Peripheral Levels of Selected Biomarkers in Patients with Post-Sarcoidosis Chronic Fatigue Syndrome, 2025, Małujło-Balcerska et al

[forestglip]

Peripheral Levels of Selected Biomarkers in Patients with Post-Sarcoidosis Chronic Fatigue Syndrome

Spoiler: Authors

Małujło-Balcerska, Elżbieta; Bączek, Karol; Górski, Witold; Kumor-Kisielewska, Anna; Gwadera, Łukasz; Białas, Adam; Piotrowski, Wojciech

[Line breaks added]

Introduction
Chronic fatigue syndrome (CFS) is characterized by persistent fatigue and multiple symptoms such as cognitive impairment and muscle pain, often linked to immune-inflammatory dysfunction. Sarcoidosis, a granulomatous disease with systemic inflammation, commonly causes fatigue, even during remission.

This study examined whether fatigue and depressive symptoms in sarcoidosis remission relate to residual inflammation or oxidative stress. Recent studies highlight parallels between post-infectious fatigue syndromes, including Long COVID, and sarcoidosis-related fatigue, emphasizing IL-6 mediated pathways.

Theoretical frameworks of immune–metabolic interactions further support the hypothesis that residual inflammation drives persistent fatigue in remission.

Materials and methods
Seventy-one sarcoidosis patients were divided into three groups: remission with fatigue (RS/CFS, n=22), remission without fatigue (R/S, n=23), and active sarcoidosis (A/S, n=26).

Fatigue was assessed with the Fatigue Assessment Scale (FAS), depressive symptoms with the Beck Depression Inventory (BDI), and quality of life with PHQ-9. Pulmonary function tests measured FEV1 and FVC. Serum biomarkers (hsCRP, IL-6, TNF-α, total antioxidant status, and 8-isoprostanes) were measured by ELISA.

Results
RS/CFS and A/S groups showed significantly higher fatigue, and depressive scores compared to R/S (P < 0.05).

HsCRP and IL-6 levels were elevated in fatigued patients (RS/CFS and A/S) versus non-fatigued (R/S) (P < 0.05). IL-6 correlated moderately with fatigue and depression scores (r =0.33). No significant differences were found in TNF-α or oxidative stress markers.

Pulmonary function was slightly reduced in fatigued patients and weakly correlated with mental fatigue (r = – 0.26).

Conclusion: Our data support a role for low-grade systemic inflammation, especially elevated hsCRP and IL-6, in fatigue and depressive symptoms during sarcoidosis remission. Further research integrating inflammatory, oxidative, metabolic, and neuroendocrine pathways is needed to elucidate fatigue pathogenesis and develop targeted interventions.

IL-6 may represent a potential biomarker of fatigue in sarcoidosis. These findings highlight the importance of persistent low-grade inflammation and may guide the development of future therapeutic strategies.

Web | DOI | PDF | Journal of Inflammation Research | Open Access

 

[forestglip]

I didn't put this in the ME/CFS forum because their definition of CFS is just high fatigue:

The diagnosis of CFS was based on a Fatigue Assessment Scale score ≥22, after systematic exclusion of alternative causes of fatigue (eg, thyroid dysfunction, anaemia, ongoing infection).

 

[V.R.T.]

Peripheral Levels of Selected Biomarkers in Patients with Post-Sarcoidosis Chronic Fatigue Syndrome

Spoiler: Authors

Małujło-Balcerska, Elżbieta; Bączek, Karol; Górski, Witold; Kumor-Kisielewska, Anna; Gwadera, Łukasz; Białas, Adam; Piotrowski, Wojciech

[Line breaks added]

Introduction
Chronic fatigue syndrome (CFS) is characterized by persistent fatigue and multiple symptoms such as cognitive impairment and muscle pain, often linked to immune-inflammatory dysfunction. Sarcoidosis, a granulomatous disease with systemic inflammation, commonly causes fatigue, even during remission.

This study examined whether fatigue and depressive symptoms in sarcoidosis remission relate to residual inflammation or oxidative stress. Recent studies highlight parallels between post-infectious fatigue syndromes, including Long COVID, and sarcoidosis-related fatigue, emphasizing IL-6 mediated pathways.

Theoretical frameworks of immune–metabolic interactions further support the hypothesis that residual inflammation drives persistent fatigue in remission.

Materials and methods
Seventy-one sarcoidosis patients were divided into three groups: remission with fatigue (RS/CFS, n=22), remission without fatigue (R/S, n=23), and active sarcoidosis (A/S, n=26).

Fatigue was assessed with the Fatigue Assessment Scale (FAS), depressive symptoms with the Beck Depression Inventory (BDI), and quality of life with PHQ-9. Pulmonary function tests measured FEV1 and FVC. Serum biomarkers (hsCRP, IL-6, TNF-α, total antioxidant status, and 8-isoprostanes) were measured by ELISA.

Results
RS/CFS and A/S groups showed significantly higher fatigue, and depressive scores compared to R/S (P < 0.05).

HsCRP and IL-6 levels were elevated in fatigued patients (RS/CFS and A/S) versus non-fatigued (R/S) (P < 0.05). IL-6 correlated moderately with fatigue and depression scores (r =0.33). No significant differences were found in TNF-α or oxidative stress markers.

Pulmonary function was slightly reduced in fatigued patients and weakly correlated with mental fatigue (r = – 0.26).

Conclusion: Our data support a role for low-grade systemic inflammation, especially elevated hsCRP and IL-6, in fatigue and depressive symptoms during sarcoidosis remission. Further research integrating inflammatory, oxidative, metabolic, and neuroendocrine pathways is needed to elucidate fatigue pathogenesis and develop targeted interventions.

IL-6 may represent a potential biomarker of fatigue in sarcoidosis. These findings highlight the importance of persistent low-grade inflammation and may guide the development of future therapeutic strategies.

Web | DOI | PDF | Journal of Inflammation Research | Open Access

There was an IL-6 finding and drug study in Long Covid was there not?

The drug was called something like Tocilzumab...

 

[Verity]

There was someone on this forum who had sarcoidosis who said post-sarcoidosis fatigue can actually look ME-like. Wish they’d used better criteria here because it would be interesting to see a group of patients like that.

 

[richie]

There was someone on this forum who had sarcoidosis who said post-sarcoidosis fatigue can actually look ME-like. Wish they’d used better criteria here because it would be interesting to see a group of patients like that.

May have been me. CS or another ME Assoc Rep has met up with some sarkies and was impressed by the degree of similarity between PEM as reported in ME/CFS and post exertional fatigue reported by current sarkies. Post sarc fatigue is certainly debilitating and may be accompanied by myalgias so it is at least colloquially ME like and puzzling as to cause, though TH1 skewing and low cortisol may be implicated. I have probed sarc sufferers on therir PEF and what they go through is certainly a profoundly disturbing phenomenon in terms of low battery, long charge time. quick discharge and stuffing knocked out after little exertion. My personal experience over 40 years is hard to assess as it may have involved sarc, tick borne infections and what I call Teitelbaum's Kitchen sink ME (so many things could be involved). Sarc itself may be a manifestation of persistent infection in some cases and commonly accompanying anergy may open sufferers to many infections which then poses the question as to whether the a symptom flare isn sarcoid or a manifestation of an infection in sb with sarcoid which may or may not be the occasion of further sarcoid. For many the fatigue of sarc is nightmarish and the post sarc syndrome can be life changing.

 

[richie]

Peripheral Levels of Selected Biomarkers in Patients with Post-Sarcoidosis Chronic Fatigue Syndrome

Spoiler: Authors

Małujło-Balcerska, Elżbieta; Bączek, Karol; Górski, Witold; Kumor-Kisielewska, Anna; Gwadera, Łukasz; Białas, Adam; Piotrowski, Wojciech

[Line breaks added]

Introduction
Chronic fatigue syndrome (CFS) is characterized by persistent fatigue and multiple symptoms such as cognitive impairment and muscle pain, often linked to immune-inflammatory dysfunction. Sarcoidosis, a granulomatous disease with systemic inflammation, commonly causes fatigue, even during remission.

This study examined whether fatigue and depressive symptoms in sarcoidosis remission relate to residual inflammation or oxidative stress. Recent studies highlight parallels between post-infectious fatigue syndromes, including Long COVID, and sarcoidosis-related fatigue, emphasizing IL-6 mediated pathways.

Theoretical frameworks of immune–metabolic interactions further support the hypothesis that residual inflammation drives persistent fatigue in remission.

Materials and methods
Seventy-one sarcoidosis patients were divided into three groups: remission with fatigue (RS/CFS, n=22), remission without fatigue (R/S, n=23), and active sarcoidosis (A/S, n=26).

Fatigue was assessed with the Fatigue Assessment Scale (FAS), depressive symptoms with the Beck Depression Inventory (BDI), and quality of life with PHQ-9. Pulmonary function tests measured FEV1 and FVC. Serum biomarkers (hsCRP, IL-6, TNF-α, total antioxidant status, and 8-isoprostanes) were measured by ELISA.

Results
RS/CFS and A/S groups showed significantly higher fatigue, and depressive scores compared to R/S (P < 0.05).

HsCRP and IL-6 levels were elevated in fatigued patients (RS/CFS and A/S) versus non-fatigued (R/S) (P < 0.05). IL-6 correlated moderately with fatigue and depression scores (r =0.33). No significant differences were found in TNF-α or oxidative stress markers.

Pulmonary function was slightly reduced in fatigued patients and weakly correlated with mental fatigue (r = – 0.26).

Conclusion: Our data support a role for low-grade systemic inflammation, especially elevated hsCRP and IL-6, in fatigue and depressive symptoms during sarcoidosis remission. Further research integrating inflammatory, oxidative, metabolic, and neuroendocrine pathways is needed to elucidate fatigue pathogenesis and develop targeted interventions.

IL-6 may represent a potential biomarker of fatigue in sarcoidosis. These findings highlight the importance of persistent low-grade inflammation and may guide the development of future therapeutic strategies.

Web | DOI | PDF | Journal of Inflammation Research | Open Access

Markers of immune disturbance have been found up to 27 yrs before sarc diagnosis in a Swedish study. Numerous sarkies will say they ahve felt unwell for years and it makes me wonder if this is rooted in pre sarc phenomena.

 

[Verity]

May have been me. CS or another ME Assoc Rep has met up with some sarkies and was impressed by the degree of similarity between PEM as reported in ME/CFS and post exertional fatigue reported by current sarkies.

I believe it was you! I recognize your username. That is very interesting. I hope whatever helps one group will end up helping the other.

 

[richie]

I believe it was you! I recognize your username. That is very interesting. I hope whatever helps one group will end up helping the other.

Quite a few sarcoid sufferers are being given a CFS diagnosis but as if it were an alternative cause for fatigue , which is questionable, or on the other hand as if it were merely a list of symptoms and if you have then you can pile in, with aetiologies counting for little of anything. It's problematic either way, but , as you say , overlap and exchange may help and sarc doctors do not know what to do about many of the ME like symptoms. Interestingly small fibre neuropathy is a frequent guest at the sarcoid table and that a can also present with vexing non specifics. Recent findings on circulating mitochondrial DNA have shown up similarities between sarc and ME but 2 day CPET results on sarc do not show 2nd day decline unlike some ME sufferers. Seen nothing on post sarc with regard to any CPET testsing.