Drug – bio-affecting and body treating compositions – Immunoglobulin – antiserum – antibody – or antibody fragment,... – Derived from – or present in – food product
Reexamination Certificate
2000-09-07
2004-03-16
Housel, James (Department: 1648)
Drug, bio-affecting and body treating compositions
Immunoglobulin, antiserum, antibody, or antibody fragment,...
Derived from, or present in, food product
C424S130100, C530S395000, C530S300000, C530S350000, C435S004000
Reexamination Certificate
active
06706267
ABSTRACT:
BACKGROUND OF THE INVENTION
Field of the Invention
The invention relates to a method of reducing inflammation in animals. More particularly, the invention relates to the combination of egg product and glucosamine to produce a synergistic effect in reducing inflammation, and particularly arthritis, in animals.
Inflammation
Inflammation, as defined in Dorland's Medical Dictionary, is “a localized protective response, elicited by injury or destruction of tissues, which serves to destroy, dilute or wall off both the injurious agent and the injured tissue.” It is characterized by fenestration of the microvasculature, leakage of the elements of blood into the interstitial spaces, and migration of leukocytes into the inflamed tissue. On a macroscopic level, this is usually accompanied by the familiar clinical signs of erythema, edema, hyperalgesia (tenderness), and pain.
During this complex response, chemical mediators such as histamine, 5-hydroxytryptamine, various chemotactic compositions, bradykinin, leukotrienes, and prostaglandins are liberated locally. Phagocytic cells migrate into the area, and cellular lysosomal membranes may be ruptured, releasing lytic enzymes. All of these events can contribute to the inflammatory response.
In the particular case of rheumatoid arthritis, the resulting inflammation likely involves the combination of an antigen with an antibody complement causing the local release of chemotactic and chemoactivating compositions that attract leukocytes. The leukocytes phagocytose the complexes of antigen-antibody and complement, and also release the many enzymes contained in their lysosomes. These lysosomal enzymes then cause injury to cartilage and other tissues, and this furthers the degree of inflammation. Cell-mediated immune reactions may also be involved. Prostaglandins, which are key intracellular regulators of cellular function, are also released during this process.
The inflammatory response is any response characterized by inflammation as defined above. It is well known, to those skilled in the medical arts, that the inflammatory response causes much of the physical discomfort (i.e., pain and loss of function) that has come to be associated with different diseases and injuries.
Arthritis
Arthritis manifests itself in a variety of forms. Some of the more common forms include rheumatoid arthritis, osteoarthritis and generalized rheumatism.
Rheumatoid arthritis is an autoimmune disease characterized by pain, swelling and stiffness in the joints. Rheumatoid arthritis is a disease which afflicts approximately 3% of Americans, and particularly women. Rheumatoid arthritis is an extremely disabling disease and usually strikes adults between the ages of 30 and 40 years, while the occurrence of clinical illness is greatest among those aged 40-60 years. Although drug therapy is somewhat effective, as many as 7% of rheumatoid arthritis sufferers are disabled to some extent as quickly as 5 years after disease onset, and within 10 years, as many as 50% are too disabled to work.
Osteoarthritis produces similar symptoms to rheumatoid arthritis. In particular, although osteoarthritis begins as a degeneration of particular cartilage whereas rheumatoid arthritis begins as inflammation in the synovium, each process approaches the other as the disease progresses. In osteoarthritis, as cartilage deteriorates and joint congruence is altered, a reactive synovitis often develops.
Conversely, as rheumatoid arthritis erodes cartilage, secondary osteoarthritis changes in bone and cartilage develop. At the end stages of both osteoarthritis and rheumatoid arthritis, the involved joints appear the same.
Some other forms of arthritis include Ankylosing Seronegative Spondyloarthropathy (ankylosing spondylitis) and reactive arthritis. These conditions are often referred to as the “B-27 associated diseases,” and are difficult to differentiate from rheumatoid arthritis. In some cases ankylosing spondylitis, Reiters syndrome or psoriatic arthritis are present coincidingly with Rheumatoid Arthritis in the same patient. In many cases, these patients are treated with the same disease modifying drugs as those suffering from progressive rheumatoid arthritis.
Onset of arthritis generally occurs after the age of 30 in those who are susceptible to such disease. However, some forms of arthritis may be initiated by different causes, such as slow virus infections. Because there is great overlap, many physicians consider these forms as “generalized rheumatism” and approach management of the diseases in the same way. Some diseases which fall into this category include Chronic Fatigue Syndrome, fibromyalgia (fibrositis) and gout. In fact, for some patients, evidence is accumulating for superimposition of rheumatoid arthritis and fibromyalgia.
Autoimmune Diseases
As stated above, rheumatoid arthritis is an autoimmune disease, and as such, its etiology is much the same as the etiology of any other autoimmune disease. The body normally recognizes the difference between its own by-products and foreign invaders (i.e. bacteria, viruses, fungi and protozoans, to name a few). When an immune cell (T or B lymphocyte) reacts to a “self-protein” during its development, that cell is deemed defective and usually destroyed or inactivated. Sometimes, however, a “self-reactive” immune cell will escape destruction. At a certain later time, that cell can be activated and trigger an immune response. Activation is thought to occur after infection with a common bacteria or virus which contains a polypeptide having a stretch of amino acids which match a stretch on the defective self-protein. Several bacteria, such as Streptococcus, Mycoplasma, and borrelia, have been implicated in the initiation of the disease, as well as certain viruses, namely retroviruses. In addition to Rheumatoid Arthritis, autoimmunity often results in such diseases as juvenile diabetes, multiple sclerosis, Graves' disease, Meneri's disease, myasthenia gravis, lupus erythematosus and psoriasis. (Medical Sciences Bulletin, September, 1994).
Autoimmunity affects specific organs. For example, some autoimmune diseases of liver bile ducts, and kidneys are: primary biliary cirrhosis, necrotizing glomerulonephritis, “idiopathic” crescentic glomerulonephritis, virus-induced liver and kidney disease, chronic hepatitis, autoimmune and drug-induced hepatitis (Gershwin, Manns, and Mackay 1992). Immune destruction of the islets of Langerhans results in diabetes mellitus (Hagopian and Lerumark 1992) and insulin autoantibodies have been described (Palmer 1987).
There are a large category of systemic vasculitides diseases in which autoimmune mechanisms have been suggested as the cause of the pathogenesis. Some of the diseases are: leukocytoclastic angitis, polyarteritis nodosa, Goodpasture's syndrome, Kawasaki disease, Wegener's granulomatosis, Churg-Struass syndrome, giant-cell arteritis, Takayasu arteritis, immune-complëx-mediated, lupus, rheumatoid, and cryoglobulinemic vasculitis, Henoch Schonlein purpura (Kallenberg, 1996; Jennette, Jones, Falk, 1992).
There is also a body of evidence that autoimmunity may play a role in many forms of heart disease including: postpericardiotomy and post myocardial infarction syndromes, myocarditis, and idiopathic dilated cardiomyopathy. Autoimmunity may be responsible for the progression of acute disease of heart muscle to degenerative (Rose, Neumann, Burek, Herskowitz 1992).
Symptomatic involvement of skeletal muscle is common in many autoimmune diseases such as polymyositis or inflammatory myopathy (which may include rheumatoid arthritis, polymyalgia rheumatica, myasthenia gravis, myasthenic myopathy, neurogenic atrophy, motor neuron disease, fibromyalgia, fibrositis, muscular dystrophy, endocrine, metabolic, and carcinomatous myopathy). (Hollingsworth, Dawkins, Thomas 1992).
Other diseases with autoimmune origins may be uveitis, Vogt-Koyanagi-Harada syndrome, (Detrick and Hooks 1992), and Sjögren's syndrome, scieroderma, ankylosing spondylitis, dermatomyositis, psoriasis, psoriatic arthritis,
Adalsteinsson Orn
Hunchar Jeffrey G.
Iyer Subramanian
Arkion Life Sciences LLC
Chen Stacy B.
Housel James
Krikelis Basil S.
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