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MEDICAL BIOLOGY: ON FIBROMYALGIA SYNDROME

The following points are made by D.L. Goldenberg et al (J. Am. Med. Assoc. 2004 292:2388):

1) At any one time, 10% to 12% of the general population report chronic generalized musculoskeletal pain that cannot be traced to a specific structural or inflammatory cause.[1] Such idiopathic widespread pain most often will fit the classification criteria for fibromyalgia syndrome (FMS).[2]

2) The diagnosis of FMS is based on a history of widespread pain, defined as bilateral, upper and lower body, as well as spine, and the presence of excessive tenderness on applying pressure to 11 of 18 specific muscle-tendon sites.[3] The 1990 American College of Rheumatology classification criteria for the diagnosis of fibromyalgia provide a sensitivity and specificity of nearly 85% in differentiating FMS from other forms of chronic musculoskeletal pain. Surveys using these criteria have found an FMS prevalence of 2% in the US, including 3.4% of women and 0.5% of men.[4-5] Fibromyalgia is the second most common disorder observed by rheumatologists (after osteoarthritis), yet rheumatologists in the US currently provide care for less than 20% of individuals with fibromyalgia.

3) Chronic pain syndromes, such as FMS, are defined by subjective symptoms and lack unique pathophysiological characteristics. Questions often arise regarding the nature and existence of illnesses like FMS. Indeed, no discrete boundary separates syndromes such as FMS, chronic fatigue syndrome, irritable bowel syndrome, or chronic muscular headaches. Furthermore, these illnesses are each comorbid with mood disturbances.

4) Defining pain syndromes like FMS, headaches, or back pain provides a common framework to study the clinical and physiological characteristics. Research during the past decade has demonstrated similar abnormal pain processing in FMS and related chronic pain syndromes. Patients with FMS have lowered mechanical and thermal pain thresholds, high pain ratings for noxious stimuli, and altered temporal summation of pain stimuli. Physiological evidence of altered pain processing in FMS has been demonstrated by brain imaging as well as by a 3-fold higher concentration of cerebrospinal fluid substance P compared with that in healthy controls.

5) The familial coaggregation and frequent comorbidity of FMS, irritable bowel syndrome, and chronic fatigue syndrome with mood disorders also suggests a major role for neuroendocrine and stress-response abnormalities. Specific polymorphisms in the serotonin transporter gene and the catechol-O-methyltransferase enzyme that inactivates catecholamines have been associated with FMS. Altered patterns of basal and stimulated activity of several neuroendocrine axes and autonomic nervous system dysfunction have also been demonstrated. Psychosocial factors contribute greatly to the clinical expression of FMS and related disorders.

6) The authors conclude: Despite the chronicity and complexity of FMS, there are pharmacological and nonpharmacological interventions available that have clinical benefit. Based on current evidence, a stepwise program emphasizing education, certain medications, exercise, cognitive therapy, or all 4 can be recommended.

References (abridged):

1. Croft P, Rigby AS, Boswell R, et al. The prevalence of chronic widespread pain in the general population. J Rheumatol. 1993;20:710-713

2. Croft P, Schollum J, Silman A. Population study of tender point counts and pain as evidence of fibromyalgia. BMJ. 1994;309:696-699

3. Wolfe F, Smythe HA, Yunus MB, et al. The American College of Rheumatology 1990 criteria for the classification of fibromyalgia: report of the Multicenter Criteria Committee. Arthritis Rheum. 1990;33:160-172

4. Wolfe F, Cathey MA. Prevalence of primary and secondary fibrositis. J Rheumatol. 1983;10:965-968

5. Wolfe F, Cathey MA. The epidemiology of tender points. J Rheumatol. 1985;12:1164-1168

J. Am. Med. Assoc. http://www.jama.com

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Related Material:

MEDICAL BIOLOGY: ON IRRITABLE BOWEL SYNDROME

The following points are made by Henry C. Lin (J. Am. Med. Assoc. 2004 292:852):

1) Irritable bowel syndrome (IBS) is a common diagnosis that affects 11% to 14% of the population.(1-2) Currently, IBS is a diagnosis made on the basis of meeting clinical criteria.(3-5) This symptom-based approach has been used because no consistent biological marker or unifying framework has been available to explain the different symptoms and findings of IBS. The varying symptoms in IBS have led to efforts that look at differences rather than similarities between patients.

2) Another way we have emphasized difference rather than similarities is in the grouping of one set of symptoms of these patients as IBS and another set of symptoms as belonging to some other diagnosis. The clinical criteria for IBS do not include the extraintestinal symptoms that are common in these patients such as fatigue or myalgia. Instead, these complaints are viewed as symptoms of other diagnoses that coexist with IBS, such as chronic fatigue syndrome and fibromyalgia. This separation may be an artifact of medical specialization. As such, a unifying framework for understanding IBS that could account for both the gastrointestinal as well as the extraintestinal symptoms of these patients would warrant serious consideration.

3) Regardless of whether an IBS patient is troubled predominantly by constipation, diarrhea, or pain, 92% of IBS patients complain of bloating and pain, with 89% having a bloating score of 5 or greater (out of 10). Although many IBS patients describe worsening of their symptoms by food intake, most are unsuccessful in identifying a food trigger. This extremely common complaint of postprandial bloating(4) supports the possibility of a unifying pathophysiology. This symptom is associated with abdominal distension and has been corroborated by direct physical evidence of increased intestinal gas as measured by abdominal films, computed tomography of the abdomen, and plethysmographic measurement showing increased abdominal girth at the end of the day but decreased girth overnight after fasting. The possibility of a unifying explanation for IBS is further supported by reproducible x-ray findings in which increased intestinal gas was noted regardless of bowel movement pattern. Of note, the increased gas was localized to the small rather than the large intestine.

4) The author concludes: The gastrointestinal and immune effects of small intestinal bacterial overgrowth provide a possible unifying framework for understanding frequent observations in irritable bowel syndrome, including postprandial bloating and distension, altered motility, visceral hypersensitivity, abnormal brain-gut interaction, autonomic dysfunction, and immune activation.

References (abridged):

1. Thompson WG. Irritable bowel syndrome: prevalence, prognosis and consequences. CMAJ. 1986;134:111-113

2. Drossman DA, Li Z, Andruzzi E, et al. US householder survey of functional gastrointestinal disorders: prevalence, sociodemography and health impact. Dig Dis Sci. 1993;38:1569-1580

3. Manning AP, Thompson WG, Heaton KW, Morris AF. Towards positive diagnosis of the irritable bowel. BMJ. 1978;2:653-654

4. Kruis W, Thieme C, Weinzierl M, Schussler P, Holl J, Paulus W. A diagnostic score for the irritable bowel syndrome: its value in the exclusion of organic disease. Gastroenterology. 1984;87:1-7

5. Thompson WG, Creed FH, Drossman DA, et al. Functional bowel disorders and functional abdominal pain. Gastroenterol Int. 1992;5:75-91

J. Am. Med. Assoc. http://www.jama.com

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