Tag: lymphadenopathy

Chronic fatigue syndrome, exercise, cortisol and lymphadenopathy

Dear Sir,

As in the past [1], the effects of exercise in the treatment of chronic fatigue syndrome (CFS) are conflicting. Indeed, while Powell et al. [2], in 2004, reported that graded exercise was beneficial to CFS patients, Black et al. [3] have lately written that ‘overall mood, muscle pain intensity, and time spent each day with fatigue worsened following increased activity’ [3] in CFS patients, despite the fact that their increase in daily physical activity was rather moderate (28%) [3]. The virtually opposite effects of exercise in different groups of CFS patients [1–3] may reflect their different cortisol levels [1], which, just as occurred some years ago [1], continue to be contradictory. For example, Inder et al. [4], in March 2005, reported that cortisol levels were normal in their patients with CFS, whereas Segal et al. [5], in the same month, reported that their subjects with CFS had hypocortisolism.

Considering that most features of CFS, such as ‘debilitating fatigue, an abrupt onset precipitated by a stressor, feverishness, arthralgias, myalgias, adenopathy, postexertional fatigue, exacerbation of allergic responses, and disturbances in mood and sleep are all characteristic of glucocorticoid insufficiency’ [6], it is not surprising that hypocortisolism has been convincingly shown to be implicated in the pathophysiology of CFS [7]. Therefore, especially the postexertional fatigue caused by glucocorticoid insufficiency [6] strongly suggests that exercise could be of benefit to CFS patients with high [1] or normal cortisol levels [4], whereas it could be harmful to CFS patients with hypocortisolism [1, 5, 6]. Unfortunately, because of the misleading coexistence of quite different diagnostic criteria for CFS [1], it is difficult to predict the patients with CFS who are more likely to have hypocortisolism and which would worsen with exercise. However, it is arguable that the presence or absence of lymphadenopathy [8], which is a sign of hypocortisolism [6, 9] and is one of the 43 clinical features that CFS shares with Addison’s disease [10–12], could reliably discriminate CFS patients who may worsen with exercise from those who may improve with it. Indeed, lymphadenopathy, unlike other symptoms of CFS [11, 12], many of which are non-specific and can also be found in depression and other affective disorders [11, 12], is far from being common in physical diseases and is absent in psychiatric conditions.

You can read the rest of this comment here: http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2796.2005.01526.x/full

 

Source: Baschetti R. Chronic fatigue syndrome, exercise, cortisol and lymphadenopathy. J Intern Med. 2005 Sep;258(3):291-2. http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2796.2005.01526.x/full (Full article)

 

Phantom lymphadenopathy. An association with chronic fatigue syndrome

Comment on: Phantom lymphadenopathy. An association with chronic fatigue syndrome. [Postgrad Med J. 2003]

 

Shee reports an association between chronic fatigue syndrome (CFS) and what he regards as a “phantom lymphadenopathy”.1 However, his failure to observe “true lymphadenopathy” in patients with CFS complaining of swollen lymph glands does not exclude a real, albeit subclinical enlargement of those glands, because he did not compare their dimensions with the ones that were measurable before the appearance of patients’ complaints.

As someone who suffered from CFS and reported on its dramatic resolution thanks to old and new drugs for Addison’s disease,2 I clearly remember that my lymph nodes, just a few days after the abrupt onset of CFS, became mildly painful and began to swell gradually. This slow process of enlargement lasted approximately one month. However, even when my lymph glands stopped swelling further (but continued to be mildly painful), their dimensions were still clinically within normal limits. This may indirectly explain why Shee found that “careful examination did not confirm lymphadenopathy” in CFS patients with “self diagnosed enlarged lymph glands”.

You can read the rest of this comment here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1742656/pdf/v079p00185a.pdf

 

Source: Baschetti R. Phantom lymphadenopathy. An association with chronic fatigue syndrome. Postgrad Med J. 2003 Mar;79(929):185. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1742656/ (Full article)

 

Phantom lymphadenopathy. An association with chronic fatigue syndrome

Abstract:

Ten patients with self diagnosed enlarged lymph glands were referred to a general medicine outpatient clinic and careful examination did not confirm lymphadenopathy. All patients also complained of severe chronic fatigue associated with aches and miscellaneous somatic symptoms, and fulfilled criteria for diagnosis of chronic fatigue syndrome (CFS). Phantom lymphadenopathy may be a symptom in some people with CFS, and possible reasons for this are discussed.

Comment in: Phantom lymphadenopathy. An association with chronic fatigue syndrome. [Postgrad Med J. 2003]

 

Source: Shee CD. Phantom lymphadenopathy. An association with chronic fatigue syndrome. Postgrad Med J. 2003 Jan;79(927):59-60. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1742587/ (Full article)

 

A computational analysis of Canale-Smith syndrome: chronic lymphadenopathy simulating malignant lymphoma

Abstract:

OBJECTIVE: The objective of this study was to simulate changes in the human T cell system representing Canale-Smith syndrome using a dynamic computer model of T cell development and comparing with available human data.

STUDY DESIGN: Physiological stepwise maturation and function of T lymphocytes in the computer model is altered by introducing functional disturbances following lymphotropic virus infection. In the present model, acute and chronic persistent infection with the human herpesvirus-6 (HHV-6) was simulated, and ensuing changes in T cell populations were compared with those measured in human patients.

RESULTS: Using our computer model we previously found that simulated acute HHV-6 infection produced T cell computer data, which resembled an infectious mononucleosis-like disease in patients. Simulated chronic persistent infection, instead, resulted in variable cell changes comparing well to patients with chronic fatigue syndrome. In one setting, however, persistent immature lymphocytosis was observed similar to what initial has been described in this journal as Canale-Smith syndrome.

CONCLUSION: Using a computer model developed by us we were able to produce simulations that resemble the immune system features of Canale-Smith syndrome. Further understanding of these simulation results may possibly guide future investigations into this disorder.

 

Source: Krueger GR, Brandt ME, Wang G, Berthold F, Buja LM. A computational analysis of Canale-Smith syndrome: chronic lymphadenopathy simulating malignant lymphoma. Anticancer Res. 2002 Jul-Aug;22(4):2365-71. http://www.ncbi.nlm.nih.gov/pubmed/12174928

 

The existence of a fatigue syndrome after glandular fever

Abstract:

This prospective cohort study was designed to test whether a distinct fatigue syndrome existed after the onset of glandular fever.

Two hundred and fifty primary care patients, with either glandular fever or an ordinary upper respiratory tract infection (URTI) were interviewed three times in the 6 months after the clinical onset of their infection. At each interview a standardized psychiatric interview was given and physical symptoms were assessed. There were 108 subjects with and Epstein-Barr virus (EBV) infection; 83 subjects had glandular fever not caused by EBV and 54 subjects had an ordinary URTI. Five subjects were excluded because they had no evidence of an infection.

Principal components analyses of symptoms supported the existence of a fatigue syndrome, particularly in the two glandular fever groups. The addition of symptoms not elicited by the standard interviews gave the full syndrome. This included physical and mental fatigue, excessive sleep, psychomotor retardation, poor concentration, anhedonia, irritability, social withdrawal, emotional lability, and transient sore throat and neck gland swelling with pain. A fatigue syndrome probably exists after glandular fever.

 

Source: White PD, Thomas JM, Amess J, Grover SA, Kangro HO, Clare AW. The existence of a fatigue syndrome after glandular fever. Psychol Med. 1995 Sep;25(5):907-16. http://www.ncbi.nlm.nih.gov/pubmed/8588009

 

Low grade pyrexia: is it chronic fatigue syndrome?

Abstract:

Eighty seven consecutive patients presenting with prolonged low grade pyrexia (99 degrees-101 +/- F) during 1984-93 were followed up for a mean duration of 2.9 years. Mean age was 37.55 years (SD + 10.16) and 66 (75.8%) were females. Onset of pyrexia was acute in 57 patients and was associated with chilly sensation (42), Fatigue (69), Arthralgias (61), myalgias (55) and several other non specific symptoms. Clinical examination showed paucity of physical signs with 7 patients showing tender lymphadenopathy, 7 showing splenomegaly, 5 hepatomegaly, and 1 phylctenular conjunctivitis. Psychiatric examination was within normal limits. Extensive investigations for any viral or other infection, autoimmune disorder or malignancy were unrewarding. Patients were followed up for an average of 2.9 (2 to 5 years). Thirteen patients had become asymptomatic within one year of onset of symptoms, 38 by two years and 45 by the end of three years. This syndrome may be a variant of chronic fatigue syndrome.

Comment in: Low grade pyrexia: is chronic fatigue syndrome a safe and justified diagnosis? [J Assoc Physicians India. 1995]

 

Source: Anand AC, Kumar R, Rao MK, Dham SK. Low grade pyrexia: is it chronic fatigue syndrome? J Assoc Physicians India. 1994 Aug;42(8):606-8. http://www.ncbi.nlm.nih.gov/pubmed/7868552

 

Gender differences in patients with chronic fatigue syndrome

Abstract:

OBJECTIVE: To determine whether there are differences between men and women patients who have chronic fatigue syndrome (CFS) and, if so, to ascertain whether a gender-related pattern exists.

DESIGN: A descriptive study of demographic, clinical, and psychosocial measures, the results of which were prospectively collected for patients who had CFS.

SETTING: A university-based referral clinic devoted to the evaluation and management of chronic fatigue.

PATIENTS: 348 CFS patients who had undergone complete medical evaluations.

MEASURES: Clinical variables included symptoms, physical examination findings, and laboratory results. Psychosocial assessment consisted of a structured psychiatric interview, the Medical Outcomes Study Short-form General Health Survey to assess functional status, the General Health Questionnaire to ascertain psychological distress, the Multidimensional Health Locus of Control, and measures of attribution, social support, and coping.

MAIN RESULTS: Overall, few gender-related differences were identified. Women had a higher frequency of tender or enlarged lymph nodes (60% versus 33%, p < or = 0.01) and fibromyalgia (36% versus 12%, p < or = 0.001) and lower scores on the physical functioning subscale of the Medical Outcomes Study Short-form General Health Survey (37.6 versus 52.2, p < 0.01); men more often had pharyngeal inflammation (42% versus 22%, p < or = 0.001) and reported a higher lifetime prevalence of alcoholism (20% versus 9%, p < or = 0.01).

CONCLUSIONS: In general, demographic, clinical, and psychosocial factors do not distinguish men from women CFS patients.

 

Source: Buchwald D, Pearlman T, Kith P, Schmaling K. Gender differences in patients with chronic fatigue syndrome. J Gen Intern Med. 1994 Jul;9(7):397-401. http://www.ncbi.nlm.nih.gov/pubmed/7931750

 

Postinfectious chronic fatigue syndrome: case history of thirty-five patients in Germany

Abstract:

Thirty-five patients with chronic fatigue syndrome according to the criteria of Holmes were followed for periods of up to eight years. The most frequent symptoms were severe fatigue, arthralgias and myalgias, recurrent oropharyngitis and various psychiatric disorders.

More than half of the patients suffered from neuropathy, lymphadenopathy, gastrointestinal complaints and recurrent low-grade fever. Recurrent or persistent activity of human herpesvirus -6 infection was seen in 73% of the patients and of Epstein-Barr virus in 34.4%. In addition, various other infections were diagnosed at lower frequency.

Initial routine immunologic screening revealed various types of deficiencies, these were yet inconsistent and variable when different patients were compared with each other. Tentative treatments included in immunoglobulins, nonspecific immunostimulation and virostatic drugs. No consistently positive results were obtained with any treatment schedule although immunoglobulins appeared the most efficient measure. In addition, psychologic care of the patients is indicated, since disturbances in the psycho-neuroimmunologic regulation may play a significant role in the pathogenesis of the disease.

 

Source: Hilgers A, Krueger GR, Lembke U, Ramon A. Postinfectious chronic fatigue syndrome: case history of thirty-five patients in Germany. In Vivo. 1991 May-Jun;5(3):201-5. http://www.ncbi.nlm.nih.gov/pubmed/1893076

 

Chronic fatigue syndrome in northern Nevada

Abstract:

The clinical and laboratory findings from studies of patients with chronic fatigue syndrome (CFS) from northern Nevada are summarized. Physicians caring for these patients have estimated that greater than 400 patients with CFS from northern Nevada and nearby communities in California were identified between 1984 and 1988.

As a result of these studies, a cluster of clinical and laboratory features associated with the illness in moderately to severely affected patients has been identified: profound fatigue of prolonged duration; cervical lymphadenopathy; recurrent sore throat and/or symptoms of influenza; loss of cognitive function manifested by loss of memory and loss of ability to concentrate; myalgia; impairment of fine motor skills; abnormal findings on magnetic resonance imaging brain scan; depressed level of antibody to Epstein-Barr virus (EBV) nuclear antigen; elevated level of antibody to EBV early antigen restricted component; elevated ratio of CD4 helper to CD8 suppressor cells; and strong evidence of association of this syndrome with infection with human herpesvirus 6.

More-serious and longer-lasting neurologic impairments, including seizures, psychosis, and dementia, have also been observed in some of these patients.

 

Source: Daugherty SA, Henry BE, Peterson DL, Swarts RL, Bastien S, Thomas RS. Chronic fatigue syndrome in northern Nevada. Rev Infect Dis. 1991 Jan-Feb;13 Suppl 1:S39-44. http://www.ncbi.nlm.nih.gov/pubmed/1850542

 

A chronic “postinfectious” fatigue syndrome associated with benign lymphoproliferation, B-cell proliferation, and active replication of human herpesvirus-6

Abstract:

A 17-year-old, previously healthy woman developed an acute “mononucleosis-like” illness with an associated “atypical” pneumonitis, followed by years of debilitating chronic fatigue, fevers, a 10-kg weight loss, night sweats, and neurocognitive symptoms. Thereafter, her sister developed a similar but less severe illness.

The patient developed marked, chronic lymphadenopathy and splenomegaly, with associated persistent relative lymphocytosis and atypical lymphocytosis and with thrombocytopenia. After 3 years of illness, a splenectomy was performed, which resulted in some symptomatic improvement, prompt weight gain, and resolution of all hematologic abnormalities. Serial immunologic studies revealed a strikingly elevated number of activated B lymphocytes and a T lymphopenia, which improved but did not return to normal postsplenectomy. No causal association was found with any of several infectious agents that could produce such a lymphoproliferative illness.

However, both the patient and her sister had evidence of active infection with the recently discovered human herpesvirus-6. Seven years after the onset of the illness, the patient and her sister remain chronically ill.

 

Source:  Buchwald D, Freedman AS, Ablashi DV, Sullivan JL, Caligiuri M, Weinberg DS, Hall CG, Ashley RL, Saxinger C, Balachandran N, et al. A chronic “postinfectious” fatigue syndrome associated with benign lymphoproliferation, B-cell proliferation, and active replication of human herpesvirus-6. J Clin Immunol. 1990 Nov;10(6):335-44. http://www.ncbi.nlm.nih.gov/pubmed/1964694