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[ back to index ]Posted to Co-Cure Tue, 18 Apr 2000 19:07:36 -0400Severe nutcracker syndrome was found to be present in all 9 of the fatigued, disabled children studied by the authors. The children were studied because they were intermittently or persistently absent from school and filled the criteria for CFS.
Does severe nutcracker phenomenon cause pediatric chronic fatigue?
Does severe nutcracker phenomenon cause pediatric chronic fatigue?
Authors: Takahashi Y, Ohta S, Sano A, Kuroda Y, Kaji Y, Matsuki M, Matsuo M
Affiliation: Department of Pediatrics, Tenri Hospital, Nara, Japan.
Journal: Clinical Nephrology (ISSN 0301-0430) 2000 Mar;53(3):174-81
NLM citations: PMID: 10749295, UI: 20210866
- The nutcracker phenomenon is a nickname for hypertension of the left renal (kidney) vein .)
- In the abstract given, the authors use the terms chronic fatigue and chronic fatigue syndrome interchangeably and do not indicate which definition they use in stating that the children fulfilled the criteria for CFS.
Posted to Co-Cure Sat, 15 Apr 2000 05:14:43 -0400[ back to index ]
Got Pain? Researchers Have Some Ideas That May Surprise You
Got Pain? Researchers Have Some Ideas That May Surprise You
Marijuana, Hot Peppers, Snails, and Frogs May Be Sources of Pain Relief
By L.A. McKeown
WebMD Medical News
April 14, 2000 (New York) -- Researchers seeking new ways to relieve the pain that persistently plagues many Americans are looking in some unusual places: a snail found in the Philippines, a poisonous frog from Ecuador, and the marijuana plant.
According to a recent Gallup survey, pain is a fact of life for many in the U.S., with 46% of women and 37% of men reporting that they experience some pain daily. Pain can be acute, or short-lived, like that experienced after an accident; or chronic, meaning it lasts long after an injury has healed or is due to persistent inflammation or nerve damage. Some diseases, such as diabetes and shingles, can cause long-term pain that is difficult to treat.
Read the full article at:
- Current therapies used to treat pain include drugs that suppress inflammation, which work for mild to moderate pain, or narcotic agents, which can be addictive.
- With so few choices for treatment, pain is often difficult to treat adequately.
- New research into pain treatments is focusing on compounds from marijuana, hot peppers, snail venom, and secretions from a poisonous frog.
[ back to index ]Posted to Co-Cure Fri, 14 Apr 2000 09:06:05 -0400The authors discuss the history and testing of three CFS patients, ages 11, 12 and 13. As measured by SPECT scan, cerebral blood flow in the left temporal and occipital lobes were markedly lower in two of the patients compared to previously-reported levels in healthy subjects. In the third case, blood flow in the left basal ganglia and thalamus was markedly higher than in healthy subjects. There was also remarkable elevation of the choline/creatine ratio in all three patients. No focal structural abnormalities were visible on the MRIs. The authors conclude that clinical CFS symptoms "may be closely related to an abnormal brain function".
Chronic fatigue syndrome in childhood may be closely related to abnormal brain function
Chronic fatigue syndrome in childhood.
Authors: Tomoda A, Miike T, Yamada E, Honda H, Moroi T, Ogawa M, Ohtani Y, Morishita S
Affiliation: Department of Child Development, Kumamoto University School of Medicine, Japan. &NBSP E-Mail: email@example.com
Journal: Brain and Development (ISSN 0387-7604) 2000 Jan;22(1):60-4
NLM citations: PMID: 10761837, UI: 20222474
Posted to Co-Cure Thu, 13 Apr 2000 21:01:08 -0400[ back to index ]
Research Points to Possible New Class of Painkillers
Researchers have found a potential new target for the development of a class of pain-killing drugs.
In a study on mice, scientists deleted a certain gene and found that the mice did not feel certain types of painful irritations.
This pain receptor is found primarily at the site of an injury, so any drugs that target this receptor would theoretically have few side effects.
Read the article at:
[ back to index ]Posted to Co-Cure Wed, 12 Apr 2000 09:51:29 -0400The authors evaluated the benefits and tolerability of opioids in the long-term management of chronic noncancer pain, including fibromyalgia. This study showed that failure of one opioid cannot predict the patient's response to another, and if a patient experiences an intolerable side effect or if the drug is ineffective, changing to a different opioid may result in a lessening or elimination of the side effect or pain.
Opioid Substitution to Improve the Effectiveness of Chronic Noncancer Pain Control: A Chart Review
Opioid Substitution to Improve the Effectiveness of Chronic Noncancer Pain Control: A Chart Review.
Authors: Quang-Cantagrel ND, Wallace MS, Magnuson SK
Affiliation: Department of Anesthesiology, University of California San Diego, San Diego, California.
Address correspondence and reprint requests to Mark S. Wallace, MD, UCSD Pain Management Medical Group, 9500 Gilman Dr. #0924, La Jolla, CA 92093-0924.
Journal: Anesthesia and Analgesia (ISSN 0003-2999) 2000 Apr;90(4):933-937
NLM citation: PMID: 10735802
The abstract does not mention which opioids were tested, but it does indicate that the original article has a chart showing each subject's specific reactions to the medications tested. Interested readers can obtain the full article via PubMed (fee service http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed), a medical or public library, or by writing the authors for a reprint (address is given above.)
The abstract can be viewed at
[ back to index ]Posted to Co-Cure Tue, 11 Apr 2000 13:10:40 -0400The authors tested 10 female FMS patients with 5 mg of tropisetron per evening for 4 weeks. They measured pain score, fatigue, sleep disturbances, and number of tender points. Half of the patients showed a statistical clinical improvement of all the above parameters starting after the first week of treatment. Two patients did not respond to the therapy; three discontinued the study because of side-effects.
Treatment of fibromyalgia with tropisetron, a 5HT3 serotonin antagonist
Treatment of fibromyalgia with tropisetron, a 5HT3 serotonin antagonist: a pilot study.
Authors: Papadopoulos IA, Georgiou PE, Katsimbri PP, Drosos AA
Affiliation: Department of Internal Medicine, Medical School, University of Ioannina, Greece.
Clinical Rheumatology (ISSN 0770-3198) 2000;19(1):6-8
NLM citations: PMID: 10752491, UI: 20214156
[ back to index ]Posted to Co-Cure Wed, 5 Apr 2000 19:04:09 -0700 by Melissa O'TooleContext: Pain often is inadequately treated due in part to reluctance about using opioid analgesics and fear that they will be abused. Although international and national expert groups have determined that opioid analgesics are essential for the relief of pain, little information has been available about the health consequences of the abuse of these drugs.
Trends in Medical Use and Abuse of Opioid Analgesics
Trends in Medical Use and Abuse of Opioid Analgesics
JAMA. 2000;283:1710-1714 (April 5, 2000)
David E. Joranson, MSSW; Karen M. Ryan, MA; Aaron M. Gilson, PhD; June L. Dahl, PhD
Objective: To evaluate the proportion of drug abuse related to opioid analgesics and the trends in medical use and abuse of 5 opioid analgesics used to treat severe pain: fentanyl, hydromorphone, meperidine, morphine, and oxycodone.
Design and Setting: Retrospective survey of medical records from 1990 to 1996 stored in the databases of the Drug Abuse Warning Network (source of abuse data) and the Automation of Reports and Consolidated Orders System (source of medical use data).
Patients: Nationally representative sample of hospital emergency department admissions resulting from drug abuse.
Main Outcome Measures: Medical use in grams and grams per 100,000 population and mentions of drug abuse by number and percentage of the population.
Results: From 1990 to 1996, there were increases in medical use of morphine (59%; 2.2 to 3.5 million g), fentanyl (1168%; 3263 to 41,371 g), oxycodone (23%; 1.6 to 2.0 million g), and hydromorphone (19%; 118,455 to 141,325 g), and a decrease in the medical use of meperidine (35%; 5.2 to 3.4 million g). During the same period, the total number of drug abuse mentions per year due to opioid analgesics increased from 32,430 to 34,563 (6.6%), although the proportion of mentions for opioid abuse relative to total drug abuse mentions decreased from 5.1% to 3.8%. Reports of abuse decreased for meperidine (39%; 1335 to 806), oxycodone (29%; 4526 to 3190), fentanyl (59%; 59 to 24), and hydromorphone (15%; 718 to 609), and increased for morphine (3%; 838 to 865).
Conclusions: The trend of increasing medical use of opioid analgesics to treat pain does not appear to contribute to increases in the health consequences of opioid analgesic abuse.
Full article at:
Posted to Co-Cure Mon, 3 Apr 2000 14:26:50 -0400 by Rich Van Konynenburg firstname.lastname@example.org[ back to index ]
Metabolic Pathogenesis Hypothesis for CFS/FM
I would like to propose a metabolic hypothesis for the pathogenesis of CFS/FM that I believe fits many of the observations.
The essential idea is that the onset of CFS/FM occurs when a chronic partial blockade is inserted somewhere in the chain of reactions that make up the intermediary metabolism, i.e. the pathway involved in burning fuel and making ATP. Intermediary metabolism includes glycolysis, the pyruvate dehydrogenase complex, the Krebs cycle, and the respiratory chain.
There are several subsets of PWCs, and each subset has a different etiology, but all the etiologies have in common the fact that they impact intermediary metabolism by inserting a chronic partial blockade somewhere within it.
Different etiologies insert the partial blockade at different places in the intermediary metabolism. This explains why subsets of PWCs differ in terms of their history of triggering factors, speed of onset, biochemical indicators, and response to various treatments, while at the same time they generally share a more or less common set of symptoms.
The symptoms arise from the common pathogenesis and pathophysiology, which flow from the various etiologies, but the etiologies are different.
One major etiology appears to be the depletion of reduced glutathione, as suggested by Dr. Cheney and Dr. Bounous. Most of the known "triggering factors" for CFS/FM are known to use reduced glutathione.
These include infections, physical trauma, surgery, lack of sleep, excessive physical exercise, emotional stress, exposure to toxins or oxidants, excessive use of alcohol, diet deficient in antioxidants and sources of the amino acids that are precursors for making glutathione, such as cysteine, etc.
If the inventory of reduced glutathione gets too low in the liver, it hoards what it needs to preserve life. The muscle cells then become deficient in reduced glutathione. This allows the peroxynitrite, an oxidizing free radical, to build up. Peroxynitrite attacks the enzyme cis-aconitase in the Krebs cycle of the muscle cells, producing a partial blockade. This causes a drop in ATP production, which robs the calcium pumps of the energy needed to pump Ca ions back into the sarcoplasmic reticulum, and it also robs the myosin heads of the ATP needed to detach them from the actin fibers.
This leads to the observed fatigue, weakness, and contractions in the muscles. Meanwhile, back in the Krebs cycle, citrate builds up (as observed by the U. of Newcastle group), because it is just upstream of the partial blockade. Citrate is transported into the Sarcoplasm, and it downregulates phosphofructokinase in the glycolysis chain, further lowering the ATP production.
This latter effect causes a glucose backlog in the blood, and the pancreas is forced to raise the insulin level to push it into the liver and fat cells, where it is converted to stored fat. This accounts for the weight gain in many PWCs. The overshoot in the control system then produces hypoglycemia in many PWCs. They consume carbohydrates again, and the cycle is repeated. (This is why a low carbohydrate diet is helpful for many PWCs. It stops this cycle.)
The resulting high average insulin level causes the fatty acids to be sequestered in the fat cells, and thus not available to be burned for fuel by the muscle cells. This accounts for the stubbornness of the weight gain in many PWCs.
Since the muscle cells cannot use glucose efficiently because of the downregulation of glycolysis by citrate, and since they cannot get fatty acids because of the high insulin, they burn amino acids for fuel, using what's left of the Krebs cycle, by anapleurosis. This causes the amino acid levels in the blood to drop (which is observed).
The shortage of amino acids in the blood then causes other problems: The lymphocytes are unable to get enough glutamine and other amino acids, so cell-mediated immunity becomes dysfunctional. Since this is the type of immunity needed to counter viruses, intracellular bacteria, and yeasts, they begin to thrive. The result is infections that spread systemically and do their damage on tissues, including the brain. This leads to cognitive problems, etc.
Another problem is that the cells of the small intestine are unable to get enough glutamine also, which is their main substrate. This leads to irritable bowel syndrome and to leaky gut syndrome. The latter produces food allergies.
There is also a shortage of tryptophan in the blood, and this leads to depletion of serotonin and melatonin, affecting mood and sleep. Etc., etc.
Another etiology is the hypercoagulability theory of Dr. David Berg. This etiology interferes with oxygen getting to cytochrome oxidase, and thus produces a partial blockade at the end of the intermediary metabolism chain. ATP production drops, and the same syndrome ensues.
A third etiology is the excess phosphate reabsorption etiology of Dr. R. Paul St. Amand. In my opinion (not his, at least yet) the excess phosphate ties up magnesium ions in the mitochondria, and this leads to downregulation of pyruvate dehydrogenase and/or isocitrate dehydrogenase, which are very magnesium dependent, thus putting partial blockades at one or both of these sites. Again, the same symptom set occurs.
I suspect that there are probably several more etiologies, based on my observations of the range of PWC subsets, but I suggest that all of them somehow impact the intermediary metabolism, and that's what brings on CFS/FM.
I have focussed here on the muscle cells, but other kinds of cells are probably also affected, including cells in the nervous system. In the case of neurons, the major use of ATP is to drive the sodium-potassium ATPase ion pumps. When these are short of ATP, they are unable to maintain the intracellular ion concentrations at the proper values.
This leads to a change in the osmotic potential inside the cells, because the pumps normally move three sodium ions out when they bring two potassium ions in. The result is increased concentration of ions inside, and this causes the cells to absorb water and swell. This may be the origin of the need to perform Chiari surgergy in some PWCs. Their brains have swollen too much for the available space allowed by the bones of the head and neck.
Another effect of the lack of ATP for the ion pumps is that the membrane potential drops, and this reduces the threshold for firing action potentials (nerve impulses). This may be one of the origins of the increased sensation of pain in FM. (The other appears to be spinal in location, and appears to be associated with lowered serotonin.)
Comments are welcome. Please mail them to: email@example.com
[ back to index ]Posted to Co-Cure Sun, 2 Apr 2000 20:17:58 -0400 by Kimberly HareLittle has been reported on prognostic indicators in children with chronic fatigue syndrome (CFS).
The course of severe chronic fatigue syndrome in childhood
The course of severe chronic fatigue syndrome in childhood.
J R Soc Med 2000 Mar;93(3):129-34
Rangel L, Garralda ME, Levin M, Roberts H
Academic Unit of Child and Adolescent Psychiatry, Imperial College School of Medicine, St Mary's Hospital, London, UK.
PMID: 10741312, UI: 20205485
We used interviews with children and parents, a mean of 45.5 months after illness onset, to follow up 25 cases of CFS referred to tertiary paediatric psychiatric clinics.
At its worst, the illness had been markedly handicapping (prolonged bed-rest and school absence in two-thirds); mean time out of school was one academic year. Two-thirds, however, had recovered and resumed normal activities--mean duration of illness to recovery/assessment 38 months--and none had developed other medical conditions.
Recovery was associated with specific physical triggers to the illness, with start of illness in the autumn school term and with higher socioeconomic status. Severe fatigue states in children can cause serious and longlasting handicap but most children recover.
[ back to index ]Posted to Co-Cure Sat, 1 Apr 2000 19:06:02 -0800 by Melissa O'TooleSUMMARY: In this study, researchers set out to get a better idea of the relationship between regions of the brain and immune activity, specifically in those with fibromyalgia. To measure this, they used a method called butanol positron emission tomography. By zeroing in on portions of the brain that registered activity correlating to natural killer cell activity, the researchers identified the culprit brain regions. Although the study sampled a relatively small number of FM patients (five), the association between the immune system with the portion of the brain involved in pain perception, emotion and attention, was striking. The findings provide clues as to how the brain understands and communicates immune activity to our body, as well as its regulatory role in the whole process.
Immune Activity in Fibromyalgia Patients Is Associated with Regions of the Brain
Neuroimmune relations in patients with fibromyalgia: a positron emission tomography study
Neurosci Lett 2000 Mar 24;282(3):193-196
Lekander M, Fredrikson M, Wik G
Department of Clinical Neuroscience, Psychology Section, Karolinska Institute and Hospital Z6, S-171 76, Stockholm, Sweden
ABSTRACT: To study relations between neural and immune activity in patients with chronic pain, we correlated regional cerebral blood flow measured with [(15)O]butanol positron emission tomography to immune function in five patients with fibromyalgia. Partly replicating previous data in healthy volunteers, natural killer cell activity correlated negatively with right hemisphere activity in the secondary somatosensory and motor cortices as well as the thalamus. Moreover, natural killer cell activity was negatively and bilaterally related to activity in the posterior cingulate cortex. Thus, immune parameters were related to activity in brain areas involved in pain perception, emotion, and attention. Implicated from a small study population, these strong neuro-immune associations are discussed in view of recent findings concerning mechanisms and adaptive values in immuno-cortical communication and regulation.
[ back to index ]Posted to Co-Cure Thu, 30 Mar 2000 19:50:55 -0500The authors followed the illness of 35 CFS patients to study the role of HHV-6 infection or reactivation in the pathogenesis of the illness. Relative to healthy controls, the CFS patients had higher levels of HHV-6 IgM and IgG antibody and higher frequency of antibody to HHV-6 early protein (p41/38). Using peripheral blood mononuclear cells (PBMCs), they found that isolates from CFS patients were predominately Variant A while those from healthy controls were predominately Variant B (67%). Persistent HHV-6 infection was found in two CFS patients over a period of 2.5 years and HHV-6 specific cellular immune responses were detected in PBMCs from ten CFS patients. The authors suggest that HHV-6 reactivation plays a role in the pathogenesis of CFS.
Frequent HHV-6 reactivation in multiple sclerosis (MS) and chronic fatigue syndrome (CFS) patients
[Moderator's note: this summary concentrates on findings for CFS. A link to the abstract is included below and includes information on MS as well.]
Frequent HHV-6 reactivation in multiple sclerosis (MS) and chronic fatigue syndrome (CFS) patients.
Authors: Ablashi DV, Eastman HB, Owen CB, Roman MM, Friedman J, Zabriskie JB, Peterson DL, Pearson GR, Whitman JE
Affiliation: Department of Microbiology and Immunology, Georgetown University, School of Medicine, Washington, DC, USA
Journal of Clinical Virology (ISSN 1386-6532) 2000 May 1;16(3):179-191
NLM citation: PMID: 10738137
[ back to index ]Posted to Co-Cure Tue, 28 Mar 2000 00:57:12 -0500 by Fred SpringfieldAbstract:
A 37 kDa 2-5A binding protein as a potential biochemical marker for CFS
A 37 kDa 2-5A binding protein as a potential biochemical marker for chronic fatigue syndrome
American Journal of Medicine, Volume 108, Issue 2 (February 2000), Pages 99-105
Kenny De Meirleir [a A], Catherine Bisbal [b], Isabelle Campine [a], Pascale De Becker [a], Tamim Salehzada [b], Edith Demettre [b] and Bernard Lebleu [b]
[a]Department of Human Physiology and Medicine (KDM, IC, PDB), Vrije Universiteit Brussel, Brussels, Belgium
[b]Molecular Genetics Institute (CB, TS, ED, BL), Université Montpellier II, Montpellier, France
[A] Requests for reprints should be addressed to Prof. Dr. K. De Meirleir, V.U.B. KRO gebouw-1, Laarbeeklaan 101, 1090 Brussel, Belgium
Manuscript received 3 August 1998 Revised 15 July 1999 Accepted 15 July 1999;
PURPOSE: Recent studies have revealed abnormalities in the ribonuclease L pathway in peripheral blood mononuclear cells of patients with the chronic fatigue syndrome. We conducted a blinded study to detect possible differences in the distribution of 2-5A binding proteins in the cells of patients with chronic fatigue syndrome and controls.
PATIENTS AND METHODS: We studied 57 patients with chronic fatigue syndrome and 53 control subjects (28 healthy subjects and 25 patients with depression or fibromyalgia). A radioactive probe was used to label 2-5A binding proteins in unfractionated peripheral blood mononuclear cell extracts and to compare their distribution in the three groups.
RESULTS: A 37 kDa 2-5A binding polypeptide was found in 50 (88%) of the 57 patients with chronic fatigue syndrome compared with 15 (28%) of the 53 controls (P <0.01). When present, the amount of 37 kDa protein was very low in the control groups. When expressed as the ratio of the 37 kDa protein to the 80 kDa protein, 41 (72%) of the 57 patients with chronic fatigue syndrome had a ratio >0.05, compared with 3 (11%) of the 28 healthy subjects and none of the patients with fibromyalgia or depression.
CONCLUSION: The presence of a 37 kDa 2-5A binding protein in extracts of peripheral blood mononuclear cells may distinguish patients with chronic fatigue syndrome from healthy subjects and those suffering from other diseases.
[ back to index ]Posted to Co-Cure Sat, 18 Mar 2000 22:10:34 -0500The authors studied the effect of vaccination with a staphylococcus toxoid compared to the effect of injections of sterile water in 28 patients with both fibromyalgia and chronic fatigue syndrome. The abstract discusses the success the authors found with those patients who received the toxoid.
Effects of staphylococcus toxoid vaccine on pain and fatigue in patients with FMS/CFS
This article was published in 1998 but just made it to MedLine, so it is being sent to our readers.
Effects of staphylococcus toxoid vaccine on pain and fatigue in patients with fibromyalgia/chronic fatigue syndrome.
Authors: Andersson M, Bagby JR, Dyrehag L, Gottfries C
Affiliation: Pain Unit, Kungalv Hospital, Sweden
European Journal of Pain 1998;2(2):133-142
NLM citation: PMID: 10700309
Note: All abstract summaries, unless otherwise noted, were prepared by Margaret Bailey.