Autoimmune Diseases Systemic Lupus
Systemic Lupus Erythematosis (SLE) is an immune-mediated disease that serves
as a model for hypersensitivity diseases. The peak incidence of SLE is in women
between the ages of 20 and 40 and who present with a typical malar rash,
lymphadenopathy, arthralgias, fever, fatigue and will often complain of
recurrent flu-like illness. As the disease advances, increased evidence of
target organ damage can be found with protein and red cells in the urine, raised
ESR, pleurisy, pericarditis, hair loss, associated with the appearance of
circulating auto-antibodies, especially antinuclear.
SLE features circulating immune complexes and fits the model of delayed
pattern food allergy (Type 3 and IV hypersensitivity mechanisms). Patients with
type 3 pattern food allergy have lupus-like symptoms and signs for years, but
only a small subgroup crosses over or decompensates into the more severe
illness, SLE. The butterfly rash is common and is associated with cervical node
enlargement. Arthralgias are associated with generalized aching and stiffness
and infrequently joint swelling occurs. The type 3 food allergy pattern appears
to be a milder manifestation of SLE and may not progress over many years. These
patients only occasionally have ANA titers above 1:40.
A number of prescription drugs and several industrial chemicals are known to
trigger autoimmune disease. Hydralazine, isoniazid, penicillamine, practolol and
other drugs can induce SLE. While they may act as incomplete antigens and
contribute to immune complex formation, the toxic effects of certain drugs on
the complement system may also interfere with immune complex clearing and induce
SLE can be considered a disease of immune complex handling - immune complexes
containing non-cellular antigens are inappropriately deposited in tissues, which
are then damaged by inflammatory responses. A general thesis would suggest that
foods, drugs and chemicals in the environment that promote the formation of
immune complexes or impair the clearing of complexes induce autoimmune disease.
Hydralazine, marketed as an anti-hypertensive drug, also occurs naturally in
tobacco, smoke, mushrooms and may enter the food supply through contamination
with plastics, dyes, and herbicides. Individual susceptibility would be
influenced by the ability to metabolize the toxic chemical. Slow acetylators,
for example, are more prone to hydralazine-induced SLE.
Bardana et al reported on autoimmune reactions induced by dietary antigens.
They recalled that Sr. Wm. Osler had first suggested that dietary proteins were
important in the pathogenesis of Henoch-Schonlein purpura and arthritis. They
reported on an investigation of alfalfa-induced illness in monkeys A
non-nutrient amino acid, L-canavanine, found in alfalfa seeds and sprouts, was
identified as a trigger of an SLE-like syndrome. The severity of illness
produced by canavanine in monkeys is remarkable; a hemolytic anemia was a
consistent effect. Cooking alfalfa-containing foods may remove the problem since
canavanine is heat labile.
In SLE-prone mice, removing milk protein, casein, from a standard laboratory
diet had a dramatic benefit - 8% of the casein-fed mice survived at 24 months;
100% of the casein-free group survived. When the milk protein, casein, is
digested, protein fragments or peptides can be potent players in immune
networks. A casein peptide, beta-casomorphin 4-9, stimulates immune activity,