Immune mediated inflammatory diseases (IMIDS) are a group of diseases characterized by chronic inflammation and organ damage.
Evaluation has moved from organ based classification to a molecular classification which better addresses pathophysiological commonalities across IMIDs affecting different organs but with substantially mechanistic differences.
IMDs are heterogeneous at multiple levels with differences in genetic features, immune pathogenesis and treatment responses.
Molecular approach to IMIDs requires particularly as the range of immune targeted therapeutics expands.
Responses to conventional drug therapy differ across IMIDs example nonsteroidal anti-inflammatory drugs work in axial spondylarthritis and psoriatic arthritis but are less effective in rheumatoid arthritis and it Crohn’s disease and ulcerative colitis they can adverse effects to the impairment of epithelial barrier function.
In addition conventional immune modularity agents have efficacy in individual IMIDs: methotrexate used in rheumatoid arthritis, sulfasalazine in psoriatic arthritis and spondylarthritis, azathioprine in inflammatory bowel disease and cyclosporine in ulcerative colitis.
Tumor necrosis factor alpha is efficacious in all major forms of arthritis as well as the two main forms of inflammatory bowel disease.
IMIDs affect the inner surface of the body: the gut with inflammatory bowel disease:Crohn’s disease and ulcerative colitis, and the joints: inflammatory arthritis rheumatoid arthritis, psoriatic arthritis, and axial spondylarthritis: affecting about 3% of the general population.
The prevalence of IMIDs has been increasing.
Both inflammatory arthritis and inflammatory bowel disease are characterized by chronicity, are often affecting people of young age, persist through adulthood, with substantial disease progression and damage and loss of function of affected organs.
The skin being the outer barrier of the body, and the body’s inner barriers the gut and joints are particularly prone to IMIDs, since they are required to maintain tissue homeostasis at sites exposed to microbial, chemical, and mechanical challenges.
Because there is a high level load of pathogen associated molecular patterns that continuously trigger immune activation barriers are equipped with regulatory systems that control, suppress, and resolve inflammation through anti-inflammatory cytokines, lipid mediators, and immune regulator cells.
That IMD’s of the joints and bowel are associated with lesions in the skin, supporting and interdisciplinary approach to the molecular pathogenesis of IMIDs.
Inflammatory bowel disease and inflammatory arthritis share a combination of genetic susceptibility loci genes and triggers.
These environmental triggers include smoking, mechanical stress, or microbiome changes.
The clinical onset of these two disorders is based on an immune response that infiltrates target tissues with activated immune cells.
Both disorders have a chronic clinical course with flares and silent phases and low potential for spontaneous resolution.
The systemic inflammatory character of both of these disorders can lead to complications: increased risk of inflammatory eye disorders-uveitis with scleritis, with skin lesions psoriasis, erythema nodosum, pyoderma, cardiovascular diseases and premature osteoporosis.
Both inflammatory arthritis and inflammatory bowel disease can have effects on the CNS by altering pain perception, and be associated with fatigue and depressive behavioral symptoms.
Biologic disease modifying antirheumatic drugs (bDMARDs) add transformed the care of patients with these diseases characterized by common inflammatory pathways leading to inflammation, such as rheumatoid arthritis, spondylarthritis, and inflammatory bowel disease.
These biologic DMARDs improve symptoms, reduce damage of joints, G.I. tract and other affected organs, reduce disability, comorbidities, and mortality.
Many patients with immune mediated inflammatory disorders do not respond to treatment, and have approximately 50% of initial responders have an adequate disease control.
Patients with secondary failure associated flares have irreversible tissue damage, glucocorticoid exposure, loss of productivity, and worsened quality of life.
It may take weeks to months to reestablish disease control after secondary failure.
The anti-inflammatory effect of TNF-alpha inhibition is based on its effect on myeloid cell activation, which is common in many forms of immune mediated inflammatory diseases.
TNF – alpha is clinical clinically effective in arthritis rather than in inflammatory bowel disease, while other types of TNF alpha can be effective in both diseases.
Rheumatoid arthritis is the only immune mediated inflammatory disease that shows combined TNF-alpha and interleukin 6 dependency.
Interleukin 6 receptor inhibition is effective in rheumatoid arthritis but it’s not effective in axial spondyloarthritis and psoriatic arthritis.
Several immune mediated diseases are associated with increased risk of cancer in the involved organs such as: inflammatory bowel disease and colorectal cancer, primary sclerosing cholangitis and hepato-biliary cancer, celiac disease and small intestine cancer.
These findings imply a local carcinogenic effect of the presence of immune dysregulation.
Rheumatoid arthritis is a systemic disease associated with the higher risk of lymphoma and lung cancer and a lower risk of breast, colorectal and prostate cancers.
Some immune mediated diseases are associated with higher cancer risk in distant organs.