Category: Overlapping Illnesses

A case of femoral arteriovenous fistula causing high-output cardiac failure, originally misdiagnosed as chronic fatigue syndrome

Abstract:

Percutaneous arterial catheterisation is commonly undertaken for a range of diagnostic and interventional procedures. Iatrogenic femoral arteriovenous fistulas are an uncommon complication of these procedures. Most are asymptomatic and close spontaneously, but can rarely increase in size leading to the development of symptoms. We report a case of an iatrogenic femoral arteriovenous fistula, causing worsening congestive cardiac failure, in a 34-year-old marathon runner. This was originally diagnosed as chronic fatigue syndrome. Following clinical examination, duplex ultrasound, and CT angiography a significant arteriovenous fistula was confirmed. Elective open surgery was performed, leading to a dramatic and rapid improvement in symptoms. Femoral arteriovenous fistulas have the potential to cause significant haemodynamic effects and can present many years after the initial procedure. Conservative, endovascular, and open surgical management strategies are available.

 

Source: Porter J, Al-Jarrah Q, Richardson S. A case of femoral arteriovenous fistula causing high-output cardiac failure, originally misdiagnosed as chronic fatigue syndrome. Case Rep Vasc Med. 2014;2014:510429. doi: 10.1155/2014/510429. Epub 2014 May 20. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4055063/ (Full article)

 

Lumbar puncture, chronic fatigue syndrome and idiopathic intracranial hypertension: a cross-sectional study

Abstract:

OBJECTIVE: Unsuspected idiopathic intracranial hypertension (IIH) is found in a significant minority of patients attending clinics with named headache syndromes, if it is specifically sought out. Chronic fatigue syndrome is frequently associated with headache. Could the same be true of chronic fatigue? Moreover, there are striking similarities between the two conditions. Could they be related? Attempting to answer these questions, we describe the results of a change in clinical practice aimed at capturing patients with chronic fatigue who might have IIH.

DESIGN: Cross-sectional.

SETTING: Hospital outpatient and radiology departments.

PARTICIPANTS: Patients attending a specialist clinic with chronic fatigue syndrome and headache who had lumbar puncture to exclude raised intracranial pressure.

MAIN OUTCOME MEASURES: Intracranial pressure measured at lumbar puncture and the effect on headache of cerebrospinal fluid drainage.

RESULTS: Mean cerebrospinal fluid pressure was 19 cm H2O (range 12-41 cm H2O). Four patients fulfilled the criteria for IIH. Thirteen others did not have pressures high enough to diagnose IIH but still reported an improvement in headache after drainage of cerebrospinal fluid. Some patients also volunteered an improvement in other symptoms, including fatigue. No patient had any clinical signs of raised intracranial pressure.

CONCLUSIONS: An unknown, but possibly substantial, minority of patients with chronic fatigue syndrome may actually have IIH. An unknown, but much larger, proportion of patients with chronic fatigue syndrome do not have IIH by current criteria but respond to lumbar puncture in the same way as patients who do. This suggests that the two conditions may be related.

 

Source: Higgins N, Pickard J, Lever A. Lumbar puncture, chronic fatigue syndrome and idiopathic intracranial hypertension: a cross-sectional study. JRSM Short Rep. 2013 Nov 21;4(12):2042533313507920. doi: 10.1177/2042533313507920. eCollection 2013. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3899735/ (Full article)

 

A role for homeostatic drive in the perpetuation of complex chronic illness: Gulf War Illness and chronic fatigue syndrome

Erratum in

  • PLoS One. 2014;9(4):e94161.
  • PLoS One. 2014;9(6):e100355.

Abstract:

A key component in the body’s stress response, the hypothalamic-pituitary-adrenal (HPA) axis orchestrates changes across a broad range of major biological systems. Its dysfunction has been associated with numerous chronic diseases including Gulf War Illness (GWI) and chronic fatigue syndrome (CFS). Though tightly coupled with other components of endocrine and immune function, few models of HPA function account for these interactions.

Here we extend conventional models of HPA function by including feed-forward and feedback interaction with sex hormone regulation and immune response. We use this multi-axis model to explore the role of homeostatic regulation in perpetuating chronic conditions, specifically GWI and CFS. An important obstacle in building these models across regulatory systems remains the scarcity of detailed human in vivo kinetic data as its collection can present significant health risks to subjects. We circumvented this using a discrete logic representation based solely on literature of physiological and biochemical connectivity to provide a qualitative description of system behavior. This connectivity model linked molecular variables across the HPA axis, hypothalamic-pituitary-gonadal (HPG) axis in men and women, as well as a simple immune network. Inclusion of these interactions produced multiple alternate homeostatic states and sexually dimorphic responses.

Experimental data for endocrine-immune markers measured in male GWI subjects showed the greatest alignment with predictions of a naturally occurring alternate steady state presenting with hypercortisolism, low testosterone and a shift towards a Th1 immune response. In female CFS subjects, expression of these markers aligned with an alternate homeostatic state displaying hypocortisolism, high estradiol, and a shift towards an anti-inflammatory Th2 activation. These results support a role for homeostatic drive in perpetuating dysfunctional cortisol levels through persistent interaction with the immune system and HPG axis. Though coarse, these models may nonetheless support the design of robust treatments that might exploit these regulatory regimes.

 

Source: Craddock TJ, Fritsch P, Rice MA Jr, del Rosario RM, Miller DB, Fletcher MA, Klimas NG, Broderick G. A role for homeostatic drive in the perpetuation of complex chronic illness: Gulf War Illness and chronic fatigue syndrome. PLoS One. 2014 Jan 8;9(1):e84839. doi: 10.1371/journal.pone.0084839. ECollection 2014. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3885655/ (Full article)

 

Impact of the fibromyalgia in the chronic fatigue syndrome

Abstract:

BACKGROUND AND OBJECTIVE: Different studies have showed association of the chronic fatigue syndrome (CFS) with other pathologies, including fibromyalgia (FM). The objective of this study is to analyze whether there are differences in the clinic and in the assessment of fatigue in CFS patients associated or not with FM.

PATIENTS AND METHODS: A cross-sectional, single-site observational study was undertaken on a consecutive cases of a register of CFS patients at CFS Unit in Vall d’Hebron Hospital, Barcelona, from January 2008 until March 2011. The variables analyzed were FM comorbidity, sleep and fatigue characteristics and cognitive, neurological and autonomic symptoms. Questionnaires of fatigue impact scale, fatigue strength and impact on quality of life SF-36 were evaluated.

RESULTS: We included 980 CFS patients (mean age: 48±9 years; 91% women). Fibromyalgia was present in 528 patients (54%). The level of fatigue (P=.001) and pain (P<.001) was higher in FM patients. Patients with CFS and FM had more prevalence of sleep-related phenomena. The percentage of patients and the degree of severity of cognitive symptoms, neurological and autonomic dysfunction was higher in FM patients (P<.001). FM patients scored higher on the fatigue impact scale (P<.001) and showed worse results in the quality of life questionnaire (P<.001).

CONCLUSIONS: FM co-morbidity worse clinical parameters, fatigue and the perception of quality of life in CFS patients.

Copyright © 2013 Elsevier España, S.L. All rights reserved.

 

Source: Faro M, Sáez-Francàs N, Castro-Marrero J, Aliste L, Collado A, Alegre J. Impact of the fibromyalgia in the chronic fatigue syndrome. Med Clin (Barc). 2014 Jun 16;142(12):519-25. doi: 10.1016/j.medcli.2013.06.030. Epub 2014 Jan 2. [Article in Spanish] https://www.ncbi.nlm.nih.gov/pubmed/24387955

 

Etiology of sicca syndrome in a consecutive series of 199 patients with chronic fatigue syndrome

Dear Sir,

Chronic fatigue syndrome (CFS) is a heterogeneous and multisystemic disorder of unknown pathogenesis and etiology. It is characterized by prolonged generalized and abnormal fatigue post-exercise (98%), recurrent headache (90%) and problems of concentration and memory (85%) that have lasted for at least 6 months. It is accompanied by such other symptoms as tender lymph nodes (80%), musculoskeletal pain (75%) and psychiatric problems (65%).1,2 The prevalence of CFS is estimated to be between 0.5 and 2.5%, predominantly in women (4:1).1,2 Many patients with CFS also complain of sicca symptoms in up to 30–87%, and are more likely to have thyroid disorder and sleep disruption;2,3 that may suggest an underlying role of the immune system in these patients. Primary Sjögren’ syndrome (PSS) is a systemic autoimmune disease, that presents chronic exocrine glands hypofunction leading to xerostomia and/or xerophthalmia, and extraglandular involvement, of which autoimmune hypothyroidism (AIHT) is the most common autoimmune disease developed4. Patients with PSS, also experience CFS-like musculoskeletal and neurocognitive symptoms more than 50%, and the two disorders share some similar immunologic defects.4 The purpose of this study was to determine the causality of sicca symptoms in 199 consecutive patients diagnosed as having CFS, and the possible association with PSS, although few studies that have examined this association (between 2010 and 2012 in our chronic fatigue unit of Joan XXIII University Hospital) according to the Fukuda’ criteria of 1994.

You can read the rest of this article here: http://www.reumatologiaclinica.org/en/etiology-sicca-syndrome-in-consecutive/articulo/S2173574314001075/

 

Source: Qanneta R, Fontova R, Pàmies A. Etiology of sicca syndrome in a consecutive series of 199 patients with chronic fatigue syndrome. Reumatol Clin. 2014 Jul-Aug;10(4):269-70. doi: 10.1016/j.reuma.2013.11.002. Epub 2013 Dec 17. http://www.reumatologiaclinica.org/en/etiology-sicca-syndrome-in-consecutive/articulo/S2173574314001075/ (Full article)

 

Conditions, controversies and contradictions between Central Sensitivity Syndrome and Depressive Disorders

Abstract:

We present a description of the Central Sensitivity Syndrome (CSS) and some of its main components such as Multiple Chemical Sensitivity Syndrome, Chronic Fatigue Syndrome and Fibromyalgia. We review the changes in pain perception, describing the physiology and pathophysiology of the painful experience from the medulla horn to the CNS. We explain the theory of central sensitization as the basis to the syndrome. We refer to the differences between fibromyalgia and depressive disorders, is spite of their frequent presentation in comorbidity.

We state the main clinical and neurobiological differences. We point out the main psychoneuroimmunoendocrinologic differences such as adrenal activity (hypoactivity vs. hyperactivity, DST hypersuppressive response vs. DST non suppression, hypersensitivity of central glucocorticoid receptors vs. desensitization of these, among others), thyroid (probable reverse T3 vs. flat stimuli TSH response curve) and growth hormone secretion (probable increase vs. disruption of normal circadian rhythm) that makes CSS resemble PTSD. We describe differential changes in sleep patterns (alpha-delta intrusion vs. altered sleep time, REM latency, and stage 3/4) and immunological disturbances almost opposite in each pathological entity. We finally argue which medical specialty should treat these complex syndromes.

 

Source: Maresca T, Covini E, Mato AM. Conditions, controversies and contradictions between Central Sensitivity Syndrome and Depressive Disorders.Vertex. 2013 Sep-Oct;24(111):373-91. [Article in Spanish] https://www.ncbi.nlm.nih.gov/pubmed/24312923

 

Myalgic encephalomyelitis/chronic fatigue syndrome and encephalomyelitis disseminata/multiple sclerosis show remarkable levels of similarity in phenomenology and neuroimmune characteristics

Abstract:

BACKGROUND: ‘Encephalomyelitis disseminata’ (multiple sclerosis) and myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) are both classified as diseases of the central nervous system by the World Health Organization. This review aims to compare the phenomenological and neuroimmune characteristics of MS with those of ME/CFS.

DISCUSSION: There are remarkable phenomenological and neuroimmune overlaps between both disorders. Patients with ME/CFS and MS both experience severe levels of disabling fatigue and a worsening of symptoms following exercise and resort to energy conservation strategies in an attempt to meet the energy demands of day-to-day living. Debilitating autonomic symptoms, diminished cardiac responses to exercise, orthostatic intolerance and postural hypotension are experienced by patients with both illnesses.

Both disorders show a relapsing-remitting or progressive course, while infections and psychosocial stress play a large part in worsening of fatigue symptoms. Activated immunoinflammatory, oxidative and nitrosative (O+NS) pathways and autoimmunity occur in both illnesses. The consequences of O+NS damage to self-epitopes is evidenced by the almost bewildering and almost identical array of autoantibodies formed against damaged epitopes seen in both illnesses.

Mitochondrial dysfunctions, including lowered levels of ATP, decreased phosphocreatine synthesis and impaired oxidative phosphorylation, are heavily involved in the pathophysiology of both MS and ME/CFS. The findings produced by neuroimaging techniques are quite similar in both illnesses and show decreased cerebral blood flow, atrophy, gray matter reduction, white matter hyperintensities, increased cerebral lactate and choline signaling and lowered acetyl-aspartate levels.

SUMMARY: This review shows that there are neuroimmune similarities between MS and ME/CFS. This further substantiates the view that ME/CFS is a neuroimmune illness and that patients with MS are immunologically primed to develop symptoms of ME/CFS.

 

Source: Morris G, Maes M. Myalgic encephalomyelitis/chronic fatigue syndrome and encephalomyelitis disseminata/multiple sclerosis show remarkable levels of similarity in phenomenology and neuroimmune characteristics. BMC Med. 2013 Sep 17;11:205. doi: 10.1186/1741-7015-11-205. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3847236/ (Full article)

 

Comorbidity of postural orthostatic tachycardia syndrome and chronic fatigue syndrome in an Australian cohort

Abstract:

OBJECTIVE: Patients with chronic fatigue syndrome (CFS) are frequently diagnosed with comorbid postural orthostatic tachycardia syndrome (POTS), suggesting a shared pathogenesis. The aim of this study was to examine the relationship between demographic characteristics, autonomic functioning and fatigue levels amongst CFS patients with and without comorbid POTS.

DESIGN AND SETTING: All patients presenting to the CFS Discovery Clinic between 2009 and 2012 completed a 20-min standing task as part of their initial assessment. Heart rate and pulse pressure were recorded at baseline, at 2-min intervals poststanding, at the end of the task and following a recovery period. Average heart rate and pulse pressure variability were calculated from this data. Age, gender, length of illness and self-reported fatigue scores were also recorded. POTS patients were diagnosed by an orthostatic increase in heart rate >30 beats per min, concomitant symptoms of orthostatic intolerance and no orthostatic hypotension. Differences in autonomic functioning between POTS and CFS patients were compared using independent samples t-tests, whilst logistic and linear regressions were performed to examine the contribution of autonomic functioning to task completion and perceived fatigue, respectively.

RESULTS:Comorbidity of CFS and POTS (CFS-POTS) was observed in 11% (33/306) of patients. CFS-POTS patients were significantly younger (P < 0.001), had a shorter length of illness (P = 0.034), experienced greater task difficulty (P = 0.002) and were able to stand for significantly shorter periods compared to the CFS-only patients (P < 0.001). CFS-POTS patients experienced significantly lower baseline diastolic blood pressure (P = 0.002), significantly higher heart rate and lower pulse pressures at each standing measurement. Early heart rate changes (P = 0.002) and overall heart rate change (P < 0.001) were significant predictors of completion status, whereas heart rate variability (P < 0.001) and female gender (P < 0.001) were significant predictors of increased perceived task difficulty.

CONCLUSIONS:Haemodynamic and demographic differences between CFS-POTS and CFS-only patients suggest that the former group reflects a distinct subgroup of the CFS population. The findings highlight the utility of screening younger patients with fatigue for POTS, and identified heart rate variability as an important marker of fatigue for CFS patients in general.

© 2013 The Association for the Publication of the Journal of Internal Medicine.

 

Source: Reynolds GK, Lewis DP, Richardson AM, Lidbury BA. Comorbidity of postural orthostatic tachycardia syndrome and chronic fatigue syndrome in an Australian cohort. J Intern Med. 2014 Apr;275(4):409-17. doi: 10.1111/joim.12161. Epub 2013 Nov 29. http://onlinelibrary.wiley.com/doi/10.1111/joim.12161/full (Full article)

 

Biological phenotypes underpin the physio-somatic symptoms of somatization, depression, and chronic fatigue syndrome

Abstract:

OBJECTIVE: Somatization is a symptom cluster characterized by ‘psychosomatic’ symptoms, that is, medically unexplained symptoms, and is a common component of other conditions, including depression and myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). This article reviews the data regarding the pathophysiological foundations of ‘psychosomatic’ symptoms and the implications that this has for conceptualization of what may more appropriately be termed physio-somatic symptoms.

METHOD: This narrative review used papers published in PubMed, Scopus, and Google Scholar electronic databases using the keywords: depression and chronic fatigue, depression and somatization, somatization and chronic fatigue syndrome, each combined with inflammation, inflammatory, tryptophan, and cell-mediated immune (CMI).

RESULTS: The physio-somatic symptoms of depression, ME/CFS, and somatization are associated with specific biomarkers of inflammation and CMI activation, which are correlated with, and causally linked to, changes in the tryptophan catabolite (TRYCAT) pathway. Oxidative and nitrosative stress induces damage that increases neoepitopes and autoimmunity that contribute to the immuno-inflammatory processes. These pathways are all known to cause physio-somatic symptoms, including fatigue, malaise, autonomic symptoms, hyperalgesia, intestinal hypermotility, peripheral neuropathy, etc.

CONCLUSION: Biological underpinnings, such as immune-inflammatory pathways, may explain, at least in part, the occurrence of physio-somatic symptoms in depression, somatization, or myalgic encephalomyelitis/chronic fatigue syndrome and thus the clinical overlap among these disorders.

© 2013 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.

Comment in

Source: Anderson G, Berk M, Maes M. Biological phenotypes underpin the physio-somatic symptoms of somatization, depression, and chronic fatigue syndrome. Acta Psychiatr Scand. 2014 Feb;129(2):83-97. doi: 10.1111/acps.12182. Epub 2013 Aug 17. https://www.ncbi.nlm.nih.gov/pubmed/23952563

 

Kynurenine Pathway Pathologies: do Nicotinamide and Other Pathway Co-Factors have a Therapeutic Role in Reduction of Symptom Severity, Including Chronic Fatigue Syndrome (CFS) and Fibromyalgia (FM)

Abstract:

The definition of dual tryptophan pathways has increased the understanding of the mind-body, body-mind dichotomy. The serotonergic pathway highlights the primary (endogenous) psychiatric disorders. The up-regulation of the kynurenine pathway by physical illnesses can cause neuropathic and immunological disorders1 associated with secondary neuropsychiatric symptoms.

Tryptophan and nicotinamide deficiencies fall within the protein energy malnutrition (PEM) spectrum. They can arise if the kynurenine pathway is stressed by primary or secondary inflammatory conditions and the consequent imbalance of available catabolic/anabolic substrates may adversely influence convalescent phase efficiency. The replacement of depleted or reduced NAD+ levels and other cofactors can perhaps improve the clinical management of these disorders.

Chronic fatigue syndrome (CFS) and fibromyalgia (FM) appear to meet the criteria of a tryptophan-kynurenine pathway disorder with potential neuroimmunological sequelae. Aspects of some of the putative precipitating factors have been previously outlined.2,3 An analysis of the areas of metabolic dysfunction will focus on future directions for research and management.

 

Source: Blankfield A. Kynurenine Pathway Pathologies: do Nicotinamide and Other Pathway Co-Factors have a Therapeutic Role in Reduction of Symptom Severity, Including Chronic Fatigue Syndrome (CFS) and Fibromyalgia (FM). Int J Tryptophan Res. 2013 Jul 21;6(Suppl 1):39-45. doi: 10.4137/IJTR.S11193. Print 2013. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3729338/ (Full article)