Systemic as well as organ-localised immuno-inflammatory diseases (including autoimmune disease) are an important cause of morbidity and mortality. They occur in approximately 5-7% of the population, mainly striking young women in the reproductive age. Most of them are chronic conditions characterised by remissions and exacerbation.
The immune system is capable of marshalling highly potent effector mechanisms for eliminating foreign antigens. A short burst of such activity is usually adequate to eliminate foreign antigens with minimal tissue damage. Only minor discomfort may occur that includes transient malaise, fever and signs of local inflammatory swelling at the site of foreign antigen along with tender enlargement of the draining lymph nodes. However, if immune response fails to eliminate the pathogen, it becomes chronic and persistent. Chronic immune response causes a persistent inflammatory reaction that is called immuno-inflammatory or hypersensitivity diseases.
Clinically, immune inflammation is characterised by constitutional symptoms consisting of fever, usually low grade, night sweats, loss of weight and appetite, fatigue and malaise. The associated laboratory abnormalities include high erythrocyte sedimentation rate (usually > 50 mm in 1st hour), high platelet count (> 400,000/ mm3), anaemia of chronic inflammation, high C-reactive protein, increase in total serum globulins associated with a fall in serum albumin level. Usually, there is also a mild elevation of serum alkaline phosphatase level. The best example of this situation is the failure of immune response to eliminate tubercle bacilli. This leads to a chronic persistent immune reaction accompanied by severe constitutional symptoms (referred as tuberculo-toxaemia) and laboratory features of chronic persistent inflammation.
Situations that may lead to immuno-inflammatory tissue damage may be summed up as:
1. Immune inflammation due to chronic persistence of antigen. The antigen may persist when
(a) It is intrinsically (relatively) resistant to immune elimination (e.g. tubercle and lepra bacilli).
(b) Immune response is weak due to either a genetic or an acquired defect (e.g. immunodeficiencies including immunoglobulin and their subclass deficiencies, complement deficiencies, defective macrophage-monocyte system, Fc- and C3b- receptor defects, etc.)
2. Inappropriate immune response
Immune response against ubiquitous environmental antigens : food items, clothing, dust, pollens, feathers, animal dander, insect particles, common chemicals of day-to-day use, etc.
b) Self antigens.
c) Transplanted organs or transfused blood.
The types of hypersensitivity mechanisms can also be classified according to time course. Thus, type I reaction is often called immediate hypersensitivity. The term subacute hypersensitivity has been used for types II and III reactions. Type IV hypersensitivity is called delayed or delayed-type hypersensitivity.
1. Auto Sensitivity (autoimmune) diseases.
2. Allo Sensitivity diseases.
3. Xenosensitivity (heterosensitivity) diseases.
Spectrum of autoimmune diseases
Hashimoto’s thyroiditis Primary myxoedema Thyrotoxicosis Pernicious anaemia Autoimmune atrophic gastritis Addison’s disease Premature menopause (few cases) Insulin-dependent diabetes mellitus Goodpasture’s syndrome Myasthenia gravis Male infertility (few cases) Pemphigus vulgaris Pemphigoid Sympathetic ophthalmia Phacogenic uveitis Multiple sclerosis Autoimmune haemolytic anaemia Idiopathic thrombocytopenic purpura Idiopathic leukopenia Primary biliary cirrhosis Chronic hepatitis (HBsAg-negative) Cryptogenic cirrhosis (some cases) Ulcerative colitis Sjogren’s syndrome Rheumatoid arthritis Dermatomyositis Scleroderma Mixed connective tissue disease Discoid lupus erythematosus Non-organ-specific Systemic lupus erythematosus.
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