Coincidental Splenectomy in Chronic Fatigue Syndrome (2011) Miller Et. Al

Sustained 20 years, zero citations. Zero.

“A unique case of coincidental splenectomy for trauma during chronic fatigue syndrome (CFS) is presented. The patient had a two-year history of CFS prior to her involvement in a road crash. Delayed rupture of the spleen ten days later necessitated urgent laparotomy. At operation, the splenic parenchyma was spongy and friable. Splenorrhaphy was considered inadvisable and a splenectomy was performed. Histological examination of the spleen revealed chronic inflammatory changes of uncertain etiology. One year post-operatively, the patient recovered from her CFS symptoms and returned to work. These histopathological changes in the spleen of a patient with CFS have not been described before.”

 

I have often thought it odd that in these days when people seem to have scans for all sorts of reasons, after almost forty years with a spleen, probably enlarged, and continuously making its presence known, no doctor has seemed vaguely interested.

 

This is curious, but I suspect it reflects lack of specificity of the CFS diagnosis, rather than a common cause amongst patients. But then you wonder, how many patients could this apply to?

 

I have a strange feeling (lots of them!) but something I read recently makes me wonder if it is an enlarged spleen. I'm never going to know as I can't bear the thought of visiting a doctor and risking hurt and humiliation, just told my family to mention it if I am in a car crash.

I doubt it is a cause of ME but could be a consequence.

 

Presumably the spleens were examined in the few autopsies of patients who died from ME?

 

Has anyone seen the text of the paper?

The abstract mentions chronic inflammatory change but in the spleen that is pretty meaningless. The spleen is normal full of inflammatory cells - that is where half of them normally live. If the spleen had been traumatised ten days earlier you would expect it to be a mess with structural damage and neutrophil accumulation.

To be honest I am not sure what they are supposed to have found that was not consistent with a car crash?

 

Sci hub link, https://sci-hub.se/10.1300/J092v04n01_05

 

Indeed, I didn't read this bit of the paper:

 

It's a very odd and perfunctory report. Large atypical T lymphoblasts do not sound much like inflammation. I wonder if by chance there was a low grade local T lymphoproliferative disorder, although T cell lymphoproliferation is rarely benign.

One wonders why a more extensive formal pathology report was not provided.

I don't think one report of some odd cells like this helps us understand ME.

 

Splenectomy in general lowers immune reservoir for B-cell production and is a focal point for herpes virus infections. It is not just general immunstimulation due to a viral infection as shown in acute splenomegaly. These cells are co-localized with cytochromes with are modulated by that by a viral infection, which would cause variations in metabolism of drugs, which should be intuitive acutely. But more specifically, ebv actually integrates with these cells and changes their morphology permanently beyond acute illness.

When you remove the tonsils of a person with psoriasis, it sometimes cures the skin lesions because it is a systemic reaction to latent staph within the tonsils.

One is to not draw hasty conclusions from the single paper but I can explain specifically why it is relevant and draw parallels.

One argument is that even a pilot trial of splenectomy is pretty harsh or even a biopsy - it is not for young people - pro athletes return to sports after Splenectomy with no sequelae.