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Increased risk of chronic fatigue syndrome following burn injuries.

Murph

:)
Messages
1,799
J Transl Med. 2018 Dec 5;16(1):342. doi: 10.1186/s12967-018-1713-2.
Increased risk of chronic fatigue syndrome following burn injuries.
Tsai SY1,2,3, Lin CL4,5, Shih SC6,7, Hsu CW8,9, Leong KH8,9, Kuo CF10, Lio CF9,11, Chen YT8,9, Hung YJ8,9, Shi L12.
Author information
Abstract

BACKGROUND:
The overlapping symptoms and pathophysiological similarities between burn injury and chronic fatigue syndrome (CFS) are noteworthy. Thus, this study explores the possible association between burn injury and the subsequent risk of CFS.

METHOD:
We used data from the Taiwan National Health Insurance system to address the research topic. The exposure cohort comprised of 17,204 patients with new diagnoses of burn injury. Each patient was frequency matched according to age, sex, index year, and comorbidities with four participants from the general population who did not have a history of CFS (control cohort). Cox proportional hazards regression analysis was conducted to estimate the relationship between burn injury and the risk of subsequent CFS.

RESULT:
The incidence of CFS in the exposure and control cohorts was 1.61 and 0.86 per 1000 person-years, respectively. The exposure cohort had a significantly higher overall risk of subsequent CFS than did the control cohort (adjusted hazard ratio
 = 1.48, 95% confidence interval [CI] = 1.41-1.56). The risk of CFS in patients with burn injury in whichever stratification (including sex, age, and comorbidity) was also higher than that of the control cohort.

CONCLUSION:
The findings from this population-based retrospective cohort study suggest that thermal injury is associated with an increased risk of subsequent CFS and provided a point of view suggesting burn injuries in sun- exposed areas such as the face and limbs had greater impact on subsequent development of CFS compared with trunk areas. In addition, extensively burned areas and visible scars were predictors of greater physiological and psychosocial that are needed to follow-up in the long run.

KEYWORDS:
Burn; Chronic fatigue syndrome; Immune system diseases; National health programs; Thermal injury

PMID:
30518392
DOI:
10.1186/s12967-018-1713-2
 

alex3619

Senior Member
Messages
13,810
Location
Logan, Queensland, Australia
We already know this cause. Its a complex epigenetic response. Burn victims are much like sepsis victims, and CFS, and potentially strictly defined ME, involves very similar epigenetic changes. Its an emergency response, the energy metabolism is shunted from general function toward the immune system. I expect to see a lot more research on this for ME in the next few years now that we know this. This research was expected.

This is why some researchers are saying that ME is chronic sepsis.

Most life threatening events can induce a similar change. In ME is usually viral, but it can be from any major damaging event. In some cases this does not switch off. That failure is in many cases a basis for ME. Its also not really understood yet. What is driving it to fail to restore to normal? Asking that question is where some of the research is looking right now, including Stanford and I think Harvard.
 

uglevod

Senior Member
Messages
220
There is a so called "sepsis"(basically endotoxin levels in blood) and there is an immune response to it, since endotoxin stimulates immune system via TLR receptors(LPS is an TLR ligand) and TLR expression is directly dependent on the vit D levels: https://www.ncbi.nlm.nih.gov/pubmed/23875738
Burn injury -> vit D drop(or already a low level) -> over-stimulation of immune system with endotoxin -> critical health condition(organ failure)

Thats why D3 supplement can help(not always) with both sepsis condition and burn injury condition(by suppressing immune system).
 
Last edited:

alex3619

Senior Member
Messages
13,810
Location
Logan, Queensland, Australia
There is a so called "sepsis"(basically endotoxin levels in blood) and there is an immune response to it, since endotoxin stimulates immune system via TLR receptors(LPS is an TLR ligand) and TLR expression is directly dependent on the vit D levels:
New research suggests this explanation is wrong. During the first day of sepsis the expressed gene profile totally changes. Its an entire epigenetic rewrite. The immune system, and toxins, might trigger sepsis, but the actual disorder is due to the body shifting to a very different genetic profile, in order to cope with a life threatening emergency. The problem, from our perspective, is not that we have a sepsis like condition, but that after the threat is gone the response remains. Similar findings are made in burns and cancer patients.

Many of us take vitamin D from low doses to insane doses. None have recovered that I am aware of, though I do not doubt that random or unknown factors might result in some rare recoveries during many different treatments, including vitamin D. Some of us probably do need vitamin D but we need to be cautious.

Another confounding factor is that many of us are prescribed vitamin D due to the test for inactive vitamin D. This is quite often a serious mistake. Inflammation and other changes trigger vitamin D activation in ME patients, leading to very high levels of active vitamin D. The active form is frequently not tested for. Hyperactivation of vitamin D leads to a depletion of the inactive form, which doctors react to. In ME both active and inactive forms of vitamin D need to be tested. The same goes for any inflammatory state.