritis – $79 million
  • Multiple sclerosis – $101 million
  • Lupus – $100 million
  • Chronic Obstructive Pulmonary Disorder – $100 million

Two Disease Trajectories?
Clearly both FM and ME/CFS deserve much, much more funding, but  ME/CFS appears to be slowly finding its way in the research world while fibromyalgia may actually be declining.

Read the full article

 

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Bedbound Cardiff woman’s heartbreak after illness

Posted on 04/27/2018 by wames

Mirror online news post, by Mark Smith & Jamie Bullen, 26 April 2018: Bedbound woman’s heartbreak after illness ‘ruins’ relationship with daughter ‘who only knows her as sick mum’

Carol Davis said her ME has “destroyed my life” after leaving her bedridden for more than 10 years and sometimes incapable of walking and talking

A mum left bedridden for more than a decade has revealed how her illness has “ruined” her relationship with her daughter.

Carol Davis, 54, once enjoyed an active life filled with travelling, parties and regular shopping trips until she was struck down with myalgic encephalomyelitis, commonly known as ME.

The former nursery manager claims the condition has “destroyed” her life, leaving her unable to leave her house and suffering from chronic fatigue bouts so severe she is unable to walk or talk, Wales Online reports.

She also told how the illness had a devastating impact on her 24-year-old daughter, who she says has only ever known her as her ‘sick mum’.

Carol, from Cardiff, said: “It has destroyed my life.

“My bed is like my office. I cannot cook for myself, change my bed, or do my own washing. My partner does everything for me.

“I have packets of jellies and bananas by the side of my bed as I’m too afraid to get out of bed.

“I have not been outside my house since last summer.

“I used to love shopping in Cardiff city centre but I don’t think I’ve been there for 15 years.”

Carol said she experienced her first ME symptoms following the birth of her daughter in 1995.

“I contracted a virus in the hospital and I was in there for a few weeks.

“After that I slept a lot of the time and the doctors thought I was experiencing postnatal depression.

“I kept going back to my GP as nothing was changing. I was tested for everything, including loads of different viruses, and they came to the conclusion that I had chronic fatigue syndrome (CFS).

“But there are differences between ME and CFS.”

Carol is promoting the organisation Invest in ME which is running the campaign #haveacuppaforme to raise funds for ME research

Read the full article

 

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‘It’s like being a slave to your own body in a way’: a qualitative study of adolescents with CFS/ME

Posted on 04/26/2018 by wames

Research abstract:

‘It’s like being a slave to your own body in a way’: a qualitative study of adolescents with chronic fatigue syndrome, by Berit Widerøe Njølstad, Anne Marit Mengshoel & Unni Sveen in Scand J Occup Ther. 2018 Apr 1:1-10.

BACKGROUND:
Chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) is a relatively common disabling illness in adolescents that may limit participation in daily life.

AIM:
This study explored interactions between the illness experiences of adolescents with CFS/ME, their occupational lives and expectations for the future.

METHODS:
Seven adolescents with CFS/ME were interviewed. The interviews were analyzed using thematic analysis.

RESULTS:
Three themes were developed. ‘Being ruled by an unfamiliar and inexplicable body’, which illustrated that altered and strange bodies seemed to separate and disrupt the participants from their former occupational lives. ‘On the sideline of life with peers’, which demonstrated that the informants spent time at home, doing undemanding activities instead of participating in activities with peers. ‘A coherent connection between present and future life’, which was reflected by how the participants eventually accepted their situation and rebuilt a meaningful occupational life and value of self.

CONCLUSION:
CFS/ME made the body unfamiliar and disconnected informants from participating in their usual daily occupations. A coherent interaction between body, occupational life and social self was achieved by taking their new body into account and adjusting their occupations accordingly. This practice enabled the participants to hope for a better future life.

Read the full article

 

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Pain, genes, drugs & you

Posted on 04/25/2018 by wames

Health rising blog post, by Cort Johnson, 20 April 2018: Pain, Genes, Drugs and You: How Your Genetic Makeup May Be Keeping You in Pain

From Dr. Trescott’s lecture given to the Physician Partners of America: “Your Genes, Your Pain Drugs and You Or “Why Every Pain Physician Should be Testing Your Genes“

When the patient says, “This doesn’t work,” or, “I’ve been too sensitive,” or, “My mother had a terrible time with medicine X and I’ve had a terrible time with medicine X”, that should really tell you there’s likely to be a genetic problem there. Trescott

Dr. Trescott is past President of the American Society of Interventional Pain Physicians.

We know that many people with fibromyalgia and chronic fatigue syndrome respond very differently to drugs. A drug that works great for one person might have no effect in another person or even make another ill.

Why such variability? I’ve long assumed this meant that many people diagnosed with ME/CFS and FM actually have a different illness, but a recent lecture presented by the Physician Partners of America suggested that’s not necessarily true.  It’s possible that underlying genetics or epigenetic changes which affect how our metabolism breaks down substances could play a role.

The Genes
How you respond to a drug partly comes down to your genes. The human race is very variable genetically. A lot of that variability lies in small genetic variations called gene polymorphisms which can alter how effectively that gene works. These polymorphisms can have no effect or cause the gene to work less or more effectively.

Most people are normal – they have two “good” copies of a gene which allows them to metabolize substances properly. A significant number of people, however, have “good” and “bad” copies of a gene which can inhibit their ability to break down drugs. A smaller number of people (poor metabolizers) have two bad copies of a gene – they hardly break down some drugs at all.

Others with multiple copies of good genes (ultra-metabolizers) can find that even normal amounts of a drug can make them sick as they metabolize the drug into substances that cause harm.  Rapid metabolizers of oxycodone, for instance, will produce high levels of oxymorphone, which causes nausea, sedation and other symptoms.

The pain field is a perfect place to look for genetic anomalies in drug metabolism because responses to pain drugs are all over the map. In fact, the process of producing a pain sensation is so complex that some despair of ever producing really effective pain drugs. Part of that complexity lies in the genes that produce the enzymes that break down pain drugs.

The lecturer, Andrea Trescott, MD, a well known pain researcher and doctor, provided a dramatic personal example of the effects a gene polymorphism can have. Her first clue that she might have some hidden genetic vulnerabilities came during a surgical procedure as she was giving birth when she was given Percocet. It had absolutely no effect on her pain.

That process repeated itself during an emergency dental procedure when she was given Percocet, once, twice, three times – and received no relief at all (nor experienced any side effects). She might as well have been eating sugar cubes.

A week later, she went back for another procedure and asked to be given Darvocet which knocked her pain levels out. Subsequently, she found out that genetic polymorphisms in her CYPD26 (or 2D6) gene left her unable to metabolize Percocet. (Ten percent of Caucasians are 2D6 deficient).

Years later, her son, who was also 2D6 deficient, was scheduled to have his wisdom teeth removed. Requesting that hydrocodone, which his genetic status suggested that he metabolized poorly, not be used, didn’t work.  Stating that, “of course, he (the surgeon) blew me off”, her son got little relief from the hydrocodone, went back to the surgeon complaining of pain, and was labeled a drug seeker.

Take codeine. Codeine is inert – by itself it has no effects on pain – and has, like many opioid pain relievers, to be metabolized to morphine by the CYP2D6 enzyme to work. Morphine is then metabolized by another enzyme called UGT2B7 to M6G (morphine-6-glucuronide), which has pain-relieving properties. During that metabolic process, though, two other factors are released which can actually increase pain levels.

If you are not metabolizing codeine, you will get little relief from it. If you’re a super metabolizer taking large amounts of codeine, this could actually make your pain worse…

Read the full article for more information about drug metabolism and interactions, a gene called COMT and genetic testing to assess a patient’s response to a drug.

 

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Mast Cell Activation may underlie CFS

Posted on 04/24/2018 by wames

Medscape blog post, 13 March 2018, by Miriam Tucker: Mast Cell Activation may underlie ‘Chronic Fatigue Syndrome’

Mast cell activation syndrome (MCAS) may be an overlooked yet potentially treatable contributor to the symptoms of chronic fatigue syndrome/myalgic encephalomyelitis (ME/CFS), say physicians who specialize in ME/CFS and its manifestations.

The subject was discussed during a 2-day clinician summit held March 2 to 3, 2018, during which 13 panelists met to begin developing expert consensus guidance for primary care and specialist physicians for the management of the complex multisystem illness ME/CFS, and to recommend research priorities.

“ME/CFS is a descriptive diagnosis of a bunch of symptoms, but it says nothing about what’s causing the symptoms, which is probably part of the reason it’s so hard for it to get recognition. So, the question becomes, What other pathology is driving this illness and making the person feel so ill? I think mast cell activation is one of those drivers, whether cause, effect, or perpetuator, I don’t know,” internist David Kaufman, MD, who practices in Mountain View, California, told Medscape Medical News.

MCAS is a recently described collection of signs and symptoms involving several different organ systems, that, as with ME/CFS itself, do not typically cause abnormalities in routine laboratory or radiologic testing. Proposed diagnostic criteria were published in 2010 in the Journal of Allergy and Clinical Immunology.

Kaufman first learned about MCAS about 5 years ago from a patient who introduced him to the published work of mast cell expert Lawrence Afrin, MD. “I spoke to him and then I started looking for it, and the more I looked, the more I found it,” Kaufman said, estimating that he has identified MCAS in roughly half his patients who meet ME/CFS criteria.

Indeed, summit panel member Charles W. Lapp, MD, who recently retired from his ME/CFS and fibromyalgia practice in Charlotte, North Carolina, told Medscape Medical News, “I see a lot of this. I think it’s one of the many overlap syndromes that we’ve been missing for years.”

Another panel member, New York City ME/CFS specialist Susan M. Levine, MD, also said she sees MCAS frequently. “I suspect 50% to 60% of ME/CFS patients have it. It’s a very new concept.”

In Levine’s experience, MCAS often manifests in patients being unable to tolerate certain foods or medications. “If we can reduce the mast cell problem, we can facilitate taking other drugs to treat ME/CFS,” she said. However, she also cautioned, “It’s going to be a subset, not all ME/CFS patients.”

Clinical Assessment and Laboratory Testing
As discussed at the summit, for patients who meet ME/CFS criteria, the next step is to drill down into individual patients’ symptoms and address treatable abnormalities. Investigation for MCAS may yield such findings among those who exhibit episodic symptoms consistent with mast cell mediator release affecting two or more of the following areas:

  • Skin: urticaria, angioedema, flushing
  • Gastrointestinal: nausea, vomiting, diarrhea, abdominal cramping
  • Cardiovascular: hypotensive syncope or near syncope, tachycardia
  • Respiratory: wheezing
  • Naso-ocular: conjunctival injection, pruritus, nasal stuffiness

Symptoms can wax and wane over years and range from mild to severe/debilitating. It is important to ask about triggers, Kaufman advised. “The patient is usually aware of what makes them feel worse.”

Routine laboratory assessments include complete blood count with differential, complete metabolic panel, magnesium, and prothrombin time/partial thromboplastin time.

More specific laboratory testing can be tricky, as the samples must be kept cold. These include serum tryptase, chromogranin A, plasma prostaglandin D2, histamine, heparin, a variety of random and 24-hour urinary prostaglandins, and urinary leukotriene E4.

For patients who have had a prior biopsy, the saved sample can be stained for mast cells.

Kaufman said that initially after he learned about MCAS, he would only run the laboratory tests in patients with suggestive clinical history, such as food sensitivities/triggers, rashes, hives, temperature intolerance, or chemical sensitivities. “But ultimately, I had patients [for whom] I couldn’t figure out what was going on; I would check, and started finding positives in patients I wasn’t suspicious of.”

So, now he just tests for it in all his patients with ME/CFS. “It’s bigger than allergy,” he remarked.

Treatment May Ease Some ME/CFS Symptoms
Treatment of MCAS involves trigger avoidance as possible; H1 receptor antagonists such as loratadine, cetirizine, or fexofenadine (up to double the usual doses); H2 histamine receptor antagonists including famotidine or ranitidine; and mast cell membrane-stabilizers such as cromolyn sodium. Slow-release vitamin C can also help in inhibiting mast cells.

Over-the-counter plant flavonoids such as quercetin also may be helpful, typically at high doses (up to 1000 mg three times daily). “There’s a long list of medications that either quiet down mast cell activation or block the receptor,” Kaufman noted.

But despite that, without controlled trials, it is difficult to determine the exact clinical effects of blocking mast cells, especially as these patients tend to be taking many other medications. And in the context of ME/CFS, the extent to which suppressing mast cell activity addresses the core symptoms of fatigue, postexertional malaise, orthostatic intolerance, and cognitive dysfunction is unclear.

Kaufman noted, “I think treatment clearly helps with the fatigue because they’re not reacting to everything. It improves gastrointestinal symptoms, so they can eat better…. I have seen [postural orthostatic tachycardia syndrome] improve, but I have to say I also give meds for dysautonomia, so I can’t be sure.”

Lapp said that in his experience, “[Patients with ME/CFS] aren’t cured, but do get better. [Blocking mast cell activity] gets rid of dizziness, fatigue, nausea, and light sensitivity.”

Levine pointed out, “We’re just at the beginning of identifying this patient subset and thinking what makes sense to try…. One thing that’s sure is that the drugs are pretty safe,” she said, adding that when it comes to working up patients with ME/CFS for MCAS, “There only seem to be good things that can happen.”

See also: Brief Summary of Mast Cell Activation Disease (MCAD) and Mast Cell Activation Syndrome (MCAS), by Margaret Williams, 14 Sep 2017

 

 

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ME, CFS & SEID: three distinct clinical entities?

Posted on 04/23/2018 by wames

Article abstract:

Myalgic Encephalomyelitis, Chronic Fatigue Syndrome, and Systemic Exertion Intolerance Disease: Three Distinct Clinical Entities, by Frank N M Twisk in Open Access Challenges 2018, 9(1), 19 [Published: 13 April 2018]

Many researchers consider chronic fatigue syndrome (CFS) to be a synonym of Myalgic Encephalomyelitis (ME). However, the case criteria of ME and CFS define two distinct clinical entities. Although some patients will meet both case criteria, other patients can meet the diagnosis of ME and not fulfil the case criteria for CFS, while the diagnosis of CFS is largely insufficient to be qualified as a ME patient.

ME is a neuromuscular disease with distinctive muscular symptoms, including prolonged muscle weakness after exertion, and neurological signs implicating cerebral dysfunction, including cognitive impairment and sensory symptoms.

The only mandatory symptom of CFS is chronic fatigue. Chronic fatigue must be accompanied by at least four out of eight nonspecific symptoms: substantial impairment in short-term memory or concentration, a sore throat, tender lymph nodes, muscle pain, multijoint pain, a new type of headaches, unrefreshing sleep, and postexertional “malaise” lasting more than 24 h.

So, regardless whether the name ME is appropriate or not, ME is not synonymous to CFS. That is not a matter of opinion, but a matter of definition. Due to the definitions of ME and CFS, “ME/CFS” does not exist and cannot be replaced by a new clinical entity (SEID: Systemic Exertion Intolerance Disease), as recently suggested.

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Pharmacological activation of AMPK & glucose uptake in… ME/CFS

Posted on 04/20/2018 by wames

Research abstract:

Pharmacological activation of AMPK and glucose uptake in cultured human skeletal muscle cells from patients with ME/CFS, by Audrey E Brown, Beth Dibnah, Emily Fisher, Julia L Newton, Mark Walker in Bioscience Reports [Preprint April 13, 2018]

Background:
Skeletal muscle fatigue and post-exertional malaise are key symptoms of Myalgic Encephalomyelitis ( ME/CFS). We have previously shown that AMPK activation and glucose uptake are impaired in primary human skeletal muscle cell cultures derived from patients with ME/CFS in response to electrical pulse stimulation, a method which induces contraction of muscle cells in vitro. The aim of this study was to assess if AMPK could
be activated pharmacologically in ME/CFS.

Methods
Primary skeletal muscle cell cultures from patients with ME/CFS and healthy controls were treated with either metformin or 991. AMPK activation was assessed by Western blot and glucose uptake measured.

Results
Both metformin and 991 treatment [antifungal] significantly increased AMPK activation and glucose uptake in muscle cell cultures from both controls and ME/CFS. Cellular ATP content was unaffected by treatment although ATP content was significantly decreased in ME/CFS compared to controls.

Conclusions
Pharmacological activation of AMPK can improve glucose uptake in muscle cell cultures from patients with ME/CFS. This suggests that the failure of electrical pulse stimulation to activate AMPK in these muscle cultures is due to a defect proximal to AMPK. Further work is required to delineate the defect and determine whether pharmacological activation
of AMPK improves muscle function in patients with ME/CFS.

Read the full article

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Metabolic abnormalities in CFS/ME: a review

Posted on 04/20/2018 by wames

Review Article abstract:

Metabolic abnormalities in chronic fatigue syndrome/myalgic encephalomyelitis: a mini-review, by Cara Tomas, Julia Newton in Biochemical Society Transactions [Published Apr 17, 2018]

Chronic fatigue syndrome (CFS), commonly known as myalgic encephalomyelitis (ME), is a debilitating disease of unknown etiology.

CFS/ME is a heterogeneous disease associated with a myriad of symptoms but with severe, prolonged fatigue as the core symptom associated with the disease. There are currently no known biomarkers for the disease, largely due to the lack of knowledge surrounding the eitopathogenesis of CFS/ME.  Numerous studies have been conducted in an attempt to identify potential biomarkers for the disease.

This mini-review offers a brief summary of current research into the identification of metabolic abnormalities in CFS/ME which may represent potential biomarkers for the disease. The progress of research into key areas including immune dysregulation, mitochondrial dysfunction, 5′-adenosine monophosphate-activated protein kinase activation, skeletal muscle cell acidosis, and metabolomics are presented here.

Studies outlined in this mini-review show many potential causes for the pathogenesis of CFS/ME and identify many potential metabolic biomarkers for the disease from the aforementioned research areas. The future of CFS/ME research should focus on building on the potential biomarkers for the disease using multi-disciplinary techniques at multiple research sites in order to produce robust data sets.

Whether the metabolic changes identified in this mini-review occur as a cause or a consequence of the disease must also be established.

Read the full article

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Weighted Standing Time test as a measure of orthostatic intolerance in ME/CFS

Posted on 04/19/2018 by wames

Research abstract:

Weighting of orthostatic intolerance time measurements with standing difficulty score stratifies ME/CFS symptom severity and analyte detection, by Alice M. Richardson, Don P. Lewis, Badia Kita, Helen Ludlow, Nigel P. Groome, Mark P. Hedger, David M. de Kretser, Brett A. Lidbury in Journal of Translational Medicine Vol 16, p 97 [Published April 12, 2018]

Background:
Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is clinically defined and characterised by persistent disabling tiredness and exertional malaise, leading to  unctional impairment.

Methods:
This study introduces the weighted standing time (WST) as a proxy for ME/CFS severity, and investigates its behaviour in an Australian cohort.

WST was calculated from standing time and subjective standing difficulty data, collected via orthostatic intolerance assessments. The distribution of WST for healthy controls and ME/CFS patients was correlated with the clinical criteria, as well as pathology and cytokine markers. Included in the WST cytokine analyses were activins A and B, cytokines causally linked to inflammation, and previously demonstrated to separate ME/CFS from healthy controls.

Forty-five ME/CFS patients were recruited from the CFS Discovery Clinic (Victoria) between 2011 and 2013. Seventeen healthy controls were recruited concurrently and identically assessed.

Results:
WST distribution was significantly different between ME/CFS participants and controls, with six diagnostic criteria, five analytes and one cytokine also significantly different when comparing severity via WST.

On direct comparison of ME/CFS to study controls, only serum activin B was significantly elevated, with no significant variation observed for a broad range of serum and urine markers, or other serum cytokines.

Conclusions:
The enhanced understanding of standing test behaviour to reflect orthostatic intolerance as a ME/CFS symptom, and the subsequent calculation of WST, will encourage the greater implementation of this simple test as a measure of ME/CFS diagnosis, and symptom severity, to the benefit of improved diagnosis and guidance for potential treatments.

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SEID diagnostic criteria applied on an adolescent CFS cohort

Posted on 04/18/2018 by wames

Research abstract:

Systemic exertion intolerance disease diagnostic criteria applied on an adolescent chronic fatigue syndrome cohort: evaluation of subgroup differences and prognostic utility, by Tarjei Tørre Asprusten, Dag Sulheim, Even Fagermoen, Anette Winger, Eva Skovlund, Vegard Bruun Wyller in BMJ Paediatrics Open 2018, Vol 2, Issue 1

What is already known on this topic?

  • There exist more than 20 diagnostic definitions of chronic fatigue syndrome (CFS).
  • A new definition and a new label (systemic exertion intolerance disease, SEID) have recently been proposed.
  • The validity of the SEID criteria has not been established, either in adults or in adolescents.

What this study hopes to add?

  • The present study questions the discriminant and prognostic validity of the SEID diagnostic criteria in adolescent CFS.
  • It suggests that the criteria tend to select patients with depressive symptoms.

Objective:

Existing case definitions for chronic fatigue syndrome (CFS) all have disputed validity. The present study investigates differences between adolescent patients with CFS who satisfy the systemic exertion intolerance disease (SEID) diagnostic criteria (SEID-positive) and those who do not satisfy the criteria (SEID-negative).

Methods:

120 adolescent patients with CFS with a mean age of 15.4 years (range 12–18 years) included in the NorCAPITAL project (ClinicalTrials ID: NCT01040429) were post-hoc subgrouped according to the SEID criteria based on a comprehensive questionnaire. The two subgroups were compared across baseline characteristics, as well as a wide range of cardiovascular, inflammatory, infectious, neuroendocrine and cognitive variables. Data from 30-week follow-up were used to investigate prognostic differences between SEID-positive and SEID-negative patients.

Results:

A total of 45 patients with CFS were SEID-positive, 69 were SEID-negative and 6 could not be classified. Despite the fact that clinically depressed patients were excluded in the NorCAPITAL project, the SEID-positive group had significantly higher score on symptoms suggesting a mood disorder (Mood and Feelings Questionnaire): 23.2 vs 13.4, difference 9.19 (95% CI 5.78 to 12.6). No other baseline characteristics showed any group differences.

When accounting for multiple comparisons, there were no statistically significant differences between the groups regarding cardiovascular, inflammatory, infectious, neuroendocrine and cognitive variables. Steps per day and Chalder Fatigue Questionnaire at week 30 showed no differences between the groups.

Conclusion:

The findings question the discriminant and prognostic validity of the SEID diagnostic criteria in adolescent CFS, and suggest that the criteria tend to select patients with depressive symptoms.

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