ME, Opioid-Antagonist NALOXONE-REVERSIBLE MONOCYTE DYSFUNCTION in CFS:DIRE

by Helen Borel,RN,MFA,PhD

   According to Prieto et al. (1989), reporting in the Scandinavian Journal of Immunology, who studied 35 consecutive patients with CFS:DIRE, 85% showed monocyte dysfunction "characterized by marked reduction in the number of monocytes displaying immuno-reactive cytoskeletal vimentin filaments, a low phagocytosis index, and reduced expression of HLA-DR antigens." This finding by Prieto and colleagues, way back in the late 1980s, demonstrates the crippling of these vital phagocytotic cells in patients suffering ME, CFS:DIRE.  Why?  Read about what normal monocytes do in healthy individuals, why and how sick monocytes harm patients with ME, CFS:DIRE.

               MONOCYTE: Part of the Immune Sytstem's 
               Leukocytes (aka White Blood cells, key cells 
               that help fight infections and allergies, but which 
               over-proliferate in the case of leukemia and other
               disease states), a monocyte is a phagocyte which 
               is an "eater" of bacteria, a destroyer of bacteria. 
               A monocyte is a large phagocytotic leukocyte 
               with basophilic cytoplasm containing faint eosino-
               philic granulations.    

               MONOCYTES travel in the blood for 6 to 9 days 
               having a critical role in immune functions.  To 
               understand their vital role in ME, CFS:DIRE, I refer 
               you to that important Prieto and collegues' research 
               paper I discussed in my 1992 book Living With and         
            Recovering From CHRONIC FATIGUE SYNDROME:
          Debilitating Immunopathic Relapsing Encephalomyelitis       

              HLA-DR = Human Leucocyte Antigen-D Related 
              (the discovery of which has led to greater success 
               and longevity in organ transplantation)  

   Specifically, in this ME, CFS:DIRE disease, one's monocytes are dysfunctional, overwrought, over-activating excess endorphins, the body's own "morphines" (endogenous opioids).  Not surprisingly,
then, these patients' monocytes responded positively, in that study, to the widely-known narcotic antagonist naloxone. 

   The Role of  Neurochemicals in the Modulation 
   of Immunochemicals and Vice Versa
   As that Prieto et al. research showed, in the presence of naloxone, those dysfunctionally low readings changed for the better, and I quote, "These values increased dramatically after incubation of the patients' monocytes with the opioid antagonist naloxone....These findings suggest that an increased opioid activity acting through a classical receptor mechanism is active on monocytes from a high proportion of patients with CFS and that this represents a novel example of immunomodulation by opioid peptides in human disease. We suggest endogenous opioids are involved in the pathogenesis of chronic fatigue syndrome." These medical scientists' assertion also proves my definition of ME, CFS:DIRE
as a disease due to ENDOGENOUS CHEMOTHERAPY, the body giving itself almost nonstop "killer treatments" of cytokines.  See my blog "ME, ENDOGENOUS CHEMOTHERAPY DISEASE".

   "To summarize," firmly state Prieto and colleagues, "a naloxone-reversible monocyte dysfunction has been found in a high percentage of patients with CFS, illustrating the immunomodulating role of opioid peptides in human disease.  Our results indicate that the study of the percentage of VF-positive monocytes in the presence and absence of naloxone might prove to be a useful clinical test in the investigation of patients with CFS and might contribute to a better understanding of the pathophysiology of this process."

    Both a Diagnostic Test AND a Specific Treatment
   As I proposed, in my book published a quarter century ago, the 
results of this study made me conclude, "Therefore, treatment with naloxone, the narcotic-antagonist usually used to reverse narcotic overdoses, may be one avenue of treatment for CFS:DIRE patients." 

(c) Copyright 1992 to 2018 by Dr. Helen Borel. All rights reserved.