A Major Fault in Diabetic Inflammation: Failure of Leucocytic Glycogen Transfer to Histiocytes

  • J. W. Rebuck
  • F. W. Whitehouse
  • S. M. Noonan
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 1)


The diabetic is allegedly more susceptible to infection than the nondiabetic. Particularly, there has been noted a frequent association of extensive local or systemic infection with the presence of diabetic acidosis. Perillie, Nolan, and Finch [18] have reviewed the humoral immunologic studies in this area and concluded that if lowered resistance to infection is present in patients with diabetes, immunologic factors did not play the essential role in impaired resistance. In contrast, these workers showed that the early neutrophilic phase of the local inflammatory response was significantly delayed and diminished in diabetic patients with acidosis in comparison with normals or nonacidotic patients. The advent of the human skin window technique [20] presents the inflammatory leucocytes with the same clarity of cytologic detail previously available only in the classic hematologic preparations of peripheral blood or marrow aspirates. With this, a new neutrophilic function of cytoplasmic shedding into the exudative fluids was apparent. Before death of the granulocyte in the later stages of inflammation, it could be demonstrated that the neutrophilic cytoplasm peripheral to its nuclear lobes was fragmented in granular or particulate form and shed into the exudative fluids.


Periodic Acid Schiff Glycogen Content Diphtheria Toxoid Phagocytic Ability Fibrin Strand 
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Copyright information

© Springer Science+Business Media New York 1967

Authors and Affiliations

  • J. W. Rebuck
    • 1
  • F. W. Whitehouse
    • 1
  • S. M. Noonan
    • 1
  1. 1.The Henry Ford Hospital DetroitUSA

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