The grey area of effort syndrome and hyperventilation: from Thomas Lewis to today

Abstract:

Lewis used the diagnosis ‘effort syndrome’ for subjects whose ability to make and sustain effort had been reduced by homeostatic failure. A major element was depletion of the body’s capacity for buffering the acids produced by exercise.

In his view this systems disorder was not to be regarded as a specific organ disease, and losing sight of the metabolic element would foster the invention of fanciful, unphysiological diagnoses. His views were dismissed because normal resting plasma bicarbonate levels were considered by others in that era to exclude serious depletion of the body’s total capacity for buffering the effects of exertion.

Today, effort syndrome is still a useful diagnosis for a condition of exhaustion and failure of performance associated with depletion of the body’s buffering systems. Other elements associated with homeostatic failure are now recognised, principally emotional hyperarousal and hyperventilation. Their physiological interrelationships are described. Effort syndrome is amenable to recovery through rehabilitation, and it may be a mistake to treat chronic fatigue syndrome and unspecific illness without including it in the differential diagnosis.

 

Source: Nixon PG. The grey area of effort syndrome and hyperventilation: from Thomas Lewis to today. J R Coll Physicians Lond. 1993 Oct;27(4):377-83. http://www.ncbi.nlm.nih.gov/pubmed/8289156

 

Serum angiotensin-converting enzyme as a marker for the chronic fatigue-immune dysfunction syndrome: a comparison to serum angiotensin-converting enzyme in sarcoidosis

Abstract:

PURPOSE: To study the reliability of a serum angiotensin-converting enzyme (ACE) assay as a marker for the chronic fatigue-immune dysfunction syndrome (CFIDS), and to compare some enzyme characteristics of ACE in CFIDS with that in sarcoidosis.

PATIENTS AND METHODS: Forty-nine patients with CFIDS and 56 endemic control subjects from Lyndonville, New York, and Charlotte, North Carolina; plus 23 untreated patients with active sarcoidosis, 24 with sarcoidosis receiving corticosteroid therapy, and 32 patient controls without sarcoidosis from California. Serum ACE levels were determined with a spectrophotometric method. The effect of freezing and thawing and the effect of storage at 4 degrees C were compared between CFIDS and sarcoidosis samples.

RESULTS: Serum ACE levels were elevated in 80% of patients with CFIDS and 30% of endemic control subjects as compared with 9.4% of nonendemic California control subjects. The ACE activity in CFIDS differed from that in sarcoidosis because of its lability with storage at 4 degrees C in CFIDS and its partial activation with freezing and thawing. Thus, ACE activity was elevated in the majority of CFIDS patients either upon initial assay or upon a subsequent assay after refreezing. ACE activity was elevated in 87% of patients with active sarcoidosis and was not affected by storage or freezing and thawing.

CONCLUSIONS: Serum ACE elevations may be a useful marker for CFIDS, especially if a method can be developed to distinguish ACE in CFIDS from that in sarcoidosis. The sensitivity for CFIDS was 80%, with 68% specificity in an endemic area. The increased prevalence of serum ACE elevations in endemic controls as compared with nonendemic controls suggests that an ACE increase may be an early manifestation of CFIDS and supports the concept that CFIDS is a definite disease state.

 

Source: Lieberman J, Bell DS. Serum angiotensin-converting enzyme as a marker for the chronic fatigue-immune dysfunction syndrome: a comparison to serum angiotensin-converting enzyme in sarcoidosis. Am J Med. 1993 Oct;95(4):407-12. http://www.ncbi.nlm.nih.gov/pubmed/8213873

 

The “anti-Ki” syndrome: major clinical features

Abstract:

OBJECTIVE: To describe the major clinical features of patients with high titers of anti-Ki antibodies.

METHOD AND RESULTS: Four of 172 patients with connective tissue diseases showed high titers (> 1/256) of anti-Ki antibodies. In these four patients, (1) the common clinical findings were alopecia, disabling chronic fatigue, muscle weakness, tenosynovitis, dry mouth, and abnormal glucose tolerance test; (2) anti-Ki antibodies were positive not only in patients with sicca lupus, but also in those with nonsicca lupus. In this case, anti-insulin receptor antibody was positive and there was a regulatory insufficiency of the pituitary. (3) Symptoms of anti-Ki antibodies share many clinical and laboratory features of chronic fatigue syndrome and fibromyalgia, that is, they may share either a common etiologic agents or a common pathogenetic pathway or both.

CONCLUSION: “Anti-Ki antibody” syndrome may be a subset of sicca lupus.

 

Source: Matsunaga K. The “anti-Ki” syndrome: major clinical features. Rinsho Byori. 1993 Aug;41(8):882-7. [Article in Japanese] http://www.ncbi.nlm.nih.gov/pubmed/8371504

 

Complications of sarcoidosis. Chronic fatigue syndrome

Abstract:

Well-recognised complications are pulmonary fibrosis, cor pulmonale, glaucoma, cataract and nephrocalcinosis causing failure of lungs, heart, vision and kidneys. Less well-recognised is the post-sarcoidosis chronic fatigue syndrome.

The afflicted join sarcoidosis patients’ associations because of their profound symptoms of myalgia, fatigue, sleep reversal and low-spiritedness. The symptoms are out of proportion to the lack of physical signs and the absence of objective evidence of sarcoidosis.

Management includes unremitting sympathy and replenishment of essential neurochemicals.
Comment in: Complications of sarcoidosis. Chronic fatigue syndrome. [Sarcoidosis. 1993]

 

Source: James DG. Complications of sarcoidosis. Chronic fatigue syndrome. Sarcoidosis. 1993 Mar;10(1):1-3. http://www.ncbi.nlm.nih.gov/pubmed/8134708

 

Fibromyalgia, sleep disorder and chronic fatigue syndrome

Abstract:

Various research studies show that the amalgam of disordered sleep physiology, chronic fatigue, diffuse myalgia, and cognitive and behavioural symptoms constitutes a non-restorative sleep syndrome that may follow a febrile illness, as in the chronic fatigue syndrome. Where rheumatic complaints are prominent such a constellation of disturbed sleep physiology and symptoms also characterizes the fibromyalgia disorder.

In contrast to the chronic fatigue syndrome, fibromyalgia is associated with a variety of initiating or perpetuating factors such as psychologically distressing events, primary sleep disorders (e.g. sleep apnoea, periodic limb movement disorder) and inflammatory rheumatic disease, as well as an acute febrile illness.

The chronic fatigue syndrome and fibromyalgia have similar disordered sleep physiology, namely an alpha rhythm disturbance (7.5-11 Hz) in the electroencephalogram (EEG) within non-rapid eye movement (NREM) sleep that accompanies increased nocturnal vigilance and light, unrefreshing sleep. Aspects of cytokine and cellular immune functions are shown to be related to the sleep-wake system.

The evidence suggests a reciprocal relationship of the immune and sleep-wake systems. Interference either with the immune system (e.g. by a viral agent or by cytokines such as alpha-interferon or interleukin 2) or with the sleeping-waking brain system (e.g. by sleep deprivation) has effects on the other system and will be accompanied by the symptoms of the chronic fatigue syndrome.

 

Source: Moldofsky H. Fibromyalgia, sleep disorder and chronic fatigue syndrome. Ciba Found Symp. 1993;173:262-71; discussion 272-9. http://www.ncbi.nlm.nih.gov/pubmed/8491102

 

Isolated diastolic dysfunction of the myocardium and its response to CoQ10 treatment

Abstract:

Symptoms of fatigue and activity impairment, atypical precordial pain, and cardiac arrhythmia frequently precede by years the development of congestive heart failure.

Of 115 patients with these symptoms, 60 were diagnosed as having hypertensive cardiovascular disease, 27 mitral valve prolapse syndrome, and 28 chronic fatigue syndrome. These symptoms are common with diastolic dysfunction, and diastolic function is energy dependent. All patients had blood pressure, clinical status, coenzyme Q10 (CoQ10) blood levels and echocardiographic measurement of diastolic function, systolic function, and myocardial thickness recorded before and after CoQ10 replacement.

At control, 63 patients were functional class III and 54 class II; all showed diastolic dysfunction; the mean CoQ10 blood level was 0.855 micrograms/ml; 65%, 15%, and 7% showed significant myocardial hypertrophy, and 87%, 30%, and 11% had elevated blood pressure readings in hypertensive disease, mitral valve prolapse and chronic fatigue syndrome respectively. Except for higher blood pressure levels and more myocardial thickening in the hypertensive patients, there was little difference between the three groups.

CoQ10 administration resulted in improvement in all; reduction in high blood pressure in 80%, and improvement in diastolic function in all patients with follow-up echocardiograms to date; a reduction in myocardial thickness in 53% of hypertensives and 36% of the combined prolapse and fatigue syndrome groups; and a reduced fractional shortening in those high at control and an increase in those initially low.(ABSTRACT TRUNCATED AT 250 WORDS)

 

Source: Langsjoen PH, Langsjoen PH, Folkers K. Isolated diastolic dysfunction of the myocardium and its response to CoQ10 treatment. Clin Investig. 1993;71(8 Suppl):S140-4. http://www.ncbi.nlm.nih.gov/pubmed/8241699

 

Atrial myxoma: a rare cause of progressive exertional dyspnoea

Abstract:

A 40 year old man suffered eight years of vague but disabling symptoms, initially thought to be related to post viral fatigue syndrome, but ameliorated by the removal of a large atrial myxoma. The diagnosis of atrial myxoma is notoriously difficult, but should be excluded by echocardiography if there are predominant symptoms of progressive exertional dyspnoea, even in the absence of cardiological signs.

 

Source: Gray JB, Bridges AB, McNeill GP. Atrial myxoma: a rare cause of progressive exertional dyspnoea. Scott Med J. 1992 Dec;37(6):186-7. http://www.ncbi.nlm.nih.gov/pubmed/1492217

 

Fatigue syndromes: new thoughts and reinterpretation of previous data

Abstract:

Recently, the author has identified 19 patients who have complained of marked fatigue that had abnormal responses to copper test bracelets or necklaces. At this time, 8 have been shown to have at least one enzyme deficiency in the heme pathway. These patients have been diagnosed with multiple sclerosis, chronic fatigue syndrome and other non-specific diagnoses. A lengthy but still limited review of the literature was performed regarding the following conditions: multiple sclerosis (MS), hepatic porphyria (HP), chronic fatigue syndrome (CFS) and paralytic polio (PP). The text will focus on similar epidemiologies, laboratory findings and clinical courses. Copper as a common but not unique etiologic agent will be discussed; as will the heme pathway, a biologic process that may be disordered in all.

 

Source: Downey DC. Fatigue syndromes: new thoughts and reinterpretation of previous data. Med Hypotheses. 1992 Oct;39(2):185-90. http://www.ncbi.nlm.nih.gov/pubmed/1461185

 

Rheumatic fever and disorders of the musculoskeletal system

Abstract:

New information provided on the pathogenesis and management of rheumatic fever is of current interest. Invasive disease by group A streptococci has been shown to be due to production of toxin A. The natural history and immunopathologic basis for chronic Lyme arthritis are reported. Attention is drawn to pyomyositis and clinical presentation of chronic fatigue syndrome in children. Patients with Sweet’s syndrome often have antineutrophil cytoplasmic autoantibodies. Biopsy specimens of panniculitis should be taken to aid treatment. Long-term outcome in chronic osteomyelitis is favorable; recommendations on the rational use of imaging have been reported.

 

Source: Coovadia HM. Rheumatic fever and disorders of the musculoskeletal system. Curr Opin Rheumatol. 1992 Oct;4(5):718-24. http://www.ncbi.nlm.nih.gov/pubmed/1419508

 

Fibromyalgia, chronic fatigue, and myofascial pain syndromes

Abstract:

During the past year many studies have been published on fibromyalgia and chronic fatigue syndromes. Randomized clinical trials using current operational diagnostic criteria were reported, but no single therapy has been highly effective in either condition. The working case definition of chronic fatigue syndrome has been criticized and suggestions for a new case definition have been made. Further understanding of the overlap of these three common disorders will also require that uniform diagnostic criteria be tested in chronic fatigue syndrome and myofascial pain syndrome.

 

Source: Goldenberg DL. Fibromyalgia, chronic fatigue, and myofascial pain syndromes. Curr Opin Rheumatol. 1992 Apr;4(2):247-57. http://www.ncbi.nlm.nih.gov/pubmed/1581154