Inflammatory Arthritis

Some Topics

  • Systemic Lupus

    Systemic lupus erythematosis (SLE) is an immune-mediated disease that serves as a model of hypersensitivity disease. 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, and 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, arthritis, hair loss, associated with the appearance of circulating autoantibodies, 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 into the more severe illness, SLE. A butterfly facial rash is common and is associated with cervical node enlargement. Arthralgias are associated with generalized aching and stiffness and infrequently joint swelling occurs. The milder versions of this process are often diagnosed as fibromyalgia. Transitory inflammatory episodes in and around joints are diagnosed as bursitis, tendonitis, synovitis and often attributed to strains and sprains. The type 3 food allergy pattern appears to be a milder manifestation of SLE and may not progress over many years. These patients do not have elevated ESR, and only occasionally have ANA titers above 1: 40. Some complain of recurrent chest pain that suggests pericarditis or pleurisy, but objective evidence is usually lacking.

    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 indirectly.

    .SLE can be considered a disease of immune complex handling: immune complexes containing non-cellular antigens are inappropriately deposited in tissues that are then damaged by inflammatory responses. A general thesis would suggest that drugs and chemicals in the environment that promote the formation of immune complexes or impair the clearing of complexes would tend to 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 cow’s milk protein, casein, from a standard laboratory diet had a dramatic benefit: 8% of the casein-fed mice survived at 24 months, while 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, creating hypersensitivity.


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