Check out the five main causes of serum sickness

The typical symptoms of serum sickness mainly include fever, skin rash, joint pain, and some patients may also experience abdominal discomfort, nausea and vomiting. When serum sickness is diagnosed, it must be treated promptly to prevent the condition from worsening and inducing shock in the patient. So what are the main causes of serum sickness? Here, the editor will give you some basic knowledge about the five main causes of serum sickness, hoping it will be helpful to everyone.

Serum sickness is a typical type III allergic reaction. The body can produce antibodies against the antigenic components of foreign serum that enter the body or against antigenic complex proteins formed by the combination of certain drugs that act as haptens and proteins in the body.

Experts say that when the amount of antibodies formed is slightly less than the antigens that have not yet disappeared in the body, immune complexes can be formed that are deposited on the blood vessel walls, which then activate the complement system, generate vascular substances, neutrophil chemotactic factors, etc., causing local congestion and edema, infiltration of neutrophils and the release of proteolytic enzymes in lysosomes, leading to tissue inflammation and damage.

How does serum sickness occur?

1. Experts point out that the antibody globulin that constitutes the immune complex of serum sickness is mainly IgG, but if there is more IgE, the increase in serum permeability will be more obvious when the disease occurs. There may also be symptoms of laryngeal edema, hypotension, and even anaphylactic shock. Those who are more likely to produce IgG and IgE antibodies under antigen stimulation are also more likely to develop serum sickness.

2. Common pathogens of serum sickness include serum proteins, and non-protein drugs include penicillins, sulfonamides, streptomycin, phenytoin sodium, and thiouracil drugs. Currently, there are very few diseases that can be treated with antisera, only 12 diseases such as diphtheria, tetanus and botulism. In addition, due to the widespread use of preventive vaccines in recent years, the incidence of such diseases has also been significantly reduced.

3. However, in recent years, due to the continuous development of clinical immunology, there are more and more biological products and non-protein drugs of various chemical structures. The incidence of serum sickness-like reactions has an increasing trend in clinical practice. This is a new problem for clinicians. The rational use of biological products and hapten drugs is crucial.

4. Currently, the serum preparations that cause serum sickness in clinical practice mainly include tetanus antitoxin, diphtheria antitoxin, various snake venom antitoxins and antilymphocyte globulin (ATG); the drugs that cause serum sickness mainly include penicillin, streptomycin, sulfonamides, salicylates, butacol, phenytoin sodium, dextran and other macromolecular drugs.

5. When pathogenic substances containing serum proteins enter the body, specific antibodies will be produced in the body after 2 to 3 weeks. At this time, if the above-mentioned pathogenic substances still remain in the human body, they can form immune complexes with these antibodies in the form of antigens or haptens and deposit on the vascular bed, activating the classical complement pathway and causing a series of inflammatory reactions. Serum sickness and serum sickness-like reactions appear clinically. The occurrence of this inflammatory process is mainly caused by the immune complexes activating phagocytes and immune active cells to secrete a large number of cytokines and inflammatory mediators.

Symptoms may not appear after the first exposure to xenogeneic serum or non-protein drugs. This is because the body still has enough antibodies to form immune complexes with foreign antigens and be cleared from the body. However, when the same antigen is exposed again, some sensitized B lymphocytes will quickly transform into plasma cells, secrete large amounts of antibodies and combine with antigens to form immune complexes, causing a rapid serum reaction.