Tag: letter

Chronic fatigue syndrome in adolescents

Dear Editor:

Chronic fatigue syndrome (CFS) or myalgic encephalomyelitis (ME) is a rare disease in adolescents, in whom the incidence is 0.5%. In adults, it has a multifactorial aetiology with no determining factor, primarily affects women (ratio, 2–3:1) aged 20–40 years, and in some cases its onset is associated with an infectious cause (usually viral). In adulthood, CFS is diagnosed based on clinical manifestations and is a diagnosis of exclusion (Table 1),1 and while the literature includes descriptions of differences in the paediatric population, few series present data on its particular features in this age group. The management is symptomatic with the goal of improving quality of life. Treatment with selective serotonin reuptake inhibitors (SSRIs), melatonin, methylphenidate, cognitive-behavioural therapy (CBT) and graded exercise has been proven to be effective in these patients.

You can read the full letter here: http://www.analesdepediatria.org/en/chronic-fatigue-syndrome-in-adolescents/articulo/S2341287916301168/

 

Source: Calle Gómez Á, Delgado Díez B, Campillo I López F, Salmerón Ruiz MA, Casas Rivero J. Chronic fatigue syndrome in adolescents. An Pediatr (Barc). 2016 Dec;85(6):318-320. doi: 10.1016/j.anpedi.2016.03.010. Epub 2016 May 20. [Article in Spanish] http://www.analesdepediatria.org/en/chronic-fatigue-syndrome-in-adolescents/articulo/S2341287916301168/ (Full article)

 

Response to: fibromyalgia and chronic fatigue syndrome caused by non-celiac gluten sensitivity

Dear Editor:

We have closely read the article published by Isasi et al.1 in Reumatologia Clínica presenting a case of fibromyalgia (FM) and chronic fatigue syndrome (CFS) caused by non-celiac sensitivity to gluten (NGCD). We would like to comment our experience with this attractive topic regarding patients with FM/CFS, which I hope will contribute to an improved knowledge of this association. The authors have reasonably ruled out celiac disease (CD) and have hypothesized that NGCD is the cause of FM and CFS in their patient; upon complete remission (CR) of symptoms, both digestive and musculoskeletal, with a gluten-free diet (GFD).

You can read the rest of this letter here: http://www.reumatologiaclinica.org/en/response-to-fibromyalgia-chronic-fatigue/articulo/S217357431400166X/

 

Source: Qanneta R, Fontova R, Castel A. Response to: fibromyalgia and chronic fatigue syndrome caused by non-celiac gluten sensitivity. Reumatol Clin. 2015 May-Jun;11(3):185. doi: 10.1016/j.reuma.2014.09.008. Epub 2014 Nov 7. http://www.reumatologiaclinica.org/en/response-to-fibromyalgia-chronic-fatigue/articulo/S217357431400166X/ (Full article)

Amitriptyline and prochlorperazine inhibit proinflammatory mediator release from human mast cells: possible relevance to chronic fatigue syndrome

CFS a complex disorder characterized by unexplained severe fatigue for over 6 months with a broad range of additional symptoms involving the nervous, endocrine and immune systems, and an estimated prevalence of 1%1. Tricyclic antidepressants (TCAs) are prescribed off label for a number of painful diseases that are often comorbid, such as chronic fatigue syndrome (CFS), fibromyalgia, interstitial cystitis, and irritable bowel syndrome, the symptoms of which are worsened by stress2. However, there is no known mechanism to explain the apparent beneficial action of TCAs3.

Mast cells and their mediators have been implicated in inflammatory diseases4, including CFS5. Mast cells are located perivascularly in close proximity to neurons in the thalamus and hypothalamus, especially the median eminence6, where they are juxtaposed to corticotropin-releasing hormone (CRH)-positive nerve processes7. CRH activates mast cells to release vascular endothelial growth factor (VEGF)8, which could participate in neurogenic inflammation and contribute to the pathogenesis of CFS. Such mediators may be released locally in the brain or may cross the blood-brain-barrier (BBB), which can be disrupted by stress, subsequent to mast cell activation9. Given the above, we hypothesized that TCAs may be helpful through inhibition of mast cell release of pro-inflammatory mediators.

You can read the rest of this letter here: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3498825/

 

Source: Clemons A, Vasiadi M, Kempuraj D, Kourelis T, Vandoros G, Theoharides TC. Amitriptyline and prochlorperazine inhibit proinflammatory mediator release from human mast cells: possible relevance to chronic fatigue syndrome. J Clin Psychopharmacol. 2011 Jun;31(3):385-7. doi: 10.1097/JCP.0b013e3182196e50. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3498825/ (Full article)

 

Heresies in textbook on psychiatry

In journal no. 5/2004( 1 ) reported Textbook of Psychiatry by Ulrik Fredrik Malt et al ( 2 ). This book contains erroneous information relating to the description of neurasthenia. The authors classify chronic fatigue syndrome (CFS), post-viral fatigue syndrome (PVFS) and myalgic encephalomyelitis (ME) as neurasthenia, diagnosis code F48.0, and has thus reclassified suffering from a neurological condition to be a psychiatric condition. This was done in Malts first textbook of psychiatry, published in 1994.

WHO has since 1969 classified Thurs the 1st as neurological disease and is not going to change that in the upcoming revision. The English psychiatrists Simon Wessely, Michael Sharpe and their counterparts, often called Wessely School, has spent countless publications in more than a decade trying to to psychiatric ME / CFS, which in part has been internationally condemned.

Leading Norwegian psychiatrists are influenced by Wessely School doctrine, and this doctrine has been continued in Textbook of Psychiatry ( 2 ). In WHO’s Guide to mental health in primary care , which Wessely has helped to develop, is ME / CFS wrongly classified under mental disorders, F48.0. Wrong classification has been debated in the British House several times. WHO were involved and confirmed that ME / CFS should continue to be classified under G93.3 and that no disease can be classified in more than one category. According to ICD-10 is to be post-viral fatigue syndrome specifically excluded before the diagnosis neurasthenia set. Secretary of State for the UK Department of Health, Lord Warner, had in the House of Lords regret their statements in support of Wessely misclassification.

Director of WHO’s Collaborating Centre at King’s College London, Professor Rachel Jenkins has had to bow and accept the WHO’s official position, namely that ME / CFS should be classified under G93.3. The book is stopped and will come in a revised edition. When a country has accepted WHO’s regulations, it is mandatory to follow ICDs classification.

Malt and employee classification of ME / CFS in Textbook of Psychiatry ( 2 ) is contrary to the WHO system. It is highly regrettable that new generations healthcare are taught in heresy by reading the chapter on psychosomatic disorders in this book. In my view, the discussion of ME / CFS is removed, the book withdrawn and come out in a revised edition.

A consensus panel of medical experts has developed new clinical criteria for ME / CFS ( 3 ) These criteria provide a more accurate description of reality.

You can read the full letter here: http://tidsskriftet.no/article/1015463

 

Source: E. Stormorken. Heresies in textbook on psychiatry. Tidsskr Nor Laegeforen. 2004 May 6;124(9):1277; author reply 1277. [Article in Norwegian] http://tidsskriftet.no/article/1015463 (Full article)

 

The chronic fatigue syndrome

Sir, Although many doctors equate chronic fatigue syndrome (Oxford definition) with what we call myalgic encephalomyelitis (ME), there are some noteworthy differences.

Firstly, in Britain, chronic fatigue syndrome is an umbrella term covering a number of different conditions including neurasthenia, effort syndrome and fibromyalgia. ME is a more specific entity (see the ‘ 10, 1992) and unlike the above, has been closely linked to a persistent infection and immune system activation.

Secondly, while profound fatigue is undeniably the most common symptom of ME, it is rather different from the type of tiredness which people normally experience after exertion. For example, it is often accompanied by feelings of illness which are so unlike anything which people have had before that patients frequently say they cannot describe it. Some have referred to the latter as a severe ‘flu-like’ malaise, others have likened it to being poisoned. Regrettably, having subsumed ME under a general heading of chronic fatigue syndrome, this important and disabling aspect of ME will almost certainly be overlooked.

You can read the rest of this letter here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2399627/pdf/postmedj00050-0083a.pdf

 

Source: Macintyre A, Hume MC. The chronic fatigue syndrome. Postgrad Med J. 1993 Feb;69(808):164. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2399627/

 

Chronic fatigue syndrome: a joint paediatric-psychiatric approach

Comment on: Chronic fatigue syndrome: a joint paediatric-psychiatric approach. [Arch Dis Child. 1992]

 

SIR,-While agreeing that physical, psychological, and social factors must all be taken into account in the management of this complex and controversial syndrome I would disagree with Dr Margaret Vereker’s statement that no organic pathology can be detected to account for any of the symptoms. This conclusion has been made without reference to a number of research papers describing persisting viral infection, neuromuscular abnormalities in both structure and function, and immune system dysfunction.

Gow et al using polymerase chain reaction techniques, have been able to demonstrate the presence of enteroviral genome in muscle biopsies from a significant number of patients (53%) compared with controls (15%). None of the healthy control group in this study had evidence of viral particles in their muscle, this was only found in those with colonic or breast malignancies. Precisely what cytopathological effect this intracellular virus is having within muscle remains open to debate. However, Behan et al have published electron microscopic evidence of structural damage to the muscle mitochondria along with type II fibre atrophy; this is a finding which is not normally considered to be consistent with simple disuse.

You can read the rest of this letter here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1793782/pdf/archdisch00632-0102a.pdf

 

Source: Shepherd C. Chronic fatigue syndrome: a joint paediatric-psychiatric approach. Arch Dis Child. 1992 Nov;67(11):1410. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1793782/

 

Fluctuations in perceived energy and mood among patients with chronic fatigue syndrome

Comment on: Fluctuations in perceived energy and mood among patients with chronic fatigue syndrome. [J R Soc Med. 1992]

 

As one who has long had a high regard for Dr Shepherd’s reasoned arguments in. the area of chronic fatigue syndrome (CFS) (September. 1992 JRSM, p 588), I am sorry to have to point out a logical inconsistency in his assessment of our work. Postinfectious patients do indeed form a sub-group of those with chronic fatigue syndrome. However, according to the ‘Oxford criteria’, in defining other groups of chronically fatigued patients, a diagnosis of previous infection is not necessary. Thus precipitating infection is not necessary for defining the syndrome itself, as we said in our paper.

Secondly, he might do well to note the way in which our results show energy and mood levels among CFS patients to be at their highest in the midmorning. This does not appear to be the pattern typically found among individuals with a primary diagnosis of depression, as we also point out. We regard this distinction as being potentially important and would hope.that the ME Association might wish to consider its implications. Unfortunately, this point was also missed in a recently unsolicited ‘abstraction’ of our work kindly prepared for us by the International Federation of ME Associations to be published in their Medical Update.

You can read the rest of this letter here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1293708/pdf/jrsocmed00106-0076.pdf

 

Source: Wood C. Fluctuations in perceived energy and mood among patients with chronic fatigue syndrome. J R Soc Med. 1992 Oct;85(10):650. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1293708/

 

Immune responsiveness in chronic fatigue syndrome

Comment on: Immune responsiveness in chronic fatigue syndrome. [Postgrad Med J. 1991]

 

Sir, The paper by Milton and colleagues (1) challenges the hypothesis that patients with postviral fatigue syndrome (myalgic encephalomyelitis) have a persisting viral infection along with consequent immune dysregulation. The protocol employed in the study suggests that their conclusions may not be valid.

Firstly, the 31 patients were selected from a group attending a ‘muscle clinic’ who complained of ‘unexplained chronic fatigue’. Of these only 15 had a clear history of a precipitating viral illness – a key diagnostic feature of postviral fatigue syndrome. Secondly, although other research groups have also demonstrated that raised levels of Coxsackie B virus IgG and IgM antibodies are not diagnostic of the syndrome, (2) these findings cannot be used to exclude the possibility of persisting viral infection within either muscle or the central nervous system.

As far as muscle is concerned, Gow and colleagues( 3) have recently detected enteroviral RNA sequences in muscle biopsies of 53% of patients with a well-defined postviral fatigue syndrome compared to 15% in a control group, and Archard et al. (4) have shown that this persisting enterovirus is poorly replicating.

Demonstrating the presence of persisting virus within the central nervous system is obviously far more difficult without autopsy material. However, Daugherty et al. (5) in America have published the results of MRI scans and cognitive function tests on 20 patients (with age and sex matched healthy controls) showing abnormalities consistent with an organic brain syndrome similar to that seen in patients who are positive for human immunodeficiency virus.

You can read the rest of this letter here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2399327/pdf/postmedj00061-0069a.pdf

 

Source: Shepherd C. Immune responsiveness in chronic fatigue syndrome. Postgrad Med J. 1992 Jan;68(795):66-7. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2399327/

 

Chronic fatigue syndrome

SIR,

Dr Anthony David and colleagues (1) cite our paper (2) as one that makes inflated claims about the chtionic fatigue syndrome.

We first reported retrospectively an association between antibodies to coxsackie virus B and a group of symptoms similar to those previously described as myalgic encephalomyelitis. (3) We were faced with an ever increasing clinical problem of which we had little understanding, and the prospective investigation of coxsackie virus B antibody titres in these patients seemed a reasonable step forward. No widely accepted definition of the chronic fatigue syndrome existed in 1983, and we did not attempt to define it. We approached the problem from the opposite direction in that we had a definable test and we tried to show what happened to the results of this test in a group of ill patients.

Since 1983 much research into this syndrome has been carried out. It has taken a long time for a consensus to be agreed defining the syndrome. We believe that today’s definition that the syndrome cannot be diagnosed before six months has elapsed is acceptable. In our study 72% of our patients were still unwell six months into the illness.

The comparison made by Dr David and colleagues of their paper with ours is invalid. They questioned 611 general practice attenders whereas we reported on a group of 140 patients presenting over six months with what we believe to be the same illness.

In retrospect we think that what we observed was the slow spread of an infective agent through our town in 1983 and through neighbouring towns in our district in 1984 and 1985. The clinical syndrome coincided with a rise in the prevalence of coxsackie virus B antibodies in the general population from 10-12% in 1973-84 (we found 25% in 1983) to 55% in 1985-6. (4) Since then our clinical impression has been one of a return to normal; we see occasional new cases but not as many as in 1983.

The prevalence of this condition seems to depend on the activity of an infective agent of some kind, be it viral or otherwise, in the area of study at the time, and further research is made difficult by the wide fluctuations of prevalence that will be found from place to place and from time to time.

~B D CALDER

~P J WARNOCK Helensburgh G84 8BW

1 David A, Pelosi A, McDonald E, et al. Tired, weak, or in need of rest: fatigue among general practice attenders. BMJ 1990;301:1199-202. (24 November.)

2 Calder BD, Warnock PJ, McCartney RA, Bell EJ. Coxsackie B viruses and post-viral syndrome J R Coll Gen Pract 1987;37: 11-4.

3 Calder BD, Warnock PJ. Coxsackie B infections in Scottish general practice. J R Coll Gen Pract 1984;34:15-9.

4 Miller NA, Carmichael HA, Calder BD, et al. Antibody to coxsackie B virus in diagnosing postviral fatigue syndrome. BMJ (in press).

 

Source: B D Calder and P J Warnock. Chronic fatigue syndrome. BMJ. 1991 Jan 19; 302(6769): 181. PMCID: PMC1668832 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1668832/

 

Life insurance MDs sceptical when chronic fatigue syndrome diagnosed

Comment on: Life insurance MDs sceptical when chronic fatigue syndrome diagnosed. [CMAJ. 1990]

 

As a physician with chronic fatigue syndrome (CFS) since the early days of the Lake Tahoe, Calif., outbreak, in 1984, I read Olga Lechky’s report (Can MedAssoc J 1990; 143: 413- 415) with particular interest. It was refreshing to hear Dr. Richard Proschek, assistant medical director of Mutual Life of Canada, admit that the industry’s attitude to CFS is one of hostility. Unfortunately for the thousands of severely debilitated patients with the condition this scepticism and hostility are not restricted to that industry, which in many instances has behaved with compassion and responsibility toward its clients. The hostile viewpoint is also widely prevalent in the medical profession and is often freely communicated to patients.

To hold that CFS is not a real disease it is necessary to imagine that in 1984 people of all ages began to manufacture a condition with clearly defined symptoms that begins as a flu-like illness, persists and evolves. How many diseases fit this description? When, before 1984, did depression present so? Can it be true that thousands of our brightest citizens, including children, Olympic aspirants, several members of some families, alarming numbers of teachers, 50% of a symphony orchestra and 10% of the population of Incline Village, Nev., abruptly and concurrently elected to drop out of life, then continued to complain in the face of widespread scepticism, hostility, marital breakdown and, frequently, isolation? What, other than an infectious agent, could cause this?

Proschek’s bias arises from his position. Physicians in practice, however, see many CFS patients who have no insurance or are quite wealthy. The degree to which imagination must extend to accommodate a diagnosis of secondary gain in these people is beyond belief. Many physicians lament the lack of a blood test for CFS. What, pray, is the test for malingering, a diagnosis we seem to have no difficulty making?

You can read the rest of this letter here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1452931/pdf/cmaj00229-0013.pdf

 

Source: Sean J. O’Sullivan, MD. Life insurance MDs sceptical when chronic fatigue syndrome diagnosed. CMAJ. 1990 Dec 15;143(12):1283-6. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1452931/