Xxiv международная медико-биологическая конференция молодых исследователей Фундаментальная наука и клиническая

ETIOPATHOGENESIS AND SANOGENESIS 
OF CHRONIC FATIGUE SYNDROME
Majetić S., demonstrator
Department of Pathophysiology, School of Medicine, University of Zagreb, 
University Hospital Centre, KBC Rebro, 
Zagreb, Croatia 
Acad. Supervisor: Prof. Z. Kovač, M.D., Ph.D., Chairman of Dept.
Introduction: 
Chronic Fatigue Syndrome (CFS) or Myalgic 
Encephalomyelitis (ME) is defined as persistent fatigue that lasts more 
than 6 months and is not relieved by sleep. CFS affects patients’ physiology 
both physically and cognitively. Physical symptoms are elevated body 
temperature, sleep disorders, headache, myalgia, arthralgia, postexertional 
malaise (PEM) and lymphadenopathy. Cognitive symptoms are “brain fog” 
and forgetfulness. Brain fog refers to a slow thinking, difficulty focusing, 
confusion, lack of concentration, haziness in thought processes. CFS is 
more common in female population, around 40 years of age. Prevalence 
varies 7-38 / 100 000. Etiology is not yet established, but it is assumed 
that long lasting process is in the background and stressful situations are 
triggers. Also, genes may be responsible for this syndrome, but not single 
mutated gene is found, so polygenic inheritance may be in question. 
Methods and materials: 
This overview is based on 8 pubmed 
downloaded papers that included over 600 original papers and researches. 
Papers contain: conclusions based on descriptions of experiments from 
previous researches, original studies, found brain pathology in one patient 
and possible treatment for CFS. 
Results and discussion: 
Several mechanisms may play role in 
etiopathogenesis of CFS/ME. They include inflammation, oxidative 
stress and mitochondrial dysfunction, dysfunction of facilitation 
system, conditioned inhibition system, dysregulation of autonomic 
nervous system, orthostatic hypotension, brain cell death, enzyme 
mutation, metabolic changes and cell acidosis. Oxidative stress can be 
measured though thiobarbituritic acid reactive substances (TBARS) and 
carbonylated proteins. In CFS patients TBARS levels were two times higher 
than in control groups (0,4 nmol/mg in CFS patients and 0,2 nmol/mg 

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in control group; [p<0,001]). Carbonylated proteins were also higher in 
CFS patient (3,18 nmol/mg in CFS patient and 1,78 nmol/mg; [p<0,002]). 
Dysregulation of facilitation system and conditioned inhibition system 
are linked to exposure to excessive stress (or overwork) without enough 
recovery, during lifetime, but also it serves as a trigger to symptomatic 
stage of the disease. This can be explained with the term allostasis. There 
are several candidate markers that can help distinguish possible CFS 
from healthy brain, such as HHV-6, tau protein, phenylalanine, telomere 
attrition, postmortem brain pathology.