Hypersensitivity and Homoeopathy
Dr. Rajneesh Kumar Sharma MD (Homoeopathy)
Dr. (Km) Ruchi Rajput BHMS
Dr. Ashutosh Kaushik BHMS
Definition, classification, factors, types- Type I Hypersensitivity, Type II Hypersensitivity, Type III Hypersensitivity, Type IV Hypersensitivity, Bibliography.
• An exaggerated response by the immune system to a drug or other substance.
• A state of altered reactivity in which the body reacts with an exaggerated immune response to a foreign agent.
• an allergy; an exaggerated or inappropriate immune response categorized based on which part of the immune system that is involved and the onset of response (i.e. Types I, II, III, IV)
• an immune reaction (allergy) in which the body has an exaggerated response to a specific antigen (e.g., food, pet dander, wasp venom).
• (hi´´per-sen´´su1-tiv´u1-te) Another name for allergy; abnormal immune response that may be immediate (due to antibodies of the IgE class) or delayed (due to cell-mediated immunity).
• An excessive immune response that results from previous exposure to an antigen. Immediate responses are antibody-mediated and occur in minutes; delayed responses are mediated by T-cells and occur about 24 hrs later.
• Hypersensitivity causes objectively reproducible symptoms or signs, initiated by exposure to a defined stimulus that is tolerated by normal subjects.
• An abnormal sensitivity to a stimulus of any kind. Allergy; a malfunction in which the immune system mounts an inappropriately large response with undesirable consequences, such as tissue damage.
• The state of being abnormally sensitive or susceptible, as to the action of allergens.
• Pathological sensitivity, extreme sensitivity.
Thus the term hypersensitivity describes the state of pathological sensitivity (Psora) caused by antigen-specific immune reactions (Psora) that are either inappropriate or excessive and result in harm to the host (Syphilis), causing objectively reproducible symptoms or signs, initiated by exposure to a defined stimulus (Psora) that is tolerated by normal subjects.
Classification of Hypersensitivity
According to Gell and Coombs’ classification, Hypersensitivity reactions are classified into four different types based on their underlying immunological mechanisms and clinical manifestations-
• Type I hypersensitivity reactions commonly occur against apparently inoffensive environmental antigens (allergens), (Psora) whereas
• types II,
• III and possibly
• IV reactions may occur against environmental (commonly infectious) agents or self-antigens in the course of autoimmune disease (Syphilis).
The term hypersensitivity is often used interchangeably with allergy (meaning altered reactivity- Psora); however, allergy is best reserved for type I hypersensitivity.
Factors to determine hypersensitivity
Multiple factors determine whether a hypersensitive rather than a normal immunological response occurs. This includes-
• the genetic make-up of the individual (Homoeopathically explained Constitution of the individual)
• the physical and chemical properties of the antigen and
• its Gell and Coombs’ classification of hypersensitivity reactions
Type I hypersensitivity
This presents the picture of clinical allergy (Psora). The antigens involved are called allergens. Type I reactions typically occur within minutes of exposure to allergen and involve the interaction of-
• allergen-specific IgE and
• tissue mast cells.
Before a type I response can occur, the immune system must previously have encountered the antigen and stimulated B cells (B Cells are nothing but a type of lymphocytes produced in bone marrow and matured within it) to produce antigen/allergen-specific IgE. IgE is normally present in very low concentrations in the serum but total IgE levels are increased in patients with parasitic infections, in most atopic patients, as well as in many apparently healthy individuals. A high total serum IgE does not, however, cause an allergic response; there must be an elevation of allergen-specific IgE. Mast cells found in the mucosa of the airways and gut as well as in connective tissues bind IgE.
Type II hypersensitivity
These reactions are also mediated by antibody, but in contrast to type I reactions, the antibodies involved are either of the IgG or IgM class. A characteristic of type II reactions is that the antibody response is directed against antigens that are expressed on cell surfaces, not against soluble antigens. These bound antibodies act as a focus for further cellular and complement-mediated damage (Syphilis) to specific cell types or organs.
Typical examples of type II hypersensitivity include transfusion reactions, autoimmune haemolytic anaemia (Syphilis), hyperacute graft rejection (Psora), Goodpasture’s syndrome (Pseudopsora) and Graves’ disease (Psora- Sycosis). Transfusion reactions (Psora) and hyperacute graft rejections involve the recognition of truly foreign antigens and ought to be preventable conditions with adequate blood grouping, tissue typing and cross-matching.
Type III hypersensitivity
This is also antibody mediated but, in contrast to type II reactions, the antigenic targets of type III reactions are soluble and not bound to the cell membrane. The combination of soluble antigen and specific antibody, of IgG or IgM class, results in the formation of immune complexes (Psora-Sycosis). These immune complexes circulate in the bloodstream and, consequently, the damage caused is not limited to one particular cell type or organ (Syphilis) but may occur at remote sites throughout the body (Syphilis). Immune complexes are formed during normal antibody responses as a means of assisting antigen disposal. These immune complexes are quickly cleared by the monocyte/macrophage system, in particular by the phagocytes (Syphilis) of the liver, the Kupffer cells. When immune complexes persist (Sycosis), either in the circulation or as deposits within tissues (Sycosis), they activate a number of inflammatory pathways and the response becomes hypersensitive (Psora). Antigens that cause immune complex formation may be either exogenous (infectious or environmental agents) or endogenous (self-antigens in autoimmune responses).
Chronic antigen exposure allows continuous immune complex formation (Sycosis). Clinical examples of conditions in which chronic antigen exposure is believed to be important in generating a type III response include infections (e.g. hepatitis B virus infection (Cancerous), bacterial endocarditis (Sycosis- syphilis)) and autoimmune conditions (e.g. systemic lupus erythematosus (Pseudopsora)).
Type IV hypersensitivity
Type IV hypersensitivity reactions differ from types I–III in that the primary immunological effectors in type IV reactions are cells — mainly lymphocytes and monocytes — and not antibody molecules as in types I–III. Type IV responses are also referred to as delayed-type hypersensitivity as the reactions occur 12 hours or more following exposure to antigen. Examples of type IV hypersensitivity are-
Contact hypersensitivity (Psora) is caused by low-molecularweight antigens, which alone are incapable of eliciting an immune response. They stimulate the immune system by binding to normal body proteins and in this form are described as haptens. The most common example is probably nickel hypersensitivity where patients develop an eczematous reaction to nickel contained in costume jewellery, watches, trouser buttons, etc. The rash that appears is typically eczematous but is usually limited to areas of skin that are in direct contact with the metal.
In contrast to contact hypersensitivity, tuberculin hypersensitivity is a phenomenon that chiefly occurs in the dermis. Koch observed that when patients suffering from tuberculosis were given an intradermal injection of tuberculin (an antigen derived from Mycobacterium tuberculosis) they suffered both a local and a systemic reaction (Pseudopsora). The local skin reaction is characterized by an area of induration and swelling, and this response is now recognized as being mediated by sensitized lymphocytes. This type IV reaction is used clinically as a means of determining the sensitization status of individuals in tests for tuberculosis and leprosy. The Mantoux test and Lepromin test involve the intradermal injection of M. tuberculosis and M. leprae extracts, respectively.
Where antigen persists, the response may develop into a granulomatous hypersensitivity (Psora- Sycosis), which is the most severe form of type IV hypersensitivity and clinically the most important. Granulomas are collections of macrophages, some of which coalesce to form giant cells, surrounded by a cuff of small lymphocytes (Sycosis). The macrophages often have the appearance of epithelial cells, and are known as epithelioid cells. Granulomas are formed when the immune system fails to remove foreign antigen (Psora), which then persists, usually within macrophages.
S. No. Rubrics found in various repertories related to Hypersensitivity No. of Remedies
1 Clarke J. H., Clinical Repertory (English) - Clinical - H - hypersensitiveness 8
2 SENSATIONS AND COMPLAINTS IN GENERAL - Insensibility, numbness, painlessness, etc. - alternating with hypersensitiveness 1
3 CHILL - Chill, etc. - concomitants - mind - sensibility - exalted (hypersensitiveness) 17
4 MIND - Mood, disposition - Hypersensitive, cannot bear contradiction, vexed at trifles 45
5 NERVOUS SYSTEM - Nervousness - Hypersensitiveness 65
6 GENERALITIES - Bones - Pain - Throbbing, jerking, darting, drawing, hypersensitiveness 1
7 GENERALS - ALLERGIC constitution - chemical hypersensitivity 5
8 GENERALS - NUMBNESS - Externally - alternating with hypersensitiveness 1
cham. nux-v. acon. coff. phos. asaf. colch. ign. plat. sep.
14 12 10 10 10 9 9 9 9 9
2 - - 1 - 1 - 2 - -
- - - - - - - - 1 -
4 3 4 4 2 - 2 - - 3
2 2 1 - 1 1 2 2 2 2
2 2 2 2 2 2 2 2 1 1
- - - - - 1 - - - -
- 1 - - 1 - - - - -
- - - - - - - - 1 -
Prevalence of miasms in inflammation:
Psora 100 %
Sycosis 100 %
Tubercular 100 %
Syphilis 75 %
Cancerous 62.5 %
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© Dr. Rajneesh Kumar Sharma MD (Homoeopathy)
Dr. (Km) Ruchi Rajput BHMS
Dr. Ashutosh Kaushik BHMS
Homoeo Cure Research Centre P. Ltd.
NH 74- Moradabad Road
Kashipur (UTTARANCHAL) - INDIA