A Proposition of an Auxiliary Treatment for Diabetes Mellitus, Type I

Kimihiko Okazaki

Published Date: 2017-04-15
DOI10.21767/2471-8041.100045

Kimihiko Okazaki*

Okazaki Medical Clinic, Ukyoku, Kyoto, Japan

*Corresponding Author:
Kimihiko Okazaki
Okazaki Medical Clinic, Ukyoku, Kyoto, Japan
Tel: 207-277-2020
E-mail: ma13081x@ma1.seikyou.ne.jp

Received Date: March 24, 2017; Accepted Date: April 13, 2017; Published Date: April 15, 2017

Citation: Okazaki K. A Proposition of an Auxiliary Treatment for Diabetes Mellitus, Type I. Med Case Rep, 3:2. DOI: 10.21767/2471-8041.100045

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Abstract

It is well known that diabetes mellitus, Type-I is an autoimmune disease. As a matter of course, all of patients of this disease should have anti-pancreatic B cell antibodies on the surface of cytolytic T lymphocytes. Few, if any, contemporary physicians seem to take this fact into consideration presumably because most, if not all, of them take it for granted that most, if not all, antibody molecules rigidly adhere to their receptors on cell-surfaces.

Introduction

It is well known that diabetes mellitus, Type-I is an autoimmune disease. As a matter of course, all of patients of this disease should have anti-pancreatic B cell antibodies on the surface of cytolytic T lymphocytes. Few, if any, contemporary physicians seem to take this fact into consideration presumably because most, if not all, of them take it for granted that most, if not all, antibody molecules rigidly adhere to their receptors on cell-surfaces.

On the other hand, approximately five decades ago, a novel concept of existence of an equilibrium state among antibody molecules in the vicinity of their receptors on cell-surfaces has been established [1-3]. It follows that every antibody molecule in the vicinity of its receptor keeps repeating attaching to and detaching from the receptors. The reason why not “receptor” but “receptors” are because each antibody molecule may change receptors. It still follows those replacements of antibody molecules on a certain receptor keep occurring all the time. Naturally, the traditional concept of rigid adhesions of antibody molecules to the receptors is irrelevant.

Conclusion

Conclusion In conclusion, progressive destruction of pancreatic B-cells could be terminated if anti-pancreatic B cell antibodies were replaced from the surface of cytolytic T lymphocytes. In order to do so, accumulations of non-specific antibodies in the patients’ bodies are necessary. Still in order to do so, repeated intradermal injections with a non-specific antigen preparation is necessary. An example of the latter preparation is Neurotropin, a product of Nippon Zohki Pharmaceutical Company (Osaka), consisting of extract of rabbit skin inflamed by inoculation of Vaccinia virus.

An alternative proposition might be intra-venous infusions of saline solution of gamma-globulin. However, repeated gamma-globulin infusions are dangerous since anti-gammaglobulin antibodies may be produced in the recipients’ bodies, which may cause an anaphylactic reaction after a large number of infusions.

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