Guillain-Barre syndrome 1N leprosy patients.

Leprosy commonly affects the peripheral and cranial nerves. This involvement often manifests with peripheral neuropathy, occurring as a result of direct invasion of the nerves by lepra bacilli. Immune-mediated neuropathy occurring in leprosy, as part of lepra reaction, has been described earlier. We report here two cases of Guillain-Barre syndrome occurring in patients with leprosy who did not have any obvious evidence of lepra reaction.

An appetite for armadillo

In October 1979, a 70-year-old man was referred and admitted to the Medical University of South Carolina Hospital. Three or four years earlier, he had begun to notice the appearance of raised, nontender lumps on his arms and legs.

On the potential usefulness of exchange plasmapheresis in the immunotherapy of cancer and of some chronic persistent infections.

In an individual sensitized to an antigen, Withdrawal of the corresponding antibody and of the accompanying antigen-antibody complexes stimulates antibody production: the end result is thus not unlike the effect of a booster dose of that antigen. Conversely, a sufficient concentration of antigen-antibody complexes will eventually shut off the antibody production to that antigen. The body is able to regulate through this mechanism the amplitude of the immune response, using the feed-back interaction of antigen-antibody complexes with the immune system. Without such a control system any antigenic stimulation would result in an uncontrolled out-pouring of antibodies, as is observed in myeloma. The regulation of cell mediated immunity is also indirectly affected by the concentration of circulating antigen-antibody complexes. Other mechanisms of immunoregulation are also at work, using the mediation of so-called suppressor cells, identified as sub-populations of T and B cells acting both specifically and non-specifically on immune effectors cells. It is likely that a major factor contributing to the pathogenesis of some persistent chronic infections such as syphilis, brucellosis, chronic viral hepatitis, leprosy, vaccinia, congenital cytomegalovirus infection persisting in childhood, and so on, and in conditions such as cancer, is an inadequate initial production of antibodies, further aggravated by the ensuing immunosuppression brought about by the formation of antigen-antibody complexes. Antigen-antibody complexes have indeed been identified as playing a prominent role in some of these diseases. It is also suggested that the magnitude of the initial antigenic dose may influence the ensuing immune response: while a large antigen dose could induce a "classic" and efficient immune response, a low antigen dose, such as an incipient neoplasm, could result in a minimal antibody response, further suppressed by the appearance of antigen-antibody complexes. Through this mechanism, a premature failure to eradicate the disease would follow. I suggest that a significant and sudden lowering of the concentration of relevant entibodies and antigen-antibody complexes through exchange plasmapheresis, would trigger a fully adequate and therapeutic immune response. This possibility is discussed.