Fw: Ref.: (LML) Median nerve damage in leprosy

 

 

 
Leprosy Mailing List – January 27,  2022

 

Ref.:  (LML) Median nerve damage in leprosy

 

From:  Zhaudat Umerov, Moscow, Russia

 

Dear Pieter,

 

 

Thanks to Wim Theuvenet  for the important question in the LML mail of January 9th.2022. The possibility of widespread use of nerve decompression techniques in the carpal canal in the early stages (loss of sensitivity, without muscle atrophy) is a very tempting program to combat disability. This can be successful with the detailed development of both indications and contraindications.  

 

It may be useful to recall the mechanism of nerve damage. The results of the study using polyclonal and monoclonal antibodies established cross reactive (mimicking) antigenic determinants of M.leprae and the myelin sheath of peripheral nerves. Consequently, the pathogen causes a cellular and humoral immune response against the pathogen and peripheral nervous tissue (CMI and autoantibodies). The normal (non-immunodeficient) host immune system protects the body by removing autoreactive T cells in the thymus and peripheral lymphatic system using a subclass of CD4+CD25 FOXP3+ T-regulatory cells. The removal of these cells suppresses the host's cellular immune response against the pathogen and the myelin sheath of Schwann cells. This is typical for multibacillary leprosy. However, T-reg. cells do not affect B-lymphocytes and the production of cross-reacting IgM and IgG antibodies.     

 

The place of doubling (reproduction) of the pathogen is the phagolysosome compartment of the host macrophages, and the cell wall of macrophages and membranes of phagolysosomes are impervious to high-molecular IgG - 150 kDa, IgM - 970 kDa autoantibodies. Consequently, the reaction of autoantibodies with intracellular pathogen and Schwann cell myelin does not occur. However, antibodies react with pathogen antigens expressed on surrounding tissues including epineurium.  An inflammatory immune response causes fibrosis, which compresses nerve fibers.

 

In these cases, the functional activity of the nerves may persist for a long time, which is an indication for performing a nerve decompression operation in the carpal tunnel. 

Stimulation of the host with low doses of the M.leprae mimicking antigen can lead to tolerance by suppression of increasing Treg cells. In this case, a strong Th1-mediated cellular immune reaction develops against the pathogen and the myelin sheath of Schwann cells, causing a decrease in the bacillary load of host tissues and damage to peripheral nerves by irreversible demyelination. This is typical for paucibacillary leprosy. Performing a nerve decompression operation in the carpal tunnel in such patients will not fulfill the expectations.  

 

I hope the above will be useful when deciding on surgical intervention.

 

   Kind regards,

 

   Zhaudat UMEROV

   Moscow and Antalya.

 

 

LML - S Deepak, B Naafs, S Noto and P Schreuder

LML blog link: http://leprosymailinglist.blogspot.it/

Contact: Dr Pieter Schreuder << editorlml@gmail.com

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