'98 Letters to Editor by Dr. sson.. Syndromes Associated with Silicone Breast Implants

[Guest guest]

" The only evidence is that of passive transfer of

immunologic stimulation of lymphocytes found in some

children of silicone breast implant mothers. All these

children have complained of arthalgias, growth

disorder, abdominal pains, exhibited esophageal

dysmobility on endoscopy and demonstrated learning

attention deficit disorders. "

------------------------

Subject Reference: '98 Letters to Editor by Dr.

sson

Sirs: In the article recently published as " Syndromes

Associated with Silicone Breast Implants " there were

several areas that were deleted, By the author, and

these sections deal directly with the issue of

Causation [1]. At the core of the issue all the

epidemiological studies on Silicone breast implants

have one thing in common; they are all designed either

to investigate or to obfuscate the issue of causation.

Unfortunately, silicone does not fulfill any of the

scientific epidemiological criteria for either

sufficient or necessary cause of the disease that

appears to be associated with silicone gel

implantation. While it is tempting to assert that

there is a direct risk from silicone there is little

scientific evidence to support that conclusion,

although it may play a secondary role in the

pathogenesis of disease. There is considerable

evidence to suggest that the indirect

(autoimmune) factor(s) is/are central to the

development of a disease from the presence of

silicone. Moreover, the biochemical activity of

silicone has been well documented by Dow Corning

Health and Environmental Sciences 1997 as an internal

animal study #1997-100000-43454 [2]. Whether

auto-antibodies are merely associated with the

development of a silicone adjuvant disease or play a

central role in the cause of the illness is often

difficult to determine.

Witebsky [3] has erected a set of postulates that are

routinely used to determine the relationship of

immunology phenomena to the etiology of a specific

disease.

(1) The autoimmune response must be regularly

associated with the disease

There is convincing evidence that polyneuropathy

(demyelinating) is associated with patients

complaining of symptoms after silicone gel

implantation. This may be associated with a variety of

autoimmune chemical phenomena. Less convincing, but an

association of demyelination of the central nervous

system and anti-thyroid antibodies may be found in

approximately 2>25% of the patients with symptoms

following implantation. Furthermore, local immune

responses may be found in the capsule surrounding the

silicone gel implants and this includes activation of

macrophages, B and T lymphocytes and selected T cell

receptor utilization and interleukin-2 antibodies.

Moreover, HLA typing has demonstrated that there is a

significant HLA-DR52-53 positivity in those

symptomatic patients with silicone gel implants.

(2) A replica of the disease must be inducible in

animals

Peritoneal inflammatory granulomatosis, foamy

conglomeration and, finally, plasmacytomagenesis in

genetically susceptible mice (BALC/C.DBA/2-IHDI-PEP3)

have been shown following intra-peritoneal injection

of silicone. In addition, experimental allergic

encephalopathy (EAE) and experimental allergic

neuropathy (EAN) have been extensively studied.

Moreover, silicone gel and

octamethylcyclotetrasiloxane (D4) have been shown to

potentiate antibody production to bovine serum in A/J

mice.

(3) Immunopathologic changes in the natural and

experimental diseases should parallel each other EAN

and EAE have been extensively studied and each of the

adjuvant dependent antigens has been identified. In

the EAN disease, produced in susceptible animals, the

Po glycoprotein, P2 lipid binding protein and the

myelin associated protein (MAG) have been,

etiologically, associated with the development and

progression of the disease which parallels that found

in silicone breast implant adjuvant disease associated

with peripheral neuropathy. The protein, PI, also

named myelin basic protein (MBP), is found only in the

central nervous system and is responsible for the

animal model of EAE. In the model of EAN, commonly

produced in rats, a maximum histocompatibility

complex MHC II response regularly occurs which is

medicated by T cells and occurs in the following

stages:

(A) Alteration of the blood-nerve barrier with the

infiltration of T cells within 72 hours after the

challenge.

( Migration of the inflammatory T cells with the

presence of edema and it is associated with a decrease

of nerve conduction. This occurs within 45 days

following the induction of EAN.

© CD4 (T) cells predominate with the production of

cytokines, which, in turn, increase the cell adhesion

molecules by endothelial cells.

(D) Finally, there is accumulation of macrophages, T

cells, polymophonuclear leukocytes which when

activated release free oxygen, hydroxyl radicals,

proteases and lipases. The damage appears to be

oxidative damage, while the protein and lipid enzymes

are produced in order to digest the damaged cells

debris. These changes have been observed in patients

with Sural nerve biopsies.

Thus, the balance between the intensity of the initial

inflammatory T cell response and the antibo

dy concentration may then determine the clinical

course of the disease.

(4) Transfer of the autoimmune illness should be

possible by the transfer of serum or lymphoid cells

from the diseased individual to a normal recipient

This study has not been performed to the knowledge of

the author. The only evidence is that of passive

transfer of immunologic stimulation of lymphocytes

found in some children of silicone breast implant

mothers. All these children have complained of

arthalgias, growth disorder, abdominal pains,

exhibited esophageal dysmobility on endoscopy and

demonstrated learning attention deficit disorders.

In conclusion, I do not believe that epidemiological

studies alone and the continuing rhetoric will be

adequate either to prove or to disprove if there is a

definitive relationship between silicone breast

implants and disease and, furthermore, adequate

biological and biochemical studies will be required.

ARTHUR DALE ERICSSON, MD

6560 Fannin, Suite 720, Houston, Texas 77030, USA

REFERENCES

[1] sson AD. Syndromes associated with silicone

breast implants: a clinical study and review. J Envir

Med 1998; 8: 35-51.

[2] Varapath S, Salyers K and Plotzke K. Non-regulated

study: identification of major metabolites of

octamethylcyclotetra-siloxane(D4) in rat urine, Dow

Coming Internal Memorandum (August 26, 1997), 1-72.

[3] Barrett J. Textbook of Immunology. St Louis, MO:

C. V. Mosby Company

1988: 36>2.